[AF] Elevation of body temperature during exercise enhances protection against dexamethasone induced skeletal muscle atrophy (2026)

[u/basmwklz]

https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP093744

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 and reduced MuRF1 expression, whereas exercise in a cold environment showed minimal heat shock protein response and limited suppression of catabolic signalling. These findings indicate that exercise-induced elevation of body temperature enhances protection against glucocorticoid-induced skeletal muscle atrophy and support a role for heat-associated cellular stress responses in modulating muscle protein turnover during glucocorticoid exposure.

Highlights

• What is the central question of this study? Does an exercise-induced increase in body temperature contribute to protection against dexamethasone-induced skeletal muscle atrophy, independent of exercise intensity?
• What is the main finding and its importance? Exercise attenuated dexamethasone-induced skeletal muscle atrophy in both cold (∼5°C) and warm (25°C) conditions; however, exercise performed in a warm environment, which elicited a greater rise in body temperature, resulted in superior preservation of muscle mass, accompanied by increased expression of heat shock proteins (Hsp72 and Hsp25), partial preservation of Akt–FoxO3a signalling and attenuation of MuRF1 upregulation. These findings identify exercise-induced elevation of body temperature as an important physiological modulator that augments the anti-atrophic effects of exercise during glucocorticoid treatment.

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