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Sleep Med Rev. 2018 Feb;37:60-68. doi: 10.1016/j.smrv.2017.01.001. Epub 2017 Jan 19.

Is exercise a viable therapeutic intervention to mitigate mitochondrial dysfunction and insulin resistance induced by sleep loss?

Author information

1
Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Australia.
2
Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Australia; School of Medicine and Health Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, 6027, Australia.
3
Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Australia. Electronic address: Jon.Bartlett@vu.edu.au.

Abstract

Sleep loss has emerged as a risk factor comparable to that of physical inactivity for the development of insulin resistance, impaired glucose tolerance and type 2 diabetes mellitus. This is a concern as it was estimated in 2012 that approximately 70 million adults in the United States are sleeping less than 6 h each night, and the average nightly sleep duration of a representative sample of the U.S. adult population is reported to be significantly less than in previous decades. The underlying mechanisms responsible for chronic sleep loss induced insulin resistance include modifications in the regulation of hormone secretion, peripheral clock gene regulation, and the cellular signaling processes associated with regulating mitochondrial respiratory function. Emerging evidence shows these mechanisms share similar biochemical signaling pathways to those underpinning exercise-induced adaptations, which together suggest exercise might be a viable, suitable, and potent treatment alternative to alleviate sleep loss induced insulin resistance and glucose intolerance. In this theoretical review, we provide a summary of the impact of reduced sleep duration and quality on mitochondrial function and insulin resistance, before detailing the possible underlying mechanisms. Finally, we propose how and why regular exercise may be a therapeutic intervention to mitigate sleep loss induced mitochondrial dysfunction and insulin resistance.

KEYWORDS:

AMP-activated protein kinase (AMPK); Clock genes; Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α); Skeletal muscle

PMID:
29056415
DOI:
10.1016/j.smrv.2017.01.001
[Indexed for MEDLINE]

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