Muscle
273
If the intensity of exercise exceeds about 70 percent of
the maximal rate of ATP breakdown, however, glycolysis con-
tributes an increasingly signifi cant fraction of the total ATP
generated by the muscle. The glycolytic pathway, although
producing only small quantities of ATP from each molecule
of glucose metabolized, can produce ATP quite rapidly when
enough enzymes and substrate are available, and it can do
so in the absence of oxygen (under anaerobic conditions).
The glucose for glycolysis can be obtained from two sources:
the blood or the stores of glycogen within the contracting
muscle fi bers. As the intensity of muscle activity increases,
a greater fraction of the total ATP production is formed by
anaerobic glycolysis. This is associated with a corresponding
increase in the production of lactic acid.
At the end of muscle activity, creatine phosphate and
glycogen levels in the muscle have decreased. To return a mus-
cle fi ber to its original state, therefore, these energy-storing
compounds must be replaced. Both processes require energy,
and so a muscle continues to consume increased amounts of
oxygen for some time after it has ceased to contract. In addi-
tion, extra oxygen is required to metabolize accumulated
lactic acid and return the blood and interstitial fl
uid oxygen
concentrations to pre-exercise values. These processes are
evidenced by the fact that you continue to breathe deeply and
rapidly for a period of time immediately following intense
exercise. This elevated oxygen consumption following exer-
cise repays the
oxygen debt
—that is, the increased produc-
tion of ATP by oxidative phosphorylation following exercise
is used to restore the energy reserves in the form of creatine
phosphate and glycogen.
Muscle Fatigue
When a skeletal muscle fi ber is repeatedly stimulated, the ten-
sion the fi ber develops eventually decreases even though the
stimulation continues (
Figure 9–23
). This decline in muscle
tension as a result of previous contractile activity is known as
muscle fatigue.
Additional characteristics of fatigued muscle
are a decreased shortening velocity and a slower rate of relax-
ation. The onset of fatigue and its rate of development depend
on the type of skeletal muscle fi ber that is active, the inten-
sity and duration of contractile activity, and the degree of an
individual’s fi
tness.
If a muscle is allowed to rest after the onset of fatigue,
it can recover its ability to contract upon restimulation (see
Figure 9–23). The rate of recovery depends upon the dura-
tion and intensity of the previous activity. Some muscle fi bers
fatigue rapidly if continuously stimulated but also recover
rapidly after a brief rest. This type of fatigue (high-frequency
fatigue) accompanies high-intensity, short-duration exercise,
such as weight lifting. In contrast, low-frequency fatigue
develops more slowly with low-intensity, long-duration exer-
cise, such as long-distance running, which includes cyclical
periods of contraction and relaxation. This type of fatigue
requires much longer periods of rest, often up to 24 hours,
before the muscle achieves complete recovery.
It might seem logical that depletion of energy in the
form of ATP would account for fatigue, but the ATP con-
centration in fatigued muscle is only slightly lower than in a
resting muscle, and not low enough to impair cross-bridge
cycling. If contractile activity were to continue without fatigue,
the ATP concentration could decrease to the point that the
cross-bridges would become linked in a rigor confi
gura-
tion, which is very damaging to muscle fi bers. Thus, muscle
fatigue may have evolved as a mechanism for preventing the
onset of rigor.
Many factors can contribute to the fatigue of skeletal
muscle. Fatigue from high-intensity, short-duration exercise
is thought to involve at least three different mechanisms:
1.
Conduction Failure.
The muscle action potential
can fail to be conducted into the fi ber along the
T-tubules, which halts the release of calcium from
the sarcoplasmic reticulum. This conduction failure
results from the buildup of potassium ions in the small
volume of the T-tubule during the repolarization
of repetitive action potentials. Elevated external
potassium concentration leads to a persistent
depolarization of the membrane potential, and
eventually causes a failure to produce action potentials
in the T-tubular membrane (due to inactivation of
sodium channels). Recovery is rapid with rest as the
accumulated potassium diffuses out of the tubule or is
pumped back into the cell, restoring excitability.
2.
Lactic Acid Buildup.
Elevated hydrogen ion
concentration alters protein conformation and activity.
Thus, the acidifi cation of muscle by lactic acid may
alter a number of muscle proteins, including actin and
myosin, as well as the proteins involved in calcium
release. The function of the Ca
2+
-ATPase pumps of
the sarcoplasmic reticulum is also affected, which may
in part explain the impaired relaxation of fatigued
muscle. Recent single-fi ber experiments performed
at body temperature suggest that high acidity does
not directly hinder contractile proteins, so effects on
calcium handling may predominate.
Stimuli
Isometric tension
Tetanus
Fatigue
Fatigue
Time
Rest
period
Figure 9–23
Muscle fatigue during a maintained isometric tetanus and recovery
following a period of rest.
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