Saner, NJ and Lee, MJC and Kuang, J and Pitchford, NW and Roach, GD and Garnham, A and Genders, AJ and Stokes, T and Schroder, EA and Huo, Z and Esser, KA and Phillips, SM and Bishop, DJ and Bartlett, JD, Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms, Molecular Metabolism, 43 pp. 1-14. ISSN 2212-8778 (2021) [Refereed Article]
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Copyright 2020 The Author(s). Published by Elsevier GmbH. This is an open access article under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Objective: Sleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Because exercise improves glucose tolerance and mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep.
Methods: To minimize between-group differences of baseline characteristics, 24 healthy young males were allocated into one of the three experimental groups: a Normal Sleep (NS) group (8 h time in bed (TIB) per night, for five nights), a Sleep Restriction (SR) group (4 h TIB per night, for five nights), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB per night, for five nights and three high-intensity interval exercise (HIIE) sessions). Glucose tolerance, mitochondrial respiratory function, sarcoplasmic protein synthesis (SarcPS), and diurnal measures of peripheral skin temperature were assessed pre- and post-intervention.
Results: We report that the SR group had reduced glucose tolerance post-intervention (mean change ± SD, P value, SR glucose AUC: 149 ± 115 A.U., P = 0.002), which was also associated with reductions in mitochondrial respiratory function (SR: -15.9 ± 12.4 pmol O2.s-1.mg-1, P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P < 0.001), and reduced amplitude of diurnal rhythms. These effects were not observed when incorporating three sessions of HIIE during this period (SR+EX: glucose AUC 67 ± 57, P = 0.239, mitochondrial respiratory function: 0.6 ± 11.8 pmol O2.s-1.mg-1, P = 0.997, and SarcPS (FSR%/day): 1.77 ± 0.22%, P = 0.971).
Conclusions: A five-night period of sleep restriction leads to reductions in mitochondrial respiratory function, SarcPS, and amplitude of skin temperature diurnal rhythms, with a concurrent reduction in glucose tolerance. We provide novel data demonstrating that these same detrimental effects are not observed when HIIE is performed during the period of sleep restriction. These data therefore provide evidence in support of the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.
|Item Type:||Refereed Article|
|Keywords:||circadian rhythms, exercise, glucose tolerance, mitochondria, sleep|
|Research Division:||Health Sciences|
|Research Group:||Sports science and exercise|
|Research Field:||Exercise physiology|
|Objective Group:||Clinical health|
|Objective Field:||Treatment of human diseases and conditions|
|UTAS Author:||Pitchford, NW (Dr Nathan Pitchford)|
|Web of Science® Times Cited:||9|
|Deposited By:||Health Sciences|
|Downloads:||6 View Download Statistics|
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