Oxygen

study guide
Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within

Key concepts

Oxygen uptake during exercise is dependent upon exercise intensity and duration,
but intensity is the primary determinant
The oxygen deficit arises due to a delay in oxygen delivery and/or mitochondrial
respiration. CP utilisation and anaerobic glycolysis provide energy during this period
VO2 drift occurs during prolonged, strenuous exercise due to factors within the
contracting skeletal muscles
Excess post-exercise oxygen consumption (EPOC) has three distinct time courses
and is due to slow decline in oxygen demands, resynthesis of key substrates and
elevated temperature and hormones.
Primary functions of the cardiovascular system are to deliver O2 to, and to remove
CO2 and heat from, contracting skeletal muscle
Increased muscle blood during exercise is primarily due to vasodilator metabolites
and action of muscle pump
Cardiac output increases due to increased heart rate and stroke volume
Control of the circulation during exercise involves "central command" and feedback
from contracting muscles and key receptors (e.g. baroreceptors), interacting with
the autonomic nervous system
Exercise training remodels the heart to enhance stroke volume and promotes
skeletal muscle angiogenesis.
The key role of ventilation is to maintain arterial O2 saturation and remove CO2
Breathing frequency and tidal volume increase during exercise
Respiratory muscles become significant consumers of oxygen themselves during
heavy exercise, can fatigue and are a source of a chemoreflex with effects on active
muscle blood flow
The regulation of ventilation during exercise is complex and far from fully described,
but involves central neural control, feedback from muscle afferents, mechanical
feedback from lungs and limbs and humoral factors.
Maximal oxygen uptake is the most commonly used measure of "cardiorespiratory
fitness"
Maximal oxygen uptake is a measure of the combined abilities of the respiratory and
cardiovascular systems to deliver oxygen and the active skeletal muscle to consume
oxygen
Maximal oxygen uptake is determined by a combination of genetic endowment and
physical training
Oxygen delivery is generally considered the rate limiting factor for maximal oxygen
uptake.

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within

Oxygen uptake kinetics

The oxidation of metabolic fuels (primarily CHO and fat) is critically dependent upon the
supply of oxygen to contracting skeletal muscle. This is the important role of the
respiratory and cardiovascular systems.
Oxygen uptake (VO2) is primarily determined by the exercise intensity and during cycling
exercise, given the mechanical efficiency is fairly constant across a wide range of
training status (~20%), there is a characteristic VO2 for a given power output the
relationship is essentially linear.

POWER VO2
(watts)
(l.min-1)
50
100
150
200
250
300

0.9
1.5
2.1
2.8
3.5
4.2

During exercise where the body mass must be supported (e.g. walking, running), the
exercise VO2 is determined not only by the speed of running (intensity), but also by body
mass and walking/running technique. Running economy, or the VO2 for a given running
speed, is an important factor in determining middle-long distance running success.

There are distinct phases in VO2 during the transition from rest to the steady-state
VO2 at a given exercise intensity and then during recovery as VO2 returns to the resting
level at a variable rate, determined by the intensity and duration of the preceding
exercise.
During the transition from rest to exercise, and from one exercise intensity to a higher
intensity, there is slow increase in VO2, necessitating the recruitment of other energy
systems to meet the energy demands of exercise. This is termed the "oxygen deficit"
and the main energy system used is creatine phosphate, with smaller contribution from
"anaerobic" glycolysis. Interestingly, a parameter termed the "maximal accumulated
oxygen deficit (MAOD)" has been used as a measure of the so-called "anaerobic
capacity". It is greater in sprint athletes compared with endurance athletes and is
increased after a period of sprint training.

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
Why an oxygen deficit?

Slow O2 delivery due to gradual increases in cardiac output, muscle blood flow
and/or tissue diffusion
Slow O2 utilisation due to slow activation of mitochondrial respiration ("metabolic
inertia")
Combination of both mechanisms?

Although there is generally a given steady-state VO2 for a given exercise power output,
as exercise duration is extended there is a progressive increase in VO2, especially at
higher exercise intensities. This is termed "VO2 drift" or the "slow component" (derived
from mathematical modelling of the increase in VO2 during exercise).
Factors contributing to the VO2 drift:

80% due to changes within active skeletal muscle

Recruitment of lower efficiency type II skeletal muscle fibres
Reduced P-O coupling efficiency
Elevated muscle temperature
Increased FFA metabolism
Elevated catecholamines
O2 cost of ventilatory and cardiac work.

Following exercise, there is reduction in VO2, with three distinct phases fast, slow and
ultra-slow. VO2 remains above the resting level for some, depending upon the intensity
and duration of the preceding exercise. The "extra" VO2 above rest during recovery is
termed the excess post-exercise oxygen consumption (EPOC). Processes contributing
to EPOC include:

Resynthesis of ATP and CP

Restoration of myoglobin O2 stores
Elevated HR, VE, temperature, catecholamines
Increased FFA metabolism
Mitochondrial uncoupling
Glycogen and protein synthesis.

A crucial metabolic process during the early recovery period, and contributing to the fast
component of EPOC, is CP resynthesis. This is a fast process, with a half time of ~60-90
sec, and is critically dependent on the availability of oxygen. The rate of post-exercise
CP resynthesis is often used a marker of muscle oxidative capacity. Dietary creatine
supplementation enhances CP synthesis and performance in high intensity exercise.
Lactate oxidation was proposed as a reason for increased VO2 during recovery;
however, there is no evidence in support of this. The metabolic fates of lactate are:

Oxidation in skeletal (type I) and cardiac muscle active recovery, below the lactate
threshold, enhances lactate removal
Susbstrate for glycogen resynthesis
Conversion to other metabolites e.g. amino acids
Lactate oxidation does not increase VO2 and lactate does not cause delayed onset
muscle soreness.

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Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
Another important metabolic process during recovery is resynthesis of muscle glycogen,
which is influenced by:

Degree of muscle glycogen depletion

Glycogen synthase activity
Muscle GLUT4 expression
Blood glucose and insulin levels, determined by amount, type and timing of postexercise CHO ingestion
Muscle damage.

Cardiovascular responses to exercise

The cardiovascular system functions during exercise to:

Increase O2 supply to active skeletal and cardiac muscle [Fick equation: VO2 = Q x
(CaO2 CVO2)]
Facilitate CO2 and heat removal
Ensure maintenance of mean arterial blood pressure: MAP = Q x TPR.
Circulation
(l.min-1)

Rest Light Heavy Max

Oxygen uptake

0.3

0.8

2.4

4.0

Cardiac output

5.8

9.5

17.5

25.0

Active skeletal muscle 1.2

4.5

12.5

22.0

Coronary

0.3

0.4

0.8

1.0

Skin

0.5

1.5

1.9

0.6

Splanchnic

1.4

1.1

0.6

0.3

Renal

1.1

0.9

0.6

0.3

Other

0.6

0.4

0.4

0.1

Cerebral

0.8

0.8

0.8

0.8

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
This table summarises the changes in VO2, Q and regional blood flow in response to
exercise of progressive increasing intensity. Note the coupling of VO2 and Q increases,
the large increase in skeletal muscle blood flow, vasoconstriction in inactive vascular
beds and the biphasic response in skin blood flow.
The increase in skeletal muscle blood flow (hyperaemia) is a fundamental event to
enhance O2 delivery to contracting skeletal muscle. Factors mediating this are:

Metabolic vasodilators released form contracting skeletal muscle, endothelium and

the red blood cell ATP, adenosine, K+, ROS, NO
Muscle pump (also important in maintaining venous return)
Conducted vasodilation spread of vasodilation via smooth muscle gap junctions
Functional sympatholysis desensitization of sympathetic vasoconstrictor action by
metabolites.

In order to maintain MAP in the face of the vasodilation in active skeletal muscle, Q is
increased due to increased HR and SV, although SV tends to level off at higher
intensities, and vasoconstriction in inactive vascular beds. Systolic blood pressure
increases as cardiac output increases; diastolic blood pressure, reflects TPR, remains
relatively constant but may decrease at higher intensities as muscle blood flow
increases; mean arterial blood pressure increases slightly. The baroreflex still operates,
but is rest to a higher level to allow simultaneous increases in MAP and HR during
exercise.
During prolonged exercise, at a given exercise intensity, there is a progressive increase
in HR ("cardiovascular drift"), decrease in blood volume, SV and Q. Factors contributing
to cardiovascular drift:

Decreased SV due to increased HR and reduced blood volume

Hyperthermia
Dehydration
Peripheral displacement of blood volume due to initial cutaneous vasodilation.

The control of the cardiovascular system involves interplay of the parasympathetic and
sympathetic arms of the autonomic nervous system.

"Central command", linked to motor cortical activation of skeletal muscle, sets basic
pattern of effector activity. This is modulated by feedback from muscle chemosensors
and mechanoreceptors and the baroreceptors.
Parasympathetic (vagus) withdrawal increases HR. Increased sympathetic activity
increases HR, cardiac contractility, muscle sympathetic nerve activity and plasma
noradrenaline, adrenaline and renin activity, and decreases splanchnic and renal blood
flow.
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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
Cardiovascular adaptations to exercise training:

Reduced HR during exercise; maximal HR unchanged or lower

Increased SV during exercise and maximal SV
Expanded blood volume
Increased heart size due to increased LV mass and chamber size
Increased adrenergic sensitivity
Increased arterial diameter and compliance
Increased capillary density and recruitment.

Respiratory responses to exercise

The respiratory system functions during exercise to:

Maintain arterial O2 saturation

Increase CO2 removal
Maintain acid-base balance
Role in fluid and temperature balance?

Increased minute/alveolar ventilation:

VE = VT x f / VA = (VT VD) x f

The increase in ventilation during incremental exercise is characterized as a continuous,

exponential function or as exhibiting distinctive "thresholds" associated with VO2 and
VCO2. The so called "ventilatory thresholds" have been shown to correlate with
endurance performance as they set levels of exercise that can be tolerated without
major respiratory/ventilator distress.
Factors involved in the regulation of exercise hyperpnea (increased VE) include:

Motor cortical activation and muscle afferents (type III and IV, spindles?)
CO2 flux to the lung (chemoreceptor?)
Increased K+, H+, lactate?, catecholamines and body temperature
Lung and chest wall mechanoreflexes
No role for O2.

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
Pulmonary gas exchange ensures adequate arterial O2 saturation and removal of CO2,
even with large increases in pulmonary blood flow (Q). However, if inspired O2 is
reduced (e.g. at altitude) or if the pulmonary transit time is reduced due to large
increases in pulmonary blood flow, arterial O2 saturation may be challenged.

There are reports in the literature of arterial desaturation during near maximal exercise in
trained subjects this has implications for locomotor muscle fatigue and exercise
limitations. It is believed that the large, training-induced increase in maximal cardiac
output (pulmonary blood flow), in the absence of any changes in the pulmonary system,
results in reduced pulmonary transit time. The factors contributing to exercise-induced
arterial desaturation:

Pulmonary diffusion limitation (reduced transit time)

VA/Q inequality
Expiratory flow limitation and inadequate VE mechanical limitation?

Increasing inspired oxygen partial pressure prevents the decrease in arterial

O2 saturation and increases maximal oxygen uptake (see later).

Respiratory muscle work during exercise:

May increase to as much as 15% of VO2 and Q during strenuous exercise
Can result in diaphragmatic fatigue during intense exercise
Diaphragmatic fatigue associated with activation of respiratory muscle
chemoreflexes that result in sympathetically mediated vasoconstriction in active
limb skeletal muscle and fatigue
Potential benefits of respiratory muscle training for exercise performance?

Following endurance training, ventilation is lower during exercise at the same exercise
power output this is associated with lower blood K+, H+ and lactate and reduced
activation of muscle afferents.

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within

Maximal oxygen uptake

Maximal oxygen uptake (VO2 max) is the most widely recognized measure of cardiorespiratory fitness. Values vary according to interactions between the level of habitual
physical activity/training and genetic endowment the highest values are recorded in
well trained endurance athletes.

VO2 max represents the combined abilities of the respiratory and cardiovascular
systems to deliver oxygen to muscle and of the muscle to consume oxygen.
Measurements of the maximal mitochondrial oxidative capacity in muscle examined in
vitro with unlimited supply of oxygen and substrates suggest that it exceeds values
recorded for VO2 max (estimating the active muscle mass). This supports the contention
that VO2 max is limited by oxygen delivery to muscle.

During maximal exercise at sea level, the respiratory system is not thought to limit
VO2 max except in those subjects who have arterial desaturation during maximal
exercise in these subjects, VO2 max is increased by breathing hyperoxic (~26% O2)
gas mixtures. Thus, most attention has focused on maximal cardiac output and
locomotor blood flow and muscle diffusing capacity as the major determinants of
oxygen delivery. Strategies to increase central blood volume (e.g. plasma volume
expanders) and total red cell mass (e.g. blood doping, EPO administration, altitude
training) have been effective in increasing VO2 max. In recent years, there has also been
discussion of the importance of the CNS and motor drive and neuromuscular
recruitment.

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
Physiological determinants of VO2 max:

CNS and motor drive

Respiration VE, VA/Q, pulmonary diffusing capacity
Circulation [Hb], MAP, Q (HR & SV), muscle blood flow, capillary density, muscle
diffusing capacity
Skeletal muscle mass, mitochondrial density & oxidative potential, [Mb], substrate
availability.

Abbreviations
ADP

adenosine diphosphate

AMP

adenosine monophosphate

ATP

adenosine triphosphate

C aO 2

arterial blood oxygen content

C vO 2

mixed venous blood oxygen content

CHO

carbohydrate

CP (PCr) creatine phosphate (phosphocreatine)

Cr

creatine

DL

diffusing capacity of the lung

DM

diffusing capacity of the muscle

DO2

diffusing capacity for oxygen

EPO

erythropoietin

breathing frequency (breaths per minute)

FFA

free fatty acid

FT

fast twitch fibre

GLUT4

glucose transporter isoform 4

Hb

haemoglobin

HbO2

oxyhaemoglobin

HR

heart rate

LV

left ventricle/ventricular

MAP

mean arterial pressure

Mb

myoglobin

MbO2

oxymyoglobin

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Oxygen study guide

Exercise Physiology:
Understanding the Athlete Within
Understanding the Athlete Within
NO

nitric oxide

P AO 2

alveolar oxygen partial pressure

P aO 2

arterial oxygen blood partial pressure

P vO 2

mixed venous blood partial pressure

P-O

ratio of ATP production per unit of oxygen consumption

Q/QT

cardiac output (product of HR and SV)

ROS

reactive oxygen species

ST

slow twitch fibre

SV

stroke volume

TPR

total peripheral resistance

VA

alveolar ventilation (accounts for dead space)

VD

dead space volume (go gas exchange in this space)

VE

minute ventilation

VCO2

carbon dioxide production

VO2

oxygen consumption

VT

tidal volume

Image credits
1.
2.
3.
4.
5.
6.

7.

muscle glycogen - The University of Melbourne

O2 image - N/A - Lecture's own material
Exercise time graph - Figure 1 from Hughson RL. Tschakovsky ME. Houston ME Regulation of
oxygen consumption at the onsent of exercise. Exc. Sport Science Review, 2001, 29 (3), 129-133,
Reproduced with permission to Lippincott Williams & Wilkins
Ventalation graph - B.D. Johnson et al. J. Physiol 460: 385-405, 1993 (with permission, Wiley)
PAO2 graph - J.A. Dempsey et al. Resp. Physiol. & Neurobiol. 151: 242-250, 2006 (with
permission, Wiley)
Exercise Power graph - B. Saltin & PO Astrand. Maximal oxygen uptake. J Appl Physiol
September 1967 23: 353-358. Reproduced with permission from the American Physiological
Society
O2 Delivery graph - R. Boushel et al. Mitochondrion 11: 303-307, 2011 (with permission, Elsevier)

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