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Proposed Mechanisms of Delayed-Onset Muscle Soreness
by Tahira Collier

INTRODUCTION

Delayed onset muscle soreness (DOMS) is a sensation felt in exercised muscles between 8 hours and 3 days following unaccustomed heavy exercise. Although muscle soreness usually occurs in less physically trained individuals, most people, including elite athletes can experience this soreness as well. The mechanisms involved in DOMS are still being studied and refined, however researchers strongly suggest that certain exercises can generally cause damage to muscle fibers, resulting in soreness. The body responds to that damage by producing the common symptoms associated with DOMS shortly after the exercise. These symptoms include pain, decreased range of motion, decreased output of muscle force, and some swelling. The body then helps repair the damage and the muscles are able to function normally again (i.e., return to their function before exercise) without pain.

The topic of delayed onset muscle soreness is of interest for two reasons. One is that most individuals who engage in some physical activity, especially one they are not accustomed to, may experience some degree of DOMS. Depending on how much time passes before exercising again, DOMS could occur several times in one individual. For those who experience DOMS, or in cases where DOMS can play a critical role in performance (i.e., sports), learning more about the mechanisms of muscle soreness can help people understand how the body responds to certain physical activities. One that has an understanding of these general mechanisms can perhaps learn to deal with the effects of muscle fiber damage.

Another reason the topic of delayed muscle soreness is of interest is because of the slight uncertainty in the mechanisms of soreness. Several studies, of which many are supported, have hypothesized the causes of soreness, which is initiated by muscle fiber damage, and the body’s response to it. For example, most studies suggest an acute inflammatory response while others find no specific indicators of such response. Although there has been much agreement on the general causes of muscle fiber damage and the body’s general response, some questions on both mechanisms remain unanswered. The goal of this paper is to explore some of the main studies on the causes of delayed onset muscle soreness. It will specifically look at the mechanical factors suggested to play a role in DOMS and how the body responds to the muscle damage from these factors.

MECHANICAL FACTORS OF DOMS-Muscle Fiber Injury

To discuss the mechanical factors involved in delayed onset muscle soreness, it is necessary to discuss the types of exercise most associated with soreness, and the effects this exercise has on muscle fibers. In general, three main types of exercise can cause muscle soreness. These include isometric, concentric, and most commonly, eccentric exercises. Isometric and concentric exercises involve contractions that make the muscle either shorten or stay the same length. Examples would be trying to lift a heavy table without actually moving it (isometric) or bringing a barbell to the chest during a biceps curl (concentric). An eccentric exercise on the other hand causes the muscle to lengthen during contraction (e.g., lowering a barbell to the thigh during a biceps curl). Eccentric exercises tend to cause more soreness than isometric and concentric exercises because the muscles endure higher forces during contraction.

Since the beginning of the twentieth century, it has been hypothesized and well supported that general muscle soreness indicates some form of damage to muscle fibers and/or connective tissue (Hough, 1902). In his study of muscle soreness and workloads, Hough hypothesized that muscle tissues were torn after performing exercise with heavy workloads and this resulted in pain. As several other studies were conducted to investigate this hypothesis, researchers have learned more specifically what parts of the fibers may become injured and have determined eccentric exercises to cause the most damage (Armstrong et al. 1983; Clarkson et al. 1986; Sargeant and Dolan, 1987). (This explains why eccentric exercises generally create soreness more often than isometric and concentric exercises).

To determine muscle fiber damage and where it occurs after doing certain exercises, many researchers use markers of certain enzyme activities in the muscle and take muscle biopsies to examine the cell patterns, before and after exercise. For example, Armstrong and his colleagues (1983) conducted a study to examine the effects of eccentric exercise on injury in skeletal muscle in rats. They examined the muscle fibers of rats that ran up a 16 incline (primarily concentric contractions), at 0 incline (similar amounts of concentric and eccentric contractions), and down a 16 incline (primarily eccentric contractions) on a treadmill.

Their study produced several results that suggested muscle fiber damage, especially from eccentric exercise. One was a significant increase in plasma enzyme activities, particularly in the rats that ran downhill. (Although there is some uncertainty on why there is an increase in these activities, this increase has been well observed in the presence of tissue damage in other studies (Altland and Highman, 1961; Evans et al., 1986; Schwane et al., 1983)). There was also an increase in serum creatine kinase (CK) activity, which studies suggest has a direct relation to the extent of fiber degeneration. The results also showed an increase in macrophages and mononuclear cells, cells usually present when tissue damage occurs. Examinations of the muscle cells following exercise, showed disruption of some muscle cell membranes (sarcolemma), as well as disruption of the bands connecting the individual muscle fibers (Z-lines). Armstrong and colleagues noted the biggest changes of enzyme activities and fiber disruption in the muscles that underwent the most eccentric contractions. They interpreted this by suggesting there was a greater tension per cross-sectional area of these fibers, causing structural damage and leakage of the muscular enzymes mentioned.

Friden and his colleagues (1981) conducted another study that showed similar results to Armstrong’s. They attempted to look at the morphological changes of cells of the soleus muscle (part of the calf muscle) in human males, before and after running down stairs (primarily eccentric exercise). Upon examination of the exercised muscle cells two days after exercise (when the subjects complained of the most soreness), their study found no rupture or fiber degeneration at the cellular level. At the subcellular level however, there were disturbances to the Z-lines, showing widening and streaming, and in some cases total disruption. The tissues adjacent to the Z-lines were also disorganized and damaged. Friden and his colleagues explained these results by suggesting that a high muscle fiber tension developed during the exercise, causing an overload in the Z-lines. They concluded that a weak link existed between the chain of muscle fibers (which is connected by the Z-lines), thereby causing disruption.

In summary, evidence from studies on skeletal muscle after heavy exercise suggests some disruption of muscle fibers. The studies by Hough, Armstrong, and Friden demonstrate muscle fiber damage especially after eccentric exercises, which place high mechanical forces on the fibers. While there seems to be enough evidence to support the hypothesis that muscle fiber injury occurs during heavy exercise, there are still questions on exactly how the fibers are disrupted and to what extent. To determine the mechanisms by which the fiber degeneration or Z-line disruption occurs, further studies have to be conducted.

PHYSIOLOGICAL FACTORS OF DOMS-Inflammation and Other Responses

In terms of the physiological factors associated with delayed onset muscle soreness, the body undergoes several changes in response to the muscle fiber damage. Most studies suggest the body undergoes an inflammatory response, which can be characterized by symptoms of pain, some swelling or tightness, and decreased function in the muscle. Inside the body, specific cells associated with the immune system provide more solid evidence of this type of response, often referred to as a classic inflammatory response. Although some studies do not support this response hypothesis, other physiological evidence shows the muscles fibers undergo repair and adaptation, such that they are temporarily protected from further damage.

When tissue damage occurs, the body responds by sending specific cells and nutrients to the injury site to get rid of damaged cells, decrease further damage, and help repair. For tissue injury, these cells generally include monocytes, neutrophils, macrophages, and lymphocytes. The body usually alerts the brain of this injury through pain receptors, which in turn may decrease the functioning of the injured area to promote healing. Swelling may also occur to help flush out any damaged cells of the area and promote nutrient and blood flow to aid in healing.

The vast majority of studies on DOMS and muscle tissue injury indicate the presence of a general inflammatory response through pain, swelling and decreased muscle function. Although the classic inflammatory response (characterized by the presence of the specific cells mentioned) is not as universally accepted, many studies do support this idea. One such study is that by Bruunsgaard and his co-workers who studied the increases in serum interleukin-6 (a type of messenger involved in the regulation of immune response) in exercise-induced muscle injury (1997). Human male subjects performed 30 minutes of concentric and eccentric exercises on a bike, two weeks apart. Examination of blood samples during and after the exercises showed significant increases in the serum interleukin-6, particularly after the eccentric exercise. More specifically, the results indicated an increase in total concentration of lymphocytes, due to a greater recruitment of natural killer (NK) cells. (NK cells, a type of lymphocyte, are responsible for killing infected cells).

Another study that supported the classic inflammatory response to muscle fiber injury looked at the possible causes of pain and the inflammatory response (Davies et al., 1979). Many studies suggest that a specific type of prostaglandin (PGE, a hormone) sensitizes pain receptors, thereby causing pain. Davies and colleagues found that under inflammatory conditions, macrophages are capable of making and releasing large quantities of PGE, thereby causing the sensation of pain. As one particular study showed increases in PGE after eccentric exercise (Smith et al., 1993), this suggests that the muscle injury from exercise elicits an inflammatory response that may cause pain.

One other study that showed support of the classic inflammatory response was by Armstrong and colleagues (1983), that examined the muscle injury from eccentric exercise in rat skeletal muscle (described earlier). Upon examination of the fibers after exercise, there was an increase in the number of macrophages and mononuclear cells (a type of lymphocyte). This increase was even more pronounced in the muscles that underwent the most eccentric contractions. (Although this study showed evidence of inflammatory responses, other results from the study do not fully support the inflammatory response, as will be explained below).

Studies that do not support the inflammatory response hypothesis are mainly those that do not show evidence of the characteristic cells (i.e., monocytes, neutrophils, macrophages, and lymphocytes). One example is a study that examined general factors in DOMS in man (Bobbert et al., 1986). Eleven subjects performed exercise to induce delayed muscle soreness in one leg while the other leg served as a control. Blood samples taken before and several times after exercise were analyzed to determine white blood cell count. The results did not show an increase in white blood cells, suggesting there was not an inflammatory response to muscle damage.

Another study that did not support the inflammatory response hypothesis was one that observed muscle fiber damage from eccentric exercise in man (Friden et al., 1983). Muscle biopsies were taken from the vastus lateralis muscle in humans (a quadriceps muscle of the thigh) after performing eccentric exercise. Although the results showed tissue damage from the exercise, they did not observe the presence of mononuclear cells or macrophages. Their absence suggested that inflammation did not occur from the tissue damage. A third study opposing the inflammatory hypothesis was Armstrong and colleagues’ study on eccentric exercise and rat skeletal muscle. As mentioned above, the study showed some evidence for an inflammatory response, however they found very small amounts of neutrophils in the muscle tissue. Since neutrophils are a major component of the inflammatory response, Armstrong and colleagues suggested that there was not a classic inflammatory response involved in the tissue damage.

Although there is still some question on the type of response the body has to muscle damage (inflammatory or other), there is strong evidence that the muscle fibers are repaired so the muscle can return to normal functioning. One study that supported the idea of muscle repair and adaptation was that conducted by Clarkson and Tremblay (1988). Eight college women performed eccentric exercises of their forearm flexors, at differing numbers of maximal contractions. Five days after exercise, Clarkson and Tremblay analyzed muscle soreness, muscle strength, and serum creatine kinase (CK) activity. Their results suggested that the muscle adapts to the exercise by becoming more resistant to muscle damage when subsequent exercise of the same kind was performed. They also concluded that any damage that did occur was repaired at a faster rate.

Chen and Hsieh (2001) conducted another study that supported the idea of muscle adapting to exercise. They examined the effects of a 7-day eccentric training period on muscle damage in college-age males. Their results referred to an effect called the repeated bout effect (RBE), where after an initial exercise bout that induces soreness, repeating the same exercises results in less muscle damage. In their study, they found that the eccentric exercises performed on days 2-7 did not cause any further damage or soreness than from the first day of exercise. They also suggested that the muscle may start to adapt as early as 24hours following the first bout of exercise.

To summarize, the body displays some inflammatory responses to muscle fiber damage caused by some exercise. These inflammatory responses are generally characterized by the presence of monocytes, neutrophils, macrophages, and lymphocytes inside the body, and felt as symptoms of pain, swelling, and loss of function. Although there is still question on whether there is a classic inflammatory response to muscle tissue injury, there is general agreement on the idea that muscle repair and adaptation occur to help prevent further damage from the same exercise repeated in the near future. Further studies have to be conducted to determine if the responses to muscle fiber injury can be classified as inflammatory.

DISCUSSION OF STUDIES

The studies discussed above are examples of studies that provide evidence supporting the proposed muscle fiber damage from certain exercise and the body’s response to that damage. Because several researchers study related topics, and the goals of their research slightly differ, it is necessary to consider those differences when attempting to understand the proposed hypotheses. More specifically, some of these experimental differences may account for the inconsistencies in the results and the unanswered questions of the topics being studied.

Regarding the studies discussed in this paper, there were three main differences amongst the studies that could have accounted for some unanswered questions. One is that Armstrong and his colleagues studied rat skeletal muscle rather than human muscle. Although several studies on rodents and other animals, such as frogs, have suggested strong correlation with very similar studies on humans, it is not well understood that specific mechanisms in rodents and humans are the same. Therefore, the mechanisms and extent of muscle fiber damage, and the presence of certain inflammatory cells following exercise in the rats may not be that reflective of what occurs in humans.

Another major difference amongst the studies was the time of data collection from the subjects after exercise. In some studies, such as those by Armstrong et al. and Bruunsgaard et al., the experimental protocol involved collecting data within the first few hours after exercise and thereafter. In other studies, such as those by Bobbert et al. and Friden et al., data collections did not begin until 24 hours or more following exercise. This difference in the studies is important because different levels of plasma enzymes and inflammatory cells, and different stages of fiber degeneration are present at different times after tissue injury. For example, neutrophils and monocytes increase in circulation within a few hours after injury and then begin to concentrate at the injury site thereafter. Thus, depending on the stage of fiber damage, or which specific cells are most present, data collection may not show much damage or indices of an inflammatory response.

A third difference amongst the studies that may need to be taken into account is the type of measurements. This difference may be more relevant to the studies that assessed the presence of an inflammatory response. In the studies presented in this paper, researchers used either muscle biopsies or blood samples to assess the presence of inflammatory cells, with the exception of Armstrong and colleagues who used both. These different measurement methods may be important because as explained above, some inflammatory cells may only be present in the blood at certain times after the injury occurs, while others may only be at the injury site. The differing methods may also be important because there may not be a precise location where the tissue injury occurred. Most muscle biopsies are taken from the belly of the muscle (the bulkier part of the muscle). However, if the injury site is more near the myotendinous junction (where the muscle and tendon meet), then there may not be any inflammatory cells present. Therefore, studies that perform muscle biopsies away from the injury site may oppose the inflammatory response hypothesis.

SUMMARY

Delayed onset muscle soreness is the result of muscle fiber injury from unaccustomed exercise, usually eccentric exercises, which put the most force on the muscle fibers. Studies suggest that the disruption to the muscle fibers occurs particularly in muscle cell membranes and the bands that connect muscle cells. In terms of the body’s response to this tissue damage, most studies suggest an acute inflammatory response. Although some question remains on whether the response is inflammatory in a classic sense (i.e., the presence of white blood cells and macrophages), the proposed inflammatory response helps explain the common characteristics of DOMS felt 8 hours to 3 days after exercise. These include pain, loss of muscle function, swelling and reduced muscle force. The purpose of the response is to prepare the fibers for repair, so that the muscle can perhaps become protected from further damage by similar exercise that might be performed in the near future.

At present, most studies agree on the general mechanisms causing muscle fiber damage. However, some questions remain on whether an inflammatory response is involved in DOMS. To understand some of the inconsistencies of the results, one should consider looking at some of the main differences amongst the studies, including the types of subjects used and the methods of measurements. Perhaps, future studies with more similar experimental methods and subjects can create more consistent data to determine the specific mechanisms of delayed onset muscle soreness.

–copyright © 2008, Tahira Collier


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