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Eur Respir J 2002; 19:1079-1086
Copyright ©ERS Journals Ltd 2002


Contribution of respiratory acidosis to diaphragmatic fatigue at exercise

S. Jonville1, N. Delpech1 and A. Denjean1,2

1 Human Performance Laboratory, Sports Sciences Dept, University of Poitiers, and 2 Exercise Respiratory Physiology, University Hospital of Poitiers, France

CORRESPONDENCE: S. Jonville, Laboratoire d'analyse de la performance motrice humaine, Faculté des Sciences du Sport, 4 allée Jean Monnet, 86000, Poitiers, France. Fax: 33 549453396. E-mail: sophie.jonville@etu.univ-poitiers.fr

Keywords: cervical magnetic stimulation, hypercapnia, mouth pressure, respiratory muscles

Received: August 1, 2001
Accepted January 16, 2002

The factors that may modulate ventilatory muscle fatigue during exercise are controversial. In this study the contribution of acidosis to exercise-induced diaphragmatic fatigue was investigated, using measurements of the twitch mouth pressure response (tw,Pmo) to cervical magnetic stimulation.

After learning sessions, 14 healthy subjects performed two cycling tests (at 60% of maximal aerobic power for 16 min), one while breathing spontaneously (mean minute ventilation (V'e) 67.9 L·min–1) and the other while hypoventilating voluntarily (meanV'E 53.8 L·min–1). Exercise was voluntarily set at a moderate power to avoid a fatiguing effect of exercise per se.

As compared with spontaneous breathing (SB), voluntary hypoventilation (VHV) significantly increased mean carbon dioxide tension in arterial blood (Pa,CO2) (51 mmHg versus 41 mmHg) and significantly decreased arterial pH (7.28 versus 7.34). After 10 min of SB test, tw,Pmo was unchanged compared to the baseline value (19.1 versus 18.5 cmH2O) whereas tw,Pmo fell significantly as compared to baseline (17.1 versus 18.5 cmH2O) and to SB (17.1 versus 19.1 cmH2O) after the VHV test.

The results of this study suggest that exposure to hypercapnia may impair respiratory muscle function. This impairment could be more clinically relevant in patients with chronic obstructive lung disease.







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