Abstract
The results regarding the effects of unaccustomed eccentric exercise on muscle tissue are often conflicting and the aetiology of delayed onset muscle soreness (DOMS) induced by eccentric exercise is still unclear. This study aimed to re-evaluate the paradigm of muscular alterations with regard to muscle sarcolemma integrity and fibre swelling in human muscles after voluntary eccentric exercise leading to DOMS. Ten young males performed eccentric exercise by downstairs running. Biopsies from the soleus muscle were obtained from 6 non-exercising controls, 4 exercised subjects within 1 hour and 6 exercised subjects at 2–3 days and 7–8 days after the exercise. Muscle fibre sarcolemma integrity, infiltration of inflammatory cells and changes in fibre size and fibre phenotype composition as well as capillary supply were examined with specific antibodies using enzyme histochemistry and immunohistochemistry. Although all exercised subjects experienced DOMS which peaked between 1.5 to 2.5 days post exercise, no significant sarcolemma injury or inflammation was detected in any post exercise group. The results do not support the prevailing hypothesis that eccentric exercise causes an initial sarcolemma injury which leads to subsequent inflammation after eccentric exercise. The fibre size was 24% larger at 7–8 days than at 2–3 days post exercise (p<0.05). In contrast, the value of capillary number per fibre area tended to decrease from 2–3 days to 7–8 days post exercise (lower in 5 of the 6 subjects at 7–8 days than at 2–3 days; p<0.05). Thus, the increased fibre size at 7–8 days post exercise was interpreted to reflect fibre swelling. Because the fibre swelling did not appear at the time that DOMS peaked (between 1.5 to 2.5 days post exercise), we concluded that fibre swelling in the soleus muscle is not directly associated with the symptom of DOMS.
Highlights
The aetiology of delayed onset muscle soreness (DOMS) induced by eccentric exercise is still unclear [1]
The prevailing hypothesis of the mechanisms of DOMS is that the excessive strain produced during eccentric muscular contraction induces extracellular or intracellular membrane disruption that may induce hydrolysis of structural proteins such as desmin intermediate filament network, leading to myofibrillar disorganization in the form of Z-band streaming or complete disruption [2,3]
Recent studies in humans provided evidence which did not support the hypothesis, e.g., voluntary eccentric exercise did not lead to desmin intermediate filament network hydrolysis [5,6], myofibrillar disruption [5,7] or muscle fibre inflammation and necrosis [5,6,8,9,10]
Summary
The aetiology of delayed onset muscle soreness (DOMS) induced by eccentric exercise (i.e., lengthening of a contracting muscle) is still unclear [1]. The prevailing hypothesis of the mechanisms of DOMS is that the excessive strain produced during eccentric muscular contraction induces extracellular or intracellular membrane disruption that may induce hydrolysis of structural proteins such as desmin intermediate filament network, leading to myofibrillar disorganization in the form of Z-band streaming or complete disruption [2,3]. This is followed by fibre necrosis and inflammatory cell infiltration that potentiate the nerve endings and perception of pain. The Z-band streaming, classically proposed to be a hallmark of muscle damage after eccentric exercise [11,12] was proved to represent myofibril remodelling [7,13,14,15,16]
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