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“Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling
We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics ([Formula: see text]) is an independent determinant of critical power (CP) when O(2) availability is not limiting, that is, during upright cycle exercise in young, healthy individuals. Whether this ca...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6234148/ https://www.ncbi.nlm.nih.gov/pubmed/30426722 http://dx.doi.org/10.14814/phy2.13916 |
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author | Goulding, Richie P. Roche, Denise M. Marwood, Simon |
author_facet | Goulding, Richie P. Roche, Denise M. Marwood, Simon |
author_sort | Goulding, Richie P. |
collection | PubMed |
description | We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics ([Formula: see text]) is an independent determinant of critical power (CP) when O(2) availability is not limiting, that is, during upright cycle exercise in young, healthy individuals. Whether this causative relationship remains when O(2) availability is impaired remains unknown. During supine exercise, which causes an O(2) availability limitation during the exercise transition, we therefore determined the impact of a raised baseline work rate on [Formula: see text] and CP. CP, [Formula: see text] , and muscle oxygenation status (the latter via near‐infrared spectroscopy) were determined via four severe‐intensity constant‐power exercise tests completed in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a moderate‐intensity baseline work rate of 90% of the gas exchange threshold (M→S). In M→S, critical power was lower (U→S = 146 ± 39 W vs. M→S = 132 ± 33 W, P = 0.023) and [Formula: see text] was greater (U→S = 45 ± 16 sec, vs. M→S = 69 ± 129 sec, P = 0.001) when compared to U→S. There was no difference in tissue oxyhemoglobin concentration ([HbO(2) + MbO(2)]) at baseline or during exercise. The concomitant increase in [Formula: see text] and reduction in CP during M→S compared to U→S shows for the first time that [Formula: see text] is an independent determinant of CP in conditions where O(2) availability is limiting. |
format | Online Article Text |
id | pubmed-6234148 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-62341482018-11-20 “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling Goulding, Richie P. Roche, Denise M. Marwood, Simon Physiol Rep Original Articles We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics ([Formula: see text]) is an independent determinant of critical power (CP) when O(2) availability is not limiting, that is, during upright cycle exercise in young, healthy individuals. Whether this causative relationship remains when O(2) availability is impaired remains unknown. During supine exercise, which causes an O(2) availability limitation during the exercise transition, we therefore determined the impact of a raised baseline work rate on [Formula: see text] and CP. CP, [Formula: see text] , and muscle oxygenation status (the latter via near‐infrared spectroscopy) were determined via four severe‐intensity constant‐power exercise tests completed in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a moderate‐intensity baseline work rate of 90% of the gas exchange threshold (M→S). In M→S, critical power was lower (U→S = 146 ± 39 W vs. M→S = 132 ± 33 W, P = 0.023) and [Formula: see text] was greater (U→S = 45 ± 16 sec, vs. M→S = 69 ± 129 sec, P = 0.001) when compared to U→S. There was no difference in tissue oxyhemoglobin concentration ([HbO(2) + MbO(2)]) at baseline or during exercise. The concomitant increase in [Formula: see text] and reduction in CP during M→S compared to U→S shows for the first time that [Formula: see text] is an independent determinant of CP in conditions where O(2) availability is limiting. John Wiley and Sons Inc. 2018-11-13 /pmc/articles/PMC6234148/ /pubmed/30426722 http://dx.doi.org/10.14814/phy2.13916 Text en © 2018 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 Articles Goulding, Richie P. Roche, Denise M. Marwood, Simon “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling |
title | “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling |
title_full | “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling |
title_fullStr | “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling |
title_full_unstemmed | “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling |
title_short | “Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling |
title_sort | “work‐to‐work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases w’ during supine cycling |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6234148/ https://www.ncbi.nlm.nih.gov/pubmed/30426722 http://dx.doi.org/10.14814/phy2.13916 |
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