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 it's 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.