Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/39453
Title: The effect of exercise-intensity on Skeletal muscle stress kinase and insulin protein signaling.
Authors: Shaw C.S.;Parker L.;Trewin A.;Levinger I.;Stepto N.K.
Institution: (Parker, Trewin, Levinger, Shaw, Stepto) Institute of Sport, Exercise and Active Living (ISEAL), College of Sport and Exercise Science, Victoria University, Melbourne, Australia (Shaw) Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Australia (Stepto) Monash Centre for Health Research and Implementation (MCHRI), School of Public Health and Preventative Medicine, Monash University and Monash Health, Clayton, Australia
Issue Date: 24-Feb-2017
Copyright year: 2017
Publisher: Public Library of Science (E-mail: plos@plos.org)
Place of publication: United States
Publication information: PLoS ONE. 12 (2) (no pagination), 2017. Article Number: e0171613. Date of Publication: February 2017.
Journal: PLoS ONE
Abstract: Background: Stress and mitogen activated protein kinase (SAPK) signaling play an important role in glucose homeostasis and the physiological adaptation to exercise. However, the effects of acute high-intensity interval exercise (HIIE) and sprint interval exercise (SIE) on activation of these signaling pathways are unclear. Method(s): Eight young and recreationally active adults performed a single cycling session of HIIE (5x4 minutes at 75% Wmax), SIE (4 x 30 second Wingate sprints), and continuous moderate-intensity exercise work-matched to HIIE (CMIE; 30 minutes at 50% of Wmax), separated by a minimum of 1 week. Skeletal muscle SAPK and insulin protein signaling were measured immediately, and 3 hours after exercise. Result(s): SIE elicited greater skeletal muscle NF-kappaB p65 phosphorylation immediately after exercise (SIE: ~40%; HIIE: ~4%; CMIE; ~13%; p < 0.05) compared to HIIE and CMIE. AS160Ser588 phosphorylation decreased immediately after HIIE (~-27%; p < 0.05), and decreased to the greatest extent immediately after SIE (~-60%; p < 0.05). Skeletal muscle JNK (~42%; p < 0.05) and p38 MAPK (~171%; p < 0.05) phosphorylation increased, and skeletal muscle AktSer473 phosphorylation (~-32%; p < 0.05) decreased, to a similar extent immediately after all exercise protocols. AS160Ser588 phosphorylation was similar to baseline three hours after SIE (~-12%; p > 0.05), remained lower 3 hours after HIIE (~-34%; p < 0.05), and decreased 3 hours after CMIE (~-33%; p < 0.05). Conclusion(s): Despite consisting of less total work than CMIE and HIIE, SIE proved to be an effective stimulus for the activation of stress protein kinase signaling pathways linked to exercise-mediated adaptation of skeletal muscle. Furthermore, post-exercise AS160Ser588 phosphorylation decreased in an exercise-intensity and post-exercise time-course dependent manner.Copyright © 2017 Parker et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
DOI: http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1371/journal.pone.0171613
Link to associated publication: Click here for full text options
PubMed URL: 28182793 [http://www.ncbi.nlm.nih.gov/pubmed/?term=28182793]
ISSN: 1932-6203 (electronic)
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/39453
Type: Article
Subjects: *mitogen activated protein kinase p38/ec [Endogenous Compound]
adaptation
adult
article
blood sampling
cycling
enzyme activation
*exercise intensity
female
human
human experiment
male
normal human
protein analysis
protein phosphorylation
signal transduction
skeletal muscle
time
volunteer
glucose/ec [Endogenous Compound]
lactic acid/ec [Endogenous Compound]
*insulin/ec [Endogenous Compound]
transcription factor RelA/ec [Endogenous Compound]
*stress activated protein kinase/ec [Endogenous Compound]
protein kinase B/ec [Endogenous Compound]
enzyme activation
*exercise intensity
female
human
time
skeletal muscle
signal transduction
protein phosphorylation
human experiment
volunteer
adaptation
adult
Article
blood sampling
cycling
protein analysis
normal human
male
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