Effects of exercise-induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes

Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exerci...

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Veröffentlicht in:The Journal of physiology 2006-04, Vol.572 (2), p.539-549
Hauptverfasser: Vogiatzis, Ioannis, Georgiadou, Olga, Giannopoulou, Ifigenia, Koskolou, Maria, Zakynthinos, Spyros, Kostikas, Konstantinos, Kosmas, Epaminondas, Wagner, Harrieth, Peraki, Eleni, Koutsoukou, Antonia, Koulouris, Nickolaos, Wagner, Peter D., Roussos, Charis
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container_end_page 549
container_issue 2
container_start_page 539
container_title The Journal of physiology
container_volume 572
creator Vogiatzis, Ioannis
Georgiadou, Olga
Giannopoulou, Ifigenia
Koskolou, Maria
Zakynthinos, Spyros
Kostikas, Konstantinos
Kosmas, Epaminondas
Wagner, Harrieth
Peraki, Eleni
Koutsoukou, Antonia
Koulouris, Nickolaos
Wagner, Peter D.
Roussos, Charis
description Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 ± 1.6 ml kg −1 min −1 ; mean ± s.e.m. ) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O 2 saturation ( S a,O 2 ): 92 ± 1%) and one hyperoxic ( F I,O 2 : 0.5% O 2 ; S a,O 2 : 97 ± 1%) 5 min exercise test at intensities equal to 80 ± 3 and 90 ± 3% of maximal work rate (WR max ), respectively, producing the same tidal volume ( V T ) and breathing frequency ( f ) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure ( P di,tw ) during recovery. Hyperoxic exercise at 90% WR max induced significantly ( P = 0.022) greater post-exercise reduction in P di,tw (15 ± 2%) than did normoxic exercise at 80% WR max (9 ± 2%), despite the similar mean ventilation (123 ± 8 and 119 ± 8 l min −1 , respectively), breathing pattern ( V T : 2.53 ± 0.05 and 2.61 ± 0.05 l, f : 49 ± 2 and 46 ± 2 breaths min −1 , respectively), mean changes in P di during exercise (37.1 ± 2.4 and 38.2 ± 2.8 cmH 2 O, respectively) and end-exercise arterial lactate (12.1 ± 1.4 and 10.8 ± 1.1 mmol l −1 , respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S a,O 2 tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.
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Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 ± 1.6 ml kg −1 min −1 ; mean ± s.e.m. ) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O 2 saturation ( S a,O 2 ): 92 ± 1%) and one hyperoxic ( F I,O 2 : 0.5% O 2 ; S a,O 2 : 97 ± 1%) 5 min exercise test at intensities equal to 80 ± 3 and 90 ± 3% of maximal work rate (WR max ), respectively, producing the same tidal volume ( V T ) and breathing frequency ( f ) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure ( P di,tw ) during recovery. Hyperoxic exercise at 90% WR max induced significantly ( P = 0.022) greater post-exercise reduction in P di,tw (15 ± 2%) than did normoxic exercise at 80% WR max (9 ± 2%), despite the similar mean ventilation (123 ± 8 and 119 ± 8 l min −1 , respectively), breathing pattern ( V T : 2.53 ± 0.05 and 2.61 ± 0.05 l, f : 49 ± 2 and 46 ± 2 breaths min −1 , respectively), mean changes in P di during exercise (37.1 ± 2.4 and 38.2 ± 2.8 cmH 2 O, respectively) and end-exercise arterial lactate (12.1 ± 1.4 and 10.8 ± 1.1 mmol l −1 , respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S a,O 2 tested. 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Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 ± 1.6 ml kg −1 min −1 ; mean ± s.e.m. ) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O 2 saturation ( S a,O 2 ): 92 ± 1%) and one hyperoxic ( F I,O 2 : 0.5% O 2 ; S a,O 2 : 97 ± 1%) 5 min exercise test at intensities equal to 80 ± 3 and 90 ± 3% of maximal work rate (WR max ), respectively, producing the same tidal volume ( V T ) and breathing frequency ( f ) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure ( P di,tw ) during recovery. 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Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 ± 1.6 ml kg −1 min −1 ; mean ± s.e.m. ) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O 2 saturation ( S a,O 2 ): 92 ± 1%) and one hyperoxic ( F I,O 2 : 0.5% O 2 ; S a,O 2 : 97 ± 1%) 5 min exercise test at intensities equal to 80 ± 3 and 90 ± 3% of maximal work rate (WR max ), respectively, producing the same tidal volume ( V T ) and breathing frequency ( f ) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure ( P di,tw ) during recovery. Hyperoxic exercise at 90% WR max induced significantly ( P = 0.022) greater post-exercise reduction in P di,tw (15 ± 2%) than did normoxic exercise at 80% WR max (9 ± 2%), despite the similar mean ventilation (123 ± 8 and 119 ± 8 l min −1 , respectively), breathing pattern ( V T : 2.53 ± 0.05 and 2.61 ± 0.05 l, f : 49 ± 2 and 46 ± 2 breaths min −1 , respectively), mean changes in P di during exercise (37.1 ± 2.4 and 38.2 ± 2.8 cmH 2 O, respectively) and end-exercise arterial lactate (12.1 ± 1.4 and 10.8 ± 1.1 mmol l −1 , respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S a,O 2 tested. 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subjects Adult
Blood Gas Analysis
Diaphragm - physiopathology
Exercise - physiology
Humans
Hypoxia - etiology
Hypoxia - physiopathology
Lactates - blood
Leg - blood supply
Leg - physiology
Male
Muscle Fatigue - physiology
Oxygen - blood
Physical Endurance - physiology
Physical Exertion - physiology
Physical Fitness
Pulmonary Ventilation - physiology
Regional Blood Flow - physiology
Respiration
Skeletal Muscle and Exercise
Tidal Volume
Time Factors
title Effects of exercise-induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes
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