Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16398
Title: Acute high-intensity interval exercise-induced redox signaling is associated with enhanced insulin sensitivity in obese middle-aged men
Austin Authors: Parker, Lewan;Stepto, Nigel K;Shaw, Christopher S;Serpiello, Fabio R;Anderson, Mitchell;Hare, David L ;Levinger, Itamar 
Affiliation: Clinical Exercise Science Research Program, Institute of Sport, Exercise and Active Living, Victoria University, Melbourne, Victoria, Australia
Centre for Physical Activity and Nutrition Research, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia
University of Melbourne and the Department of Cardiology, Austin Health, Heidelberg, Victoria, Australia
Issue Date: 16-Sep-2016
metadata.dc.date: 2016-09-16
Publication information: Frontiers in Physiology 2016; online first: 16 September 2016
Abstract: Background: Obesity and aging are associated with increased oxidative stress, activation of stress and mitogen activated protein kinases (SAPK), and the development of insulin resistance and metabolic disease. In contrast, acute exercise also increases oxidative stress and SAPK signaling, yet is reported to enhance insulin sensitivity and reduce the risk of metabolic disease. This study explored this paradox by investigating the effect of a single session of high-intensity interval-exercise (HIIE) on redox status, muscle SAPK and insulin protein signaling in eleven middle-aged obese men. Methods: Participants completed a 2 h hyperinsulinaemic-euglycaemic clamp at rest, and 60 min after HIIE (4 × 4 mins at 95% HRpeak; 2 min recovery periods), separated by 1-3 weeks. Results: Irrespective of exercise-induced changes to redox status, insulin stimulation both at rest and after HIIE similarly increased plasma superoxide dismutase activity, plasma catalase activity, and skeletal muscle 4-HNE; and significantly decreased plasma TBARS and hydrogen peroxide. The SAPK signaling pathways of p38 MAPK, NF-κB p65, and JNK, and the distal insulin signaling protein AS160Ser588, were activated with insulin stimulation at rest and to a greater extent with insulin stimulation after a prior bout of HIIE. Higher insulin sensitivity after HIIE was associated with higher insulin-stimulated SOD activity, JNK, p38 MAPK and NF-κB phosphorylation (r = 0.63, r = 0.71, r = 0.72, r = 0.71; p < 0.05, respectively). Conclusion:These findings support a role for redox homeostasis and SAPK signaling in insulin-stimulated glucose uptake which may contribute to the enhancement of insulin sensitivity in obese men 3 h after HIIE
URI: http://ahro.austin.org.au/austinjspui/handle/1/16398
DOI: 10.3389/fphys.2016.00411
ORCID: 0000-0001-9554-6556
PubMed URL: 27695421
Type: Journal Article
Subjects: High-intensity exercise
Insulin resistance
Obesity
Oxidative stress
Appears in Collections:Journal articles

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