Exertional Heat Stroke Causes Long‐Term Satellite Cell Dysfunction and Delayed Muscle Repair

Exertional heat stroke (EHS) is an acute life-threatening event that appears to lead long-term health problems such as cardiovascular disease and immunosuppression. However, how skeletal muscle (SKM) affected in the long term by EHS not well understood. One well-known effect of on SKM rhabdomyolysis (RM), caused damage. To regain function, this damage requires effective repair response, which likely include a robust contribution progenitor satellite cell (SCs). We hypothesized SCs display EHS-induced phenotype changes contribute delay process. Purpose determine whether exposure alters SC after 30 d recovery mice evaluate impairs repair. Methods Thirty-two female were either subjected standardized protocol using forced running wheel (environmental temp: 37.5°C, 40% humidity) or matched exercise control trial (EXC)(22.5°C). The achieved peak core temps ~42.2°C accompanied transient loss consciousness. Mice sacrificed at recovery. In one cohort (N=8/group), was collected isolate for quantification proliferation patterns every 24 h over 96 their myogenic ability. Of eight isolations, three unable proliferate all following isolation, response seen any populations. Since significant portion samples did respond, we used nominal stratification classification statistical analysis. second cohort, sequence mRNA perform Western protein analyses. Results found significantly less than EXC 72 & time points (P=0.0273); however, ability differentiate into myotubes different. analysis gastroc elucidated robust, ongoing oxidative transcriptional process included upregulation genes Myh6, Myh7, Atp2a2, Casq2, Tnnc1, Tnnt1, Tnni1. This isoforms associated with fast glycolytic genes. encoding embryonic myosin, Myh3, upregulated, indicator regeneration. encoded adult myosin (Myh7) be (P<0.01), whereas Myh4 different Myh3 undetectable group. Conclusions from single incidence attenuated mice. phenomenon has potential hinder renewal pool, depletion, leading delayed may apparent through lower Myh7 gene transcription program.