Submitted on November 1, 2007
Accepted on May 19, 2008
PHASE I DYNAMICS OF CARDIAC OUTPUT, SYSTEMIC O2 DELIVERY AND LUNG O2 UPTAKE AT EXERCISE ONSET IN MEN IN ACUTE NORMOBARIC HYPOXIA
Frederic Lador1, Enrico Tam2, Marcel Azabji Kenfack1, Michela Cautero3, Christian Moia1, Denis R Morel4, Carlo Capelli3, and Guido Ferretti5*
1 Neurosciences Fondamentales, Centre Medical Universitaire, Geneva 4, Switzerland
2 Neurosciences Fondamentales, Centre Medical Universitaire, Geneva 4, Switzerland; Fisiologia Umana e Generale, Universita di Bologna, Bologna, Italy
3 Scienze Neurologiche e della Visione, Universita di Verona, Verona, Italy
4 Anesthesiologie, Pharmacologie et Soins Intensifs, Hopital Cantonal Universitaire, Geneva 4, Switzerland
5 Neurosciences Fondamentales, Centre Medical Universitaire, Geneva 4, Switzerland; Scienze Biomediche e Biotecnologie, Universita di Brescia, Brescia, Italy
* To whom correspondence should be addressed. E-mail: guido.ferretti{at}medecine.unige.ch.
We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, on five males (24.6 ± 3.4 years, 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 (FIO2 = 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Qst, by modelflow) and heart rate (fH, electrocardiography), QaO2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared to normoxia, steady state fH and Q were higher, Qst and VO2 unchanged. QaO2 was unchanged at rest, lower at exercise. During transients, phase I amplitude (A1) for VO2 was unchanged. For fH, Q and QaO2, A1 was lower. Phase I time constant (
1) for QaO2 and VO2 was unchanged. This was so also for Q at 100 W and fH at 50 W. Qst kinetics was 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. The dual origin of phase I of Q and QaO2 - neural (vagal) and mechanical (venous return increase by muscle pump action) - would rather be confirmed.
