Myofiber structure, sarcoplasmic reticulum Ca²⁺ handling, and contractile function after muscle‐damaging exercise in humans

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 Ca 2+ ‐activated force generation, Ca 2+ sensitivity, and myofiber Ca 2+ 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 Ca 2+ ‐activated force in MHC I‐fibers, but not MHC II‐fibers 48 h after exercise. Further, Ca 2+ 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 Ca 2+ uptake rate, with no effects on SR vesicle leak or SR vesicle Ca 2+ release rate. T‐tubules showed a progressive increase in the density of longitudinal tubules by 96 h after exercise. In conclusion, MHC II‐fiber Ca 2+ sensitivity was increased 48 h after exercise, attributed to changes in the REDOX status. 96 h after exercise SR vesicle Ca 2+ 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.