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Exercise Physiology:
Understanding the Athlete Within

Key concepts

The energy systems responsible for ATP generation during exercise are high energy
phosphates, glycolysis and oxidative metabolism

The relative ATP generating power and capacity of these energy systems are
inversely related

During high intensity exercise, rest-exercise transitions and prolonged endurance


exercise, the contribution of the energy systems is determined by exercise intensity
and duration

The relative importance of CHO and fat for oxidative metabolism is determined
primarily by exercise intensity and duration, with training status, preceding diet,
environmental temperature, sex and age exerting modifying influences.

Muscle glycogen and blood-borne glucose are major CHO fuels for contracting
skeletal muscle

Muscle glycogenolysis, muscle glucose uptake, CHO oxidation and liver glucose
output during exercise are influenced by intensity and duration

Muscle glycogenolysis is regulated by local and hormonal factors

Muscle glucose uptake is regulated at several steps, but increased blood flow and
GLUT4 translocation reduce delivery and sarcolemmal transport as barriers

Liver glucose output is subject to multiple, redundant controls

The interaction of pyruvate oxidation and lactate production and the importance of
PDH activity in determining rate of CHO oxidation

Training reduces reliance on CHO as fuel source mechanisms include increased


mitochondrial density and changes in hormones.

Free fatty acids (FFA) derived from adipose tissue and muscle triglycerides are the
major lipid substrate for contracting skeletal muscle

Key lipases (ATGL and HSL) break down adipose tissue and muscle triglycerides

Muscle takes up FFA via both simple and facilitated diffusion, the latter mediated
transport proteins

FFA availability, FFA transport capacity and muscle oxidative capacity are the major
determinants of fat oxidation

Training increases lipid oxidation both FFA uptake and oxidation and muscle
triglyceride utilisation.

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Exercise Physiology:
Understanding the Athlete Within

Overview of exercise metabolism


The energy systems in skeletal muscle are:

high energy phosphates


anaerobic glycolysis (glucose lactate)
oxidative metabolism of CHO and fat (with only a very minor contribution from
protein).

Substrate level phosphorylayion


PCr + ADP + H+ ATP + creatine (catalysed by creatine kinase)
2ADP ATP + AMP (catalysed by adenylate kinase)
Glycogen + 3ADP + 3Pi 2Lactate + H+ + 3ATP (glycolysis)

Oxidative phosphorylation requires O2, ADP and Pi, and electron donors (NADH,
FADH2) produced from CHO and fat metabolism
Glucose + 6O2 + 36ADP 6CO2 + 6H2O + 36ATP
Palmitate + 23O2 + 130ADP 16CO2 + 16H2O + 130ATP

The respiratory exchange ratio (RER = VCO2/VO2) can be calculated from pulmonary
gas exchange measurements of oxygen uptake (VO2) and carbon dioxide production
(VCO2) to estimate the contribution of CHO and fat to oxidative metabolism:
RER = 1.0 = 100% CHO (6CO2/6O2)
RER = 0.7 = 100% fat (16CO2/23O2)
The power of an energy system is the rate of ATP generation; the capacity is the total
amount of ATP that can be produced the two parameters are inversely related:
Power: PCr > Glycolysis > CHO oxidation > fat oxidation
Capacity: fat oxidation > CHO oxidation > Glycolysis > PCr
During the transition from rest to exercise, and from low intensity exercise to higher
intensity, there is a lag in oxygen uptake (oxygen deficit) during this period the energy
deficit is covered by PCr breakdown and glycolysis.

During high intensity, short duration ("sprint") exercise, the major energy systems are
PCr and glycolysis, with a progressive rise in oxidative metabolism of glycogen.

Refer to Figure 7a in the article by Michelle L. Parolin, Alan Chesley, Mark P. Matsos,
Lawrence L. Spriet, Norman L. Jones, and George J. F. Heigenhauser. Regulation of
skeletal muscle glycogen phosphorylase and PDH during maximal intermittent
exercise Am J Physiol Endocrinol Metab November 1, 1999 277:E890-E900:

http://ajpendo.physiology.org/content/277/5/E890.long

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Exercise Physiology:
Understanding the Athlete Within

During more prolonged, submaximal exercise, the major fuels for oxidative metabolism
are muscle glycogen, blood glucose (derived from liver glycogen and gluconeogenesis,
and the gut when glucose is ingested), and fatty acids derived from triglycerides stored
in the muscle and adipose tissue.

The relative contribution of CHO and fat is primarily determined by exercise intensity
and duration.

Refer to Figure 8 in the article by J. A. Romijn, E. F. Coyle, L. S. Sidossis, A. Gastaldelli,


J. F. Horowitz, E. Endert, and R. R. Wolfe. Regulation of endogenous fat and
carbohydrate metabolism in relation to exercise intensity and duration Am J Physiol
Endocrinol Metab September 1, 1993 265:E380-E391

http://ajpendo.physiology.org/content/265/3/E380.reprint

Unless otherwise indicated, this material is The University of Melbourne. You may save,
print or download this material solely for your own information, research or study.

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Exercise Physiology:
Understanding the Athlete Within

Refer to Figure 3 in the article by Damien J. Angus, Mark A. Febbraio, and Mark
Hargreaves Plasma glucose kinetics during prolonged exercise in trained humans when
fed carbohydrate Am J Physiol Endocrinol Metab September 1, 2002 283:E573-E577

http://ajpendo.physiology.org/content/283/3/E573.long

Factors influencing substrate metabolism during exercise:

Exercise intensity
Exercise duration
Training status
Preceding diet
Environmental temperature
Sex
Age.

These effects are mediated by substrate availability, hormone levels and the
biochemical characteristics of skeletal muscle.

CHO metabolism during exercise


Muscle glycogen and blood-borne glucose (derived from liver glycogen and
gluconeogenesis, and the gut when glucose is ingested) are the key CHO substrates
utilized during exercise. Lactate, a breakdown product of glycolysis (derived from
glycogen and glucose), is a substrate for oxidation within skeletal muscle, as well as for
gluconeogenesis in the liver. Again, the major determinants of the rates of muscle
glycogen use and glucose uptake are exercise intensity and duration.
Muscle glycogenolysis (breakdown) is catalysed by the enzyme glycogen phosphorylase
which is regulated by local factors within the contracting skeletal muscle and the
circulating hormone adrenaline.

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Exercise Physiology:
Understanding the Athlete Within

Regulation of muscle glycogenolysis during exercise:

Calcium
Inorganic phosphate
Circulating adrenaline
Muscle [glycogen]
Blood FFA availability
Temperature.

Following endurance training, muscle glycogen use is reduced lower aerobic utilization
and lactate production.
Major sites of regulation of glucose uptake during exercise:

Delivery blood flow and [glucose]


Sarcolemmal glucose transport GLUT4 translocation, glucose gradient
Metabolism activation of glycolytic and oxidative enzymes.

Increased muscle blood flow and rapid GLUT4 translocation during exercise, essentially
remove delivery and transport as limiting factors.
Regulation of muscle glucose uptake during exercise:

Increased muscle blood flow and glucose delivery


GLUT4 translocation to sarcolemma (and t-tubules)
Increased glucose disposal notably increased hexokinase activity
Blood [glucose]
FFA availability? "glucose fatty acid cycle"
Muscle [glycogen]
Insulin (additive to exercise)
Adrenaline?

Contraction signalling to glucose transport (GLUT4 translocation) during exercise:

Calcium CaMKII, PKC


AMPK
Nitric oxide
Reactive oxygen species.

Following endurance training, glucose uptake and oxidation by skeletal muscle are
reduced.
The pattern of liver glucose output during exercise is very similar to that of muscle
glucose uptake, being influenced by both exercise intensity and duration. Most of the
glucose output is derived from liver glycogenolysis as exercise duration increases,
there is a greater contribution from gluconeogenesis.

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Exercise Physiology:
Understanding the Athlete Within
Regulation of liver glucose output during exercise:

Feedforward and feedback mechanisms


Decreased insulin
Increased glucagon
Increased adrenaline
Sympathetic nerves?
Liver [glycogen]
Blood [glucose].

The rate of carbohydrate oxidation during exercise is related to the activity of the
pyruvate dehydrogenase enzyme complex its activation is related to exercise intensity
and duration.
Muscle and blood lactate increase exponentially during exercise of increasing intensity.
Regulation of lactate metabolism during exercise:

Production is determined by the balance between rates of pyruvate formation and


oxidation
Blood lactate levels are determined by the rates of lactate production and clearance
Muscle oxidative capacity
LDH isoenzyme profile
Oxygen supply to contracting skeletal muscle
Adrenaline
Muscle [glycogen].

Fat metabolism during exercise


Fatty acids, derived from adipose tissue triglycerides and transported in the plasma
bound to albumin and from intramuscular triglycerides, are the key fat substrates for
contracting skeletal muscle during exercise. Fatty acids from triglycerides within
circulating chylomicrons and very low density lipoproteins only contribute to a very small
extent.
Initially, the intramuscular triglycerides are utilized and there is a progressive increase in
plasma fatty acid oxidation if the mobilization of fatty acids into the blood is inhibited,
there is a greater reliance on intramuscular triglycerides.
Glycerol is released into the circulation from both adipose tissue and contracting
skeletal muscle and is often used as a measure of overall lipolysis.
Triglycerides are broken down by lipases that are generally specific for triglycerides
(adipose triglyceride lipase ATGL), diglycerides (hormone sensitive lipase HSL) and
monoglycerides (monoglyceride lipase MGL). Both ATGL and HSL are regulated by
phosphorylation.

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Exercise Physiology:
Understanding the Athlete Within
Regulation of adipose tissue lipolysis during exercise:

Mediated by ATGL and HSL


-adrenergic stimulation
Decreased plasma insulin
Adipose tissue blood flow
FFA/albumin ratio
Blood [glucose] and [lactate]
Caffeine.

Regulation of skeletal muscle lipolysis during exercise:

Mediated by ATGL and HSL


-adrenergic stimulation (via PKA)
Calcium via ERK
Blood [glucose]
Plasma FFA availability.

For many years it was thought that fatty acid uptake into contracting skeletal muscle
occurred by simple diffusion; however, it has become clear that there is a major
component that occurs by facilitated diffusion, mediated via a number of fatty acid
transporters.
Determinants of skeletal muscle fatty acid uptake during exercise:

Arterial plasma [FFA]


Ability of muscle to oxidise fatty acids
Sarcolemmal, cytosolic and mitochondrial fatty acid transporters (FABP, FAT/CD36,
FATP)
Carnitine and CPT activity
-oxidative capacity mitochondrial density and HAD activity.

Carnitine is critical for the transport of long chain fatty acids into the mitochondria and
interacts with the enzymes CPT and CAT. There is also evidence that the fatty acid
transporter FAT/CD36 is also involved in the mitochondrial uptake of fatty acids.
Medium chain triglycerides (MCTs) do not rely on the carnitine-CPT system and can be
taken up directly by the mitochondria for this reason there has been interest in
including MCTs in sports supplements to enhance fat oxidation, although results are
equivocal and they can cause gastrointestinal distress at higher concentrations.
Carnitine is at the "crossroads" of CHO and fat metabolism and can act as a buffer for
acetyl units generated during high rates of carbohydrate breakdown, resulting in
increased acetylcarnitine and reduced free carnitine this is one potential explanation
for the reduction in fat oxidation at higher exercise intensities when there is a greater
reliance on CHO.
Why is fat oxidation reduced with increasing exercise intensity?

Reduced plasma fatty acid availability associated with reduced adipose tissue
blood flow which impairs fatty acid mobilization
Increased glycolytic flux inhibits CPT activity and mitochondrial fatty acid uptake
due to increased malony-CoA and decreased pH
Reduced carnitine availability
Oxidation of CHO requires less oxygen for given ATP production.

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Exercise Physiology:
Understanding the Athlete Within
Following endurance training, there is increased fat oxidation both plasma FFA and
intramuscular triglyceride oxidation are increased. Muscle adaptations that facilitate
increased fat oxidation include:

Increased mitochondrial density and HAD activity


Increased expression of sarcolemmal, cytosolic and mitochondrial fatty acid
transporters
Increased CPT activity.

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print or download this material solely for your own information, research or study.

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Exercise Physiology:
Understanding the Athlete Within

Abbreviations
ADP

adenosine diphosphate

AMP

adenosine monophosphate

AMPK

AMP-activated protein kinase

ATGL

adipose triglyceride lipase

ATP

adenosine triphosphate

CaMKII

calcium/calmodulin-dependent kinase II

CAT

carnitine acyltranferase

CHO

carbohydrate

CoA

co-enzyme A

CP (PCr)

creatine phosphate (phosphocreatine)

CPT

carnitine palmitoyltransferase

Cr

creatine

ERK

extracellular signal-regulated kinase

ETC

electron transport chain

FABPc

fatty acid binding protein (cytosolic)

FADH2

flavin adenine dinucleotide

FAT/CD36 fatty acid transporter


FATP

fatty acid transport protein

FFA

free fatty acid

FT

fast twitch fibre

G-1-P

glucose-1-phosphate

G-6-P

glucose-6-phosphate

GLUT4

glucose transporter isoform 4

Gly

glycogen

GLY

glycogenolysis

GNG

gluconeogenesis

HAD

-hydroxy acyl-CoA dehydrogenase

HSL

hormone sensitive lipase

IM

inner mitochondrial membrane

IMTG

intramyocellular triglyceride

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Exercise Physiology:
Understanding the Athlete Within
LDH

lactate dehydrogenase

LFA

long chain fatty acid

LT

lactate threshold

MCT

monocarboxylate transporter

NAD

oxidised nicotinamide adenine dinucleotide

NADH

reduced nicotinamide adenine dinucleotide

NO

nitric oxide

OM

outer mitochondrial membrane

PDC

pyruvate dehydrogenase complex

PDH

pyruvate dehydrogenase

PKA

protein kinase A

PKC

protein kinase C

PM

plasma membrane

Rd

rate of disappearance/disposal

Rox

rate of oxidation

ROS

reactive oxygen species

SR

sarcoplasmic reticulum

ST

slow twitch fibre

TCA

tricarboxylic acid

TG

triglyceride/triacylglycerol

Image credits
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6.

Graph- ATP turnover vs. Time - Figure 7a in the article by Michelle L. Parolin, Alan Chesley, Mark
P. Matsos, Lawrence L. Spriet, Norman L. Jones, and George J. F. Heigenhauser. Regulation of
skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise Am J
Physiol Endocrinol Metab November 1, 1999 277:E890-E900:
liver glycogen - The University of Melbourne
adipose tissue - The University of Melbourne
muscle glycogen - The University of Melbourne
Graph- cal kg vs. % VO2 max - Figure 8 in the article by J. A. Romijn, E. F. Coyle, L. S. Sidossis,
A. Gastaldelli, J. F. Horowitz, E. Endert, and R. R. Wolfe. Regulation of endogenous fat and
carbohydrate metabolism in relation to exercise intensity and duration Am J Physiol Endocrinol
Metab September 1, 1993 265:E380-E391
Graph- % energy vs. % time - Figure 3 in the article by Damien J. Angus, Mark A. Febbraio, and
Mark Hargreaves Plasma glucose kinetics during prolonged exercise in trained humans when fed
carbohydrate Am J Physiol Endocrinol Metab September 1, 2002 283:E573-E577

Unless otherwise indicated, this material is The University of Melbourne. You may save,
print or download this material solely for your own information, research or study.

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