Human Physiology, 14th edition (2016)

382 Chapter 12

significantly in fast-twitch fibers during high-intensity

exercise, but does not decline enough to produce rigor

complexes (as in rigor mortis). ATP does not measurably

decline in slow-twitch fibers during exercise.

3. Depletion of muscle glycogen. The mechanisms by which

this contributes to fatigue are not fully understood, but it

appears to decrease the release of Ca^2 1 from the sarcoplas-

mic reticulum.

4. Increased ADP in the cytoplasm. This causes a decrease in

the velocity of muscle shortening during muscle fatigue.

The foregoing is a description of the reasons that muscle

tissue can fatigue during exercise. When humans exercise,

however, we often experience fatigue before our muscles them-

selves have fatigued sufficiently to limit exercise. Put another

way, our maximum voluntary muscle force is often less than

the maximum force that our muscle is itself capable of pro-

ducing. This demonstrates central fatigue —muscle fatigue

caused by changes in the CNS rather than by fatigue of the

muscles themselves.

Evidence suggests that central fatigue is complex. In part,

it involves a reduced ability of the “upper motoneurons” (inter-

neurons in the brain devoted to motor control) to drive the

“lower motoneurons” (in the spinal cord). Muscle fatigue thus

has two major components: a peripheral component (fatigue

in the muscles themselves) and a central component (fatigue

in the CNS that causes reduced activation of muscles by

motoneurons).

Adaptations of Muscles to Exercise Training

The maximal oxygen uptake, obtained during very strenuous

exercise, averages 50 ml of O 2 per minute per kilogram body

weight in males between the ages of 20 and 25 (females aver-

age 25% lower). For trained endurance athletes (such as swim-

mers and long-distance runners), maximal oxygen uptakes

can be as high as 86 ml of O 2 per minute per kilogram. These

considerable differences affect the lactate threshold, and thus

can become particularly high in the narrow spaces of the trans-
verse tubules. (Remember that K^1 leaves axons and muscle
fibers during the repolarization phase of action potentials.) This
depolarizes the membrane potential of muscle fibers, inter-
fering with their ability to produce action potentials. Fatigue
under these circumstances lasts only a short time, and maximal
tension can again be produced after less than a minute’s rest.
Muscle fatigue that occurs during other types of exer-
cise appears to have different causes. Chiefly, there is
depletion of muscle glycogen and a reduced ability of the
sarcoplasmic reticulum to release Ca^2 1 , leading to failure of
excitation- contraction coupling. Although failure of excitation-
contraction coupling is known to produce muscle fatigue, the
reasons for that failure—despite nearly a century of study—are
incompletely understood.
It has been known from the early twentieth century that
fatigue occurs when lactate accumulates, and that restoring
aerobic respiration allows muscle glycogen and contractile
ability to recover. This led to the widespread belief that low-
ered muscle pH is caused by H^1 released from lactic acid,
and that the lowered pH produced in this way causes muscle
fatigue. However, ongoing research suggests that lactate pro-
duction may be more coincidental with muscle fatigue than a
cause of it.
Several other changes during exercise may produce mus-
cle fatigue through their effects on Ca^2 1 release from the sar-
coplasmic reticulum and Ca^2 1 stimulation of contraction.
The relative contribution of each of these changes to muscle
fatigue depends on the type of exercise performed. The muscle
changes with exercise that may contribute to fatigue include
the following:

1. Increased concentration of PO 4 3 2 , derived from the break-
   down of phosphocreatine, in the cytoplasm. This is cur-
   rently believed to reduce the force developed by cross
   bridges and to be a major contributor to muscle fatigue.


2. A decline in ATP, particularly around the junction of
   the transverse tubules and sarcoplasmic reticulum, that
   may hinder the action of the Ca^2 1 pumps. ATP declines

Figure 12.26 Relative abundance of
different muscle fiber types in different
people. The percentage of slow type I fibers,
fast type IIX fibers, and intermediate fast type
IIA fibers in the muscles of different people
varies tremendously. This is due to differences in
genetics and to the effects of physical training.

100

80

60

40

20

0

Person

with

spinal

injury

Percent of total muscle

World-

class

sprinter

Average

couch

potato

Average

active

person

Slow type I

Fast type IIA

Fast type IIX

Middle-

distance

runner

World-

class

marathon

runner

Extreme

endurance

athlete