A brief bout of exercise in hypoxia reduces ventricular filling rate and stroke volume response during muscle metaboreflex activation

Gabriele Mulliri,Gianmarco Sainas,Giorgio Nughedu,Giovanna Ghiani,Antonio Crisafulli,Fabio Sechi,Sara Magnani,Silvana Roberto,Seyed Alireza Hosseini Kakhak,Pier Paolo Bassareo

doi:10.1007/s00421-020-04435-0

Abstract

PurposeThe hemodynamic consequences of exercise in hypoxia have not been completely investigated. The present investigation aimed at studying the hemodynamic effects of contemporary normobaric hypoxia and metaboreflex activation.MethodsEleven physically active, healthy males (age 32.7 ± 7.2 years) completed a cardiopulmonary test on an electromagnetically braked cycle-ergometer to determine their maximum workload (Wmax). On separate days, participants performed two randomly assigned exercise sessions (3 minutes pedalling at 30% of Wmax): (1) one in normoxia (NORMO), and (2) one in normobaric hypoxia with FiO2 set to 13.5% (HYPO). After each session, the following protocol was randomly assigned: either (1) post-exercise muscle ischemia (PEMI) to study the metaboreflex, or (2) a control exercise recovery session, i.e., without metaboreflex activation. Hemodynamics were assessed with impedance cardiography.ResultsThe main result was that the HYPO session impaired the ventricular filling rate (measured as stroke volume/diastolic time) response during PEMI versus control condition in comparison to the NORMO test (31.33 ± 68.03 vs. 81.52 ± 49.23 ml·s−1,respectively, p = 0.003). This caused a reduction in the stroke volume response (1.45 ± 9.49 vs. 10.68 ± 8.21 ml, p = 0.020). As a consequence, cardiac output response was impaired during the HYPO test.ConclusionsThe present investigation suggests that a brief exercise bout in hypoxia is capable of impairing cardiac filling rate as well as stroke volume during the metaboreflex. These results are in good accordance with recent findings showing that among hemodynamic modulators, ventricular filling is the most sensible variable to hypoxic stimuli.

Highlights

Hypoxia triggers numerous adaptive mechanisms at cellular, tissue, and systemic level
There was a significant reduction in both S O2 and cerebral tissue oxygenation (Cox) during the hypoxic sessions compared to the normoxic ones
These differences started at the third minute of rest for S O2 and at the second minute of rest for Cox to continue throughout tests duration

Summary

Introduction

Hypoxia triggers numerous adaptive mechanisms at cellular, tissue, and systemic level. The motor cortical areas reflexively activate the cardiovascular control centres located in the medulla oblongata, inducing an increase in HR and in mean blood pressure (MAP) proportional to motor drive. This mechanism, termed “central command”, produces its effects by increasing SNS activity and by withdrawing vagal tone. At muscle level, type III and IV nerve endings collect information about the mechano and metabolic status of the contracting muscle and convey this information to the cardiovascular control areas, thereby triggering a SNS-mediated reflex termed “exercise pressor reflex” (EPR). The metabolic part of the EPR is commonly termed “metaboreflex”, whereas the mechanical one is known as “mechanoreflex” (Crisafulli et al 2015; Nobrega et al 2014)

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