Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

V. Exercise and Adaptations to Training
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slow, a reversal of contractile properties occurs—that is,
fast-twitch muscles become slow, and slow-twitch muscles
become fast. Accompanying this is a corresponding
change in the enzyme histochemical profiles of the myofibers.
Therefore, the motor neuron influences (1) the type
of energy metabolism employed by a myofiber and all the
structural changes in fiber organelles that this implies and
(2) the myofiber’s physiological properties of contraction.
More recent cross-innervation studies, however, demonstrate
that the embryogenic determination of muscle fiber types
provides an inherent bias toward an original phenotype.
Transplantation of myoblasts from cat jaw muscles (type
2 m fibers) into the fast-twitch extensor digitorum limb muscle
results in expression of their 2 m myosin isoform even
when enervated by the extensor digitorum nerve ( Hoh and
Hughes, 1988 ). Conversely, when jaw muscle myoblasts are
transplanted into the slow-twitch soleus muscle, the soleus
nerve can override type 2 m expression and switch fibers to
myosin heavy chain type 1 expression. Taken together, these
studies suggest that muscle fiber type is determined by competitive
interactions between endogenous programming and
exogenous cues from motor neurons that require continual
reinforcement ( Rubenstein and Kelly, 2004 ).
V . EXERCISE AND ADAPTATIONS TO
TRAINING
A . Exercise Intensity and Sources of Energy
The rate of energy utilization during intense exercise can
be as much as 200 times greater than at rest and the rate of
ATP utilization is closely associated with the rate of ATP
synthesis ( Holloszy, 1982a ). Hence, the availability of ATP
is a central requirement for sustaining the rate and duration
of exercise. Because the stores of creatine phosphate
and ATP available for immediate use within myofibers are
small, the metabolic pathways for ATP synthesis serve a
vital function in the maintenance of exercise. A number
of interdependent factors appear to influence the metabolic
pathways used for energy production during exercise.
These include the speed and duration of exercise, the
muscle fiber composition, the metabolic properties of the
muscle fibers recruited, and the availability of oxygen and
different energy substrates.
Aerobic pathways such as the Krebs cycle, β oxidation
of free fatty acids (FFA) and the electron transport chain are
located within mitochondria and provide the bulk of ATP for
the cell as long as oxygen is plentiful. The efficiency of mitochondrial
pathways is demonstrated by the ability to generate
38 molecules of ATP from oxidation of one molecule of glucose
or the generation of up to 146 molecules of ATP from
β oxidation of an FFA. Anaerobic pathways such as glycolysis,
creatine phosphate, and the purine nucleotide cycle
are found within the cell cytoplasm. Anaerobic glycolysis
converts glucose to pyruvate, and then lactate provides only
two molecules of ATP for each molecule of glucose metabolized.
Anaerobic glycolysis, although less efficient, rapidly
supplies ATP even when oxygen is not available.
The main fuels for aerobic muscular contraction are
FFA and glucose, which are supplied by intramuscular
(lipid droplets, β glycogen particles) and extramuscular
(liver and adipose tissue) depots during exercise. The
rate-limiting factor in the supply of plasma free fatty acid
(FFA) to muscle appears to be the rate of FFA release from
adipose tissues ( Bennard et al. , 2005 ). The rate-limiting
factor in the extramuscular supply of glucose to working
muscle is glucose uptake by the myofibers. It is estimated
that 65% or more of the oxygen utilization during moderate
to heavy exercise is accounted for by the oxidation of
carbohydrates ( Holloszy, 1982a ; Sahlin, 1986 ). Glycogen
is the primary fuel metabolized to synthesize ATP during
anaerobic metabolism ( Holloszy, 1982a ).
At rest, oxidation of FFA and stored triglycerides contributes
the bulk of the fuel used for maintaining muscle
tone, whereas the oxidation of glucose accounts for only
10% to 20% of the CO 2 produced ( Havel et al. , 1967 ). At
the onset of exercise, energy is initially derived from creatine
phosphate and anaerobic glyco(geno)lysis. However, as the
duration of exercise is increased and blood flow increases,
there is a shift to aerobic metabolism in which glucose, FFA,
and triglycerides are oxidized. At low to moderate exercise
intensities, the oxidation of fatty acids provides the major
source of energy. At moderate to high aerobic exercise
intensities, the oxidation of fatty acids decreases and carbohydrates
account for 50% or more of the amount of substrate
utilized ( Wahren, 1977 ). At moderately high aerobic
exercise intensities, muscle glycogen accounts for the majority
of the glucose oxidized, and oxidized FFA are primarily
derived from muscle triglyceride depots. By using FFA,
intramuscular glycogen stores are spared. Metabolic events
within skeletal muscle, which are believed to contribute to
fatigue during prolonged submaximal exercise, involve a
combination of the following: intramuscular glycogen concentrations
become depleted, muscle temperatures become
markedly elevated, electrolyte concentrations are altered, or
neuromuscular fatigue occurs. Very little lactic acid accumulates
at fatigue during submaximal exercise.
At maximal exercise speeds, oxygen consumption peaks,
oxidative energy metabolism is maximal, and further energy
must be generated by anaerobic glycolysis or deamination
of ATP. Glycogen serves as the major fuel utilized at maximal
speeds and exponential accumulation of lactate results.
Depletion of glycogen stores normally does not appear to
limit maximal exercise because marked depletion is not
observed before the onset of fatigue. Conventional theories
regarding muscle fatigue with maximal exercise have hypothesized
that an acidosis, arising from accumulation of lactic
acid, is the primary determinant of muscle fatigue. Lactic
acid was said to inhibit the activity of phosphofructokinase,