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Exercises and
Possible Causes of Delayed Muscle Soreness
There are three common hypothetical explanations of the soreness
that occurs usually a day or two after strenuous exercise-the
lactic acid accumulation hypothesis, the muscle spasm hypothesis,
and the tissue damage hypothesis.
The Lactic Acid Accumulation Hypothesis.
It is well established that lactic acid accumulates to a greater
extent in more intensive types of exercise and that more intensive
exercise generally causes the greatest delayed muscle soreness.
However, there are several lines of evidence which
suggest that lactic acid has little to- do with delayed
soreness. First, lactic acid does not remain elevated above
resting values more than 15-30 minutes after exercise, yet
soreness typically is delayed until 24-48 hours following
exercise. The onset of soreness is so far removed from the.
d of elevated lactic acid that it is difficult to believe
that lactic acid c6uld cause the soreness. Second,
the greatest soreness accompanies eccentric contractions, which
are associated with relatively slight lactic acid accumulation..
Third, there are some activities which produce much soreness but
essentially no lactic acid. As an example, consider an
overweight, middle-aged, unfit person who begins a training
program with a few vigorous straight-legged toe touching
exercises. Within a day after the stretching, which causes little
or no lactic acid production, the backs of the trainee's legs
would be very sore. Finally, patients who have a hereditary
absence of phosphorylase, an enzyme required for breaking down
glycogen to lactic acid, still experience great muscle pain after
strenuous contractions, in spite of a lack of lactic acid
accumulation. Accordingly, it seems extremely unlikely
that lactic acid accumulation can explain delayed muscular
soreness after unaccustomed exercise.
The Muscle Spasm Hypothesis.
Those
who believe in the muscle spasm hypothesis say: a) that strenuous
contractions cause a reduction in blood flow (ischemia) to the
working muscles, b) that this ischemia in turn triggers the
release of pain substances out of the muscle fibres into the
tissue fluid where the pain substances stimulate nerve endings,
and c) that the pain receptors cause reflex spastic contractions
of the painful muscle fibres to produce further ischemia and
continued release of pain substances to renew the pain cycle.
This hypothesis is sometimes, but not always, supported by
electro-myographic evidence that under some circumstances fatigued
muscles may indeed continue to contract after exercise. Also,
stretching of the muscles may reduce the contractile activity and
the associated pain. However, it seems very unlikely that
ischemia and post-exercise spasms occur after all types of
exercise that can result in pain. For example, in untrained
persons the mere act of stretching in limbering-up exercises
surely does not cause ischemia but can result in pain the next
day. Therefore, the spasm-pain substance hypothesis is not a
completely satisfactory explanation of all muscle pain caused by
exercise.
The Tissue Damage Hypothesis.
A
more persuasive hypothesis is that free nerve endings are
stimulated by swelling (oedema) of muscle tissue after microscopic
damage to a relatively few muscle fibres or their surrounding
connective tissue. There are several reasons for believing that
strenuous, unaccustomed exercise may cause some minor damage to
muscle tissue.
First,
microscopic disruptions of myofibrils, especially of the Z-Iines,
have been observed in biopsy specimens from the calf muscles of
men ho ran down 10 flights of stairs 10 times. (Note that running
down stairs re- quires eccentric contractions of the calf
muscles.) All of the subjects in this experiment suffered intense
muscle discomfort, especially 2-3 days following the exercise. In
addition, animal studies have shown evidence of muscle fibre
damage after exhaustive exercise,
Second, myoglobin
appears in the blood and urine of subjects who participate in
strenuous activity. Since myoglobin is a large protein found
only in muscle, its appearance in blood and urine suggests
muscle damage. After training, there is less exercise-induced
soreness; there is also less myoglobin released into the blood.
Third,
large enzyme molecules such as lactic acid dehydrogenase and
creatine phosphokinase leak out of the muscles into the blood to a
much greater extent after eccentric exercise than after concentric
exercise at the same absolute load. The appearance of these
enzymes in the blood is widely viewed as an index of muscle fibre
damage. Since delayed soreness is also much greater after the
eccentric exercise, it therefore seems likely that tissue damage
is a precursor to delayed soreness after exercise.
Fourth,
there is substantial evidence that muscle protein degradation is
accelerated for at least 6 hours after treadmill running or weight
lifting. This increased degradation of muscle protein may be a
reflection of increased activity of lysozymes, enzymes
which become especially active in response to cellular damage.
Finally,
it has been reported that connective tissue in skeletal muscle may
be degraded by exercise that produces soreness. This may be
especially important in view of the suggestion that eccentric
exercise (which causes the greatest soreness) places more stress
on connective tissue than does concentric exercise.
Summary.
There is little evidence to support the view that lactic acid
accumulation is causally related to delayed muscle soreness.
Muscle spasms may accompany soreness after certain types of
exercise, but it is unlikely that ischemia and spasms occur in
mild eccentric exercise which produces soreness. Such spasms may
be a result of tissue damage and not the direct cause of
soreness. Most of the evidence suggests that minor damage to
muscle and/or connective tissue causes a gradual increase (over
12-48 hours) in the leakage of chemicals into the extra-cellular
spaces of the muscle. These chemicals may directly stimulate free
nerve endings in the tissues or cause a progressive swelling of
the tissues that places pressure on the nerve endings and causes
the discomfort reported as "stiffness," "soreness," or "pain."
Delayed Soreness After Unaccustomed. Exercise-The Role of
Eccentric Contractions
It is curious that the greatest delayed soreness in muscles occurs
in response to eccentric (lengthening) contractions, which are
less difficult to perform with the same load than concentric
contractions. In a bench press, for example, soreness is much
more likely to occur in a person who repeats only the lowering
(eccentric) phase of the movement than in one who only raises the
load, even though it is much more difficult to raise than to lower
a given load. Because there is less electro-myographic activity
and less oxygen uptake with eccentric exercise, it appears that
fewer (or different) motor units are activated or there is a lower
frequency of motor unit recruitment during eccentric contractions
than during concentric contractions. Therefore, each individual
muscle fibre may produce greater force while lengthening than
while shortening. If this is so, it seems probable that the
individual fibres and their connective tissue attachments are
under greater stress during the eccentric exercise and are thus
more subject to disruption.
Minimizing Muscle Soreness.
Whatever the exact mechanism underlying muscle soreness may be,
there are enough facts known about soreness to enable us to
minimize its development. It is known that soreness is more apt
to occur with relatively intense, phasic, or jerking movements
which involve strenuous eccentric contractions. Also, soreness is
more common in those who are undertaking an exercise program after
a long period of inactive living. Therefore, a rational approach
to the initiation of a fitness program is: Begin with extremely
light activity that does not require any lunging or thrusting
movements, conduct the exercise periods for only 15-20 minutes
during the first few sessions, and progressively and slowly
increase both the intensity and duration of the exercise
sessions. This will allow the muscle fibres and the connective
tissue in the muscle to have a chance to become toughened as an
adaptive response to the training.
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