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Review Article
Interaction among Skeletal Muscle Metabolic Energy Systems
during Intense Exercise
Julien S. Baker,1 Marie Clare McCormick,1 and Robert A. Robergs2
1
Health and Exercise Science Research Laboratory, School of Science, University of the West of Scotland, Hamilton Campus,
Almada Street, Hamilton ML3 0JB, UK
2 School of Human Movement Studies, Charles Sturt University, Bathurst, NSW 2795, Australia
Correspondence should be addressed to Julien S. Baker, julien.baker@uws.ac.uk
Received 15 July 2010; Revised 5 October 2010; Accepted 7 October 2010
Academic Editor: Michael M. Muller
Copyright 2010 Julien S. Baker et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
High-intensity exercise can result in up to a 1,000-fold increase in the rate of ATP demand compared to that at rest (Newsholme
et al., 1983). To sustain muscle contraction, ATP needs to be regenerated at a rate complementary to ATP demand. Three
energy systems function to replenish ATP in muscle: (1) Phosphagen, (2) Glycolytic, and (3) Mitochondrial Respiration. The
three systems dier in the substrates used, products, maximal rate of ATP regeneration, capacity of ATP regeneration, and
their associated contributions to fatigue. In this exercise context, fatigue is best defined as a decreasing force production during
muscle contraction despite constant or increasing eort. The replenishment of ATP during intense exercise is the result of a
coordinated metabolic response in which all energy systems contribute to dierent degrees based on an interaction between the
intensity and duration of the exercise, and consequently the proportional contribution of the dierent skeletal muscle motor
units. Such relative contributions also determine to a large extent the involvement of specific metabolic and central nervous system
events that contribute to fatigue. The purpose of this paper is to provide a contemporary explanation of the muscle metabolic
response to dierent exercise intensities and durations, with emphasis given to recent improvements in understanding and research
methodology.
1. Introduction
Muscle contraction and, therefore, all exercise are dependent
on the breakdown of adenosine triphosphate (ATP) and
the concomitant release of free energy (1). This free energy
release is coupled to the energy requirements of cell work, of
which muscle contraction is just one example
ATPase
as glycogen and triacylglycerols, and more importantly, having a sensitive control system to rapidly increase metabolism
during times of energy (ATP) demand. Muscle tissue is
unique in that it can vary its metabolic rate to a greater extent
than any other tissue depending on the demands placed
upon it [1]. The study of bioenergetics provides a rationale
explanation for this scenario, where the concentrations of
muscle ATP, ADP, AMP, and Pi during rest conditions are
optimal for supporting free energy transfer to and from ATP.
All cells function to maintain the resting condition
adenylate metabolite concentrations as best as possible in the
face of increasing ATP demand. The best example of this trait
of cellular energy metabolism is the relatively stable muscle
ATP concentration despite more than a 1,000-fold increase
in ATP demand, which can occur during short-term intense
exercise (Figure 1). For example, muscle ATP decreases by
only 1 to 2 mmol/kg wet wt during these conditions, and
even with involuntary maximal contraction to contractile
failure, muscle ATP does not get lower than 5 mmol/kg wet
wt [2]. In short, the muscle ATP concentration is not an
energy store, but collectively with each of ADP, AMP, and
Pi is an essential requirement for optimal cell function.
Furthermore, any reduction in muscle ATP coincides with
cellular conditions associated with the rapid development of
fatigue, defined as a reduction in the ability of a muscle to
produce force or power, or a reduction in ATP turnover of
skeletal muscle [3, 4]. Fatigue is vital to the physiological
function of the human body as it prevents ATP falling to such
low levels that could cause muscle rigor or irreversible muscle
damage [59].
How then can cells detect, rapidly respond to, and
successfully meet sudden increases in ATP demand? The
answers lie in an understanding of the systems by which cells
regenerate ATP. There are three major energy systems which
are responsible for the resynthesis of ATP (Figure 2). These
systems can be categorised as follows: (1) The Phosphagen
System, (2) The Glycolytic System, and (3) Mitochondrial
Respiration.
The purpose of this paper is to re-explain the simultaneous and coordinated contributions of all energy systems
to meet muscle ATP demand during dierent intensities and
durations of exercise. It is important to provide a contemporary perspective of muscle metabolism given recent advances
in understanding of energy system interaction, novel findings
from advanced technologies such as magnetic resonance
spectroscopy (MRS), and consensus from current debates
on the biochemistry and cellular implications of metabolic
acidosis.
(2)
AMP deaminase
3
35
Increasing
fatigue
1.25
30
Creatine phosphate
(mmol/L muscle water)
1.5
1
0.75
0.5
0.25
25
20
15
10
5
0
0
0.5
1.5
Time (min)
2.5
0.5
2.5
(b)
30
11
25
Inorganic phosphate
(mmol/L muscle water)
(a)
1.5
Time (min)
20
15
10
5
7
5
3
1
0
0
0.5
1.5
Time (min)
2.5
(c)
0.5
1.5
Time (min)
2.5
(d)
Figure 1: Stack plots of the change in (a) ATP turnover and key phosphagen system metabolites during 3 minutes of intense exercise to
volitional exhaustion. (b) Creatine phosphate, (c) inorganic phosphate, and (d) ATP. Note the well maintained preservation of muscle ATP
for most of the duration of the exercise bout.
Glycogen + HPi
Glycolytic
ATP
G1P
Fatty acids
ADP
G6P
Pyruvate
2 HPi + 3 ADP
Acetyl CoA
3 ATP
TCA
cycle
Phosphagen
ATP + HPi
CrP + ADP + H+
ADP + ADP
AMP + H+
ATP + AMP
IMP + NH4 +
ADP + HPi
e H+
ATP
O + 2H+ + 2e
Mitochondrial respiration
H2O
Acetyl CoA
-ketoglutarate
TCA
cycle
Mitochondrial matrix
NH4 +
Bicarbonate (HCO3 )
2 ATP
Aspartate
2 ADP
Carbamoyl phosphate
Pi
Citrulline
ATP
Cytosol
Ornithine
2 Pi
Urea cycle
AMP
Argininosuccinate
Arginine
Fumarate
Figure 3: The urea cycle of the liver, showing the connections between the TCA cycle in the mitochondria, ammonia, and the production
of urea. Note that the conversion of glutamate to -ketoglutarate (top central region of figure) is condensed for clarity (oxaloacetate +
glutamate -ketoglutarate + aspartate [aspartate aminotransferase]) and is therefore also a source of aspartate. The direct conversion of
glutamate to -ketoglutarate is catalyzed by glutamate dehydrogenase.
Mitochondrial
fat
5
4
Energy systems
3
2
Mitochondrial
CHO
Glycolytic
Phosphagen
0
0
0.5
1.5
Time (min)
2.5
0.5
1
1.5
2
ATP turnover rate (mmol/kg/s)
2.5
5
CrP
27
24
ATP
21
18
HPi
Rest
15
12
9
6
3
Exercise
30
Intense exercise
0
10 12 14 16
Time (min)
18 20 22 24
Exhaustion
6
only slightly increased further to 85.5 3.5%. Mathematical
models predicted that CrP resynthesis would not reach even
95% of resting value until 13.6 minutes after exercise. More
recently Forbes et al. [31] studied CrP recovery kinetics in
humans and in rats using 31 P MRS. They found that in the
majority of humans there was indeed an initial fast recovery
component in skeletal muscle following intense exercise.
Nevertheless the evidence for the biphasic nature of CrP
recovery is not conclusive. Although it seems unlikely that
after intense exercise the model of recovery will follow a
monoexponential pattern, it could be that a biphasic model
may not be adequate to describe the resynthesis pattern.
Advances in technology (e.g., 31 P MRS) have shown that even
in the first 3s of recovery the slope was significantly dierent
to the slope in the first 0.5 s (P = .001) [32]. This suggests
that there could be more than 2 distinct phases in the CrP
recovery process.
There is conflicting evidence in the literature over
the importance of oxygen during the resynthesis of CrP
following high-intensity exercise. A number of studies have
looked at recovery of muscle following high intensity exercise
under ischaemic conditions. Sahlin and colleagues [25] and
Harris and his coworkers [30] have found these conditions
to substantially suppress the resynthesis of CrP. This therefore suggests that CrP resynthesis is reliant on oxidative
metabolism [30, 33, 34]. However, Crowther and colleagues
[35] found that following high-intensity exercise under
ischaemic conditions, glycolytic flux remained elevated for
a short period of time; it remained high for 3 seconds and
had decreased to baseline levels within 20 seconds. If this
was the case and glycolytic ATP production was making
a considerable contribution to energy supply during the
recovery phase, then an initial fast phase of CrP recovery
would be expected immediately following the cessation of
high-intensity exercise. This ties in with the work discussed
previously. Work done by Forbes et al. [31] also suggests
that glycolytic ATP production may have contributed the CrP
resynthesis during the initial fast phase of recovery following
high-intensity exercise. If CrP is only partially restored
during the recovery phase, this can lead to a compromised
performance in subsequent exercise bouts, for example, a
decrease in power output.
3. Glycolysis
When exercise continues longer than for a few seconds,
the energy to regenerate ATP is increasingly derived from
blood glucose and muscle glycogen stores [36]. This near
immediate activation of carbohydrate oxidation after the
onset of exercise [37] is caused by the production of AMP,
the increases in intramuscular free calcium and inorganic
phosphate (both increase the rate of the phosphorylase
reaction as calcium is an activator of phosphorylate and
inorganic phosphate is a substrate), and the near spontaneous increase in blood glucose uptake into muscle caused
by muscle contraction. The increased rate of glucose6-phosphate (G6 P) production from glycogenolysis and
increased glucose uptake provides a rapid source of fuel for
Glycogen
Pi
Phosphorylase Glucose
Glucose-1-phosphate
Hexokinase ATP
Phase 1
ADP + H+
Glucose-6-phosphate
Phosphoglucomutase
Phosphoglucose
isomerase
Fructose-6-phosphate
Phosphofructokinase
ATP
(PFK)
ADP + H+
Fructose-1,6-bisphosphate
Aldolase
Phase 2
Glyceraldehyde-3-phosphate + dihydroxyacetone phosphate
Pi
NAD+
Glyceraldehyde-3-phosphate
Pi
Glyceraldehyde-3-phosphate
NAD+
dehydrogenase
NADH + H+
1,3-bisphosphoglycerate
1,3-bisphosphoglycerate
ADP
ADP
Phosphoglycerate kinase
ATP
ATP
3-Phosphoglycerate
3-Phosphoglycerate
NADH + H+
Phosphoglycerate mutase
2-Phosphoglycerate
H2O
2-Phosphoglycerate
Enolase
H2O
Phosphoenolpyruvate
Phosphoenolpyruvate
ADP
ADP
Pyruvate kinase
ATP
ATP
Pyruvate
Pyruvate
Figure 8: The glycolytic pathway. Note the duplication of phase 2 3-carbon metabolite reactions to account for the 6 carbons of each
metabolite from phase 1.
40
H H
C
Phosphagen
35
30
25
Glycolytic
O
+
H-C-H
20
Mitochondrial respiration
+ H+
Adenine
15
Pyruvate
10
NH 2
NADH
Lactate dehydrogenase
10
20
30
40
50 60
Time (s)
70
80
90
100
C
NH2
C
HO
H
+
H-C-H
Adenine
H
Lactate
NAD+
2 lactate + 2 NAD+
2 NAD+ +
Glucose + 2 Pi + 2 ADP
2 Pyruvate + 2 NADH + 2 H+
+ 2 ATP + 2H2O
Cell work
2 Pi + 2 ADP
+ 2 H+
2 ATP + 2H2O
Figure 11: The changes and cycling of substrates, products, and protons during the glycolytic-lactate energy system. Adapted from Robergs
et al. [45].
Glycogen
2
Glucose
ATP
ADP
NAD+
2 NADH + H+
3 ADP
3 ATP
2 Pyruvate
Glycolysis
Cytosol
NAD+
2 CO2
Mitochondrial matrix
2 NADH + H+
2 acetyl CoA
NADH + H+
2 citrate
NAD+
2H2O
2 oxaloacetate
FADH2
2H2O
2 NADH + H+
FAD+
2 NAD+
TCA
cycle
2 NAD+
2 NADH + H+
2H2O
2 NAD+
n 1/2 O2 + ne + nH+
2 FADH2
2 FAD+
nH2 O
2 NADH +
H+
2 CO2
2 -ketoglutarate
2 CO2
2 GTP 2 GDP + 2 Pi
Mitochondrial respiration
Figure 12: The biochemical connections between the cytosol and mitochondria of skeletal muscle for the complete oxidation of
carbohydrate. Note that the TCA cycle as shown is not complete for all substrates and products. Also, the ATP yield from carbohydrate
oxidation is greater for the substrate glycogen than glucose. For skeletal muscle, there are 37 molecules of ATP produced from one Glucose6-phosphate derived from glycogen, assuming the presence of the glycerol-3-phosphate shuttle.
6. Mitochondrial Respiration
The resynthesis of ATP by mitochondrial respiration occurs
in mitochondria and involves the combustion of fuel in the
presence of sucient oxygen. The fuel can be obtained from
sources within the muscle (free fatty acids and glycogen),
and outside the muscle (blood free fatty acids [from adipose
tissue], and blood glucose [from dietary ingestion or the
liver]).
We will comment on the reactions involved in mitochondrial respiration structured by the source of substrate.
10
O
R C Fatty-acyl Co-A
S-coenzyme A
CAT II
Carnitine
Carnitine
O
SH-coenzyme A
R C
R C
Carnitine
Carnitine
SH-coenzyme A
Matrix
CAT I
Intermembranous space
Figure 13: Transport of long chain (>15 carbons) fatty acyl CoA molecules into the mitochondria via the carnitine shuttle.
S-Co-A
7 SH-Co-A
C
H2C
O
H3C
1
CH2
H2C
H3C
H3C
O
C
CH2
3
CH2
H2C
H3C
H3C
O
C
H3C
O
C
H3C
4
CH2
H2C
5
CH2
H2C
CH2
H2C
O
2
H2C
CH2
H3C
H3C
S-Co-A
O
Palmitoyl CoA
CO2
TCA
cycle
ADP + Pi
ATP
1/2 O2 + 2H+ + 2e
H2O
Figure 14: The sequential degrading of fatty acyl CoA molecules, as occurs in the -oxidation pathway, within the mitochondria.
11
Cytosol
NADH
Dihydroxyacetone
phosphate
NAD+
FADH2
FAD+
Glycerol-3-phosphate
Mitochondrion
(4)
tion. When cytosolic NADH transported by the glycerol-3phosphate shuttle is oxidised by the respiratory chain 1.5 ATP
is produced, rather than 2.5 ATP. This is due to FAD, not
NAD+, being the electron acceptor. FAD allows NADH to be
transported into the mitochondria against a concentration
gradient; this occurs at a cost of 1ATP molecule per 2
electrons [17]. The higher ATP yield means that for a given
rate of ATP regeneration there would be less demand for
oxygen consumption. In addition, such ATP regeneration
occurs with a higher CO2 production, explaining the lower
respiratory exchange ratio (RER) during exercise for a greater
reliance on lipid than carbohydrate oxidation.
6.3. Amino Acid Oxidation. Muscle has an available supply of
amino acids for use in catabolism, and these comprise what
is known as the free amino acid pool. However, continued
muscle contraction, especially when carbohydrate supply
and/or provision is inadequate, requires protein catabolism
to sustain free amino acids. Thus, prolonged exercise in
times of poor carbohydrate nutrition increases protein
breakdown and amino acid oxidation. Intense exercise also
increases amino acid oxidation, but involves negligible
protein catabolism due to the short-term nature of intense
exercise.
7. Conclusions
The interaction and relative contribution of the 3 energy
systems during incremental exercise and periods of maximal exhaustive exercise are of considerable theoretical and
practical interest. The energy systems respond dierently
in relation to the high, often sustained and usually diverse
energy demands placed on them during daily and sporting
activities. Analysis of the current literature suggests that
virtually all physical activities derive some energy from each
of the 3 energy-supplying processes. There is no doubt that
each system is best suited to providing energy for a dierent
type of event or activity, yet this does not imply exclusivity.
Similarly, the energy systems contribute sequentially but in
an overlapping fashion to the energy demands of exercise.
The anaerobic (nonmitochondrial) system is capable of
responding immediately to the energy demands of exercise
and is able to support extremely high muscle force application and power outputs. Unfortunately the anaerobic system
is limited in its capacity, such that either a cessation of
work or a reduction in power output to a level that can be
met by aerobic metabolism is seen during extended periods
of intense exercise. The aerobic energy system responds
surprisingly quickly to the demands of intense exercise, yet
due to a relatively low rate of ATP turnover, is incapable of
meeting the energy demands at the beginning of exercise,
irrespective of the exercise intensity, or intense exercise.
Nevertheless, it now seems evident that the aerobic system
plays a significant role in determining performance during
high-intensity exercise, with a maximal exercise eort of
75 seconds deriving approximately equal energy from the
aerobic and anaerobic energy systems.
12
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