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Am J Physiol Regul Integr Comp Physiol 295: R624-R632, 2008. First published May 21, 2008; doi:10.1152/ajpregu.00797.2007
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EXERCISE AND RESPIRATORY PHYSIOLOGY

Phase I dynamics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men in acute normobaric hypoxia

Frédéric Lador,1 Enrico Tam,1,2 Marcel Azabji Kenfack,1 Michela Cautero,3 Christian Moia,1 Denis R. Morel,4 Carlo Capelli,3 and Guido Ferretti1,5

1Département des Neurosciences Fondamentales, Centre Médical Universitaire, Genève, Switzerland; 2Dipartimento di Fisiologia Umana e Generale, Università di Bologna, Bologna; 3Dipartimento di Scienze Neurologiche e della Visione, Facoltà di Scienze Motorie, Università di Verona, Verona, Italy; 4Département d'Anesthésiologie, Pharmacologie et Soins Intensifs, Hôpital Cantonal Universitaire, Genève, Switzerland; and 5Sezione di Fisiologia Umana, Dipartimento di Scienze Biomediche e Biotecnologie, Università di Brescia, Brescia, Italy

Submitted 1 November 2007 ; accepted in final form 19 May 2008

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 ± 3.4 yr, 82.1 ± 13.7 kg, maximal aerobic power 330 ± 67 W), we determined beat-by-beat cardiac output (Q), oxygen delivery (QaO2), and breath-by-breath lung oxygen uptake (VO2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2 = 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Qst, by model flow) and heart rate (fH, electrocardiography), and QaO2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q were higher, and Qst and VO2 were unchanged. QaO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for VO2 was unchanged. For fH, Q and QaO2, A1 was lower. Phase I time constant ({tau}1) for QaO2 and VO2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q and QaO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

cardiovascular response


Address for reprint requests and other correspondence: G. Ferretti, Département de Neurosciences Fondamentales, Centre Médical Universitaire, 1 rue Michel Servet, CH-1211 Genève 4, Switzerland (e-mail: guido.ferretti{at}medecine.unige.ch)






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