Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice

This study was designed to (1) investigate the effects of acute short‐duration intermittent hypoxia on muscle mRNA and microRNA expression levels; and (2) clarify the mechanisms by which short‐duration intermittent hypoxia improves endurance capacity. Experiment‐1: Male mice were subjected to either...

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Main Author: Suzuki, Junichi
Format: Online
Language:English
Published: John Wiley and Sons Inc. 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831319/
id pubmed-4831319
recordtype oai_dc
spelling pubmed-48313192016-04-20 Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice Suzuki, Junichi Original Research This study was designed to (1) investigate the effects of acute short‐duration intermittent hypoxia on muscle mRNA and microRNA expression levels; and (2) clarify the mechanisms by which short‐duration intermittent hypoxia improves endurance capacity. Experiment‐1: Male mice were subjected to either acute 1‐h hypoxia (12% O2), acute short‐duration intermittent hypoxia (12% O2 for 15 min, room air for 10 min, 4 times, Int‐Hypo), or acute endurance exercise (Ex). The expression of vascular endothelial growth factor‐A mRNA was significantly greater than the control at 0 h post Ex and 6 h post Int‐Hypo in the deep red region of the gastrocnemius muscle. miR‐16 expression levels were significantly lower at 6 and 10 h post Int‐Hypo. Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) mRNA levels were significantly greater than the control at 3 h post Ex and 6 h post Int‐Hypo. miR‐23a expression levels were lower than the control at 6–24 h post Int‐Hypo. Experiment‐2: Mice were subjected to normoxic exercise training with or without intermittent hypoxia for 3 weeks. Increases in maximal exercise capacity were significantly greater by training with short‐duration intermittent hypoxia (IntTr) than without hypoxia. Both 3‐Hydroxyacyl‐CoA‐dehydrogenase and total carnitine palmitoyl transferase activities were significantly enhanced in IntTr. Peroxisome proliferator‐activated receptor delta and PGC‐1α mRNA levels were both significantly greater in IntTr than in the sedentary controls. These results suggest that exercise training under normoxic conditions with exposure to short‐duration intermittent hypoxia represents a beneficial strategy for increasing endurance performance by enhancing fatty acid metabolism in skeletal muscle. John Wiley and Sons Inc. 2016-04-06 /pmc/articles/PMC4831319/ /pubmed/27044851 http://dx.doi.org/10.14814/phy2.12744 Text en © 2016 The Author. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Suzuki, Junichi
spellingShingle Suzuki, Junichi
Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
author_facet Suzuki, Junichi
author_sort Suzuki, Junichi
title Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
title_short Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
title_full Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
title_fullStr Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
title_full_unstemmed Short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
title_sort short‐duration intermittent hypoxia enhances endurance capacity by improving muscle fatty acid metabolism in mice
description This study was designed to (1) investigate the effects of acute short‐duration intermittent hypoxia on muscle mRNA and microRNA expression levels; and (2) clarify the mechanisms by which short‐duration intermittent hypoxia improves endurance capacity. Experiment‐1: Male mice were subjected to either acute 1‐h hypoxia (12% O2), acute short‐duration intermittent hypoxia (12% O2 for 15 min, room air for 10 min, 4 times, Int‐Hypo), or acute endurance exercise (Ex). The expression of vascular endothelial growth factor‐A mRNA was significantly greater than the control at 0 h post Ex and 6 h post Int‐Hypo in the deep red region of the gastrocnemius muscle. miR‐16 expression levels were significantly lower at 6 and 10 h post Int‐Hypo. Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) mRNA levels were significantly greater than the control at 3 h post Ex and 6 h post Int‐Hypo. miR‐23a expression levels were lower than the control at 6–24 h post Int‐Hypo. Experiment‐2: Mice were subjected to normoxic exercise training with or without intermittent hypoxia for 3 weeks. Increases in maximal exercise capacity were significantly greater by training with short‐duration intermittent hypoxia (IntTr) than without hypoxia. Both 3‐Hydroxyacyl‐CoA‐dehydrogenase and total carnitine palmitoyl transferase activities were significantly enhanced in IntTr. Peroxisome proliferator‐activated receptor delta and PGC‐1α mRNA levels were both significantly greater in IntTr than in the sedentary controls. These results suggest that exercise training under normoxic conditions with exposure to short‐duration intermittent hypoxia represents a beneficial strategy for increasing endurance performance by enhancing fatty acid metabolism in skeletal muscle.
publisher John Wiley and Sons Inc.
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831319/
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