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

Saner, Nicholas J.; Bishop, David J.; Bartlett, Jonathan D.

doi:10.1016/j.smrv.2017.01.001

Cited by 41Circadian rhythm and melatoninSleep and related disordersSleep and Work-Related Fatigue

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

Saner, Nicholas J., Bishop, David J., Bartlett, Jonathan D.·2018·Sleep Medicine Reviews

DOI 10.1016/j.smrv.2017.01.001

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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.

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Sleep-loss-induced reductions in glucose tolerance may in part be a consequence of changes in mitochondrial content, function, or processes that regulate these properties, including mitochondrial dynamics and mitochondrial protein synthesis.
“Therefore, sleep-loss-induced reductions in glucose tolerance may, in part, be a consequence of changes in mitochondrial content, function, or the processes that regulate these properties, including mitochondrial dynamics and mitochondrial protein synthesis [17].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [17]
One approach to mitigate or ablate the impact of reduced sleep duration on glucose tolerance is via exercise.
“One approach to mitigate or ablate the impact of reduced sleep duration on glucose tolerance is via exercise [17].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [17]
High-intensity interval exercise may mitigate the detrimental effects of sleep loss on glucose metabolism by increasing mitochondrial content and function and preventing changes in circadian rhythmicity.
“Consequently, HIIE may mitigate the detrimental effects of sleep loss on glucose metabolism by increasing mitochondrial content and function and preventing changes in circadian rhythmicity [17].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [17]
Exercise has potential benefits in the context of circadian misalignment and sleep loss.
“Considering the negative metabolic consequences, such as reduction in insulin sensitivity and mitochondrial function, attributed to both circadian misalignment and sleep loss [21,67] and the potential benefits of exercise in this context [17,68], further research is warranted.”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [17]

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Authors: Saner, N. J., Bishop, D. J., & Bartlett, J. D.
Affiliations: Victoria University (AU)
Edith Cowan University (AU)
Corresponding author: Bartlett, Jonathan D.
ORCID: Saner, Nicholas J.
Bishop, David J.
Bartlett, Jonathan D.
Venue: Sleep Medicine Reviews
Publisher: Elsevier BV
Published: 2018-02
Volume: 37
Pages: 60-68
ISSN: 1087-0792 (ISSN-L)
DOI: 10.1016/j.smrv.2017.01.001
OpenAlex: W2574522861
Cited by: 41
References: 97
Citations by year: 2026: 2 · 2025: 5 · 2024: 8 · 2023: 6 · 2022: 8 · 2021: 1 · 2020: 6 · 2019: 2 · 2018: 3
FWCI: 0.36
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Sleep Medicine Reviews (publishedVersion)
PubMed (publishedVersion)
Victoria University Research Repository (Victoria University) (submittedVersion)
Research Online (Edith Cowan University) (submittedVersion)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords: sleep deprivation, physical activity, insulin resistance, mitochondrial dysfunction, type 2 diabetes, impaired glucose tolerance, clock genes, hormone secretion, mitochondrial respiratory function, exercise therapy
MeSH terms: Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Mitochondria, Sleep Deprivation, Exercise, AMP-Activated Protein Kinases, CLOCK Proteins

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

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