This is an excerpt from Physiology of Sport and Exercise 8th Edition With HKPropel Access by W. Larry Kenney,Jack H. Wilmore & David L. Costill.
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:
- 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.
- 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.
- Within a few hours there is a significant elevation in circulating neutrophils that participate in the inflammatory response.
- 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.
- Fluid and electrolytes shift into the area, creating edema, which causes tissue swelling and activates pain receptors. Muscle spasms may also be present.
DOMS 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, the affected muscles are not able to exert as much force when the person is asked to apply maximal force, as in the performance of a 1-repetition maximum strength test. Maximal force-generating capacity gradually returns over days or weeks. The loss of strength is the result of
- the physical disruption of the muscle as illustrated in figure 6.9,
- failure within the excitation–contraction coupling process, see figure 1.8, and
- loss of contractile protein.
Failure in excitation–contraction coupling appears to be the most important, particularly during the first 5 days. This is illustrated in figure 6.10.
Muscle glycogen resynthesis also is impaired when a muscle is damaged. Resynthesis is generally normal for the first 6 to 12 h after exercise, but it slows or stops completely as the muscle undergoes repair, thus limiting the fuel storage capacity of the injured muscle. Figure 6.11 illustrates the time sequence of the various markers of muscle damage associated with intense eccentric exercise of the elbow flexor muscles as compared with concentric exercise. As shown in the figure, changes in function (MVC and range of motion), muscle swelling (circumference), soreness, and molecular indicators of damage (creatine kinase activity and myoglobin concentration) persist for several days.
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 an exhaustive high-intensity 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.