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

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⁺

SUBMITTER: Handegard V 

PROVIDER: S-EPMC11788311 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature