Author(s): KITAOKA, Y., SHIRAI, T., EBISUDA, Y., TAKAHASHI, Y., SUGIYAMA, F., MUKAI, K., Institution: KANAGAWA UNIVERSITY, Country: JAPAN, Abstract-ID: 1819

INTRODUCTION:
It is known that repeated exposure to heat leads to acclimation, which improves whole-body thermoregulatory mechanisms and enhances exercise performance in hot conditions. However, the impact of heat stress on equine skeletal muscle is not yet fully understood. In this study, we examined the direct effects of heat stress treatment on mitochondrial respiratory function and transcriptomic responses using primary equine skeletal muscle culture cells.
METHODS:
Ten Thoroughbred horses performed incremental exercise tests (IET) under hot conditions (wet bulb globe temperature: 30°C). Biopsies from the gluteus medius muscle were taken before IET, and cultured myoblasts were incubated at 37°C (control) or 43°C (heat) for 1 h. Oxygen consumption rate was measured using a Seahorse XF96 Extracellular Flux Analyzer. At 3 h after the heat treatment, differential gene expression was identified using DESeq2 (false discovery rate cutoff: 0.05, minimal fold change: 1.5).
RESULTS:
There was a trend of correlation between exercise duration during IET and maximal respiration of cultured myoblasts from each horse (r=0.59, p=0.07). Immediately following heat treatment, both basal and maximal respiration decreased significantly while proton leak remained unchanged. Heat exposure upregulated 331 genes and downregulated 414 genes in equine myoblasts compared with control cells. Pathway analysis revealed heat-induced upregulation of outer mitochondrial membrane organization and downregulation of mitophagy.
CONCLUSION:
Our results suggest that hyperthermia transiently decreases the efficiency of cellular respiration and triggers mitochondrial remodeling in equine skeletal muscle. These observations may provide insights for improving exercise performance in hot conditions.