Elevation of body temperature during exercise enhances protection against dexamethasone‑induced skeletal muscle atrophy

作者：Berkay Ozerklig, Şenay Akın, Seda Olgaz Bingol, B. O. Yildiz, Scott K. Powers, Ibrahim Turkel, H. Demirel · 发表于：Experimental Physiology · 年份：2026 · DOI：10.1113/ep093744 · 研究领域：Medicine

Abstract Prolonged glucocorticoid exposure induces skeletal muscle atrophy through suppression of protein synthesis and activation of catabolic signalling pathways. Although exercise attenuates glucocorticoid‐induced muscle loss, whether exercise‐induced increases in body temperature contribute remains unclear. In this study, we examined whether exercise in different thermal conditions modulates skeletal muscle atrophy and intracellular signalling during glucocorticoid exposure. Female Sprague–Dawley rats (n = 48) were assigned to six groups: control (CON), dexamethasone‐treated (DEX), cold exercise (∼5°C; CE), cold exercise with dexamethasone (CED), warm exercise (25°C; WE) and warm exercise with dexamethasone. Exercise protocols were matched, and dexamethasone was administered for 5 days. Dexamethasone reduced plantaris muscle mass (by 17%, P < 0.0001) and fibre cross‐sectional area (27%, P < 0.0001). During dexamethasone treatment, exercise in a cold environment provided partial protection, with muscle mass higher than DEX (P = 0.0476), but both muscle mass and fibre CSA remained lower than CON (P = 0.0096 and P = 0.0215, respectively). In contrast, exercise in a warm environment preserved muscle mass and fibre CSA (no difference vs. CON) and resulted in higher muscle mass (P = 0.0070) and fibre CSA (P < 0.0001) than DEX. Exercise‐induced increases in rectal temperature were associated with higher Hsp72 and Hsp25 expression, partial preservation of Akt–FoxO3a signalling an...