Delayed onset muscle soreness (DOMS) is a familiar experience for the elite and novice athletes. Symptoms can range from muscle tenderness to severe deliberating pain. It is generally believed that eccentric contractions produce higher tension on muscle fibres and connective tissues than concentric and isometric contractions. This higher mechanical stress induces initial injury, and subsequent damage is linked to inflammatory process and to changes in the excitation-contraction coupling within the muscles. Classically myofibrillar ultrastrctural changes in DOMS muscles are mainly related with myofibrillar Z-disc. Z-disc streaming and broadening have long been deemed as the hallmarks of DOMS muscles. Recent studies on rabbit models have shown a rapid loss of the intermediate filament protein desmin after eccentric contractions and this was believed to be the initial event which triggers a subsequent muscle fibre necrosis. Even though numerous studies have been conducted on both human muscles and animal models following eccentric exercise, the mechanisms responsible for the perception of DOMS have not been clearly identified.
To re-evaluate the exercise-induced muscle soreness with respect to the muscle fibre structural changes, in the present study three different modes of eccentric exercise were used as a model to introduce DOMS in healthy young subjects. Biopsies from the soleus muscle and vastus lateralis muscle were taken from control subjects and those who had taken part in the exercise, at different time intervals after exercise. The biopsies were analyzed with general histology, enzymehistochemistry, immunohistochemistry and electronmicroscopy.
All the three exercise protocols induced DOMS, which reached its peak value at 24-48 hour post exercise. Examination of the biopsies taken after the three exercise modes showed no loss of desmin or fibre necrosis of any biopsy. However, in biopsies taken 1 hour post exercise, some influx of fibrinogen into muscle fibres was observed. Despite that, the sarcolemma integrity revealed by stainings with dystrophin and laminin was seemingly not destroyed. Further analysis of the biopsies taken after the downstairs running with high-resolution immunohistochemistry revealed the following alterations: 1) F-actin and desmin were in much greater amounts and distributed differently from normal muscle; 2) alpha-actinin, nebulin and titin were initially lacking in focal areas and were subsequently reappearing. These changes were mainly observed in the 2-3 days and 7-8 days post exercise biopsies. The staining patterns were proposed to represent different stages of sarcomere formation. These findings therefore support the suggestion that myofibrils in muscles subjected to eccentric contractions adapt to unaccustomed activity by the addition of new sarcomeres. Electronmicroscopy showed ultrastructural changes also mainly in biopsies taken 2-3 days and 7-8 days post exercise. These changes were classified into four types on bases of their different staining patterns. For each of the four types of changes, there was a corresponding type of changes revealed by the immunohistochemical method. It was concluded that alterations revealed by electronmicroscopy were suggestive of myofibrillar remodeling rather than the conventionally suggested injury.
The present study will change the dogma that myofibrillar disruption/damage is a hallmark of DOMS. The findings of this study is of clinical importance as the myofibrils contrary to becoming weakened, are reinforced by cytoskeletal elements during the addition of new sarcomeres. The latter gives for the first time a mechanistic explanation for the lack of further damage upon additional exercise (second bout effect). Furthermore, the current methods of analysis of biopsies from eccentric exercised subjects can be used as an in situ model to analyze the molecular changes taking place in the muscle fibres affected by DOMS.