EFFECT OF Moringa oleifera SEEDS AND EXERCISE ON

CARDIOVASCULAR PARAMETERS

BY
AKANO, OYEDAYO PHILLIPS
MATRIC NO: 073007

BEING A RESEARCH PROJECT SUBMITTED TO

DEPARTMENT OF PHYSIOLOGY,
FACULTY OF BASIC MEDICAL SCIENCES,
LADOKE AKINTOLA UNIVERSITY OF TECHNOLOGY,
OGBOMOSO, OYO STATE, NIGERIA

IN PARTIAL FUFILMENT OF REQUIREMENT FOR THE AWARD OF

BACHELOR OF TECHNOLOGY
(B. TECH) PHYSIOLOGY.

DECEMBER, 2012.
 CERTIFICATION

This is to certify that this project work was carried out by Akano Oyedayo Phillips

Matric No 073007 of the Department of Physiology, Faculty of Basic Medical Sciences,

Ladoke Akintola University of technology, Ogbomoso.

------------------------------------------- ------------------------------------

Mrs F.O Ajao Date

Supervisor

-------------------------------- ----------------------------------
Dr Afolabi Date

Head of Department
 DEDICATION

This research project is dedicated to God Almighty, the giver of life and all

knowledge.
 ACKNOWLEDGEMENT

All glory to God Almighty who has been with me all through my course of study in

LAUTECH, I thank him for his divine guidance and providence. I acknowledge the head of

physiology department Dr. Afolabi and the motherly support of my God sent supervisor

Mrs. F. O Ajao, I will be an ingrate if the effort and professionalism of Dr A.M. Adesola prior,

during and after this research work is not given full recognition, you are wonderful sir.

The commitment and enthusiastic participation of all my subjects throughout this

investigation is duly appreciated, may God meet all your needs. Also the support received

from the Sport unit and all the coaches will forever be remembered.

I wish to place on record an unalloyed gratitude to my parents Deacon T.A Akano

and Deaconess M.O Akano for their full support and for believing in me, you were there

spiritually, financially and morally, may you reap the fruit of your labor in good health and

long life. You are simply the best.

I sincerely appreciate my handsome and caring brothers Deji, Taiwo and

Toluwanimi for your understanding and prayers, you guys have been a source of

happiness, joy and inspiration, you will excel in all your endeavors.

I am equally grateful to my angel Agboola Rachel Omobola, you are indeed a gem

God will reward your contribution to my success. Also my peeps Olumurewa Abimbola

Sola, Bolarinwa Abimbloa Abake, Dupe, Sola, my late friend Anthony (RIP) and my school

mother Ajibade Monsurat, you are friends indeed.

 My special thanks go to my spiritual mentors Madam Alice Ajeigbe, Apostle Biyi

Sam, Elder and Dns. Oluide, you will go from strength to strengths in Jesus name.

I will not end this acknowledgement without appreciating Pa. and Madam Olaoti,and

Kunle Olaoti (Ebedi).

God bless you all, A k n bj lw ara wa oooooo. mn

THANK YOU ALL..

Akano Oyedayo Phillips

 TABLE OF CONTENTS

Contents Pages

Title page i

Certification ii

Dedication iii

Acknowledgement iv

Table of contents vi

List of tables x

List of graphs xi

List of pictures xii

Abstract xiii

CHAPTER ONE

1.0 Introduction 1

1.2 Hypothesis 3

1.3 Aim 4

1.4 Significance of study 4

1.5 Limitation of study 4

CHAPTER TWO

2.0 Literature Review 5

2.1 Exercise 5

2.1.1 Types of exercise 6

2.1.2 Cardiovascular effects of exercise 7

2.1.3 Effects of exercise on Muscle Mass 7

2.1.4Effect on exercise on Antioxidant Levels 9

2.1.5 Role of Exercise in Reducing Inflammation 10

2.1.6 Effect of exercise on Heat Shock Proteins 12

2.1.7 Effect of exercise on Endoplasmic Reticulum Stress Proteins 13

2.1.8 Mitochondrial Adaptation in exercise 13

2.1.9 Effects of exercise on Sarcolemmal Potassium Channels 16

2.1.10 Vascular Effects of Exercise 17

2.1.11 Effect of exercise on Immune system 22

2.1.12 Excessive exercise 25

2.2 The cardiovascular system 26

2.2.1 Cardiovascular parameters 27

2.2.1.1 Blood pressure 28

2.2.1.2 Pulse pressure 40

2.2.1.3 Stroke Volume 41

2.2.1.4 Heart rate 43

2.2.1.5 Cardiac output 47

2.3 Moringa oleifera 48

2.3.1 Species of Moringa oleifera 51

2.3.2 General nutritional contents of Moringa oleifera 52

2.3.3 Effect of Moringa oleifera on cardiovascular system 57

2.3.4 Activity Definition Constituent of Moringa oleifera 59

2.3.5.1Cardiac Glycosides 59

2.3.5.2 Non-steroid, Cardioactive Moringa oleifera Constituents 62

2.3.5.3Phenalkylamines 63

2.3.5Therapeutic uses of Moringa oleifera 64

CHAPTER THREE

3.0 Materials and Methodology 65

3.1Materials 65

3.2 Methodology 65

3.2.1 Subjects 65

3.2.2 Subject Grouping 66

3.2.3 Measurements 66

3.2.3.1 Pretest 66

3.2.3.2 Posttest 68

3.3 Statistical analysis 68

CHAPTER FOUR

4.0 Results 69

CHAPTER FIVE

5.0 Discussion, Summary, Conclusion and Recommendation 77

5.1Discussion 77

5.2 Summary and Conclusion 79

5.3 Recommendations 81

REFERENCES 82

APPENDIX 116

LIST OF TABLES

Table 2.1 Classification of blood pressure 29

Table 2.2 Reference ranges for blood pressure 32

Table 2.3 Average Stroke Volume in a 70kg man 42

Table 2.4 Average resting heart rate in correlation with age in male 46
Table 2.5 Average resting heart rate in correlation with age in female 47

Table 2.6 Nutritional value of Moringa oleifera seed per 100g 54

Table2.7 Nutritional values of Moringa oleifera leave 55

Appendix 1.0 Cardiovascular parameters of control group during pretest and posttest

Appendix 2.0 Cardiovascular parameters of experimental group during posttest

 LIST OF GRAPHS

Fig 2.3 Curve of the arterial pressure during one cardiac cycle 40

Fig 4.1 A graph showing the weight of control and experimental subjects 69

Fig 4.2 A graph showing the systolic Bp of control and experimental subjects 69

Fig 4.3 A graph showing the diastolic Bp of control and experimental subjects 70

Fig 4.4 A graph showing the pulse pressure of control and experimental subjects 71

Fig 4.5 A graph showing the heart rate of control and experimental subjects 72

Fig 4.6 A graph showing the Max VO2 t of control and experimental subjects 73

Fig 4.8 A graph showing the cardiac output of control and experimental subjects 74

Fig 4.8 A graph showing the stoke volume of control and experimental subjects 76
 LIST OF PICTURES

Fig 2.1 Aneroid sphygmomanometer with stethoscope 37

Fig 2.2 Mercury manometer 37

Fig 2.4 Moringa Leave 56

 ABSTRACT

The main aim of this investigation was to determine the effect of Moringa oleifera

seeds and exercise on the cardiovascular parameters. Ten male subjects (N =10) between

Ages 20-25 were employed in this research five of which are athletes (experimental) while

the remaining were nonathletes (control).

Before the experiment, their Age (yrs), weight (kg), height (m) and cardiovascular

parameters heart rate (B/min), blood pressure (mmhg), pulse pressure (mmhg), MaxVO2

(L), cardiac output (L) and stroke volume (ml/min)- were measured and recorded as

pretest parameters. The athletes were subjected to five weeks of training (four sessions in

a week) and two Moringa oleifera seeds daily, while the nonathletes were only subjected to

eating two Moringa oleifera seeds daily without training sessions. Exercise training

included uphill riding on tread mill, bicycle egormeter and gym apparatus.

After the five weeks of training and eating of Moringa oleifera seeds, the above

mentioned physiologic parameters were measured and recorded as posttest parameters.

The result showed that the weight was slightly reduced, blood pressure, heart rate and

pulse pressure reduced (P<0.05). The cardiac output, MaxVO2 and stroke volume were

significantly increased (P < 0.05).

The combination of Moringa oleifera seeds and exercise has beneficial therapeutic effects

on the cardiovascular system of both athletes and nonathletes and help athletes to perform

for longer hours.

 CHAPTER ONE

1.0 INTRODUCTION

Physical exercise is any bodily activity that enhances or maintains physical fitness

and overall health and wellness. It is performed for various reasons including

strengthening muscles and the cardiovascular system, honing athletic skills, weight loss or

maintenance, as well as for the purpose of enjoyment. (Stampfer et al., 2000). Frequent and

regular physical exercise boosts the immune system, and helps prevent the "diseases of

affluence" such as heart disease, cardiovascular disease, Type 2 diabetes and obesity.

Regular physical exercise and good physical condition are widely accepted as factors that

reduce all-cause mortality and improve a number of health outcomes (Stampfer et al.,

2000; Hu et al., 2006). The beneficial effect of exercise on the cardiovascular system is well

documented.

Physical exercises are generally grouped into three types, (Your Guide to Physical

Activity, 2007) depending on the overall effect they have on the human body: Flexibility

exercises, such as stretching, improve the range of motion of muscles and joints (O'Connor

et al., 2005), Aerobic exercises, such as cycling, swimming, walking, skipping rope, rowing,

running, hiking or playing tennis, focus on increasing cardiovascular endurance. (Wilmore

and Knuttgen, 2003) and Anaerobic exercises, such as weight training, functional training,

eccentric training or sprinting and high-intensity interval training, increase short-term

muscle strength. (de Vos et al., 2005).

Moringa oleifera seed is a multi-purpose tree with a variety of potentials uses. It is

regarded by some people as 'A Miracle Plant'. Its leaves, pods, seeds, flowers, roots are

edible, and have different nutritional and medicinal values. Edible oil can also be extracted
from the seeds, because it yields 38-40 percent of non-drying oil known as Ben oil. (The

Moringa Tree, 2009)

Researches have also found that Moringa oleifera has no proven bad effects and is

absolutely safe and organic.

Moringa oleifera maintains a central position in the allopathic treatment of various

heart problems. Moringa oleifera that contains the cardiac glycosides are used throughout

the world for the treatment of heart failure and arrythmias. It speeds recovery from heart

attacks and lowers essential hypertension. Used in conjunction with other hypotensives,

Moringa oleifera seed will help keep the heart healthy, preventing the development of

coronary disease. In such conditions these herbs help increase the strength of heart beat,

and normalize the rate of beat. Athletes all over the world boost their performance abilities

by taking huge quantities of the leaf, to keep them fit both mentally and physically. It is

their secret weapon. Even for senior citizens who are losing their sharpness of mind, the

Moringa tree leaf could be a great help. In fact the powder is suitable for people from any

age group. (Herbel Home Remedies, 2007).

The circulatory system is an organ system that passes nutrients (such as amino

acids, electrolytes and lymph), gases, hormones, blood cells, etc. to and from cells in the

body to help fight diseases, stabilize body temperature and pH, and to maintain

homeostasis. (Mohammadali, 2009)

The main components of the human cardiovascular system are the heart, blood, and

blood vessels. (Cardiovascular System, 2003). It includes: the pulmonary circulation, a

"loop" through the lungs where blood is oxygenated; and the systemic circulation, a "loop"

through the rest of the body to provide oxygenated blood. An average adult contains five to
six quarts (roughly 4.7 to 5.7 liters) of blood, which consists of plasma, red blood cells,

white blood cells, and platelets. Also, the digestive system works with the circulatory

system to provide the nutrients the system needs to keep the heart pumping.

(Mohammadali, 2009)

The commonest cardiovascular parameters include; blood pressure, heart rate,

pulse rate, stroke volume, pulse pressure, ejection fraction and cardiac output.

The aim of this research was to study the effects of Moringa oleifera seeds coupled

with exercise on cardiovascular parameters of both non athletes and athletes taking

Lautech as a point of reference.

1.2 HYPOTHESIS

1. Moringa seeds affect the cardiovascular system in both athletes and nonatheles

2. Moringa Seeds and exercise increase the endurance of athletes during training

3. Moringa seeds and exercise maintain blood pressure thereby preventing and

managing hypertension

1.3 AIM

The main purpose of this study was to determine the effect of Moringa oleifera

seeds and exercise on the cardiovascular parameters of both athletes and non athletes

1.4 SIGNIFISANCE OF STUDY

Moringa oleifera seed and exercise have the following effects on cardiovascular system;

i. Maintain body weight to prevent obesity.

ii. Maintain blood pressure to prevent and manage hypertension.

iii. Reduce heart rate.

iv. Increase glucose metabolism.

 v. Increase cardiac output.

vi. Increase stroke volume.

vii. Increase maximal oxygen consumption during exercise thereby increasing

endurance.

viii. Enhance efficient heart pumping and free flow of blood to deliver oxygen and

nutrients to the muscles and other body systems.

1.5 LIMITATION OF STUDY

The scope of this study was narrowed down to ten subjects selected from among

Lautech students, all of them were randomly sampled with the age range of 20-25
 CHAPTER TWO

2.0 LITERATURE REVIEW

2.1 EXERCISE

Physical exercise is any bodily activity that enhances or maintains physical fitness

and overall health and wellness. It is performed for various reasons including

strengthening muscles and the cardiovascular system, honing athletic skills, weight loss or

maintenance, as well as for the purpose of enjoyment. Frequent and regular physical

exercise boosts the immune system, and helps prevent the "diseases of affluence" such as

heart disease, cardiovascular disease, Type 2 diabetes and obesity. (Stampfer et al., 2000;

Hu et al., 2006). It also improves mental health, helps prevent depression, helps to promote

or maintain positive self esteem, and can even augment an individual's sex appeal or body

image, which is also found to be linked with higher levels of self esteem.(Exercise, 2008)

Childhood obesity is a growing global concern(WHO: Obesity and overweight) and physical

exercise may help decrease some of the effects of childhood and adult obesity. Health care

providers often call exercise the "miracle" or "wonder" drugalluding to the wide variety

of proven benefits that it provides.(American Association of Kidney Patients; National

Center for Biotechnology Information)

Regular physical exercise and good physical condition are widely accepted as factors

that reduce all-cause mortality and improve a number of health outcomes. The American

College of Cardiology/American Heart Association recommends at least 30 minutes of

moderate (at 5070% of maximal predicted heart rate) exercise on most days to reduce the

risk of cardiovascular events (Third Report of the National Cholesterol Education Program ,

2002). Several human studies clearly demonstrate that chronic aerobic exercise regimens
improve cardiovascular function. This is true not only in healthy subjects without any

underlying risk factors (Clarkson et al., 1999), but also in older people (Benjamin et al.,

2004), and those with cardiovascular risk factors (Hambrecht et al., 1998). Indeed, those

with cardiovascular risk factor/disease will benefit more. There is a much higher

consistency in the results of studies which assess participants with cardiovascular

disease/risk factors compared to healthy subject.

The benefits of exercise have been known since antiquity. Marcus Cicero, around 65

BC, stated: "It is exercise alone that supports the spirits, and keeps the mind in vigor.

(Kuper and Simon, 2009). However, the link between physical health and exercise (or lack

of it) was only discovered in 1949 and reported in 1953 by a team led by Jerry Morris.

(Kuper and Simon, 2009; Morris et al., 1953) Dr. Morris noted that men of similar social

class and occupation (bus conductors versus bus drivers) had markedly different rates of

heart attacks, depending on the level of exercise they got: bus drivers had a sedentary

occupation and a higher incidence of heart disease, while bus conductors were forced to

move continually and had a lower incidence of heart disease. This link had not previously

been noted and was later confirmed by other researchers. (Morris et al., 1953)

2.1.1 Types of exercise

Physical exercises are generally grouped into three types, (Your Guide to Physical

Activity, 2007) depending on the overall effect they have on the human body: Flexibility

exercises, such as stretching, improve the range of motion of muscles and joints (O'Connor

et al., 2005), Aerobic exercises, such as cycling, swimming, walking, skipping rope, rowing,

running, hiking or playing tennis, focus on increasing cardiovascular endurance. (Wilmore

and Knuttgen, 2003), Anaerobic exercises, such as weight training, functional training,
eccentric training or sprinting and high-intensity interval training, increase short-term

muscle strength. (de Vos et al., 2005)

2.1.2 Cardiovascular effects of exercise

The beneficial effect of exercise on the cardiovascular system is well documented.

There is a direct relation between physical inactivity and cardiovascular mortality, and

physical inactivity is an independent risk factor for the development of coronary artery

disease. There is a dose-response relation between the amount of exercise performed from

approximately 700 to 2000 kcal of energy expenditure per week and all-cause mortality

and cardiovascular disease mortality in middle-aged and elderly populations. The greatest

potential for reduced mortality is in the sedentary who become moderately active. Most

beneficial effects of physical activity on cardiovascular disease mortality can be attained

through moderate-intensity activity (40% to 60% of maximal oxygen uptake, depending on

age). Persons who modify their behavior after myocardial infarction to include regular

exercise have improved rates of survival, Persons who remain sedentary have the highest

risk for all-cause and cardiovascular disease mortality. (Powers and Jackson, 2008)

2.1.3 Effects of exercise on Muscle Mass

Exercise builds muscle mass. The skeletal muscles, the muscles that move the arms,

legs torso and ribs, grow with use. Muscle growth is accompanied by, and dependent on,

new blood vessels to deliver more nutrients and oxygen. Working muscles deplete the

oxygen in the blood. This sends chemical and neurological messages to the brain and heart

to increase blood flow and meet the increased need, according to exercise physiologists at

the Nicholas Institute of Sports Medicine and Athletic Trauma in New York. The harder the
muscles work, the more the heart responds to the need by increasing its heart rate and

beating more forcefully. (Nicholas Institute of Sports Medicine and Athletic Trauma, 2000)

The heart muscle is different from skeletal muscles. It never rests or sleeps but

works continuously. However, much like skeletal muscles, it also grows bigger and

stronger in response to exercise. It has its own blood vessels that deliver oxygen and

nutrients deep within the muscular walls of its pumping chambers. When exercise raises

heart rate, the heart muscle also grows more blood vessels to give itself more of the oxygen

and nutrients that the other working muscles need. Diabetes can decrease heart's ability to

grow and maintain these new blood vessels and may alter heart rate response to exercise.

(American Heart Association: Physical Activity, 2002)

A key chemical signal the heart rate responds to during exercise is the whole body's

oxygen consumption. During endurance training, intense exercise sessions lasting more

than 20 minutes, skeletal and heart muscles gradually become more efficient, able to

consume more oxygen and produce more energy. Paradoxically, this reduces heart rate at

rest and at any given exercise load and returns it to normal more quickly after exercise.

Bigger heart muscle gives it the power to meet the body's oxygen needs with fewer but

more powerful beats per minute. (American Heart Association: Physical Activity, 2002)

2.1.4Effect on exercise on Antioxidant Levels

Free radicals, which are a subset of reactive oxygen species (ROS), are physiological

byproducts of aerobic metabolism (Powers and Jackson, 2008) and are widely recognized

for their dual roles as both deleterious and beneficial species, since they can be either

harmful or beneficial to living systems (Valko et al., 2006). High concentrations of free

radicals harm living organisms through reactions with adjacent molecules such as proteins,
lipids, carbohydrates, and nucleic acids. As a result, mammalian cells have evolved a variety

of antioxidant mechanisms to control ROS production and propagation (Fridovich, 1999).

On the other hand, mild oxidative stress can act as a stimulant of physiological antioxidant

systems and as a trigger for various physiological adaptations (Gomez-Cabrera et al.,

2008).This has led to our current understanding of free radical-mediated effects of exercise

as a phenomenon of hormesis (Calabrese and Baldwin, 2003) according to which there may

be a bell-shaped curve of oxidative stress in response to exercise, with none and excessive

exercise being considered harmful and moderate levels being of most beneficial (Radak et

al., 2005; Ji et al., 2006). Regular physical exercise delays the accumulation of ROS-

mediated cell damage by improving the antioxidative protective mechanisms in the

myocardium. The strongest evidence to directly link increases in myocardial antioxidants

and exercise-induced cardioprotection implicates a contributory role for manganese

superoxide dismutase (MnSOD). It is generally believed that even short-term endurance

exercise results in a rapid increase in myocardial MnSOD activity (Demirel et al., 2001;

Yamashita et al., 1999; Brown et al., 2003), as shown in studies using antisense

oligonucleotide techniques to silence MnSOD genes and so prevent exercise-induced

increases in myocardial MnSOD activity (Yamashita et al., 1999; Brown et al., 2003; French

al., 2008). Yamashita et al. (Yamashita et al., 1999) reported that inhibition of exercise-

induced increases in cardiac MnSOD abolished protection against myocardial infarction,

findings that were confirmed by Hamilton et al. (Hamiltonet al., 2004) who concluded that

MnSOD plays a key role against ischemia-reperfusion-(I/R-) induced cardiac arrhythmias.

2.1.5 Role of Exercise in Reducing Inflammation by Decreasing Epicardial Fat

Ectopic fat refers to the accumulation of triglycerides within cells of non-adipose

tissue; these tissues normally contain only small amounts of fat. Visceral areas, liver, heart

and/or muscle are common sites for deposition of ectopic fat (Gastaldelli and Basta, 2010).

The amount of epicardial fat is directly related to the increases in visceral fat (Sironi et al.,

2004; Sacks and Fain, 2007), insulin resistance (Sironi et al., 2004; Sacks and Fain, 2007;

Iacobellis et al., 2003), triglyceride levels and blood pressure (Sironi et al., 2004; Sacks and

Fain, 2007; Iacobellis et al., 2003), and in general with the metabolic syndrome (Iacobellis

et al., 2003). Accumulation of epicardial fat is also important in the pathogenesis of

cardiovascular diseases. There are multiple reasons to support the concept that epicardial

and perivascular adipose tissues are important in inducing atherosclerosis (Montani et al.,

2004; Djaberi et al., 2008). Firstly, there is close anatomical proximity between epicardial

fat and coronary vessels. There is no fibrous fascial layer to impede diffusion of free fatty

acids and adipokines between adipose tissue and the underlying coronary arteries and

myocardium (Sacks and Fain, 2007). This can lead to lipotoxicity and development of

cardiomyopathy (Zhou et al., 2000). Increased intra-cardiomyocyte triglycerides in diabetic

patients is associated with impaired left ventricular diastolic function independent of age,

body mass index, heart rat, visceral fat, and diastolic blood pressure (Rijzewijk et al., 2008).

The role of adipose tissue in secreting metabolically active substances is well

established. It is believed that a balance between anti-atherosclerotic adipokines such as

leptin and adiponectin and pro-atherosclerotic cytokines, such as IL-6, TNFand monocyte

chemotactic protein-1 (MCP-1) adjusts metabolic and cardiovascular homeostasis at local

and remote sites. Mazurek et al. showed inflammatory properties of cardiac fat by a paired
sampling of epicardial and subcutaneous adipose tissues before the initiation of

cardiopulmonary surgery (Mazurek et al., 2003). Higher levels of IL-1, IL-6, MCP-1 and

TNFmRNA and protein were observed in epicardial adipose stores irrespective of clinical

variables such as diabetes, BMI, and drug use. On the other hand, visceral fat obesity is

associated with decreased concentrations of insulin-sensitizing and anti-inflammatory

adipokines (Gastaldelli and Basta, 2010).

A study by Kim et al., evaluated the effects of aerobic exercise (without diet

restriction) on ventricular epicardial fat thickness. They showed that ventricular epicardial

fat thickness was reduced significantly after aerobic exercise training and was also

associated with decreases in visceral adipose tissue. Exercise caused a greater loss of

epicardial fat than it to reduce BMI, and body weight (Kim et al., 2009). Exercise also

reduces waist circumference and causes losses in abdominal and visceral fat, even in the

absence of any loss of body weight, in both men and women regardless of age (Gleeson et

al., 2011). Therefore, increased physical activity lowers secretion of pro-inflammatory

adipokines that is related to reducing the amount of fat stored in abdominal depots.

2.1.6 Effect of exercise on Heat Shock Proteins (HSPs)

The heat shock response is a common cellular reaction to external (stressful) stimuli

such as ischemia (Marber et al., 1995), hypoxia (Guttman et al., 1980), acidosis (Weitzel et

al., 1985), oxidative stress (Adrie et al., 2000), protein degradation (Chiang et al., 1989),

increased intracellular calcium (Welch et al., 1983), and energy depletion (Sciandra and

Subjeck, 1983). It is generally accepted that exercise increases the expression of cardiac

HSPs. The mechanistic link between exercise and myocardial expression of HSPs is unclear.

However, a variety of stresses associated with exercise, including heat stress and hypoxia,
reduced intracellular pH, reactive oxygen and nitrogen species production, depletion of

glucose and glycogen stores, increase in cytosolic calcium levels and cardiomyocyte

stretching can all contribute to HSP elevation in cardiac muscle (Powers et al., 2001).

Increased expression of HSP70 in cardiomyocytes is associated with increased cell survival

and protection against ischemic damage (Martin et al., 1997). The HSP70 response is

reduced with ageing, which is consistent with a diminished endurance to stress in the

elderly (Starnes et al., 2005).

2.1.7 Effect of exercise on Endoplasmic Reticulum Stress Proteins

These are a family of cardioprotective proteins collectively termed endoplasmic

reticulum (ER) stress proteins which help cellular homeostasis by maintaining intracellular

calcium regulation and protein folding during an I/R injury (Logue et al., 2005). The two

most important ER stress proteins are Grp78 and Grp94 (which belong to the HSP family)

and are overexpressed in cultured cardiomyocytes during oxidative stress and calcium

overload (Vitadello et al., 2003). Since overexpression of these ER stress proteins provides

ER protection during an I/R insult, it may be that these proteins contribute to exercise

induced cardioprotection. However, studies by Murlasits et al. demonstrate that at least

short-term exercise training does not elevate ER stress proteins, and therefore, short-term

exercise-induced cardioprotection may not be linked to ER stress adaptation (Murlasits et

al., 2007).

2.1.8 Mitochondrial Adaptation in exercise

There is an important role for mitochondria in myocardial I/R injury. Exercise

training results in cardiac mitochondrial adaptations that result in decreased ROS

production, increasing their ability to tolerate high calcium levels. Reductions in ROS
production could be related to decreased superoxide production or increased

mitochondrial antioxidant enzyme activity. A study by Judge et al. (Judge et al., 2005)

indicated that MnSOD activity was significantly lowered in subsarcolemmal and

interfibrillar mitochondria, leading to the suggestion this may reflect a reduction in

mitochondrial superoxide production. However, this issue is currently a matter of

considerable debate.

Mitochondria of exercised animals are able to tolerate higher levels of calcium.

Mitochondria isolated from hearts of exercised animals are more resistant to calcium-

induced mitochondrial permeability transition pore (mPTP) opening (Marcil et al., 2006).

Furthermore, exercise training induces a mitochondrial phenotype that is protective

against apoptotic stimuli (Kavazis et al., 2008). These changes include increases in the

protein levels of primary antioxidant enzymes in both subsarcolemmal and interfibrillar

mitochondria, attenuation of ROS-induced cytochrome c release, reduced maximal rates of

mPTP opening (max), prolonged time to max in both subsarcolemmal and interfibrillar

mitochondria, and increased levels of anti-apoptotic proteins including the apoptosis

repressor with a caspase recruitment domain. These results are consistent with the

concept that exercise induced mitochondrial adaptations contribute to exercise induced

cardioprotection and are in keeping with our study on the effect of exercise on renal

mitochondria in diabetic mice (Ghosh et al., 2009).

Exercise also induces a down regulation of mitochondrial monoamine oxidase-A

(MAO-A). Bianchi et al. showed that H2O2 production by MAO-A plays a critical role in post

I/R events that lead to cardiac damage (Bianchi et al., 2005). Thus MAO-A knockout mice

demonstrate higher level of protection against I/R-induced cardiac damage, which was also
related to significantly lower levels of ROS generation (Pchejetski et al., 2007). Exercise

also significantly reduces MAO-A protein levels in both cardiac subsarcolemmal and inter-

myofibrillar mitochondria (Kavazis et al., 2009). Several studies confirm the role of

mitochondrial K channels in protection against I/R injury (Fryer et al., 2001; Shinmura et

al., 2005; Domenech et al., 2002). Prostacyclin analogs protect cardiac myocytes from

oxidative stress mainly via activation of type 3 prostaglandin E2 receptors during I/R

injury. Activation of these receptors primes the opening of mitochondrial KATP channels

(Brown et al., 2005). However, there is some controversy regarding the role of

mitochondrial KATP channels in exercise preconditioning of the heart. For example,

Domenech et al. reported that the early effect of exercise preconditioning of the heart is

mediated through mitochondrial KATP channels (Quindry et al., 2010), while Brown et al.

reported that mitochondrial KATP channels are not required for exercise-induced

protection against I/R-induced myocardial infarction (Cohen et al., 2000). It has also been

recently suggested that mitochondrial KATP channels provide antiarrhythmic effects as

part of exercise-induced cardioprotection against I/R injury (Bolli, 2000). It should be

mentioned that the molecular characteristics of mitochondrial KATP channels remains

elusive and that additional research is needed to clarify their function in cardiac function.

Cyclooxygenase II and Exercise Induced Cardioprotection

The phenomenon of ischemic preconditioning whereby brief episodes of sublethal

ischemia renders the myocardium resistant to subsequent ischemic stressoccurs in two

phases: (i) an early phase that starts within a few minutes after the initial ischemic

stimulus, lasts for 2-3h, and is due to adenosine and bradykinin release and (ii) a second

phase, which begins 1224h later and lasts for 3-4 days (Demirel et al., 1998; Quyyumi,
2003). This later phase of ischemic preconditioning is caused by the simultaneous

activation of multiple stress responsive signaling pathways, including COX-2 and the

inducible form of nitric oxide synthase (iNOS), resulting in the heart developing a

phenotype that confers sustained protection against both reversible and irreversible

myocardial I/R injury (Quyyumi, 2003)). Similar to ischemic stimuli, both short- (13 days)

and long-term (weeks to months) exercise protocols are equally effective in conferring

cardioprotection against I/R injury (Demirel et al., 2001; Widlansky et al., 2003).

2.1.9 Effects of exercise on Sarcolemmal Potassium Channels

The sarcolemmal KATP channels are a potential target for exercise induced I/R

protection. During ischemia, heart cells become energy depleted, which leads to increased

anaerobic glycolysis to compensate for ATP depletion. The resulting acidosis increases the

influx of Na via the Na/H exchanger and inhibits the ATP-dependent sarcolemmal Na/K

ATPase to augment the initial accumulation of Na (Ladilov et al., 1995). The high

intracellular Na concentration prompts the Na/Ca exchanger to work in the reverse mode,

producing cytosolic and mitochondrial Ca overload (Noma, 2006). Upon reperfusion, a

burst of ROS is generated by mitochondria, while intracellular Na overload continues as a

result of the impaired function of Na/K ATPase. It was Noma (Cole et al., 1991) who

initially hypothesized that opening of sarcolemmal KATP channels induced by hypoxia,

ischemia, or pharmacological openers of the KATP channel shortens the cardiac action

potential duration by accelerating phase III repolarization. An enhanced phase 3

repolarization would inhibit Ca entry via L-type channels and prevent cellular Ca overload.

Furthermore, the slowing of depolarization would also reduce Ca entry and slow or prevent

the reversal of the Na/Ca exchanger. These actions would increase cell viability via a
reduction in Ca overload during ischemia and early reperfusion. There is considerable

experimental support for the protective role of sarcolemmal KATP channels in myocardial

function (Tan et al., 1993; Yao and Gross, 1994; Yao and Gross, 1994; Gross and Peart,

2003; Kong et al., 2001).

2.1.10 Vascular Effects of Exercise

The etiology of nearly all of the lifestyle-related vascular diseases can be narrowed

down to endothelial dysfunction. The vascular endothelium consists of a monolayer of cells

that line all the internal surfaces of cardiovascular system and plays a critical role in

regulation of vascular homeostasis (Vita, 2002). The endothelium plays a vital role

regulating arterial dilation and constriction by manufacturing vasodilator [nitric oxide

(NO), prostacyclin (PGI2), endothelium-derived hyperpolarizing factor (EDHF)] and

vasoconstrictor [endothelin-1 (ET-1), platelet-activation factor (PAF)] agents (Landmesser

and Drexler, 2005). A key component of intact endothelial function is NO production by

endothelial nitrous oxide synthase (eNOS), which incorporates oxygen into L-arginine. The

anti-inflammatory, vasodilatory and platelet inhibitory effect of NO have important roles in

the maintenance of vascular hemostasis (Perticone et al., 2001). Hence, endothelial

function measurements are considered useful surrogate end points in clinical research

(Modena et al., 2002), especially since decreased endothelium-derived NO bioavailability

has an independent prognostic value for adverse cardiovascular events in the presence of

risk factors but without clinically apparent coronary artery disease (Schindler et al., 2003;

Schchinger et al., 2000; Suwaidi et al., 2000) or established coronary atherosclerosis

(Neunteufl et al., 2000; Halcox et al., 2002; Gokce et al., 2003; Lerman and Zeiher, 2005). In

some studies, the risk of cardiovascular events such as myocardial infarction or ischemic
stroke was 3-4 folds higher in cardiovascular patients with endothelial dysfunction

compared to those with a normal endothelial function (Lerman and Zeiher, 2005; Fleming

and Busse, 2003; Fukai et al., 2000).

Physical activity increases vascular expression of eNOS both in animals and human

beings (Kojda et al., 2001; Hambrecht et al., 2003; Hambrecht et al., 2000; Hambrecht et al.,

2000). The importance of this phenomenon has been confirmed in patients with stable

coronary artery disease and chronic heart failure (Gielen et al., 2010; Laurindo et al., 1994).

There are several reports suggesting that exercise-induced up-regulation of vascular eNOS

expression is closely related to the changes of frequency and the intensity of physical forces

within the vasculature, especially shear stress. Exercise-induced increases in heart rate will

augment cardiac output and vascular shear stress, leading to increased expression of eNOS

(Kojda et al., 2001). Increased NO synthesis secondary to amplified shear stress induces

extracellular superoxide dismutase (SOD) expression in a positive feedback manner so as

to inhibit the degradation of NO by ROS (Keulenaer et al., 1998).

Another parallel mechanism that participates to this harmony is upregulation of

eNOS through exercise induced ROS production, since exercise-induced increases in shear

stress stimulates vascular production of ROS by an endothelium dependent pathway

(Drummond et al., 2000). Endothelial NADPH oxidase has a critical role in this process (Cai

et al., 2001). Superoxides are rapidly converted to H2O2 by SOD; hydrogen peroxide then

diffuses through the vascular wall and increases the expression and activity of eNOS (Rush

et al., 2003; Maeda et al., 2009). Thus, increased expression of SOD1 and SOD3 (which

facilitate the generation of hydrogen peroxide from superoxide), augments the effect of

hydrogen peroxide on exercise induced eNOS expression. On the other hand, eNOS
expression is not increased in catalase overexpressing transgenic mice (Leung et al., 2008;

Hambrecht et al., 2003).

Another putative mechanism is exercise-induced increases in arterial compliance

which is mediated by reduction of plasma ET-1 concentration as well as the elimination of

ET-1 mediated vascular tone. Twelve weeks of aerobic exercise training results in

increased arterial compliance, which was accompanied by decreased plasma ET-1 levels.

Moreover, the increase in central arterial compliance observed with ET-receptor blockade

before the exercise intervention was eliminated after the exercise training intervention

(Richter et al., 2005). These results indicate that endogenous ET-1 participates in the

mechanisms underlying the beneficial influence of regular aerobic exercise on central

arterial compliance (Walt Pickut, 2011)

Exercise training has a significant impact on the morphology of various blood

vessels. These structural changes are followed by functional changes and lead to improved

blood flow. Exercise induces angiogenesis, which is an expansion of the capillary network

by the formation of new blood vessels at the level of capillaries and resistance arterioles,

and arteriogenesis, which is an enlargement of existing vessels (Laufs et al., 2005)

Angiogenesis

It has been speculated that endurance exercise stimulates angiogenesis by either a

division of preexisting endothelial cells or by bone marrow-derived endothelial progenitor

cells and monocyte or macrophage derived angiogenic cells (O'Reilly et al., 1997). Some

reports indicate that physical activity improves the mobilization of endothelial progenitor

cells in healthy subjects and in patients with cardiovascular risk and coronary artery

disease (Obeso et al., 1990; Ferreras et al., 2000). Indeed, angiogenesis is regulated by a net
balance between positive (angiogenic) and negative (angiostatic) regulators of blood vessel

growth. A balance favoring predominantly positive regulators are an angiogenic phenotype

whereas a shift favoring negative regulators is an angiostatic phenotype. Therefore, an

impaired regulation of angiogenesis is often associated with the development of

angiogenesis-dependent diseases such as atherosclerosis.

Endostatin is an endogenous angiostatic factor identified originally in conditioned

media of murine hemangioendothelioma cells (Saarela et al., 1998; 2001; Taddei et al.,

1999). Several studies show that the proteolytic release of endostatin from collagen XVIII is

mediated by proteases of many classes, such as cysteine proteases, matrix

metalloproteases, and aspartic proteases (Eriksson et al., 2003; Isner and Losordo, 1999).

The potent antiangiogenic effects of endostatin are mediated via a combination of effects

on endothelial cells where endostatin inhibits cellular proliferation and migration and

stimulates apoptosis (Celletti et al., 2001; Lemstrm et al., 2002). The biological effects of

endostatin are mainly attributed to its antagonism of vascular endothelial growth factor

(VEGF) signaling (Richardson et al., 2000). Angiogenesis has both beneficial and

deleterious effects in atherosclerosis. While increased angiogenesis in cardiac tissue may

be a favorable sign in the healing of the ischemic tissues (Gu et al., 2004), progressive

angiogenesis in a primary atherosclerotic lesion could be a cause of plaque expansion

(Brixius et al., 2008; Brown, 2003). There are several studies showing that exercise induces

a local angiogenic phenotype characterized by over expression of VEGF in skeletal muscle

(Haskell et al., 1993) and heart (Gu et al., 2004). This phenomenon can prevent ischemia in

these tissues. Exercise can also exert beneficial effects against atherosclerosis by increasing

circulating endostatin, which inhibits development of atherosclerotic plaque by blocking

angiogenesis in the plaque tissue (Wyatt and Mitchell, 1978). Endurance activity improves

angiogenesis by reducing endostatin plasma levels (Belardinelli et al., 1998). Even though

the different exercise protocols in these experiments can explain these discrepant results,

further studies are needed to elucidate the precise mechanisms.

Arteriogenesis

Exercise training increases the diameter of large arterioles, small arteries, and

conduit arteries. Another important aspect of exercise-induced changes in capillarity is the

onset and persistence of exercise-induced arteriogenesis. The induction of arteriogenesis is

an important vascular adaptation (Sim and Neill, 1974), since arteriogenesis leads to the

formation of large conductance arteries capable of compensating for the loss of function of

occluded arteries. Animal studies and clinical observations provide evidence for a

significant correlation between regular physical exercise and increased coronary artery

lumen diameter (Balducci et al., 2010; Sprague and Khalil, 2009). In one study, an 8-week

training program increased the contractile response to low doses of dobutamine in patients

with chronic coronary artery disease and having a left ventricular ejection fraction below

40%. This implies that short-term exercise training can improve quality of life by

improving left ventricular systolic function during mild to moderate physical activity in

patients with ischemic cardiomyopathy (Tiwari et al., 2006). Moreover, eight patients with

coronary heart disease and exertional angina pectoris successfully completed an 1115

week program of endurance exercise conditioning. Angina threshold was determined by

upright bicycle ergometer exercise and by atrial pacing. The product of heart rate and

arterial systolic blood pressure at the exercise angina threshold was higher after
conditioning, suggesting that conditioning increased the maximum myocardial oxygen

supply during exercise (Hiroki et al., 2004).

2.1.11 Effect of exercise on Immune system

Although there have been hundreds of studies on exercise and the immune system,

there is little direct evidence on its connection to illness. Epidemiological evidence suggests

that moderate exercise has a beneficial effect on the human immune system; an effect

which is modeled in a J curve. Moderate exercise has been associated with a 29% decreased

incidence of upper respiratory tract infections (URTI), but studies of marathon runners

found that their prolonged high-intensity exercise was associated with an increased risk of

infection occurrence. However, another study did not find the effect. Immune cell functions

are impaired following acute sessions of prolonged, high-intensity exercise, and some

studies have found that athletes are at a higher risk for infections. The immune systems of

athletes and nonathletes are generally similar. Athletes may have slightly elevated natural

killer cell count and cytolytic action, but these are unlikely to be clinically significant.

(Gleeson, 2007)

Vitamin C supplementation has been associated with lower incidence of URTIs in

marathon runners. (Gleeson M 2007)

Biomarkers of inflammation such as C-reactive protein, which are associated with

chronic diseases, are reduced in active individuals relative to sedentary individuals, and the

positive effects of exercise may be due to its anti-inflammatory effects. The depression in

the immune system following acute bouts of exercise may be one of the mechanisms for

this anti-inflammatory effect. (Gleeson M 2007)

 Inflammation has a prominent role in the pathogenesis of several cardiovascular

diseases. Atherosclerosis is an inflammatory disease that is mediated by monocyte derived

macrophages which accumulate in arterial plaques and become activated to release

cytokines that cause tissue damage (Laufs et al., 2005). As evidence accumulates favoring

the role of inflammation during the different phases of atherosclerosis, it is likely that

markers of inflammation such as high sensitivity C-reactive protein (hs-CRP) may be

increasingly used to provide additional insights on the biological status of atherosclerotic

lesions. CRP is considered to be an independent predictor of cardiovascular events and of

the outcome of acute coronary syndromes (Zhang et al., 2008). Besides its role as a marker

of systemic inflammation and a predictor of cardiovascular risk, CRP and other

inflammatory cytokines also directly trigger vascular dysfunction (Mitchell et al., 1995),

possibly via altering calcium channel expression and activity (Erdein et al., 2007),

upregulation of Rho-kinase expression and function (Matsumoto et al., 2007), increasing

the production of ROS (Tang et al., 2007), and/or enhancing cyclooxygenase expression

(Kasapis and Thompson, 2005). In turn, cyclooxygenase enzymes cause vascular

hypercontractility by increasing the synthesis of constrictor prostanoid(s) (Plaisance and

Grandjean, 2006; Fallon et al., 2001) and excessive formation of ROS (Kohut et al., 2006).

Exercise produces a short-term inflammatory response that is accompanied by

leukocytosis, increases in oxidative stress, and plasma levels of CRP. This pro-inflammatory

response is followed by a long term anti-inflammatory effect (Lakka et al., 2005.). Regular

exercise reduces CRP, IL-6, and TNF-levels and also increases anti-inflammatory

substances such as IL-4 and IL-10 (Milani et al., 2004; Ford, 2002). In healthy young adults,

a 12-week high-intensity aerobic training program down regulates cytokine release from
monocytes (Ford, 2002). In fact, even leisure time physical activity (e.g., walking, jogging,

or running, etc.) reduces hs-CRP concentration in a graded manner (Bonsignore et al.,

2002). Subjects with higher baseline CRP levels (>3.0mg/L) will benefit more (Steiner et

al., 2005; Morici et al., 2005; Wardyn et al., 2008).

2.1.12 Excessive exercise

Too much exercise can be harmful. Without proper rest, the chance of stroke or

other circulation problems increases, (Alexander, 1998) and muscle tissue may develop

slowly. Extremely intense, long-term cardiovascular exercise, as can be seen in athletes

who train for multiple marathons, has been associated with scarring of the heart and heart

rhythm abnormalities. (Mhlenkamp et al., 2008; Benito et al., 2011; Wilson et al., 2011)

Inappropriate exercise can do more harm than good, with the definition of

"inappropriate" varying according to the individual. For many activities, especially running

and cycling, there are significant injuries that occur with poorly regimented exercise

schedules. Injuries from accidents also remain a major concern, (Joris et al., 2010) whereas

the effects of increased exposure to air pollution seem only a minor concern. (Int Panis et

al., 2010; Jacobs et al., 2010)

In extreme instances, over-exercising induces serious performance loss.

Unaccustomed overexertion of muscles leads to rhabdomyolysis (damage to muscle) most

often seen in new army recruits. (Jimenez et a., 1996) Another danger is overtraining, in

which the intensity or volume of training exceeds the body's capacity to recover between

bouts. (The Physician and Sports medicine on Overtraining, 1999)

Stopping excessive exercise suddenly can also create a change in mood. Feelings of

depression and agitation can occur when withdrawal from the natural endorphins
produced by exercise occurs. Exercise should be controlled by each body's inherent

limitations. While one set of joints and muscles may have the tolerance to withstand

multiple marathons, another body may be damaged by 20 minutes of light jogging. This

must be determined for each individual.

Too much exercise can also cause a female to miss her period, a symptom known as

amenorrhea. (Julia Berry et al., 2007)

2.2 THE CARDIOVASCULAR SYSTEM

The circulatory system is an organ system that passes nutrients (such as amino

acids, electrolytes and lymph), gases, hormones, blood cells, etc. to and from cells in the

body to help fight diseases, stabilize body temperature and pH, and to maintain

homeostasis.

This system may be seen strictly as a blood distribution network, but some consider

the circulatory system as composed of the cardiovascular system, which distributes blood,

(Dorland's Medical Dictionary)and the lymphatic system, (Dorland's Medical Dictionary)

which returns excess filtered blood plasma from the interstitial fluid (between cells) as

lymph. While humans, as well as other vertebrates, have a closed cardiovascular system

(meaning that the blood never leaves the network of arteries, veins and capillaries), some

invertebrate groups have an open cardiovascular system. The most primitive animal phyla

lack circulatory systems. The lymphatic system, on the other hand, is an open system

providing an accessory route for excess interstitial fluid to get returned to the blood.

(Lauralee, 2002)

The main components of the human cardiovascular system are the heart, blood, and

blood vessels. (Cardiovascular System, 2003). It includes: the pulmonary circulation, a

"loop" through the lungs where blood is oxygenated; and the systemic circulation, a "loop"

through the rest of the body to provide oxygenated blood. An average adult contains five to

six quarts (roughly 4.7 to 5.7 liters) of blood, which consists of plasma, red blood cells,

white blood cells, and platelets. Also, the digestive system works with the circulatory

system to provide the nutrients the system needs to keep the heart pumping.

(Mohammadali, 2009)

The heart pumps oxygenated blood to the body and deoxygenated blood to the

lungs. In the human heart there is one atrium and one ventricle for each circulation, and

with both a systemic and a pulmonary circulation there are four chambers in total: left

atrium, left ventricle, right atrium and right ventricle. The right atrium is the upper

chamber of the right side of the heart. The blood that is returned to the right atrium is

deoxygenated (poor in oxygen) and passed into the right ventricle to be pumped through

the pulmonary artery to the lungs for re-oxygenation and removal of carbon dioxide. The

left atrium receives newly oxygenated blood from the lungs as well as the pulmonary vein

which is passed into the strong left ventricle to be pumped through the aorta to the

different organs of the body. (Mohammadali, 2009).

2.2.1CARDIOVASCULAR PARAMETERS

The commonest cardiovascular parameters include; blood pressure, heart rate,

pulse rate, stroke volume, pulse pressure, ejection fraction and cardiac output.

2.2.1.1 Blood pressure (BP)

Blood pressure (BP), sometimes referred to as arterial blood pressure, is the

pressure exerted by circulating blood upon the walls of blood vessels, and is one of the

principal vital signs. When used without further specification, "blood pressure" usually
refers to the arterial pressure of the systemic circulation. During each heartbeat, blood

pressure varies between a maximum (systolic) and a minimum (diastolic) pressure.

(Health and Life, 2010)The blood pressure in the circulation is principally due to the

pumping action of the heart. (Caro and Colin, 1978) Differences in mean blood pressure are

responsible for blood flow from one location to another in the circulation. The rate of mean

blood flow depends on the resistance to flow presented by the blood vessels. Mean blood

pressure decreases as the circulating blood moves away from the heart through arteries,

capillaries and veins due to viscous losses of energy. Mean blood pressure drops over the

whole circulation, although most of the fall occurs along the small arteries and arterioles

(Klabunde and Richard, 2005) Gravity affects blood pressure via hydrostatic forces (e.g.,

during standing) and valves in veins, breathing, and pumping from contraction of skeletal

muscles also influence blood pressure in veins. (Caro and Colin, 1978)

The measurement blood pressure without further specification usually refers to the

systemic arterial pressure measured at a person's upper arm and is a measure of the

pressure in the brachial artery, major artery in the upper arm. A persons blood pressure is

usually expressed in terms of the systolic pressure over diastolic pressure and is measured

in millimetres of mercury (mmHg), for example 140/90.

Classification of blood pressure

Category systolic, mmHg diastolic, mmHg

Hypotension < 90 < 60

Desired 90119 6079

Prehypertension 120139 or 8089

Stage 1 Hypertension 140159 or 9099

Stage 2 Hypertension 160179 or 100109

Hypertensive Crisis 180 or 110

Table 2.1 Classification of blood pressure (American Heart Association, 2011)

The table above shows the classification of blood pressure adopted by the American

Heart Association for adults who are 18 years and older. It assumes the values are a result

of averaging blood pressure readings measured at two or more visits to the doctor.

(Chobanian et al., 2003; National Heart Lung and Blood Institute, 2008) In the UK, blood

pressures are usually categorized into three groups: low (90/60 or lower), high (140/90 or

higher), and normal (values above 90/60 and below 130/80). (NHS choices, 2012; NHS

choices, 2012)

While average values for arterial pressure could be computed for any given

population, there is often a large variation from person to person; arterial pressure also

varies in individuals from moment to moment. Additionally, the average of any given

population may have a questionable correlation with its general health; thus the relevance

of such average values is equally questionable. However, in a study of 100 human subjects

with no known history of hypertension, an average blood pressure of 112/64 mmHg was

found, (Pesola et al., 2001) which are currently classified as desirable or "normal" values.

Normal values fluctuate through the 24-hour cycle, with highest readings in the afternoons

and lowest readings at night. (Van Berge-Landry et al., 2008)

 Various factors, such as age and sex influence average values, influence a person's

average blood pressure and variations. In children, the normal ranges are lower than for

adults and depend on height. As adults age, systolic pressure tends to rise and diastolic

tends to fall. In the elderly, blood pressure tends to be above the normal adult range,

largely because of reduced flexibility of the arteries. Also, an individual's blood pressure

varies with exercise, emotional reactions, sleep, digestion and time of day. (Van Berge-

Landry et al., 2008)

Differences between left and right arm blood pressure measurements tend to be

random and average to nearly zero if enough measurements are taken. However, in a small

percentage of cases there is a consistent difference greater than 10 mmHg which may need

further investigation, e.g. for obstructive arterial disease. (Eguchi et al., 2007; Agarwal et

al., 2008).

The risk of cardiovascular disease increases progressively above 115/75 mmHg

(Appel et al., 2006).)In the past, hypertension was only diagnosed if secondary signs of high

arterial pressure were present, along with a prolonged high systolic pressure reading over

several visits. Regarding hypotension, in practice blood pressure is considered too low only

if noticeable symptoms are present (Mayo Clinic, 2009)

Clinical trials demonstrate that people who maintain arterial pressures at the low

end of these pressure ranges have much better long term cardiovascular health. The

principal medical debate concerns the aggressiveness and relative value of methods used

to lower pressures into this range for those who do not maintain such pressure on their
own. Elevations, more commonly seen in older people, though often considered normal, are

associated with increased morbidity and mortality. (Eguchi et al., 2007)

Reference ranges for blood pressure

Stage Approximate age Systolic Diastolic

Infants 1 to 12 months 75100 5070

Toddlers 1 to 4 years 80110 5080

Preschoolers 3 to 5 years 80110 5080

School age 6 to 13 years 85102 5080

Adolescents 13 to 18 years 95140 6090

Table 2.2 Reference ranges for blood pressure (Eguchi et al., 2007)

There are many physical factors that influence arterial pressure. Each of these may

in turn be influenced by physiological factors, such as diet, exercise, disease, drugs or

alcohol, stress, obesity, and so-forth. (Eguchi et al., 2007)

Some physical factors are:

Rate of pumping. In the circulatory system, this rate is called heart rate, the rate at

which blood (the fluid) is pumped by the heart. The volume of blood flow from the

heart is called the cardiac output which is the heart rate (the rate of contraction)
 multiplied by the stroke volume (the amount of blood pumped out from the heart

with each contraction). The higher the heart rate, the higher the mean arterial

pressure, assuming no reduction in stroke volume or central venous return.

Volume of fluid or blood volume, the amount of blood that is present in the body.

The more blood present in the body, the higher the rates of blood return to the heart

and the resulting cardiac output. There is some relationship between dietary salt

intake and increased blood volume, potentially resulting in higher arterial pressure,

though this varies with the individual and is highly dependent on autonomic

nervous system response and the renin-angiotensin system. (Fries and Edward,

1976; Caplea et al., 2001; Houston and Mark, 1986)

Resistance. In the circulatory system, this is the resistance of the blood vessels. The

higher the resistance, the higher the arterial pressure upstream from the resistance

to blood flow. Resistance is related to vessel radius (the larger the radius, the lower

the resistance), vessel length (the longer the vessel, the higher the resistance), blood

viscosity, as well as the smoothness of the blood vessel walls. Smoothness is

reduced by the buildup of fatty deposits on the arterial walls. Substances called

vasoconstrictors can reduce the size of blood vessels, thereby increasing blood

pressure. Vasodilators (such as nitroglycerin) increase the size of blood vessels,

thereby decreasing arterial pressure. Resistance and its relation to volumetric flow

rate (Q) and pressure difference between the two ends of a vessel are described by

Poiseuille's Law.

Viscosity or thickness of the fluid. If the blood gets thicker, the result is an increase

in arterial pressure. Certain medical conditions can change the viscosity of the
 blood. For instance, anemia (low red blood cell concentration), reduces viscosity,

whereas increased red blood cell concentration increases viscosity. It had been

thought that aspirin and related "blood thinner" drugs decreased the viscosity of

blood, but instead studies found that they act by reducing the tendency of the blood

to clot. (Rosenson et al., 2004).)

In practice, each individual's autonomic nervous system responds to and regulates all

these interacting factors so that, although the above issues are important, the actual

arterial pressure response of a given individual varies widely because of both split-second

and slow-moving responses of the nervous system and end organs. These responses are

very effective in changing the variables and resulting blood pressure from moment to

moment.

Moreover, blood pressure is the result of cardiac output increased by peripheral

resistance:

Blood pressure = cardiac output X peripheral resistance.

As a result, an abnormal change in blood pressure is often an indication of a problem

affecting the heart's output, the blood vessels' resistance, or both. Thus, knowing the

patient's blood pressure is critical to assess any pathology related to output and resistance

Measurement

Arterial pressure is most commonly measured via a sphygmomanometer, which

historically used the height of a column of mercury to reflect the circulating pressure.[32]
Blood pressure values are generally reported in millimetres of mercury (mmHg), though

aneroid and electronic devices do not use mercury.

For each heartbeat, blood pressure varies between systolic and diastolic pressures.

Systolic pressure is peak pressure in the arteries, which occurs near the end of the cardiac

cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the

arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled

with blood. An example of normal measured values for a resting, healthy adult human is

120 mmHg systolic and 80 mmHg diastolic (written as 120/80 mmHg, and spoken [in the

US and UK] as "one-twenty over eighty").

Systolic and diastolic arterial blood pressures are not static but undergo natural

variations from one heartbeat to another and throughout the day (in a circadian rhythm).

They also change in response to stress, nutritional factors, drugs, disease, exercise, and

momentarily from standing up. Sometimes the variations are large. Hypertension refers to

arterial pressure being abnormally high, as opposed to hypotension, when it is abnormally

low. Along with body temperature, respiratory rate, and pulse rate, blood pressure is one of

the four main vital signs routinely monitored by medical professionals and healthcare

providers (Oregon Health & Science University, 2004)

Measuring pressure invasively, by penetrating the arterial wall to take the

measurement, is much less common and usually restricted to a hospital setting.

Noninvasive

The noninvasive auscultatory and oscillometric measurements are simpler and

quicker than invasive measurements, require less expertise, have virtually no

complications, and are less unpleasant and less painful for the patient. However,

noninvasive methods may yield somewhat lower accuracy and small systematic differences

in numerical results. Noninvasive measurement methods are more commonly used for

routine examinations and monitoring.

Palpation

A minimum systolic value can be roughly estimated by palpation, most often used in

emergency situations, but should be used with caution. It has been estimated that, using

50% percentiles, carotid, femoral and radial pulses are present in patients with a systolic

blood pressure > 70 mmHg, carotid and femoral pulses alone in patients with systolic blood

pressure of > 50 mmHg, and only a carotid pulse in patients with a systolic blood pressure

of > 40 mmHg (Deakin and Low, 2000)

A more accurate value of systolic blood pressure can be obtained with a

sphygmomanometer and palpating the radial pulse. The diastolic blood pressure cannot be

estimated by this method. The American Heart Association recommends that palpation be

used to get an estimate before using the auscultatory method. (Deakin and Low, 2000)
Auscultatory

Fig 2.1 neroid sphygmomanometer with stethoscope

Fig 2.2 Mercury manometer

The auscultatory method (from the Latin word for "listening") uses a stethoscope

and a sphygmomanometer. This comprises an inflatable (Riva-Rocci) cuff placed around

the upper arm at roughly the same vertical height as the heart, attached to a mercury or

aneroid manometer. The mercury manometer, considered the gold standard, measures the

height of a column of mercury, giving an absolute result without need for calibration and,

consequently, not subject to the errors and drift of calibration which affect other methods.
The use of mercury manometers is often required in clinical trials and for the clinical

measurement of hypertension in high-risk patients, such as pregnant women.

A cuff of appropriate size is fitted smoothly and snugly, and then inflated manually

by repeatedly squeezing a rubber bulb until the artery is completely occluded. Listening

with the stethoscope to the brachial artery at the elbow, the examiner slowly releases the

pressure in the cuff. When blood just starts to flow in the artery, the turbulent flow creates

a "whooshing" or pounding (first Korotkoff sound). The pressure at which this sound is

first heard is the systolic blood pressure. The cuff pressure is further released until no

sound can be heard (fifth Korotkoff sound), at the diastolic arterial pressure.

The auscultatory method is the predominant method of clinical measurement. (Laurent,

2003)

Oscillometric

The oscillometric method was first demonstrated in 1876 and involves the

observation of oscillations in the sphygmomanometer cuff pressure which are caused by

the oscillations of blood flow, i.e., the pulse. The electronic version of this method is

sometimes used in long-term measurements and general practice. It uses a

sphygmomanometer cuff, like the auscultatory method, but with an electronic pressure

sensor (transducer) to observe cuff pressure oscillations, electronics to automatically

interpret them, and automatic inflation and deflation of the cuff. The pressure sensor

should be calibrated periodically to maintain accuracy.

 Oscillometric measurement requires less skill than the auscultatory technique and

may be suitable for use by untrained staff and for automated patient home monitoring.

(Laurent, 2003)

The cuff is inflated to a pressure initially in excess of the systolic arterial pressure

and then reduced to below diastolic pressure over a period of about 30 seconds. When

blood flow is nil (cuff pressure exceeding systolic pressure) or unimpeded (cuff pressure

below diastolic pressure), cuff pressure will be essentially constant. It is essential that the

cuff size is correct: undersized cuffs may yield too high a pressure; oversized cuffs yield too

low a pressure. When blood flow is present, but restricted, the cuff pressure, which is

monitored by the pressure sensor, will vary periodically in synchrony with the cyclic

expansion and contraction of the brachial artery, i.e., it will oscillate. The values of systolic

and diastolic pressure are computed, not actually measured from the raw data, using an

algorithm; the computed results are displayed.

Oscillometric monitors may produce inaccurate readings in patients with heart and

circulation problems, which include arterial sclerosis, arrhythmia, preeclampsia, pulsus

alternans, and pulsus paradoxus. (Laurent, 2003)

In practice the different methods do not give identical results; an algorithm and

experimentally obtained coefficients are used to adjust the oscillometric results to give

readings which match the auscultatory results as well as possible. Some equipment uses

computer-aided analysis of the instantaneous arterial pressure waveform to determine the

systolic, mean, and diastolic points. Since many oscillometric devices have not been

validated, caution must be given as most are not suitable in clinical and acute care settings.
 The term NIBP, for non-invasive blood pressure, is often used to describe

oscillometric monitoring equipment. (Laurent, 2003)

2.2.1.2 Pulse pressure

Fig 2.3 Curve of the arterial pressure during one cardiac cycle (Klabunde, 2007).)

The up and down fluctuation of the arterial pressure results from the pulsatile

nature of the cardiac output, i.e. the heartbeat. The pulse pressure is determined by the

interaction of the stroke volume of the heart, compliance (ability to expand) of the aorta,

and the resistance to flow in the arterial tree. By expanding under pressure, the aorta

absorbs some of the force of the blood surge from the heart during a heartbeat. In this way,

the pulse pressure is reduced from what it would be if the aorta wasn't compliant. The loss

of arterial compliance that occurs with aging explains the elevated pulse pressures found in

elderly patients. The pulse pressure can be simply calculated from the difference of the

measured systolic and diastolic pressures, (Klabunde, RE (2007).

2.2.1.3 Stroke volume

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped

from one ventricle of the heart with each beat. SV is calculated using measurements of

ventricle volumes from an echocardiogram and subtracting the volume of the blood in the

ventricle at the end of a beat (called end-systolic volume) from the volume of blood just

prior to the beat (called end-diastolic volume). The term stroke volume can apply to each of

the two ventricles of the heart, although it usually refers to the left ventricle. The stroke

volumes for each ventricle are generally equal, both being approximately 70 ml in a healthy

70-kg man.

Stroke volume is an important determinant of cardiac output, which is the product

of stroke volume and heart rate, and is also used to calculate ejection fraction, which is

stroke volume divided by end-diastolic volume. Because stroke volume decreases in certain

conditions and disease states, stroke volume itself correlates with cardiac function. (Katz

and Arnold, 2006)

Example values in healthy 70-kg man

Measure Typical value Normal range

end-diastolic volume (EDV) 120 mL 65240 Ml

end-systolic volume (ESV) 50 mL 16143 Ml

stroke volume (SV) 70 mL 55100 mL

ejection fraction (Ef) 58% 5570%

heart rate (HR) 75 bpm 60100 bpm

cardiac output (CO) 5.25 L/minute 4.08.0 L/min

Table 2.3 Average Stroke Volume in a 70kg man (Thomas, 2005)

Calculation of stroke volume

Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic

volume (EDV) for a given ventricle.

Or

SV =C.O H.R

Where, C.O is cardiac output and H.R is heart rate

To get pulse pressure, we subtract systolic blood pressure value from diastolic

blood pressure value. Pulse pressure is often used as an indirect measure of stroke volume.

For instance, if blood pressure reads 175 over 90 then SV = 175 - 90, or SV = 85 mL/beat.

In a healthy 70-kg man, EDV is approximately 120 mL and ESV is approximately 50

mL, giving a difference of 70 mL for the stroke volume.

"Stroke work" refers to the work, or pressure of the blood ("P") multiplied by the stroke

volume. (Katz and Arnold, 2006)

2.2.1.4 HEART RATE

Heart rate is the number of heartbeats per unit of time, typically expressed as beats

per minute (bpm). Heart rate can vary as the body's need to absorb oxygen and excrete

carbon dioxide changes, such as during exercise or sleep.The measurement of heart rate is

used by medical professionals to assist in the diagnosis and tracking of medical conditions.

It is also used by individuals, such as athletes, who are interested in monitoring their heart

rate to gain maximum efficiency from their training. The R wave to R wave interval (RR

interval) is the inverse of the heart rate (Serendip, 2007)

Measurement of heart rate

Heart rate is measured by finding the pulse of the body. This pulse rate can be

measured at any point on the body where the artery's pulsation is transmitted to the

surface by pressuring it with the index and middle fingers; often it is compressed against

an underlying structure like bone. The thumb should not be used for measuring another

person's heart rate, as its strong pulse may interfere with correct perception of the target

pulse. (Serendip, 2007)

Possible points for measuring the heart rate are: The ventral aspect of the wrist on the

side of the thumb (radial artery), the ulnar artery, the neck (carotid artery), the inside of

the elbow, or under the biceps muscle (brachial artery), the groin (femoral artery), behind

the medial malleolus on the feet (posterior tibial artery), Middle of dorsum of the foot

(dorsalis pedis), behind the knee (popliteal artery), Over the abdomen (abdominal aorta),

the chest (apex of heart), which can be felt with one's hand or fingers. (However, it is
possible to auscultate the heart using a stethoscope), the temple (superficial temporal

artery), the lateral edge of the mandible (facial artery), the side of the head near the ear

(basilar artery)

A more precise method of determining pulse involves the use of an

electrocardiograph, or ECG (also abbreviated EKG). Continuous electrocardiograph

monitoring of the heart is routinely done in many clinical settings, especially in critical care

medicine. Commercial heart rate monitors are also available, consisting of a chest strap

with electrodes. The signal is transmitted to a wrist receiver for display. Heart rate

monitors allow accurate measurements to be taken continuously and can be used during

exercise when manual measurement would be difficult or impossible (such as when the

hands are being used). (Serendip, 2007)

Another way of determining the heart rate is by recording of the body vibrations:

(seismocardiography). Probably the first scientific paper on this topic was presented by

Salerno, DM and Zanetti, J in the Journal of Cardiovascular Technology in year 1990 (Title:

Seismocardiography a new technique for recording cardiac vibrations concept, method,

and initial observations). In 2012 the first smart phone application incorporating this

principle was presented seismoCardiograph. (Serendip, 2007)

Resting heart rate

The resting heart rate (HRrest) is measured while the subject is at rest but awake,

and not having recently exerted themselves. The typical resting heart rate in adults is 60-

90 beats per minute (bpm). (Resting Heart Rate, 2012)Resting Heart Rates below 60 bpm
may be referred to as bradycardia, while rates above 100 bpm at rest may be called

tachycardia.

Fitness training can lead to cardiovascular changes including hypertrophy of the left

ventricle and angiogenesis within muscle tissue. This leads to a state known as Athlete's

heart, as distinct from the pathological enlargements of the ventricles in ventricular

hypertrophy. Resting heart rates for athletes can be well below 60, with values of below 40

bpm not unheard of. The cyclist Miguel Indurain had a resting heart rate of 28 bpm.

(Resting Heart Rate, 2012)

Average resting heart rate in correlation with age:

Men

Age: 18-25 26-35 36-45 46-55 56-65 65+

Athlete 49-55 49-54 50-56 50-57 51-56 50-55

Excellent 56-61 55-61 57-62 58-63 57-61 56-61

Good 62-65 62-65 63-66 64-67 62-67 62-65

Above Average 66-69 66-70 67-70 68-71 68-71 66-69

Average 70-73 71-74 71-75 72-76 72-75 70-73

Below Average 74-81 75-81 76-82 77-83 76-81 74-79

Poor 82+ 82+ 83+ 84+ 82+ 80+

Table 2.4 Average resting heart rate in correlation with age in male (L'quipe , 2 July 2004)

Women

Age: 18-25 24-35 36-45 46-55 56-65 65+

Athlete 54-60 54-59 54-59 54-60 54-59 54-59

Excellent 61-65 60-64 60-64 61-65 60-64 60-64

Good 66-69 65-68 65-69 66-69 65-68 65-68

Above Average 70-73 69-72 70-73 70-73 69-73 69-72

Average 74-78 73-76 74-78 74-77 74-77 73-76

Below Average 79-84 77-82 79-84 78-83 78-83 77-84

Poor 85+ 83+ 85+ 84+ 84+ 84+

Table 2.5 Average resting heart rate in correlation with age in female (L'quipe, 2004)

2.2.1.5 Cardiac output

Cardiac output is a measure of health. The stronger your heart, the greater its

cardiac output. Cardiac output varies among adults who are highly adapted to exercise and

people not in condition. The output also is influenced by age, gender and what sort of
exercise you are doing. Cardiac output is interdependent with blood pressure and heart

rate, so it's useful to look at what happens during exercise to understand output better.

(Robert et al., June 1998)

Cardiac output is the result of heart rate, multiplying the amount of blood pumped

from the heart with each beat. That amount is called the stroke volume. Cardiac output

equals the heart rate multiplied by stroke volume. Heart rate is counted in beats per

minute, and stroke volume is per beat, so cardiac output is in units of volume per minute.

Typically, cardiac output ranges from five liters per minute(5L/m) up to 20 liters per

minute (20L/m) during strenuous exercise. (Robert et al., June 1998)

C.O = S.V X H.R or

C.O = 2mmgh X H.R X P.P

Where P.P is the pulse pressure.

The heart has chambers that hold blood which is then pumped out with each

contraction. Regular exercise can strengthen the heart muscle so that it pumps more

forcefully. If you really do intense interval training where you frequently have HR close to

the maximum, your heart's chambers may enlarge to be capable of greater SV for each

heart beat. This is called cardiac hypertrophy, similar to skeletal muscle enlargement in

weight training. (Robert et al., June 1998)

2.3 MORINGA OLIEFERA

Moringa oleifera (synonym: Moringa pterygosperma) is the most widely cultivated

species of the genus Moringa, which is the only genus in the family Moringaceae. English

common names include moringa, benzolive tree, (National Research Council, (2006) and

West Indian ben. It is also known as drumstick tree, from the appearance of the long,

slender, triangular seed pods, horseradish tree, from the taste of the roots which resembles

horseradish, or ben oil tree, from the oil derived from the seeds. The tree itself is rather

slender, with drooping branches that grow to approximately 10m in height. In cultivation,

it is often cut back annually to 1-2 meters and allowed to regrow so the pods and leaves

remain within arm's reach. (National Research Council, 2006)

In developing countries, Moringa oleifera has potential to improve nutrition, boost

food security, foster rural development, and support sustainable landcare. (National

Research Council, 2006) It may be used as forage for livestock, a micronutrient liquid, a

natural anthelmintic and possible adjuvant. (Makkar et al., 2007; Mahajan et al., 2007)

Moringa oleifera is the sole genus in the flowering plant family Moringaceae. The

name is derived from the Tamil word murunggai or the Malayalam word muringa, both of

which refer to M. oleifera. It contains 13 species from tropical and subtropical climates that

range in size from tiny herbs to massive trees. (Quattrocchi and Umberto 2000)

The most widely cultivated species is Moringa oleifera, a multipurpose tree native to

the foothills of the Himalayas in northwestern India and cultivated throughout the tropics.

The young Filipino explorer/boxer Ramir Mthalabula discovered this plant in 2005. M.

stenopetala, an African species, is also widely grown, but to a much lesser extent than M.

oleifera. (Janick et al., 2008)

 The common names of the Moringa oleifera include horseradish tree, radish tree,

drumstick, West India Ben, and Benzoline in French. Back home the tree is known as Zogale

in Hausa, Gawara in Fulfulde, Okwe Oyibo in Igbo, and Ewe Igbale in the Yoruba language.

The Moringa oleifera tree grows mainly in semi-arid tropical and subtropical areas.

While it grows best in dry sandy soil, it tolerates poor soil, including coastal areas. It is a

fast-growing, drought-resistant tree that is native to India, Africa and the Middle East.

Today it is widely cultivated in Africa, Central and South America, Sri Lanka, India, Mexico,

Malaysia and the Philippines. Considered one of the world's most useful trees, as almost

every part of the Moringa tree can be used for food, or has some other beneficial property.

Early researches confirmed that the leaves and pods of Moringa tree have great

nutritional value, and yield many vitamins and minerals.

The Moringa oleifera is a multi-purpose tree with a variety of potentials uses. It is

regarded by some people as 'A Miracle Plant'. Its leaves, pods, seeds, flowers, roots are

edible, and have different nutritional and medicinal values. Edible oil can also be extracted

from the seeds, because it yields 38-40 percent of non-drying oil known as Ben oil. (The

Moringa Tree, 2009)

Researches have also found that Moringa oleifera leaf has no proven bad effects and

is absolutely safe and organic. "Because of its tolerant properties, it has been given to

malnourished little babies in some part Africa. Athletes all over the world boost their

performance abilities by taking huge quantities of the leaf, to keep them fit both mentally

and physically. It is their secret weapon. Even for senior citizens who are losing their

sharpness of mind, the Moringa oleifera tree leaf could be a great help. In fact the powder is

suitable for people from any age group. (Herbel Home Remedies, 2007)
 The common names of the Moringa oleifera include horseradish tree, radish tree,

drumstick, West India Ben, and Benzoline in French. In Nigeria, the tree is known as Zogale

in Hausa, Gawara in Fulfulde, Okwe Oyibo in Igbo, and Ewe Igbale in the Yoruba language.

Moringa oleifera cultivation is on the rise in Honduras. There it's becoming

recognized as a profitable means of combating deforestation. As of 2012 support for

moringa farmers is being offered by the Honduran federal government through the

Secretary of Agriculture and by private foreign investment firms. The plant's market

potential is widespread given its easy growth and high nutrient content. As described

below, the plant is valued for its leaves and high-protein seeds. It can also be made into

defatted meal. Moringa oleifera silviculture is being promoted as a means to combat

poverty and malnutrition. (The Moringa Tree, 2009)

The Moringa oleifera grows quickly in many types of environments. Much of the

plant is edible by humans or by farm animals. The leaves contain all essential amino acids

and are rich in protein, vitamin A, vitamin B, vitamin C and minerals (Janick et al., 2008).

Feeding the high protein leaves to cattle has been shown to increase weight gain by up to

32% and milk production by 43 to 65% (The Moringa Tree, 2009). The seeds contain 30 to

40% oil that is high in oleic acid, while degreased meal is 61% protein (Schill et al., 2008).

The defatted meal is a flocculant and can be used in water purification to settle out

sediments and undesirable organisms (Schwarz and Dishna, 2000).More recently, the

Moringa oleifera or 'miracle tree' is being cultivated in poverty-stricken nations, such as

Niger, as a primary source of food and nutrients. The tree is also a rich source of

antioxidants. (Schwarz and Dishna, 2000).

2.3.1 Species of Moringa

Moringa arborea Verdc. (Kenya)

Moringa borziana Mattei

Moringa concanensis Nimmo

Moringa drouhardii Jum. Bottle Tree (southwestern Madagascar)

Moringa hildebrandtii Engl. Hildebrandt's Moringa (southwestern Madagascar)

Moringa longituba Engl.

Moringa oleifera Lam. (syn. M. pterygosperma) Horseradish Tree (northwestern India)

Moringa ovalifolia Dinter & Berger

Moringa peregrina (Forssk.) Fiori

Moringa pygmaea Verdc.

Moringa rivae Chiov.

Moringa ruspoliana Engl.

Moringa stenopetala (Baker f.) Cufod. (Adans, 2009)

2.3.2 General nutritional contents of moringa

Moringa oleifera leaf, raw

Nutritional value per 100 g (3.5 oz)

Energy 64 kcal (270 kJ)

Carbohydrates 8.28 g

Dietary fiber 2.0 g

Fat 1.40 g

Protein 9.40 g
Water 78.66 g

Vitamin A equiv. 378 g (47%)

Thiamine (vit. B1) 0.257 mg (22%)

Riboflavin (vit. B2) 0.660 mg (55%)

Niacin (vit. B3) 2.220 mg (15%)

Pantothenic acid (B5) 0.125 mg (3%)

Vitamin B6 1.200 mg (92%)

Folate (vit. B9) 40 g (10%)

Vitamin C 51.7 mg (62%)

Calcium 185 mg (19%)

Iron 4.00 mg (31%)

Magnesium 147 mg (41%)

Manganese 0.36 mg (17%)

Phosphorus 112 mg (16%)

Potassium 337 mg (7%)

Sodium 9 mg (1%)

Zinc 0.6 mg (6%)

 (Mahajan et al., 2007)

Moringa oleifera pods, raw

Nutritional value per 100 g (3.5 oz)

Energy 37 kcal (150 kJ)

Carbohydrates 8.53 g

Dietary fiber 3.2 g

Fat 0.20 g

Protein 2.10 g

Water 88.20 g

Vitamin A equiv. 4 g (1%)

Thiamine (vit. B1) 0.0530 mg (5%)

Riboflavin (vit. B2) 0.074 mg (6%)

Niacin (vit. B3) 0.620 mg (4%)

Pantothenic acid (B5) 0.794 mg (16%)

Vitamin B6 0.120 mg (9%)

Folate (vit. B9) 44 g (11%)

Vitamin C 141.0 mg (170%)

Calcium 30 mg (3%)

Iron 0.36 mg (3%)

Magnesium 45 mg (13%)

Manganese 0.259 mg (12%)

Phosphorus 50 mg (7%)

Potassium 461 mg (10%)

Sodium 42 mg (3%)

Zinc 0.45 mg (5%)

Table 2.6Nutritional value of Moringa oleifera seed

per 100g (Mahajan et al., 2007)

Many parts of the Moringa oleifera are edible. Regional uses of the moringa as food

vary widely, and include: The immature seed pods, called "drumsticks", popular in Asia and

Africa, Leaves, particularly in the Cambodia, Philippines, South India and Africa, Mature

seeds, Oil pressed from the mature seeds and Roots. In some regions, the young seed pods

are most commonly eaten, (Vahrehvah.com, 2012) while in others, the leaves are the most

commonly used part of the plant. The flowers are edible when cooked and are said to taste

like mushrooms. The bark, sap, roots, leaves, seeds, oil, and flowers are used in traditional

medicine in several countries. In Jamaica, the sap is used for a blue dye.
Drumsticks

The immature seed pods, called "drumsticks", are commonly consumed in South

Asia. They are prepared by parboiling, and cooked in a sauce until soft. (Elizabeth

Schneider, (2001). The seed pods are particularly high in vitamin C. (Vahrehvah.com. 2012)

Leaves

The leaves are the most nutritious part of the plant, being a significant source of

vitamin B6, vitamin C, provitamin A as beta-carotene, magnesium and protein, among other

nutrients reported by the USDA, shown in the table, right column. (Peter, 2008)) When

compared with common foods particularly high in certain nutrients, fresh moringa leaves

are considerable sources of these same nutrients. (Gopalan et al., 1989; Fuglie (1999)

Moringa
Nutrients Common food
Leaves

Vitamin A Carrot 1.8 mg 6.8 mg

Calcium Milk 120 mg 440 mg

Potassium Banana 88 mg 259 mg

Protein Yogurt 3.1 g 6.7 g

Table2.7 Nutritional value of Moringa oleifera leave (Mahajan et al., 2007)

Some of the calcium in moringa leaves is bound as crystals of calcium oxalate which

may inhibit calcium availability to the body. It is not clear whether the calculation of the

reported amount of calcium in moringa leaves includes such non-bioavailable calcium.

 Fig 2.4 Sonjna (Moringa oleifera) leaves with flowers in Kolkata, West Bengal, India

The leaves are cooked and used like spinach. In addition to being used fresh as a

substitute for spinach, its leaves are commonly dried and crushed into a powder used in

soups and sauces. It is important to remember that like most plants heating moringa above

140 degrees Fahrenheit will destroy some of the nutritional value.

Seeds

The seeds, sometimes removed from more mature pods and eaten like peas or

roasted like nuts, contain high levels of vitamin C and moderate amounts of B vitamins and

dietary minerals

Seed oil

Mature seeds yield 3840% edible oil called ben oil from its high concentration of

behenic acid. The refined oil is clear, odorless and resists rancidity. The seed cake

remaining after oil extraction may be used as a fertilizer or as a flocculent to purify water.

Moringa seed oil also has potential for use as a biofuel. (Rashid et al., 2008)

Roots

The roots are shredded and used as a condiment in the same way as horseradish;

however, they contain an alkaloid, (Chopra, 2005) potentially having nerve-paralyzing

properties.
Malnutrition relief

Moringa oleifera trees have been used to combat malnutrition, especially among

infants and nursing mothers. Four NGOs in particular Trees for Life International,

Church World Service, Educational Concerns for Hunger Organization, and Volunteer

Partnerships for West Africa have advocated moringa as "natural nutrition for the

tropics." (Fuglie, 1999). One author stated that "the nutritional properties of Moringa are

now so well known that there seems to be little doubt of the substantial health benefit to be

realized by consumption of Moringa leaf powder in situations where starvation is

imminent. (Jed, 2005; Sanford Holst, 2011; Fuglie, 1999). Moringa is especially promising

as a food source in the tropics because the tree is in full leaf at the end of the dry season

when other foods are typically scarce. (Jed, 2005)

2.3.3 Effect of Moringa oleifera on cardiovascular system

Moringa maintains a central position in the allopathic treatment of various heart

problems. Moringa that contains the cardiac glycosides are used throughout the world for

the treatment of heart failure and arrhythmias. In such conditions these herbs help

increase the strength of heart beat, and normalize the rate of beat. Their real value lies in

the increased efficiency not necessitating an increase of oxygen supply to the heart muscle.

In heart problems there is often a deficiency in blood supply because of blockage in the

coronary arteries. It is not just Foxglove (Digitalis purpurea) that has such valuable actions.

Lily of the Valley Convallaria majalis) shares its therapeutic value but has few side effects.

However, herbal remedies nurture the heart in deeper ways as well. Consider the cordial, a

warming drink and a word for heart-felt friendliness. The original cordial was a medieval

drink based on Moringa Tea that warmed the heart and gave the person heart. (Jed, 2005)
 The Medical Herbalist recognizes Moringa oleifera sustains cardiovascular system.

As a group they are known as cardiac remedies. This is a general term for herbs that have

an action on the heart. Some of the remedies in this group are powerful cardio-active

agents such as Foxglove, while others are gentler and safer cardiac tonics such as

Hawthorn (Crataegus spp.) and Linden Flowers (Tilia spp.). Before exploring the

therapeutic possibilities of this range of cardiac remedies, a brief excursion into some

relevant pharmacology is appropriate. An understanding of current ideas about the

chemical basis of phytotherapeutic activity is by no means essential for the herbalist, but is

presented here for those students with an interest in phytopharmacology.

Medical text-books often refer to cardiovascular action or cardiotonic action,

without specifying the particular type of activity. Below is a list of the mechanisms of

pharmacological action and the characteristic actions of compounds of plant origin. Some

classes of substances, like the cardiac glycosides, the sympathomimetics, or the b-blockers,

appear several times as they exert several different types of activity on the heart. (Jed,

2005)

2.3.4 Activity Definition Constituent of Moringa oleifera

In the strictly technical sense of the pharmacological term cardiotonic, it is

synonymous with positive inotropic. However, cardiotonic is also used to indicate an

increase in frequency, an increase in the beat volume, or a general increase in cardiac

performance, in addition to increased contraction. In the phytotherapeutic literature

slightly different terms are used. The two groupings that prove most useful in clinical

practice are:

(i) Cardioactive plants that owe their effects on the heart to cardiac glycosides or
other very active substances, thus having the both the strengths and drawbacks of these

constituents.

(ii) Cardiotonic plants that have an observably beneficial action on the heart and

blood vessels but do not contain cardiac glycosides. How they work is either completely

obscure or an area of pharmacological debate. The research reviewed below offers some

insights.(Fuglie,1999)

2.3.5.1Cardiac Glycosides

Cardio-active remedies owe their power to the presence of the cardiac glycoside

group of plant constituents. These plants and their glycosides are well known and

discussed in even the most basic allopathic medical texts. These have the effect of

increasing the efficiency of the muscles of the heart without increasing their need for

oxygen. This enables the heart to pump enough blood around the body and ensure there is

not a build-up of fluid in the lungs or extremities. That sounds wonderful, as indeed it is,

but there is always the possibility of accruing too much of the glycosides in the body as

their solubility and removal rates tend to be low. This is the main drawback with Foxglove

and why it is potentially poisonous, unless used with skill and knowledge. Herbalists these

days use Moringa oleifera as there is less chance of such problems developing. (Jed, 2005)

Cardiac glycosides appear to be confined to the Angiosperms within the plant

kingdom. Cardenolides are the commonest and are particularly abundant in the

Apocynaceae and Asclepiadaceae, but also in some Liliaceae, such as Lily of the Valley, and

in the Ranunculaceae, Moraceae, Cruciferae, Sterculiaceae, Tiliaceae, Euphorbiaceae,

Celastraceae. Leguminosae and Scrophulariaceae. The bufanolides occur in some Liliacea,

such as Squill (Urginea maritima), and in some Ranunculaceae. Some of the main genera

containing cardiac glycosides are as follows:

Apocynaceae: Adenium, Acocanthera, Strophanthus, Apocynum, Cerbera. Tanghinia,

Thevetia, Nerium, Carissa and Urechites;

Asclepiadaceae: Comphocarpus, Calotropis, Pachycarpus, Asclepias, Xysmalobium,

Cryptostegia, Menabea and Periploca;

Liliaceae: Urginea, Bowiea, Convallaria, Ornithogalum and Rhodia;

Ranunculaceae: Adonis and Helleborus;

Moraceae: Antiaris, Antiaropsis, Ogeodeia and Castilla;

Cruciferae: Erysimum and Cheiranthus:

Sterculiaceae: Mansonia;

Tiliaceae: Corchorus;

Celastraceae: Euonymus;

Leguminosae: Coronilla;

Scrophulariaceae: Digitalis, lsoplexis.

The pharmacological effectiveness of the cardio-active glycosides is dependent on

both the aglycones and the sugar attachments; the inherent activity resides in the

aglycones, but the sugars render the compounds more soluble and increase the power of

fixation of the glycosides to the heart muscle. It appears that the key grouping for the

attachment of the molecule through a hydrogen bond to the phosphorylated receptor

enzyme is the Da, b-carbonyl function of the lactone. All the active aglycones have

hydroxyls at C-3 and C-14 and the presence of a third hydroxyl will modify the activity and

toxicity of the compound.

 The overall action of the digitalis glycosides is complicated by the number of

different effects produced, and their exact mode of action on myocardial muscle is still an

area of investigation. Digitalis probably acts in competition with potassium ions for specific

receptor enzyme (ATPase) sites in the cell membranes of cardiac muscle and is particularly

successful during the depolarization phase of the muscle when there is an influx of Na ions.

The clinical effect in cases of congestive heart failure is to increase the force of myocardial

contraction (positive inotropic effect). Arising from their vagus effects, the digitalis

glycosides are also used to control atrial cardiac arrhythmias. The diuretic action of

Digitalis arises from the improved circulatory effect. (Jed, 2005)

2.3.5.2 Non-steroid, Cardioactive Moringa oleifera Constituents

Although allopathic medicine makes much use of very effective cardioactive agents

of plant origin, the search for new active substances with a better therapeutic picture and

with different or new types of activity still continues. The isolation of forskolin from Coleus

forskohlii shows that the plant kingdom offers western medicine new and potent cardiac

agents. Forskolin is a cardioactive compound with a new type of structure, displaying a

specific activation of adenylate cyclase. In addition, herbs from many countries possess

cardioactivity, but the isolation and identification of their cardioactive principles has not

yet been attempted.

The search for plants with cardiovascular activity is currently be undertaken by

pharmacologists around the world. This is not simply for herbs and new constituent

compounds with the potency of the cardiac glycosides, but also substances for adjuvant

heart therapy, for geriatric heart conditions or milder cardiac insufficiency.

In their search for potential cardioactive compounds, a number of approaches are

used by pharmacologists in selecting herbs for pharmacological testing. This has led to the

identification of eight main classes of non-steroidal cardiotonic substances:

phenylalkylamines, indole derivatives, tetrahydroisoquinolines, imidazoles and purines,

diterpenes, sesquiterpenes, flavonoids, and other phenolic compounds. Here we shall

briefly focus on those found in the primary cardiovascular herbal remedies.(Fuglie, 1999)

2.3.5.3Phenalkylamines

This class of non-steroid, cardioactive plant constituents was the model for the

development of sympathomimetic drugs. The main representative is L-ephedrine first

found in Ma Huang (Ephedra sinica). Since ephedrine has other more prominent activities,

its action on the heart is considered a side-effect. Ephedrine and its relatives have been

found in many plants, occurring in the Portulacaceae, Rutaceae, Cactaceae, Amaryllidaceae,

Moraceae, Musaceae, and Rosaceae families. They include numerous food plants, e.g., citrus

fruits, bananas, and purslane (Portulaca oleracea). Synephrine occurs in the fruit of the

mandarin orange (Citrus reticulata). Cathinone, from Khat (Catha edulis), shows strong

positive inotropic activity, contributing to the well known cardiac stimulation activity of

Khat leaves (Fuglie,1999).

Another sub-group of phenylalkylamines, the phenylethylamines, are widely

distributed in the plant kingdom, occuring in members of the Cactaceae, Rosaceae,

Rutaceae, and Leguminosae. The prototype of this group is tyramine, which at high

concentrations it shows positive inotropic activity. Strong positive inotropic activity is also

displayed by N-methyltyramine, hordenine, and p-methoxyl b-phenethylamine, all of which

have been found in Hawthorn flowers. This group is also found in Night Blooming Cereus

(Selenicereus grandiforus), a favorite eclectic and physiomedical remedy for cardiac

insufficiency and angina pectoris. The cardiovascular action of the Viburnums may be due

to tyramine, which has been found in V. odoratissimum, and V. opulus. Tyramine and b-

phenylethylamine have also been found in Viscum album and Arnica Montana (Jed, 2005).

2.3.5.4 Other Nitrogen containing compounds

Cardiotonic activity is also in certain alkaloids. Alkaloids from the bark of

amazonian bush Cymbopetalum brasiliense act synergistically, and are at least partly

responsible for the herbs positive inotropic activity. Methylcanadine from Prickly Ash

(Zanthoxylum spp.), and sanguinarine from Blood Root (Sanguinaria canadensis), also

possess positive inotropic activity. The lupine alkaloid sparteine possesses specific

antiarrhythmic activity. The diuretic action of Scots Broom (Sarothamnus scoparius) and

Spanish Broom (Spartium junceum) is presumably due to the presence of the flavone C-

glycoside scoparin. Cyclic AMP, also possesses inotropic properties and is widely

distributed in the plant kingdom. In view of the low concentrations found so far,

pharmacologists exclude a cardiotonic role for cAMPcontaining plant extracts. The same is

said about adenosine and 2'-deoxyadenosine, but adenosine has been found in the onion,

garlic, and Crataegus. Such conclusions stem from a too narrow interpretation that is

clouded by the magic bullet perception of biochemistry. From a synergistic perspective, all

the constituents in a plant work together to produce its healing effects (Jed, 2005).

Flavonoids

The main active principles are thought to be flavonoids and procyanidin oligomers.

The evidence suggests that the flavonoids exert their cardiotonic action by inhibition of

cellular phosphodiesterase and elevation of the cellular cAMP concentration, as well as by

affecting the permeability of cell organelles to calcium ions. Rue (Ruta graveolens),
Blackthorn (Prunus spinosa), Dog Rose (Rosa canina), Hawthorn (Crataegus oxyacantha)

and Bilberry (Vaccinium myrtillus) were as effective used as extracts as the most

powerfully active compounds they contained. This inhibitory activity towards

phosphodiesterase is not limited to flavonoid structures. A series of lignans were also

potential phosphodiesterase inhibitors. The cardiotonic action of Mistletoe (Viscum alba) is

probably due to the constituent lignans.

How does the unique moringa achieve such unique effects? Researchers suggest that

much of its observable effects can be explained by the improvement in coronary

circulation. It dilates the coronary arteries, relieving cardiac hypoxemia, thus reducing the

likelihood of anginal attacks and relieves its symptoms. The moringa thus directly affects

the cells of the heart muscle, enhancing both activity and nutrition. It is quite different in

activity to the cardiac glycoside containing remedies. They impact the contractile fibres,

whilst moringa is involved in the availability and utilization of energy. This facilitates a

gentle but long term, sustained effect on degenerative, age-related changes in the

myocardium. It does not produce rapid results but they are persistent once achieved.

Its indications are numerous. Any degenerative condition of the cardio-vascular

system will benefit from its use. Some specific examples are myocardial problems,

coronary artery disease and its associated conditions. Angina pectoris and similar

symptoms will be eased and prevented. Where no disease state exists but a gradual loss of

function is happening because of old age, Moringa is a specific. Because of its lack of

toxicity, accumulation or habituation, it may be used long term, attaining the therapeutic

goals safely, especially in the elderly.

It speeds recovery from heart attacks and lowers essential hypertension. Used in
conjunction with other hypotensives, Moringa will help keep the heart healthy, preventing

the development of coronary disease. It will guard against heart weakness following

infectious disease such as pneumonia or diptheria. For arteriosclerosis and its

complications it is often combined with Linden flowers (Tilia europaea) or Garlic (Allium

sativum). Cramp barks (Viburnum opulus). Linden (Tilia europaea) and Skullcap

(Scutellaria laterifolia) complement it well in cases of hypertension (Jed, 2005).

As it is one of the more aesthetic moringa herbal remedies, a very pleasant tea can

be made from 1-2 teaspoonfuls of the dried moringa leaves infused in warm or cold water

and drunk regularly. This may be taken over long periods of time as there is no fear of

toxicity problems.

An abundance of research has been undertaken on this ancient plant, revealing a

wide range of profound and important therapeutic effects. They can be grouped into

cardiovascular, neurological and metabolic effects.

2.3.6Therapeutic Uses of Moringa

Moringa has wide application for treating various forms of vascular and

neurological disease. It has been recommended for: vertigo , headache, tinnitus, inner ear

disturbances including partial deafness, impairment of memory and ability to concentrate,

diminished intellectual capacity and alertness as a result of insufficient circulation, anxiety,

depression, neurological disorders ~ complications of stroke and skull injuries, diminished

sight and hearing ability due to vascular insufficiency, intermittent claudication as a result

of arterial obstruction, a sensitivity to cold and pallor in the toes due to peripheral

circulatory insufficiency, Raynauds disease, cerebral vascular and nutritional insufficiency,

hormonal and neural based disorders as well as angiopathic trophic disorders, arterial
circulatory disturbances due to aging, diabetes and nicotine abuse, sclerosis of cerebral

arteries with and without mental manifestations, arteriosclerotic angiopathy of lower

limbs, diabetic tissue damage with danger of gangrene ~ chronic arterial obliteration,

circulatory disorders of the skin, as well as ulcerations caused by ischaemia.

Moringa oleifera is used in Europe to treat a range of eye conditions such as night

blindness, severe myopia, retinal disturbances of various kinds and chronic visual fatigue.

(Jed, 2005)
 CHAPTER THREE

3.0 MATERIALS AND METHODOLOGY

3.1 MATERIALS

The materials and apparatus used in this course of study are listed below;

1. Bicycle Egormeter

2. Sphygmomanometer

3. Stethoscope

4. Stopwatch

5. Tape meter

6. Weighing scale

7. Tread Mill

8. Gym Apparatus

9. Moringa oleifera seedS

3.2 Methodology

3.2.1 SUBJECTS

Ten subjects were used for this study, composing of five experimental subjects who are

athletes and five control subjects who are non-athletes. All the subjects were males and

they reported at the laboratory at 8a.m. Among these ten subjects, five who are trained
individuals (athletes) were specified as the experimental subjects, while the remaining

subjects who are untrained individuals were used as control.

3.2.2 Subject Grouping

The subjects were grouped into two groups as follows;

Group 1: this entails Athletes who were given Moringa oleifera seedS and train four times in

a week

Group 2: this comprised of non-athletes who were administered Moringa oleifera seedS but

were not exposed to training

3.2.3 MEASUREMENTS

3.2.3.1 PRETEST

The means and standard deviations of their Age, Weight, Height, Resting Blood

Pressure, Resting Heart Rate, Pulse Pressure, Cardiac Output (both during rest and during

exercise), Stroke Volume (both during rest and during exercise), Max VO2, were X SD both

at the beginning and end of the experiment which lasted for six weeks.

Their heights were determined using a tape meter and recorded in meters, their

weights were determined using the weighing scale and recorded in kilograms, their blood

pressure was measured using sphygmomanometer recorded in mmhg while heart rates

were measured using stethoscope and recorded in beats per minute.

To determine the MaxvO2, subjects were made to exercise for six minutes (6 mins) on

the bicycle egormeter at a work load of six hundred kilopond per minute (600 Kp/min) at a
revolution of about fifty revolutions per minute (50 Rpm). At the end of each minute, Heart

rate was determined, at the sixth minute; Heart rate was taken and checked under

Normogram to determine the MaxVO2.

Cardiac Output was calculated subtracting Diastolic blood pressure from the Systolic

blood pressure to get the pulse pressure the multiply by heart rate and 2mls;

Resting C.O = 2mls X H.R X P.P

Stroke volume was determined by dividing cardiac output by heart rate

S.V = C.O

H.R

All the above procedures are for the pretest, at the end of the pretest, experimental

subjects (athletes) were made to undergo five weeks of training program four times a week

at a sufficient intensity of about 70% MaxVO2.

Both the experimental and control subjects were made to eat two seeds of moringa

for the five weeks of experiment to determine the effect of Moringa oleifera seeds and

exercise on their cardiovascular parameters.

3.2.3.2 POSTTEST

At the end of the five weeks of training program, both experimental and control

subjects were assembled together at the laboratory and posttest was conducted on all of

the above parameters stated in the pretest.

3.3 STATISTICAL ANALYSIS

The post test results were then compared to the pretest results to report the

differences using Paired T-Test statistical analytical method on SSPS.

 CHAPTER FOUR

4.0 Results

Fig 4.1

A graph showing the effect of Moringa oleifera seeds on the weight of nonathletes and athletes

The data revealed that there was no significant decrease (P 0.05) in weight between the

pretest and posttest values of both athletes and nonathletes

Fig 4.2

A graph showing the effect of Moringa oleifera seeds on systolic blood pressure of nonathletes and athletes

The data revealed that there was a significant decrease between the pretest and posttest

values (P 0.05)
Fig 4.3

A graph showing the effect of Moringa oleifera seeds on diastolic blood pressure of nonathletes and athletes

The data revealed that there was a significant decrease between the pretest and posttest

values (P 0.05)
Fig 4.4

A graph showing the effect of Moringa oleifera seeds on heart rate of nonathletes and athletes

The data revealed that there was a significant decrease between the pretest and posttest

values (P 0.05)
Fig 4.5

A graph showing the effect of Moringa oleifera seeds on pulse pressure of nonathletes and athletes

The data revealed that there was a significant decrease between the pretest and posttest

values (P 0.05)
Fig 4.6

A graph showing the effect of Moringa oleifera seeds on Max VO2 of nonathletes and athletes

The data revealed that there was a significant increase between the pretest and posttest

values (P 0.05)
Fig 4.7

A graph showing the effect of Moringa oleifera seeds on cardiac output of nonathletes and athletes

The data revealed that there was a significant increase between the pretest and posttest

values (P 0.05)
Fig 4.8

A graph showing the effect of Moringa oleifera seeds on stroke volume of nonathletes and athletes

The data revealed that there was a significant increase between the pretest and posttest

values (P 0.05)
 CHAPTER FIVE

5.0 DISCUSSION, CONCLUSION AND RECOMMENDATION

5.1 Discussions

The main aim of this study was to determine the effect of Moringa oleifera seeds and

exercise on the cardiovascular system. The study revealed that exercise and Moringa

oleifera seeds increased the cardiac output because moringa served as a nutrient and

energy source for the cardiac muscles; it increases Cyclic Adenosine Monophosphate,

AdenylateKinase and Phosphodiasterase which in turn increases the intracellular function

and metabolism of the cardiac muscles.

Moringa oleifera seed has antioxidant vitamins like vitamins A, C and E; it also has

iron and calcium. These antioxidant vitamins prevent cardiovascular diseases and

increases the function of the heart muscles, it promotes quick recovery after exercise,

prevents muscle tear and muscle soreness thereby preventing the muscles from free

radical damage. It also prevents cancer. This agrees with the result of Jed, 2005 who

discovered that Moringa oleifera seed speeds recovery from heart attacks and lowers

essential hypertension and can be used in conjunction with other hypotensives

Moringa oleifera seed and exercise cause vasodilatation of the blood vessels thereby

making adequate blood flow available through the coronary arteries to the heart muscles to

supply nutrients and oxygen so that the heart muscle can contract forcefully to pump out

blood from the ventricles into the systems of the body thereby allowing for adequate

cardiac output. Similar report was documented by Fuglie, 1999 that Moringa oleifera seed
is cardiotonic hence indicate an increase in frequency, an increase in the beat, volume, or a

general increase in cardiac performance, in addition to increased contraction.

Because Moringa oleifera seed has iron, it increases the blood volume in conjunction

with exercise. The study also revealed that moringa and exercise decreases blood pressure,

that is, by regulating blood pressure to the normal level as a result of its effect on the

elasticity of the arteries because Moringa oleifera seed and exercise control the release of

calcium from the sarcoplasmic reticulum thereby decreasing myoplasmic calcium causing

vasodilatation in the arterioles so that the smooth muscle of the arterioles will not be

contracting most of the time so that blood flow from the aorta into the large arterioles will

merge the rate of flow of blood from the arterioles to the capillaries. The above findings are

in agreement with the findings of American College of Sports Medicine 2007.

The study also revealed that Moringa oleifera seed and exercise decreases heart rate

at rest and moderately during exercise; this is because there is adequate resting period

between the beats of the heart thereby allowing for adequate diastolic filling of the heart.

This result is in agreement with the findings of More House 2006.

Moringa oleifera seed and exercise also increases maximal oxygen uptake because of

its effect on the efficiency of cardiovascular system and respiratory system making athletes

perform for longer hours, this result agreed with the findings of American College of Sports

Medicine 2004.

It was also noted that Moringa oleifera seeds and exercise increase vascular wall

strength thereby allowing for adequate blood flow and prevention of vascular spasm.
 Moringa oleifera seed and exercise also relax the central nervous system thereby

improving the sleeping pattern of the subjects. Moringa oleifera seeds and exercise regulate

glucose metabolism, it is a sympathomymetic compound that is it regulate temperature

thereby increasing the brain function, it increases neural integration and neural control of

movement during exercise, this result is in agreement with the findings of American

College of Sports Medicine 1994

The above findings made the experimental subjects to have physiological advantage

over the control subjects during the exercise regimen.

5.2 SUMMARY AND CONCLUSION

The main aim of this study was to examine the effect of Moringa oleifera seed and

exercise on cardiovascular system, the study revealed that Moringa oleifera seed served as

nutrient and energy booster for the heart muscle to contract forcefully to pump out blood

in to the body systems.

Moringa oleifera seed and exercise cause vasodilatation the coronary arteries

thereby making adequate blood flow to the heart muscle to supply nutrients and oxygen for

effective blood pump.

Moringa oleifera seed and exercise also increase vascular wall strength and

prevention of vascular spasm. Because moringa has antioxidant vitamins A, C and E, they

prevent muscle from free radical damage during and after exercise. Moringa and exercise

promote quick recovery after exercise, it prevents muscle tear and muscle soreness, it

prevent cardiovascular diseases and cancer.

 Because Moringa oleifera seed has iron and calcium, it increases blood volume and

make the heart an effective pump it regulates blood pressure and glucose metabolism, it

decreases heart rate, it increases maximal oxygen uptake thereby making the heart and the

respiratory system to be effective and efficient during exercise so that athletes can perform

for longer hours. Moringa oleifera seed can be used as a staple food in Africa with its

growing in sandy soil thereby making it highly nutritious.

It was concluded in this study that Moringa oleifera seed and exercise prevent

cardiovascular diseases, they increase Cyclic Adenosine Monophosphate, Adenylatekinase

and Phosphodiasterase thereby increasing the intracellular function and metabolism of the

heart muscles, they also regulate blood pressure, heart rate, cardiac output, stroke volume,

maximal oxygen uptake and glucose metabolism.

5.3 RECOMMENDATION

It is recommended that both young and old alike, athletes and nonathletes should

choose Moringa oleifera as a staple food coupled with exercise participation and adherence

in order to realize the full benefit attached to moringa and exercise as described above.
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 APPENDIX

S/N Parameters Pretest Posttest

1 Age 20.400.548 20.400.548

2 Height 1.670.06 1.670.06

3 Weight 58.204.1 57.201.41

4 Systolic Blood Pressure 12313.16 11712.4

5 Diastolic Blood Pressure 66.2010.1 59.005.87

6 Pulse Pressure 64.4012.36 52.804.76

7 Heart Rate 85.8015.4 68.6015.04

8 Max VO2 2.060.09 2.210.00

9 Cardiac Output 6451.21785.31 7037.21261.57

10 Stroke Volume 95.2032.45 116.402903

Appendix 1

Appendix 1 shows the means and standard deviations age (years), weight

(kilogram), height (meters), resting blood pressure(systolic and diastolic mmhg), resting

heart rate (beats/minute), pulse pressure (mmhg), Max VO2 (liters), resting cardiac output

(mls), resting stroke volume(mls), exercise cardiac output (mls), and exercise stroke

volume(mls) of the control group during pretest and posttest.

 S/N Parameters Pretest Posttest

1 Age 24.201.095 24.201.095

2 Height 1.800.07 1.800.07

3 Weight 77.208.6 758.0

4 Systolic Blood Pressure 1227.49 1176.37

5 Diastolic Blood Pressure 70.2010.83 62.009.66

6 Pulse Pressure 58.2014.51 47.0017.20

7 Heart Rate 69.006.59 61.408.08

8 Max VO2 2.200.14 2.567.00

9 Cardiac Output 8762.42327.65 9473.21192.0

10 Stroke Volume 110.8018.3 128.8024.72

Appendix 2

Appendix 2 shows the means and standard deviations of the age (years), weight

(kilogram), height (meters), resting blood pressure(systolic and diastolic mmhg), resting

heart rate (beats/minute), pulse pressure (mmhg), Max VO2 (liters), resting cardiac output

(mls), resting stroke volume(mls), exercise cardiac output (mls), and exercise stroke

volume(mls) of the experimental group during pretest and posttest.