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Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists

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Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists. / Vogiatzis, Ioannis; Athanasopoulos, Dimitris; Boushel, Robert Christopher; Guenette, Jordan A; Koskolou, Maria; Vasilopoulou, Maroula; Wagner, Harrieth; Roussos, Charis; Wagner, Hans Peter; Zakynthinos, Spyros.

I: Journal of Physiology, Bind 586, Nr. 22, 2008, s. 5575-5587.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Vogiatzis, I, Athanasopoulos, D, Boushel, RC, Guenette, JA, Koskolou, M, Vasilopoulou, M, Wagner, H, Roussos, C, Wagner, HP & Zakynthinos, S 2008, 'Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists', Journal of Physiology, bind 586, nr. 22, s. 5575-5587. https://doi.org/10.1113/jphysiol.2008.162768

APA

Vogiatzis, I., Athanasopoulos, D., Boushel, R. C., Guenette, J. A., Koskolou, M., Vasilopoulou, M., Wagner, H., Roussos, C., Wagner, H. P., & Zakynthinos, S. (2008). Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists. Journal of Physiology, 586(22), 5575-5587. https://doi.org/10.1113/jphysiol.2008.162768

Vancouver

Vogiatzis I, Athanasopoulos D, Boushel RC, Guenette JA, Koskolou M, Vasilopoulou M o.a. Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists. Journal of Physiology. 2008;586(22):5575-5587. https://doi.org/10.1113/jphysiol.2008.162768

Author

Vogiatzis, Ioannis ; Athanasopoulos, Dimitris ; Boushel, Robert Christopher ; Guenette, Jordan A ; Koskolou, Maria ; Vasilopoulou, Maroula ; Wagner, Harrieth ; Roussos, Charis ; Wagner, Hans Peter ; Zakynthinos, Spyros. / Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists. I: Journal of Physiology. 2008 ; Bind 586, Nr. 22. s. 5575-5587.

Bibtex

@article{03febfa0dd7211ddb5fc000ea68e967b,
title = "Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists",
abstract = "We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P <0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.",
keywords = "Acidosis, Adult, Anoxia, Bicycling, Cardiac Output, Diaphragm, Exercise Test, Humans, Male, Muscle Fatigue, Respiratory Muscles",
author = "Ioannis Vogiatzis and Dimitris Athanasopoulos and Boushel, {Robert Christopher} and Guenette, {Jordan A} and Maria Koskolou and Maroula Vasilopoulou and Harrieth Wagner and Charis Roussos and Wagner, {Hans Peter} and Spyros Zakynthinos",
year = "2008",
doi = "10.1113/jphysiol.2008.162768",
language = "English",
volume = "586",
pages = "5575--5587",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "22",

}

RIS

TY - JOUR

T1 - Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists

AU - Vogiatzis, Ioannis

AU - Athanasopoulos, Dimitris

AU - Boushel, Robert Christopher

AU - Guenette, Jordan A

AU - Koskolou, Maria

AU - Vasilopoulou, Maroula

AU - Wagner, Harrieth

AU - Roussos, Charis

AU - Wagner, Hans Peter

AU - Zakynthinos, Spyros

PY - 2008

Y1 - 2008

N2 - We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P <0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.

AB - We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P <0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.

KW - Acidosis

KW - Adult

KW - Anoxia

KW - Bicycling

KW - Cardiac Output

KW - Diaphragm

KW - Exercise Test

KW - Humans

KW - Male

KW - Muscle Fatigue

KW - Respiratory Muscles

U2 - 10.1113/jphysiol.2008.162768

DO - 10.1113/jphysiol.2008.162768

M3 - Journal article

C2 - 18832419

VL - 586

SP - 5575

EP - 5587

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 22

ER -

ID: 9586940