Muscle soreness

Muscle soreness generally results from exhaustive or very high intensity exercise. This is particularly true when people perform a specific exercise for the first time. While muscle soreness can be felt at any time, there is generally a period of mild muscle soreness that can be felt during and immediately after exercise, and then a more intense soreness felt a day or two later.

Acute muscle soreness

Pain felt during and immediately after exercise can result from accumulation of the end products of exercise, such as H⁺, and from tissue edema, mentioned earlier, which is caused by fluid shifting from the blood plasma into the tissues. Edema is the cause of the pumped-up sensation that people feel after heavy endurance or strength training. The pain and soreness usually disappear within a few minutes to several hours after the exercise. Thus, this soreness is often referred to as acute muscle soreness.

Delayed-onset muscle soreness and injury

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 the pain does not occur immediately, it is reffered to as delayed-onset muscle soreness(DOMS). Here will be discussed 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 was clearly demonstrated in a study of the relationship of muscle soreness to eccentric, concentric, and static actions. This study showed that a group who trained solely with eccentric actions experienced extreme muscle soreness, whereas the static- and concentric- action groups experienced little soreness. This idea was 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.

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 48h, even though blood lactate levels, previously thought to cause muscle soreness, were much higher with level running.

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 levels increase from 2 to 10 times their normal levels 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.

Although the effects of muscle damage on performance are not fully understood, experts generally agree that this damage is responsible in part for the localized muscle pain, tenderness, and swelling associated with DOMS. However, blood enzyme levels 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 threated 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.

Researchers have tried to use drugs to block the inflammatory reaction, but these efforts have been unsuccessful in reducing the amount of muscle soreness or the degree of inflammation. Because both effects remain, conclusions about the role of inflammation in muscle soreness cannot be drawn from this research. More recent studies, however, are beginning to establish a link between muscle soreness and inflammation. For example, 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. 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.

Sequence of events in DOMS

In 1984, Armstrong reviewed possible mechanisms for exercise-induced DOMS. He concluded that DOMS is associated with:

• Elevations in plasma enzymes,
• Myoglobinemia(presence of myoglobin in the blood), and
• Abnormal muscle histology and ultrastructure.

He developed a model of DOMS that proposed the following sequence of events:

1.            High tension in the contractile-elastic system of muscle results in structural damage to the muscle and its cell membrane.

2.            The cell membrane damage disturbs calcium homeostasis in the injured fiber, resulting in necrosis(cell death) that peaks about 48h after exercise.

3.            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. 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. 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 or interstitial or intracellular fluid increases the tissue fluid pressure within the muscle compartment, which in turn activates pain receptors within the muscle.

Delayed-onset muscle soreness and performance

With DOMS comes a reduction in the force-generating capacity of the affected muscles. Whether the DOMS is the result of injury to the muscle or edema independent of muscle injury, the affected muscles are not able to exert as much force when the person is asked to apply maximal force, such as in the performance of a 1RM strength test. Maximal force-generating capacity gradually returns over days or weeks. It has been proposed that the loss in strength is the result of three factors:

1. The physical disruption of the muscle ,
2. Failure within the excitation – contraction coupling process,
3. Loss of contractile protein.

Failure in excitation – contraction coupling appears to be the most important, particularly during the first five days.

Muscle glycogen resynthesis also is impaired when a muscle is damaged. Resynthesis is generally normal for the first 6 to 12h after exercise, but it slows or stops completely as the muscle undergoes repair, thus limiting the fuel-storage capacity of the injured muscle. Figure below illustrates the time sequence of the various factors associated with intense eccentric exercise, including pain, edema, plasma creatine kinase( a plasma enzyme marker of muscle fiber damage), glycogen depletion, ultrastructural damage in the muscle, and muscular weakness.

Reducing the negative effects of DOMS

Reducing the negative effects of DOMS is important for maximizing training gains. The eccentric component of muscle action could be minimized during early training, but this is not possible for athletes in most sports. An alternative approach is to start training at a very low intensity and progress slowly through the first few weeks. Yet another approach is to initiate the training program with a high-intensity, exhaustive training bout. Muscle soreness would be great for the first few days, but evidence suggests that subsequent training bouts would cause considerably less muscle soreness. Because the factors associated with DOMS are also potentially important in stimulating muscle hypertrophy, DOMS is most likely necessary to maximize the training response.