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The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise
Ischemic preconditioning (IPC) has been suggested to preserve neural drive during fatiguing dynamic exercise, however, it remains unclear as to whether this may be the consequence of IPC‐enhanced muscle oxygenation. We hypothesized that the IPC‐enhanced muscle oxygenation during a dynamic exercise t...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6483935/ https://www.ncbi.nlm.nih.gov/pubmed/31025549 http://dx.doi.org/10.14814/phy2.14063 |
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author | Halley, Samuel L. Marshall, Paul Siegler, Jason C. |
author_facet | Halley, Samuel L. Marshall, Paul Siegler, Jason C. |
author_sort | Halley, Samuel L. |
collection | PubMed |
description | Ischemic preconditioning (IPC) has been suggested to preserve neural drive during fatiguing dynamic exercise, however, it remains unclear as to whether this may be the consequence of IPC‐enhanced muscle oxygenation. We hypothesized that the IPC‐enhanced muscle oxygenation during a dynamic exercise task would subsequently attenuate exercise‐induced reductions in voluntary activation. Ten resistance trained males completed three 3 min maximal all‐out tests (AOTs) via 135 isokinetic leg extensions preceded by treatments of IPC (3 × 5 min bilateral leg occlusions at 220 mmHg), SHAM (3 × 5 min at 20 mmHg) or CON (30 min passive rest). Femoral nerve stimulation was utilized to assess voluntary activation and potentiated twitch torque during maximal voluntary contractions (MVCs) performed at baseline (BL), prior to the AOT (Pre), and then 10 sec post (Post). Tissue oxygenation (via near‐infrared spectroscopy) and sEMG activity was measured throughout the AOT. MVC and twitch torque levels declined (MVC: −87 ± 23 Nm, 95% CI = −67 to −107 Nm; P < 0.001, twitch: −30 ± 13 Nm; 95% CI = −25 to −35 Nm; P < 0.001) between Pre and Post without reductions in voluntary activation (P = 0.72); there were no differences between conditions (MVC: P = 0.75, twitch: P = 0.55). There were no differences in tissue saturation index (P = 0.27), deoxyhemoglobin concentrations (P = 0.86) or sEMG activity (P = 0.92) throughout the AOT. These findings demonstrate that IPC does not preserve neural drive during an all‐out 3 min isokinetic leg extension task. |
format | Online Article Text |
id | pubmed-6483935 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64839352019-05-02 The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise Halley, Samuel L. Marshall, Paul Siegler, Jason C. Physiol Rep Original Research Ischemic preconditioning (IPC) has been suggested to preserve neural drive during fatiguing dynamic exercise, however, it remains unclear as to whether this may be the consequence of IPC‐enhanced muscle oxygenation. We hypothesized that the IPC‐enhanced muscle oxygenation during a dynamic exercise task would subsequently attenuate exercise‐induced reductions in voluntary activation. Ten resistance trained males completed three 3 min maximal all‐out tests (AOTs) via 135 isokinetic leg extensions preceded by treatments of IPC (3 × 5 min bilateral leg occlusions at 220 mmHg), SHAM (3 × 5 min at 20 mmHg) or CON (30 min passive rest). Femoral nerve stimulation was utilized to assess voluntary activation and potentiated twitch torque during maximal voluntary contractions (MVCs) performed at baseline (BL), prior to the AOT (Pre), and then 10 sec post (Post). Tissue oxygenation (via near‐infrared spectroscopy) and sEMG activity was measured throughout the AOT. MVC and twitch torque levels declined (MVC: −87 ± 23 Nm, 95% CI = −67 to −107 Nm; P < 0.001, twitch: −30 ± 13 Nm; 95% CI = −25 to −35 Nm; P < 0.001) between Pre and Post without reductions in voluntary activation (P = 0.72); there were no differences between conditions (MVC: P = 0.75, twitch: P = 0.55). There were no differences in tissue saturation index (P = 0.27), deoxyhemoglobin concentrations (P = 0.86) or sEMG activity (P = 0.92) throughout the AOT. These findings demonstrate that IPC does not preserve neural drive during an all‐out 3 min isokinetic leg extension task. John Wiley and Sons Inc. 2019-04-25 /pmc/articles/PMC6483935/ /pubmed/31025549 http://dx.doi.org/10.14814/phy2.14063 Text en © 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Halley, Samuel L. Marshall, Paul Siegler, Jason C. The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
title | The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
title_full | The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
title_fullStr | The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
title_full_unstemmed | The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
title_short | The effect of IPC on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
title_sort | effect of ipc on central and peripheral fatiguing mechanisms in humans following maximal single limb isokinetic exercise |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6483935/ https://www.ncbi.nlm.nih.gov/pubmed/31025549 http://dx.doi.org/10.14814/phy2.14063 |
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