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Recent research provides insight into muscle soreness

This is an excerpt from Physiology of Sport and Exercise, Fifth Edition by W. Larry Kenney, Jack Wilmore, and David Costill.


Delayed-Onset Muscle Soreness

Muscle soreness felt a day or two after a heavy bout of exercise is not totally understood, yet researchers are continuing to give us greater insight into this phenomenon. Because this pain does not occur immediately, it is referred to as delayed-onset muscle soreness (DOMS). DOMS is classified as a type I muscle strain and can vary from slight muscle stiffness to severe, debilitating pain that restricts movement. In the following sections, we discuss some theories that attempt to explain this form of muscle soreness.

Almost all current theories acknowledge that eccentric action is the primary initiator of DOMS. This has been clearly demonstrated in a number of studies examining the relationship of muscle soreness to eccentric, concentric, and static actions. In studies, individuals who train solely with eccentric actions experience extreme muscle soreness, whereas those who train using static and concentric actions experience little soreness. This idea has been further explored in studies in which subjects ran on a treadmill for 45 min on two separate days, one day on a level grade and the other day on a 10% downhill grade.16, 17 No muscle soreness was associated with the level running. But the downhill running, which required extensive eccentric action, resulted in considerable soreness within 24 to 48 h, even though blood lactate concentrations, previously thought to cause muscle soreness, were much higher with level running.

In the following section we examine some of the proposed explanations for exercise-induced DOMS.

Structural Damage

The presence of increased concentrations of several specific muscle enzymes in blood after intense exercise suggests that some structural damage may occur in the muscle membranes. These enzyme concentrations in the blood increase from 2 to 10 times following bouts of heavy training. Recent studies support the idea that these changes might indicate various degrees of muscle tissue breakdown. Examination of tissue from the leg muscles of marathon runners has revealed remarkable damage to the muscle fibers after both training and marathon competition. The onset and timing of these muscle changes parallel the degree of muscle soreness experienced by the runners.



The electron micrograph in figure 10.8 shows muscle fiber damage as a result of marathon running.10 In this case, the cell membrane appears to have been totally ruptured, allowing the cell’s contents to float freely between the other normal fibers. Fortunately, not all damage to muscle cells is as severe.

Figure 10.9 shows changes in the contractile filaments and Z-disks before and after a marathon race. Recall that Z-disks are the points of contact for the contractile proteins. They provide structural support for the transmission of force when the muscle fibers are activated to shorten. Figure 10.9b, after the marathon, shows moderate Z-disk streaming and major disruption of the thick and thin filaments in a parallel group of sarcomeres as a result of the force of eccentric actions or stretching of the tightened muscle fibers.



Although the effects of muscle damage on performance are not fully understood, it is generally agreed that this damage is responsible in part for the localized muscle pain, tenderness, and swelling associated with DOMS. However, blood enzyme concentrations might increase and muscle fibers might be damaged frequently during daily exercise that produces no muscle soreness. Also, remember that muscle damage appears to be a precipitating factor for muscle hypertrophy.

Inflammatory Reaction

White blood cells serve as a defense against foreign materials that enter the body and against conditions that threaten the normal function of tissues. The white blood cell count tends to increase following activities that induce muscle soreness. This observation led some investigators to suggest that soreness results from inflammatory reactions in the muscle. But the link between these reactions and muscle soreness has been difficult to establish.

In early studies, researchers attempted to use drugs to block the inflammatory reaction, but these efforts were unsuccessful in reducing either the amount of muscle soreness or the degree of inflammation. These early results did not support a link between simple inflammatory mediators and DOMS. However, more recent studies have begun to establish a link between muscle soreness and inflammation. It is now recognized that substances released from injured muscle can act as attractants, initiating the inflammatory process. Mononucleated cells in muscle are activated by the injury, providing the chemical signal to circulating inflammatory cells. Neutrophils (a type of white blood cell) invade the injury site and release cytokines (immunoregulatory substances), which then attract and activate additional inflammatory cells. Neutrophils possibly also release oxygen free radicals that can damage cell membranes. The invasion of these inflammatory cells is also associated with the incidence of pain, thought to be caused by a release of substances from the inflammatory cells stimulating the pain-sensitive nerve endings. Macrophages (another type of cell of the immune system) then invade the damaged muscle fibers, removing debris through a process known as phagocytosis. Last, a second phase of macrophage invasion occurs, which is associated with muscle regeneration.23

Sequence of Events in DOMS

The general consensus among researchers is that a single theory or hypothesis cannot explain the mechanism causing DOMS. Instead researchers have proposed a sequence of events that may explain the DOMS phenomenon, including the following:

1. High tension in the contractile-elastic system of muscle results in structural damage to the muscle and its cell membrane. This is also accompanied by excessive strain of the connective tissue.

2. The cell membrane damage disturbs calcium homeostasis in the injured fiber, inhibiting cellular respiration. The resulting high calcium concentrations activate enzymes that degrade the Z-lines.

3. Within a few hours is a significant elevation in circulating neutrophils that participate in the inflammatory response.

4. The products of macrophage activity and intracellular contents (such as histamine, kinins, and K+) accumulate outside the cells. These substances then stimulate the free nerve endings in the muscle. This process appears to be accentuated in eccentric exercise, in which large forces are distributed over relatively small cross-sectional areas of the muscle.

Recent comprehensive reviews have provided much greater insight into the cause of muscle soreness. We now are confident that muscle soreness results from injury or damage to the muscle itself, generally the muscle fiber and possibly the plasmalemma.1, 4 This damage sets up a chain of events that includes the release of intracellular proteins and an increase in muscle protein turnover. The damage and repair process involves calcium ions, lysosomes, connective tissue, free radicals, energy sources, inflammatory reactions, and intracellular and myofibrillar proteins. But the precise cause of skeletal muscle damage and the mechanisms of repair are not well understood. As we have discussed previously, some evidence suggests that this process is an important step in muscle hypertrophy.

Up to this point, our discussion of DOMS has focused on muscle injury. Edema, or the accumulation of fluids in the muscular compartment, also can lead to DOMS. This edema is likely the result of muscle injury but could occur independently of muscle injury. An accumulation of interstitial or intracellular fluid increases the tissue fluid pressure within the muscle compartment, which in turn activates pain receptors within the muscle.

 

Read more about Physiology of Sport and Exercise, Fifth Edition by W. Larry Kenney, Jack Wilmore, and David Costill.



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