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July 1, 1998Medicine & Science in Sports & Exercise18 citations

Cardiovascular function following reduced aerobic activity

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PRPeter B. RavenRWR. M. Welch-O’ConnorXSXiangrong Shi

Structured PICO

Does physical deconditioning alter cardiovascular regulatory function in young, healthy volunteers?

P
Population
19 young, healthy volunteers
I
Intervention
Sustained reduction of physical activity (physical deconditioning) for 8 weeks
C
Comparator
Pre-deconditioning baseline
O
Outcome
Cardiovascular regulatory function (responses of heart rate, mean arterial pressure, central venous pressure, stroke volume, and forearm blood flow during lower body negative pressure; carotid and aortic baroreflex function)surrogate

Physical deconditioning in young healthy individuals reduces orthostatic tolerance due to functional modification of the cardiac pressure-volume relationship, despite accentuated baroreflex function.

Abstract

PURPOSE: The aim of this study was to test the hypothesis that a sustained reduction of physical activity (deconditioning) would alter the cardiovascular regulatory function. METHODS: Nineteen young, healthy volunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the responses of heart rate (HR), mean arterial pressure (MAP, measured by Finapres), central venous pressure (CVP), stroke volume (SV, Doppler), and forearm blood flow (FBF, plethysmography) were determined during lower body negative pressure (LBNP). The carotid baroreflex (CBR) function was assessed using a train of pulsatile neck pressure (NP) and suction, and the aortic baroreflex control of HR was assessed during steady-state phenylephrine (PE) infusion superimposed by LBNP and NP to counteract the PE increased CVP and carotid sinus pressure, respectively. RESULTS: Active physical deconditioning significantly decreased maximal oxygen uptake (-7%) and LBNP tolerance (-13%) without a change in baseline hemodynamics. Plasma volume (-3% at P = 0.135), determined by Evans Blue dilution, and blood volume (-4% at P = 0.107) were not significantly altered. During LBNP -20 to -50 torr, there was a significantly greater drop of SV per unit decrease in CVP in the post- (14.7 +/- 1.6%/mm Hg) than predeconditioning (11.2 +/- 0.7%/mm Hg) test accompanied by a greater tachycardia. Deconditioning increased the aortic baroreflex sensitivity (pre vs post: -0.61 +/- 0.12 vs -0.84 +/- 0.14 bpm.mm-1 Hg, P = 0.009) and the slope of forearm vascular resistance (calculated from MAP-CVP/FBF) to CVP (-2.75 +/- 0.26 vs -4.94 +/- 0.97 PRU/mm Hg, P = 0.086). However, neither the CBR-HR (-0.28 +/- 0.03 VS -0.39 +/- 0.10 bpm.mm-1 Hg) nor the CBR-MAP (-0.37 +/- 0.16 vs -0.25 +/- 0.07 mm Hg/mm Hg) gains were statistically different between pre- and postdeconditioning. CONCLUSIONS: We concluded that the functional modification of the cardiac pressure-volume relationship resulted in the reduced LBNP tolerance, despite the accentuated aortic and cardiopulmonary baroreflex function following deconditioning.

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Cite This Study

Raven et al. (1998) studied this question.

synapsesocial.com/papers/6a77dda76789de8d0af77b99https://doi.org/10.1097/00005768-199807000-00004
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