A more current and well-supported theory is the Muscle Damage theory, which is based on the disruption of the contractile component of muscle tissue after eccentric exercise. Type II fibers have the narrowest z-lines and are particularly susceptible to this type of disruption. Nociceptors located in the muscle connective tissue and in the surrounding tissues are stimulated, which leads to the sensation of pain that we know as DOMS. In practice, muscle soluble enzymes can be used as an indicator of z-line disruption and sarcolemma damage. Creatine Kinase (CK) is used as one of these muscle permeability indicators; any disruption of the z-lines and damage to the sarcolemma will enable the diffusion of CK into the interstitial fluid, where it can be measured.
Explanation :
This study goes on to explain that during the recovery phase post-contraction, accumulated lactate gets oxidized by lactate dehydrogenase (LDH) into pyruvate. This pyruvate is either oxidized in the mitochondria where it contributes to the resynthesis of ATP, or it is transported in the blood to be used or disposed of elsewhere in the body. It has been observed that for test subjects whose lactate levels were monitored for 72 hours before, during, and after exercise, their lactic acid levels returned to pre-exercise levels within 1 hour of the cessation of exercise[2]. Since DOMS does not set in for 24-48 hours, it is very unlikely that lactic acid accumulation is the cause of the pain and other symptoms associated with this disease.
These researchers did note some conditions however that were noted to affect the lactate levels of those participating in the study. For example, a participant with a diet rich or low in carbohydrate concentrations can cause lactate levels to decrease or increase respectively. Further, participants who had undergone strenuous exercise the day before are likely to show signs of glycogenic depletion, which could cause them to have irregular lactate levels. Further, the type of exercise performed was also shown to have an effect on not only lactate levels but also on the time frame required for levels to return to normal. To improve this study and potentially get better results it would be best to make sure that all test subjects were undergoing the same exercise regimens. It would also be beneficial if the amount of carbohydrates (based on body weight) was held standard, and that they all experienced 48 hours of rest before data collection. However, even given these potential weaknesses, given that the lactate levels return to below normal within an hour of exercise cessation, it can be said with reasonable certainty that lactic acid is not the cause of DOMS.
A more current and well-supported theory is the Muscle Damage theory, which is based on the disruption of the contractile component of muscle tissue after eccentric exercise. Type II fibers have the narrowest z-lines and are particularly susceptible to this type of disruption. Nociceptors located in the muscle connective tissue and in the surrounding tissues are stimulated, which leads to the sensation of pain that we know as DOMS. In practice, muscle soluble enzymes can be used as an indicator of z-line disruption and sarcolemma damage. Creatine Kinase (CK) is used as one of these muscle permeability indicators; any disruption of the z-lines and damage to the sarcolemma will enable the diffusion of CK into the interstitial fluid, where it can be measured.
