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

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 Ϯ 3.4 yr, 82.1 Ϯ 13.7 kg, maximal aerobic power 330 Ϯ 67 W), we determined beat-by-beat cardiac output (Q ), oxygen delivery (Q a O 2 ), and breathby-breath lung oxygen uptake (V O2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O 2 ϭ 0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Q st, by model flow) and heart rate (fH, electrocardiography), and Q a O 2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state f H and Q were higher, and Qst and V O2 were unchanged. Q a O 2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A 1) for V O2 was unchanged. For fH, Q and Q a O 2 , A1 was lower. Phase I time constant (1) for Q a O 2 and V O2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Q st 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 A 1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Q st. Thus the dual origin of the phase I of Q and Q a O 2 , neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed. cardiovascular response ALTHOUGH OUR KNOWLEDGE of the central (neural) control of the cardiovascular system at the exercise steady state is quite well established (19,42,57), how the circulatory readjustments upon exercise onset occur and match the increase in pulmonary oxygen uptake (V O 2 ) is less understood, as are the mechanisms underlying this matching. The kinetics of V O 2 at exercise onset were seen for a long time as reflecting essentially the metabolic adaptations in the working muscles (15,31,33). Some authors, however, soon identified two components of the V O 2 kinetics: 1) a rapid, almost immediate phase (phase I) (5, 54, 55), which they attributed to an immediate increase in cardiac output (Q ) at exercise start; and 2) a subsequent slower phase (phase II), to which they restricted the influence of muscle metabolic adjustments. The strongest support to this view came from the demonstration that the kinetics of Q (12, 13, 16, 60) and arterial O 2 flow (Q a O 2 ) (27) are very rapid.The concept of a close correspondence between V O 2 and muscle O 2 consumption was further undermined by the recent demonstration that, upon the onset of light exercise, the V O 2 kinetics are faster than the kinetics of muscle O 2 consumption estimated from the monoexponential decrease in phosphocreatine concentration (7,14,43). This would imply dissociation of the kinetics of V O 2 and muscle O 2 consumption, which should respond to different control mechanisms.Our postulate is that the V O 2 kinetics are dictated by ...

Non-invasive haemodynamic assessments using Innocor™ during standard graded exercise tests

“…2) lends further credence to earlier studies investigating the haemodynamic response to rest-to-exercise transitions. In these studies, it was shown that a steady state for cardiac output is attained between 30 (Lador et al 2006(Lador et al , 2008 and 60 s (De Cort et al 1991). Also, Davies et al (1972) found a rapid adjustment of cardiac output after increasing power (i.e.…”

“…Evidence for quick adjustments of cardiac output to increased power comes from the examination of haemodynamics during rest-to-exercise transitions in healthy participants by determining cardiac function on a beat-by-beat basis, using Doppler ultrasound (De Cort et al 1991) or the model flow method (Lador et al 2006(Lador et al , 2008. These studies showed that when increasing power from rest to 50, 80, or 100 W (i.e., "rest-to-exercise" transitions), a steady state for cardiac output is quickly reached (e.g., within the first minute).…”

Exercise Transients

“…This being the case, the _ Q increase at exercise onset would be due only to the increase in f H . Yet a rapid increase in Q s was also demonstrated (Faisal et al 2009;Lador et al 2006Lador et al , 2008, clearly opening the way to a possible role for the Frank-Starling mechanism in the Q s increase at exercise start, likely activated by the sudden blood displacement from lower limbs to the heart due to muscle pump action. If this is so, then _ Q would be under dual control, neural (f H increase via vagal withdrawal) and mechanical (Q s increase via Frank-Starling mechanism).…”

“…Vagal blockade with atropine is known to suppress in fact the rapid component of the f H increase (Fagraeus and Linnarsson 1976). Coherently in hypoxia, when vagal activity is already reduced at rest, the amplitude of the f H increase in phase I is smaller than in normoxia (Lador et al 2008).…”

“…The time constants of the phase I _ Q response are associated with an extremely rapid, and functionally instantaneous, phase I τ of _ V O 2 kinetics (Lador et al 2006(Lador et al , 2008Faisal et al 2009). This would correspond to a practically immediate upward translation of _ V O 2 that is apparent since the first breath.…”