Vagal blockade suppresses the phase I heart rate response but not the phase I cardiac output response at exercise onset in humans

Timothée Fontolliet,Aurélien Bringard,Anna Taboni,Nazzareno Fagoni,Enrico Tam,Guido Ferretti,Alessandra Adami

doi:10.1007/s00421-021-04769-3

Abstract

PurposeWe tested the vagal withdrawal concept for heart rate (HR) and cardiac output (CO) kinetics upon moderate exercise onset, by analysing the effects of vagal blockade on cardiovascular kinetics in humans. We hypothesized that, under atropine, the φ1 amplitude (A1) for HR would reduce to nil, whereas the A1 for CO would still be positive, due to the sudden increase in stroke volume (SV) at exercise onset.MethodsOn nine young non-smoking men, during 0–80 W exercise transients of 5-min duration on the cycle ergometer, preceded by 5-min rest, we continuously recorded HR, CO, SV and oxygen uptake ( dot{V} O2) upright and supine, in control condition and after full vagal blockade with atropine. Kinetics were analysed with the double exponential model, wherein we computed the amplitudes (A) and time constants (τ) of phase 1 (φ1) and phase 2 (φ2).ResultsIn atropine versus control, A1 for HR was strongly reduced and fell to 0 bpm in seven out of nine subjects for HR was practically suppressed by atropine in them. The A1 for CO was lower in atropine, but not reduced to nil. Thus, SV only determined A1 for CO in atropine. A2 did not differ between control and atropine. No effect on τ1 and τ2 was found. These patterns were independent of posture.ConclusionThe results are fully compatible with the tested hypothesis. They provide the first direct demonstration that vagal blockade, while suppressing HR φ1, did not affect φ1 of CO.

Highlights

The oxygen uptake (V O2) kinetics at the onset of a moderate-intensity exercise is characterised by two distinct phases (Whipp et al 1982), which have been modelled as a sum of two exponentials (Barstow and Molé 1987)
Application of the double exponential model to the analysis of the cardiac output (CO) kinetics at exercise onset led to the demonstration that the φ1 for V O2 kinetics may be entirely explained by the φ1 for CO (Faisal et al 2009; Lador et al 2006, 2008)
At rest in the supine position and during exercise in both postures, stroke volume (SV) was lower under atropine than in control (p < 0.05)

Summary

Introduction

The oxygen uptake (V O2) kinetics at the onset of a moderate-intensity exercise is characterised by two distinct phases (Whipp et al 1982), which have been modelled as a sum of two exponentials (Barstow and Molé 1987). Some authors postulated that at exercise start there is a rapid increase in venous return, due to sudden displacement of blood from the contracting muscles to the heart by muscle pump action. This would lead to an immediate increase in stroke volume (SV) and, in CO (Laughlin 1987; Leyk et al 1994; Linnarsson et al 1996; Wieling et al 1996; Sundblad et al 2000; Schneider et al 2002; Stenger et al 2012). This would lead to an immediate increase in stroke volume (SV) and, in CO (Laughlin 1987; Leyk et al 1994; Linnarsson et al 1996; Wieling et al 1996; Sundblad et al 2000; Schneider et al 2002; Stenger et al 2012). Fagoni et al (2020) argued that these two postulated mechanisms may coexist and are not mutually exclusive, one driven by HR, and the other by SV

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