Muscle Soreness Delayedonset Muscle Soreness Doms

Muscle soreness is one of the many common symptoms that can be successfully treated by dry needling, even when the usual physical procedures such as massage, stretching exercises, or manipulation have had no effect. A sore muscle becomes inflamed, shortened, and weak, and this can lead to tendinitis, avulsion of muscular attachment, or abnormal bone growth. Early treatment by needling, especially right after exercise, is necessary and very effective for preventing the injury of muscle and soft tissues.

Muscle soreness results from exhaustive, high-intensity, or repetitive exercise. Mild muscle soreness is usually felt during and immediately after exercise; then a more intense soreness is felt a day or two later and may last for weeks (Fig. 5-3).

Acute muscle soreness during and immediately after exercise can result from accumulation of the end products of exercise, such as H+, and also from tissue edema, which is caused by fluid shifting from blood plasma into the tissue when venous and lymphatic circulation become insufficient. Some acute soreness disappears within a few hours after exercise, and some can last for days or weeks if ignored or not properly treated.

Muscle soreness that is not felt until a day or two after heavy exercise is referred to as delayed-onset muscle soreness (DOMS). According to the



Plasma CK


Glycogen depletion

Ultrastructural damage

7 14 21

Days after exercises Figure 5-3 The delayed responses to exercise-induced muscle damage. These valuable data show that, under natural conditions, more than 3 weeks is necessary for complete histologic recovery from the ultrastructural damage (microtrauma or microtear).

author's clinical experience, the muscles that will later exhibit DOMS are already more sensitive to needling therapy than are those that will not. Thus needling therapy provides both early diagnosis and treatment of DOMS. The author has also observed that if the athlete receives ISDN treatment immediately or within 1 day after the exercise or competition, the DOMS symptoms are greatly reduced or even not felt by the athlete.

Knowledge of DOMS is limited, but almost all current research has demonstrated a connection between DOMS and eccentric muscle activ-ity.7 The levels of several specific muscle enzymes in blood, including myoglobin, increase from 2 to 10 times their normal levels after intensive exercise. This suggests that some structural damage may occur in muscle fibers after heavy training. Studies8 support the idea that these changes might indicate some degree of muscle tissue breakdown. Examination of tissue from the leg muscles of marathon runners has revealed remarkable damage to the muscle fibers after intensive training and competition. Electron micrographs provide evidence of damage to the membrane of the muscle fibers and other cellular microstructural damage, such as Z-discs, after marathon running. Experts believe that this damage is responsible in part for localized muscle pain, tenderness, and swelling associated with DOMS.

DOMS also triggers an inflammatory reaction. The white blood cell count tends to increase after activities that induce muscle soreness; accordingly, some investigators believe that soreness results from inflammatory reactions in the muscle. In fact, substances released from injured muscle can act as attractants, initiating typical inflammatory processes. Monocytes in muscle are activated by the injury and provide chemical signals to circulating inflammatory cells. Neutrophils invade the injury site and release cytokines. Cytokines are immuno-regulatory substances, which attract and activate additional inflammatory cells. Neutrophils possibly also release oxygen free radicals that can damage cell membranes. Macrophages invade the damaged muscle fibers and phagocytize debris. After the dead tissues are removed, muscle regeneration starts to replace the injured cells.

It is clear now that muscle soreness results from injury or damage to the muscle fiber and possibly the plasmalemma.9 This damage sets up a chain of events at the cellular level to activate the repair process, involving energy sources, inflammatory reactions, and other molecular mechanisms. The precise cause of skeletal muscle damage and the mechanisms of repair, however, are not well understood.

Edema, or the accumulation of fluids in the muscular compartment, also can lead to DOMS. This edema is probably the result of muscle injury. An accumulation of interstitial or intracellular fluid increases the tissue fluid pressure within the muscle compartment, which irritates pain receptors within the muscle.

DOMS and related edema result in failure in the excitation-contraction coupling process and loss of contractile protein, which reduce the force-generating capacity of the affected muscles. Failure in excitation-contraction coupling appears to be the most important, particularly during the first 5 days after injury. Muscle glycogen resyn-thesis is also impaired when a muscle is damaged. Resynthesis is not affected for the first 6 to 12 hours after exercise, but it gradually stops completely as the muscle undergoes repair. This energy redistribution reduces the fuel-storage capacity of the injured muscle and makes it weak, such that muscle retraining may be needed. Maximal forcegenerating capacity gradually returns over days or weeks.

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Essentials of Human Physiology

Essentials of Human Physiology

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