European journal of applied physiology · 2026
Running in the heat reduces time to task failure, attenuates biomarkers of muscle microtrauma, and exacerbates low-frequency force depression and cardiac vagal withdrawal over 72-h post-exercise.
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Dutra Yago Medeiros, Mendonça Paloma Tavares, Lopes João Pedro Fialho, Esco Michael R, de Souza Malta Elvis, de Poli Rodrigo Araújo Bonetti, Zagatto Alessandro Moura
Аннотация
PURPOSE: As exercise in the heat becomes increasingly common, a better understanding of post-exercise responses is essential to guide the appropriate use of fatigability monitoring tools and recovery strategies. Therefore, this study investigated the effect of running in the heat on neuromuscular function, cardiac autonomic modulation, and plasma markers of muscle microtrauma during post-exercise recovery.
METHODS: Twelve participants (V̇O2max: 44.8 ± 3.5 mL/kg/min) ran to task failure at a velocity associated with the respiratory compensation point (vRCP) in temperate (22.4 ± 0.9 °C) and hot (38.8 ± 0.7 °C) environments. Voluntary and evoked contractions of the knee-extensors, heart rate variability (HRV), and plasma creatine kinase (CK) and lactate dehydrogenase (LDH) concentrations were assessed pre-exercise, within the first hour post-exercise, and at 24-, 48, and 72-h post-exercise.
RESULTS: Running in the heat reduced time to task failure (TTF, 17.8 ± 4.4 min vs. 42.3 ± 20.1, p < 0.01, d = 1.96) and attenuated the increase in plasma CK at 24 h post-exercise (condition×time interaction, post-hoc p < 0.05). Neuromuscular function and cardiac autonomic modulation were impaired within the first hour post-exercise (time effects, p < 0.05) and returned to baseline values at 24-h post-exercise in both conditions (post-hoc p > 0.05). Aggregated data (condition effects, post-hoc p < 0.05) over the 72-h monitoring time evidenced exacerbation of low-frequency force depression (reduced Db10Force/Db100Force) and cardiac vagal withdrawal (reduced high-frequency HRV power) after running in the heat.
CONCLUSION: Running in the heat at vRCP reduced TTF. Although heat reduced exercise duration, it specifically exacerbated low-frequency force depression and cardiac vagal withdrawal for 72-h post-exercise while attenuating the increase in plasma markers of muscle microtrauma at 24-h post-exercise.
METHODS: Twelve participants (V̇O2max: 44.8 ± 3.5 mL/kg/min) ran to task failure at a velocity associated with the respiratory compensation point (vRCP) in temperate (22.4 ± 0.9 °C) and hot (38.8 ± 0.7 °C) environments. Voluntary and evoked contractions of the knee-extensors, heart rate variability (HRV), and plasma creatine kinase (CK) and lactate dehydrogenase (LDH) concentrations were assessed pre-exercise, within the first hour post-exercise, and at 24-, 48, and 72-h post-exercise.
RESULTS: Running in the heat reduced time to task failure (TTF, 17.8 ± 4.4 min vs. 42.3 ± 20.1, p < 0.01, d = 1.96) and attenuated the increase in plasma CK at 24 h post-exercise (condition×time interaction, post-hoc p < 0.05). Neuromuscular function and cardiac autonomic modulation were impaired within the first hour post-exercise (time effects, p < 0.05) and returned to baseline values at 24-h post-exercise in both conditions (post-hoc p > 0.05). Aggregated data (condition effects, post-hoc p < 0.05) over the 72-h monitoring time evidenced exacerbation of low-frequency force depression (reduced Db10Force/Db100Force) and cardiac vagal withdrawal (reduced high-frequency HRV power) after running in the heat.
CONCLUSION: Running in the heat at vRCP reduced TTF. Although heat reduced exercise duration, it specifically exacerbated low-frequency force depression and cardiac vagal withdrawal for 72-h post-exercise while attenuating the increase in plasma markers of muscle microtrauma at 24-h post-exercise.