Abstract
Exercise-induced muscle damage (EIMD) is characterized by a severe and prolonged decline in force-generating capacity. However, the precise cellular mechanisms underlying the observed long-lasting decline in force-generating capacity associated with EIMD are still unclear. We investigated in vivo force generation and ex vivo Ca2+-activated force generation, Ca2+ sensitivity, and myofiber Ca2+ handling systems (SR and t-tubules) in human biceps brachii before and 2, 48, and 96 h after eccentrically muscle-damaging contractions and in non-exercised control arm. The force-generating capacity declined by 50 ± 13% 3 h after exercise and was still not recovered after 96 h. The force-Ca relationship of skinned myofibers revealed an impaired maximal Ca2+-activated force in MHC I-fibers, but not MHC II-fibers 48 h after exercise. Further, Ca2+ sensitivity was increased in MHC II-fibers, which was reversed after incubation with a strong reductant. There was a biphasic increase in SERCA sulfonylation, and a parallel reduction in the SR Ca2+ uptake rate, with no effects on SR vesicle leak or SR vesicle Ca2+ release rate. T-tubules showed a progressive increase in the density of longitudinal tubules by 96 h after exercise. In conclusion, MHC II-fiber Ca2+ sensitivity was increased 48 h after exercise, attributed to changes in the REDOX status. 96 h after exercise SR vesicle Ca2+ uptake was impaired, and an increased number of longitudinal tubules were observed. These alterations may contribute to the impaired force generation evident at the late stage of recovery.