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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
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 glucose uptake is regulated at several steps, but increased blood flow and
GLUT4 translocation reduce delivery and sarcolemmal transport as barriers
The interaction of pyruvate oxidation and lactate production and the importance of
PDH activity in determining rate of CHO oxidation
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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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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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.
http://ajpendo.physiology.org/content/265/3/E380.reprint
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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
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.
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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:
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:
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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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:
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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:
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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Abbreviations
ADP
adenosine diphosphate
AMP
adenosine monophosphate
AMPK
ATGL
ATP
adenosine triphosphate
CaMKII
calcium/calmodulin-dependent kinase II
CAT
carnitine acyltranferase
CHO
carbohydrate
CoA
co-enzyme A
CP (PCr)
CPT
carnitine palmitoyltransferase
Cr
creatine
ERK
ETC
FABPc
FADH2
FFA
FT
G-1-P
glucose-1-phosphate
G-6-P
glucose-6-phosphate
GLUT4
Gly
glycogen
GLY
glycogenolysis
GNG
gluconeogenesis
HAD
HSL
IM
IMTG
intramyocellular triglyceride
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lactate dehydrogenase
LFA
LT
lactate threshold
MCT
monocarboxylate transporter
NAD
NADH
NO
nitric oxide
OM
PDC
PDH
pyruvate dehydrogenase
PKA
protein kinase A
PKC
protein kinase C
PM
plasma membrane
Rd
rate of disappearance/disposal
Rox
rate of oxidation
ROS
SR
sarcoplasmic reticulum
ST
TCA
tricarboxylic acid
TG
triglyceride/triacylglycerol
Image credits
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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
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