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Update on the effects of physical activity on insulin sensitivity in humans
  1. Stephen R Bird1,
  2. John A Hawley2,3
  1. 1School of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia
  2. 2Mary MaKillop Institute for Health Research, Centre for Exercise and Nutrition, Australian Catholic University, Melbourne, Victoria, Australia
  3. 3Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK
  1. Correspondence to Professor Stephen R Bird; Stephen.bird{at}rmit.edu.au

Abstract

Purpose and methods This review presents established knowledge on the effects of physical activity (PA) on whole-body insulin sensitivity (SI) and summarises the findings of recent (2013–2016) studies.

Discussion and conclusions Recent studies provide further evidence to support the notion that regular PA reduces the risk of insulin resistance, metabolic syndrome and type 2 diabetes, and SI improves when individuals comply with exercise and/or PA guidelines. Many studies indicate a dose response, with higher energy expenditures and higher exercise intensities, including high intensity interval training (HIIT), producing greater benefits on whole-body SI, although these findings are not unanimous. Aerobic exercise interventions can improve SI without an associated increase in cardiorespiratory fitness as measured by maximal or peak oxygen consumption. Both aerobic and resistance exercise can induce improvements in glycaemic regulation, with some suggestions that exercise regimens including both may be more efficacious than either exercise mode alone. Some studies report exercise-induced benefits to SI that are independent of habitual diet and weight loss, while others indicate an association with fat reduction, hence the debate over the relative importance of PA and weight loss continues. During exercise, muscle contraction stimulated improvements in SI are associated with increases in AMPK activity, which deactivates TCB1D1, promoting GLUT4 translocation to the cell membrane and thereby increasing glucose uptake. Postexercise, increases in Akt deactivate TCB1D4 and thereby increase GLUT4 translocation to the cell membrane. The reduction in intramuscular saturated fatty acids and concomitant reductions in ceramides, but not diacylglycerols, provide a potential link between intramuscular lipid content and SI. Increased skeletal muscle capillarisation provides another independent adaptation through which SI is improved, as does enhanced β cell activity. Recent studies are combining exercise interventions with dietary and feeding manipulations to investigate the potential for augmenting the exercise-induced improvements in SI and glycaemic control.

  • Physical Activity
  • Insulin Sensitivity (SI)
  • Diabetes

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

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Footnotes

  • Acknowledgements The authors thank the reviewers for their helpful and constructive comments that assisted with the finalising of the manuscript.

  • Contributor SRB undertook the initial search of the published literature and writing of the paper. JAH provided expert specialist input into the molecular sections, the identification of recent reviews that were used to present the established knowledge and contributed to the writing and revisions to the final manuscript.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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