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Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms

journal contribution
posted on 27.08.2021, 01:01 by Nicholas J Saner, Matthew J-C Lee, Jujiao Kuang, Nathan W Pitchford, Gregory RoachGregory Roach, Andrew Garnham, Amanda J Genders, Tanner Stokes, Elizabeth A Schroder, Zhiguang Huo, Karyn A Esser, Stuart M Phillips, David J Bishop, Jonathan D Bartlett
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.

History

Volume

43

Start Page

1

End Page

14

Number of Pages

14

eISSN

2212-8778

ISSN

2212-8778

Location

Germany

Publisher

Elsevier

Publisher License

CC BY-NC-ND

Additional Rights

CC BY NC ND 4.0

Language

eng

Peer Reviewed

Yes

Open Access

Yes

Acceptance Date

29/10/2020

External Author Affiliations

Victoria University; Baker Heart & Diabetes Institute, Vic.; University of Tasmania; McMaster University, Canada; University of Kentucky, USA;

Author Research Institute

Appleton Institute

Era Eligible

Yes

Medium

Print-Electronic

Journal

Molecular Metabolism

Article Number

101110