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Effects of exercise‐induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes
Author(s) -
Vogiatzis Ioannis,
Georgiadou Olga,
Giannopoulou Ifigenia,
Koskolou Maria,
Zakynthinos Spyros,
Kostikas Konstantinos,
Kosmas Epamidas,
Wagner Harrieth,
Peraki Eleni,
Koutsoukou Antonia,
Koulouris Nickolaos,
Wagner Peter D.,
Roussos Charis
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2005.102442
Subject(s) - diaphragmatic breathing , medicine , ventilation (architecture) , heart rate , cardiology , respiratory rate , endurance training , population , respiratory minute volume , tidal volume , arterial blood , work rate , anesthesia , blood pressure , respiratory system , mechanical engineering , alternative medicine , environmental health , pathology , engineering
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 2tested. 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.