4.7 Article

Effects of curtailed sleep on cardiac stress biomarkers following high-intensity exercise

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MOLECULAR METABOLISM
卷 58, 期 -, 页码 -

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DOI: 10.1016/j.molmet.2022.101445

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High-intensity exercise; Cardiomyocyte; Cardiovascular strain; Heart muscle; Sleep loss; Troponin

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Short-term sleep restriction may increase the cardiac stress response to acute high-intensity exercise in healthy young individuals, although no significant differences were observed in resting conditions. This suggests that sleep plays a significant role in the body's performance during exercise.
Objective: Physical exercise-especially at high intensity-is known to impose cardiac stress, as mirrored by, e.g., increased blood levels of cardiac stress biomarkers such as cardiac Troponin T (cTnT) and NT-proBNP. We examined healthy young participants to determine whether a few nights of short sleep duration alter the effects of acute exercise on these blood biomarkers. Methods: Sixteen men participated in a randomized order in a crossover design, comprising three consecutive nights of a) normal sleep duration (NS, 8.5 h of sleep/night) and b) sleep restriction (SR, 4.25 h of sleep/night). Blood was repeatedly sampled for determination of NT-proBNP and cTnT serum levels before and after a high-intensity exercise protocol (i.e., 75% VO2maxReserve cycling on an ergometer). Results: Under pre-exercise sedentary conditions, blood levels of cTnT and NT-proBNP did not significantly differ between the sleep conditions (P > 0.10). However, in response to exercise, the surge of circulating cTnT was significantly greater following SR than NS (+37-38% at 120-240 min post-exercise, P <= 0.05). While blood levels of NT-proBNP rose significantly in response to exercise, they did not differ between the sleep conditions. Conclusion: Recurrent sleep restriction may increase the cardiac stress response to acute high-intensity exercise in healthy young individuals. However, our findings must be further confirmed in women, older subjects and in patients with a history of heart disease. (c) 2022 The Author(s). Published by Elsevier GmbH.This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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