Medicine and science in sports and exercise · 2026
Sleep Deprivation Selectively Alters Cellular Stress Responses During Exercise in the Heat in Young and Older Males.
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McCormick James J, McCormick Kelli E, Koetje Nicholas J, Kenny Glen P
Аннотация
INTRODUCTION: Older adults are at heightened risk of heat-related morbidity, particularly in occupational settings where insufficient sleep and heat exposure commonly coincide. Autophagy and other proteostatic pathways are essential for maintaining cellular homeostasis during acute physiological stress; however, whether acute sleep deprivation modifies these responses during exercise-heat stress remains unknown.
METHODS: Ten young (23±3 years) and 10 older (61±4 years) males completed an exercise-heat stress test following normal sleep and after 24 h of total sleep deprivation in which participants performed three 30-min cycling bouts at fixed rates of metabolic heat production (150, 200, and 250 W·m -2), each separated by 15 min rest in the heat (40°C, ~13% relative humidity). Autophagy and related cellular stress pathways were assessed before and after exercise.
RESULTS: Sleep deprivation did not alter macroautophagy-related proteins, including LC3-II, the LC3-II/I ratio, ULK1 phosphorylation, or beclin-2 in either age group. However, p62 was reduced at end-exercise in young males following sleep deprivation (p=0.010), whereas the corresponding reduction in older males did not reach statistical significance. Sleep deprivation differentially altered proteins involved in chaperone-mediated autophagy, with LAMP-2A decreasing in young males but increasing in older males (both, p≤0.004). In older males, sleep deprivation reduced HSP90 and increased cleaved-caspase-3 and TNF-α (both, p≤0.048), indicating greater apoptotic and inflammatory signaling.
CONCLUSIONS: Our findings indicate that 24 h of sleep deprivation does not broadly alter markers of macroautophagy during exercise-heat stress but selectively modifies cellular stress pathways in older males, with distinct responses observed in young and older males.
METHODS: Ten young (23±3 years) and 10 older (61±4 years) males completed an exercise-heat stress test following normal sleep and after 24 h of total sleep deprivation in which participants performed three 30-min cycling bouts at fixed rates of metabolic heat production (150, 200, and 250 W·m -2), each separated by 15 min rest in the heat (40°C, ~13% relative humidity). Autophagy and related cellular stress pathways were assessed before and after exercise.
RESULTS: Sleep deprivation did not alter macroautophagy-related proteins, including LC3-II, the LC3-II/I ratio, ULK1 phosphorylation, or beclin-2 in either age group. However, p62 was reduced at end-exercise in young males following sleep deprivation (p=0.010), whereas the corresponding reduction in older males did not reach statistical significance. Sleep deprivation differentially altered proteins involved in chaperone-mediated autophagy, with LAMP-2A decreasing in young males but increasing in older males (both, p≤0.004). In older males, sleep deprivation reduced HSP90 and increased cleaved-caspase-3 and TNF-α (both, p≤0.048), indicating greater apoptotic and inflammatory signaling.
CONCLUSIONS: Our findings indicate that 24 h of sleep deprivation does not broadly alter markers of macroautophagy during exercise-heat stress but selectively modifies cellular stress pathways in older males, with distinct responses observed in young and older males.