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Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans

Repeated bouts of ischemia followed by reperfusion, known as ischemic preconditioning (IPC), is found to improve exercise performance. As redistribution of blood from the inactive areas to active skeletal muscles during exercise (i.e., functional sympatholysis) is important for exercise performance,...

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Autores principales: Horiuchi, Masahiro, Endo, Junko, Thijssen, Dick H J
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BlackWell Publishing Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4393211/
https://www.ncbi.nlm.nih.gov/pubmed/25713329
http://dx.doi.org/10.14814/phy2.12304
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author Horiuchi, Masahiro
Endo, Junko
Thijssen, Dick H J
author_facet Horiuchi, Masahiro
Endo, Junko
Thijssen, Dick H J
author_sort Horiuchi, Masahiro
collection PubMed
description Repeated bouts of ischemia followed by reperfusion, known as ischemic preconditioning (IPC), is found to improve exercise performance. As redistribution of blood from the inactive areas to active skeletal muscles during exercise (i.e., functional sympatholysis) is important for exercise performance, we examined the hypothesis that IPC improves functional sympatholysis in healthy, young humans. In a randomized study, 15 healthy young men performed a 10-min resting period, dynamic handgrip exercise at 10% maximal voluntary contraction (MVC), and 25% MVC. This protocol was preceded by IPC (IPC; 4 × 5-min 220-mmHg unilateral occlusion) or a sham intervention (CON; 4 × 5-min 20-mmHg unilateral occlusion). Near-infrared spectroscopy was used to assess changes in oxygenated hemoglobin and myoglobin in skeletal muscle (HbO(2) + MbO(2)) in response to sympathetic activation (via cold pressor test (CPT)) at baseline and during handgrip exercise (at 10% and 25%). In resting conditions, HbO(2) + MbO(2) significantly decreased during CPT (−11.0 ± 1.0%), which was significantly larger during the IPC-trial (−13.8 ± 1.2%, P = 0.006). During handgrip exercise at 10% MVC, changes in HbO(2) + MbO(2) in response to the CPT were blunted after IPC (−8.8 ± 1.5%) and CON (−8.3 ± 0.4%, P = 0.593). During handgrip exercise at 25% MVC, HbO(2) + MbO(2) in response to the CPT increased (2.0 ± 0.4%), whereas this response was significantly larger when preceded by IPC (4.2 ± 0.6%, P = 0.027). Collectively, these results indicate that IPC-induced different vascular changes at rest and during moderate exercise in response to sympathetic activation. This suggests that, in healthy volunteers, exposure to IPC may alter tissue oxygenation during sympathetic stimulation at rest and during exercise.
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spelling pubmed-43932112015-04-20 Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans Horiuchi, Masahiro Endo, Junko Thijssen, Dick H J Physiol Rep Original Research Repeated bouts of ischemia followed by reperfusion, known as ischemic preconditioning (IPC), is found to improve exercise performance. As redistribution of blood from the inactive areas to active skeletal muscles during exercise (i.e., functional sympatholysis) is important for exercise performance, we examined the hypothesis that IPC improves functional sympatholysis in healthy, young humans. In a randomized study, 15 healthy young men performed a 10-min resting period, dynamic handgrip exercise at 10% maximal voluntary contraction (MVC), and 25% MVC. This protocol was preceded by IPC (IPC; 4 × 5-min 220-mmHg unilateral occlusion) or a sham intervention (CON; 4 × 5-min 20-mmHg unilateral occlusion). Near-infrared spectroscopy was used to assess changes in oxygenated hemoglobin and myoglobin in skeletal muscle (HbO(2) + MbO(2)) in response to sympathetic activation (via cold pressor test (CPT)) at baseline and during handgrip exercise (at 10% and 25%). In resting conditions, HbO(2) + MbO(2) significantly decreased during CPT (−11.0 ± 1.0%), which was significantly larger during the IPC-trial (−13.8 ± 1.2%, P = 0.006). During handgrip exercise at 10% MVC, changes in HbO(2) + MbO(2) in response to the CPT were blunted after IPC (−8.8 ± 1.5%) and CON (−8.3 ± 0.4%, P = 0.593). During handgrip exercise at 25% MVC, HbO(2) + MbO(2) in response to the CPT increased (2.0 ± 0.4%), whereas this response was significantly larger when preceded by IPC (4.2 ± 0.6%, P = 0.027). Collectively, these results indicate that IPC-induced different vascular changes at rest and during moderate exercise in response to sympathetic activation. This suggests that, in healthy volunteers, exposure to IPC may alter tissue oxygenation during sympathetic stimulation at rest and during exercise. BlackWell Publishing Ltd 2015-02-23 /pmc/articles/PMC4393211/ /pubmed/25713329 http://dx.doi.org/10.14814/phy2.12304 Text en © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Horiuchi, Masahiro
Endo, Junko
Thijssen, Dick H J
Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
title Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
title_full Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
title_fullStr Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
title_full_unstemmed Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
title_short Impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
title_sort impact of ischemic preconditioning on functional sympatholysis during handgrip exercise in humans
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4393211/
https://www.ncbi.nlm.nih.gov/pubmed/25713329
http://dx.doi.org/10.14814/phy2.12304
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