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 (Q˙aO2), and breath-by-breath lung oxygen uptake (V˙O2) 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 Q˙aO2 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 V˙ O2 were unchanged.Q˙aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V˙O2 was unchanged. For fH, Q˙and Q˙aO2, A1 was lower. Phase I time constant (tau1) forQ˙aO2 and V˙O2 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 Q˙aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.

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

TAM, ENRICO;
2008

Abstract

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 (Q˙aO2), and breath-by-breath lung oxygen uptake (V˙O2) 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 Q˙aO2 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 V˙ O2 were unchanged.Q˙aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V˙O2 was unchanged. For fH, Q˙and Q˙aO2, A1 was lower. Phase I time constant (tau1) forQ˙aO2 and V˙O2 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 Q˙aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.
F. Lador; E. Tam; M. Azabji Kenfack; M. Cautero; C. Moia;D.R. Morel; C. Capelli;G. Ferretti;
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/69643
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