Muscle 383protein (UCP1; chapter 5, section 5.4), previously thought
to be produced only by brown adipose tissue. By uncoupling
oxidative phosphorylation, UCP1 reduces ATP production and
increases metabolic rate, which may help to reduce weight and
improve glucose tolerance. There is also evidence that regu-
lar exercise has a general anti-inflammatory effect, helping
to reduce the risk of cardiovascular and pulmonary diseases,
colon cancer, and other pathological conditions promoted by
inflammation. The anti-inflammatory effects of exercise may
partly be due to exercising muscles’ release of interleukin-6
and other myokines.
Endurance training does not increase the size of muscles.
Muscle enlargement is produced only by frequent periods of
high-intensity exercise in which muscles work against a high
resistance, as in weightlifting. As a result of resistance training,
type II muscle fibers become thicker, and the muscle therefore
grows by hypertrophy (an increase in cell size rather than num-
ber of cells). This happens first because the myofibrils within
a muscle fiber thicken due to the synthesis of actin and myo-
sin proteins and the addition of new sarcomeres. Then, after a
myofibril has attained a certain thickness, it may split into two
myofibrils, each of which may become thicker as a result of the
addition of sarcomeres. Muscle hypertrophy, in short is associ-
ated with an increase in the size of the myofibrils and then in
the number of myofibrils within the muscle fibers.
The decline in physical strength of older people is associ-
ated with a reduced muscle mass, which is due to a loss of
muscle fibers and to a decrease in the size of fast-twitch muscle
fibers. Aging is also associated with a reduced density of blood
capillaries surrounding the muscle fibers, leading to a decrease
in oxidative capacity. Resistance training can cause the surviv-
ing muscle fibers to hypertrophy and become stronger, par-
tially compensating for the decline in the number of musclethe amount of exercise that can be performed before lactic
acid production increases and muscles begin to fatigue. In
addition to having a higher aerobic capacity, well-trained ath-
letes also have a lactate threshold that is a higher percentage
of their V
·
o 2 max. The lactate threshold of an untrained person,
for example, might be 60% of the V
·
o 2 max, whereas the lac-
tate threshold of a trained athlete can be up to 80% of the V
·
o 2
max. These athletes thus produce less lactic acid at a given
level of exercise than the average person and are less subject
to fatigue.
Because the depletion of muscle glycogen places a limit
on exercise, any adaptation that spares muscle glycogen will
improve physical endurance. Trained athletes have a slower
depletion of their stored glycogen because they derive a higher
proportion of their muscle energy from the aerobic respiration
of fatty acids. The greater the level of physical training, the
higher the proportion of energy derived from the oxidation of
fatty acids during exercise below the V
·
o 2 max.
All fiber types adapt to endurance training by an increase
in mitochondria, and thus in aerobic respiratory enzymes. In
fact, the maximal oxygen uptake can be increased by as much
as 20% through endurance training. There is a decrease in type
IIX (fast glycolytic) fibers, which have a low oxidative capac-
ity, accompanied by an increase in type IIA (fast oxidative)
fibers, which have a high oxidative capacity. Although the
type IIA fibers are still classified as fast-twitch, they show an
increase in the slow myosin ATPase isoenzyme form, indicat-
ing that they are in a transitional state between the type II and
type I fibers.
Skeletal muscles can store triglycerides both within the
muscle fibers and in adipocytes between muscle fibers. The fat
storage outside of the fibers is increased in obesity and type 2
diabetes mellitus (chapter 19) and reduced by aerobic exercise.
The triglycerides within the muscle fibers are also increased in
obesity, and in this case are associated with increased insulin
resistance and type 2 diabetes. Insulin resistance (decreased
insulin sensitivity) in an obese person is promoted because the
skeletal muscle fibers take in fatty acids but have a reduced
ability to oxidize them. Endurance-trained athletes, who have a
lower risk of insulin resistance and diabetes, surprisingly also
have elevated intracellular triglycerides within their skeletal
muscle fibers ( table 12.4 ). This is possible because adaptations
within the muscle fibers of these athletes allow the fibers to
completely oxidize fatty acids. As a result, diglycerides and
long-chain fatty acids cannot accumulate where they can inter-
fere with the insulin signaling of glucose uptake.
The beneficial effects of a moderate exercise program
and a modest weight loss on insulin sensitivity are well doc-
umented. In this regard, even low-intensity exercise greatly
increases rates of lipolysis and fatty acid oxidation, and more
intense exercise has relatively little additional benefit on these
rates. In addition, scientists recently reported that regular exer-
cise stimulates human and mouse muscles to produce a newly
discovered myokine (cytokine produced by muscles, which
may also be secreted as a hormone) named irisin. Irisin stimu-
lates the white adipose cells of mice to produce uncoupling
- Improved ability to obtain ATP from oxidative phosphorylation
- Increased size and number of mitochondria
- Less lactic acid produced per given amount of exercise
- Increased myoglobin content
- Increased intramuscular triglyceride content
- Increased lipoprotein lipase (enzyme needed to utilize lipids
from blood) - Increased proportion of energy derived from fat; less from
carbohydrates - Lower rate of glycogen depletion during exercise
- Improved efficiency in extracting oxygen from blood
- Decreased number of type IIX (fast glycolytic) fibers; increased
number of type IIA (fast oxidative) fibers
Table 12.4 | Effects of Endurance Training
on Skeletal Muscles