Based on results from small animal studies, damage to the cytoskeletal proteins seen after eccentric exercise has been implicated as a trigger for muscle hypertrophy. Despite recent reports (Huijing et al. 1999), describing the importance of the intramuscular collagen in force transmission, the role collagen plays in skeletal muscle adaptation has largely been ignored. The aim of this study was to identify the histological alterations in the cytoskeletal proteins and collagen after a single bout of intense eccentric exercise.

This study was approved by the Ethics Committees of the Municipalities of Copenhagen and Frederiksberg. Eight untrained males (22-30 years) performed 210 maximum eccentric contractions (50 single leg ‘drop jumps’; 8 X 10 RM -30 deg s^-1 eccentric contractions and 8 X 10 RM -180 deg s^-1 eccentric contractions) utilizing an isokinetic dynamometer on one leg only, the contralateral leg acted as the control. Muscle biopsies were taken from the middle of the right and left vastus lateralis muscle on days 0, 2, 4 and 8 after the exercise bout. A venous blood sample and muscle tenderness assessment was obtained on each visit to the laboratory. Numerical data are shown as means ± standard deviation. Isometric force was reduced by 45 ± 19 % after the eccentric exercise bout. Standard assessments of muscle damage, creatine kinase concentration (9628 ± 16 151 U l^-1) and muscle tenderness (8 ± 2, arbitrary scale of 1 and 10), indicated muscle damage had occurred within the exercising muscle. However, seven of the subjects showed no alteration in the cytoskeletal proteins (desmin, dystrophin and fibronectin) in any biopsy taken. Only one individual, with a creatine kinase level of 51 000 U l^-1 on day 4, showed cytoskeletal damage (desmin -ve cells, dystrophin -ve cells, fibronectin +ve cells) in the exercising leg at days 2, 4 and 8. The only constant histological finding in all subjects was an increase in the number of inflammatory cells seen within the perimysial connective tissue space at days 2 and 4 in the exercising leg.

This study suggests that damage to cytoskeletal proteins is not a dominating signalling mechanism for muscle pain or for triggering muscle adaptive responses in muscle fibres. Rather it is suggested that the perimysial connective tissue may play a more dynamic role in post-exercise muscle adaptation than previously reported.