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Acute exercise alters skeletal muscle mitochondrial respiration and H2O2 emission in response to hyperinsulinemic-euglycemic clamp in middle-aged obese men

Trewin, Adam J, Levinger, Itamar, Parker, Lewan, Shaw, Christopher, Serpiello, Fabio R, Anderson, Mitchell J, McConell, Glenn K, Hare, David L and Stepto, Nigel K 2017, Acute exercise alters skeletal muscle mitochondrial respiration and H2O2 emission in response to hyperinsulinemic-euglycemic clamp in middle-aged obese men, PLoS one, vol. 12, no. 11, pp. 1-18, doi: 10.1371/journal.pone.0188421.

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Title Acute exercise alters skeletal muscle mitochondrial respiration and H2O2 emission in response to hyperinsulinemic-euglycemic clamp in middle-aged obese men
Author(s) Trewin, Adam J
Levinger, Itamar
Parker, Lewan
Shaw, ChristopherORCID iD for Shaw, Christopher orcid.org/0000-0003-1499-0220
Serpiello, Fabio R
Anderson, Mitchell J
McConell, Glenn K
Hare, David L
Stepto, Nigel K
Journal name PLoS one
Volume number 12
Issue number 11
Article ID e0188421
Start page 1
End page 18
Total pages 18
Publisher Public Library of Science
Place of publication San Francisco, Calif.
Publication date 2017-11-21
ISSN 1932-6203
Keyword(s) electron transport complex I
exercise therapy
glucose clamp technique
hydrogen peroxide
hyperinsulinism
insulin
insulin resistance
male
middle aged
mitochondria, muscle
obesity
respiration
Summary Obesity, sedentary lifestyle and aging are associated with mitochondrial dysfunction and impaired insulin sensitivity. Acute exercise increases insulin sensitivity in skeletal muscle; however, whether mitochondria are involved in these processes remains unclear. The aim of this study was to investigate the effects of insulin stimulation at rest and after acute exercise on skeletal muscle mitochondrial respiratory function (JO2) and hydrogen peroxide emission (JH2O2), and the associations with insulin sensitivity in obese, sedentary men. Nine men (means ± SD: 57 ± 6 years; BMI 33 ± 5 kg.m2) underwent hyperinsulinemic-euglycemic clamps in two separate trials 1-3 weeks apart: one under resting conditions, and another 1 hour after high-intensity exercise (4x4 min cycling at 95% HRpeak). Muscle biopsies were obtained at baseline, and pre/post clamp to measure JO2 with high-resolution respirometry and JH2O2 via Amplex UltraRed from permeabilized fibers. Post-exercise, both JO2 and JH2O2 during ADP stimulated state-3/OXPHOS respiration were lower compared to baseline (P<0.05), but not after subsequent insulin stimulation. JH2O2 was lower post-exercise and after subsequent insulin stimulation compared to insulin stimulation in the rest trial during succinate supported state-4/leak respiration (P<0.05). In contrast, JH2O2 increased during complex-I supported leak respiration with insulin after exercise compared with resting conditions (P<0.05). Resting insulin sensitivity and JH2O2 during complex-I leak respiration were positively correlated (r = 0.77, P<0.05). We conclude that in obese, older and sedentary men, acute exercise modifies skeletal muscle mitochondrial respiration and H2O2 emission responses to hyperinsulinemia in a respiratory state-specific manner, which may have implications for metabolic diseases involving insulin resistance.
Language eng
DOI 10.1371/journal.pone.0188421
Field of Research 110602 Exercise Physiology
MD Multidisciplinary
HERDC Research category C1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2017, Trewin et al
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30108800

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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.