Handegard V, Lunde P K, Frisk M, Seynnes O, Ørtenblad N, Louch W E, Paulsen G, Raastad T
Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway.
Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
Physiol Rep. 2025 Feb;13(3):e70204. doi: 10.14814/phy2.70204.
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-activated force generation, Ca sensitivity, and myofiber Ca 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-activated force in MHC I-fibers, but not MHC II-fibers 48 h after exercise. Further, Ca 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 uptake rate, with no effects on SR vesicle leak or SR vesicle Ca 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 sensitivity was increased 48 h after exercise, attributed to changes in the REDOX status. 96 h after exercise SR vesicle Ca 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.
运动诱导的肌肉损伤（EIMD）的特征是力量产生能力严重且持续下降。然而，与EIMD相关的力量产生能力长期下降背后的确切细胞机制仍不清楚。我们研究了人体肱二头肌在进行离心性肌肉损伤收缩前、收缩后2小时、48小时和96小时以及未运动的对照手臂中体内力量产生、体外钙激活力量产生、钙敏感性和肌纤维钙处理系统（肌浆网和横管）的情况。运动后3小时力量产生能力下降了50±13%，96小时后仍未恢复。运动48小时后，去表皮肌纤维的力量-钙关系显示，MHC I型纤维的最大钙激活力量受损，但MHC II型纤维未受损。此外，MHC II型纤维的钙敏感性增加，在用强还原剂孵育后这种增加被逆转。肌浆网钙ATP酶（SERCA）的磺酰化呈双相增加，同时肌浆网钙摄取率平行降低，对肌浆网囊泡渗漏或肌浆网囊泡钙释放率无影响。运动96小时后，横管的纵向管密度逐渐增加。总之，运动48小时后MHC II型纤维的钙敏感性增加，这归因于氧化还原状态的变化。运动96小时后，肌浆网囊泡钙摄取受损，并且观察到纵向管数量增加。这些改变可能导致恢复后期明显的力量产生受损。
