Open Access
CC BY-NC-ND 4.0 · Int J Sports Med 2020; 41(04): 209-218
DOI: 10.1055/a-1028-7496
Physiology & Biochemistry
Eigentümer und Copyright ©Georg Thieme Verlag KG 2018

Effect of Lower Body Negative Pressure on Phase I Cardiovascular Responses at Exercise Onset

Nazzareno Fagoni
1   Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy
,
Paolo Bruseghini
1   Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy
,
Alessandra Adami
2   Department of Kinesiology, University of Rhode Island, United States
,
Carlo Capelli
3   Department of Physical Performances, Norwegian School of Sport Sciences, Oslo, Norway
,
Frederic Lador
4   Division de Pneumologie, Département des Spécialités de Médecine, Hôpitaux Universitaires de Genève, Geneva, Switzerland
,
Christian Moia
5   Département des Neurosciences Fondamentales, Université de Genève Centre Médical Universitaire, Geneve, Switzerland
,
Enrico Tam
6   Dipartimento di Scienze Neurologiche e della Visione, University of Verona, Verona, Italy
,
Aurélien Bringard
7   University Medical Center, Basic Neurosciences, Geneva, Switzerland
,
Guido Ferretti
5   Département des Neurosciences Fondamentales, Université de Genève Centre Médical Universitaire, Geneve, Switzerland
› Institutsangaben

Funding This study was supported by Swiss National Science Foundation Grants 32003B_127620 and 3200B0-114033 to Guido Ferretti.
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Publikationsverlauf



accepted 30. September 2019

Publikationsdatum:
20. Januar 2020 (online)

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Abstract

We hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), −15, −30 and −45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to −45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.