CARDIOVASCULAR CONSEQUENCES OF BED REST - EFFECT ON MAXIMAL OXYGEN-UPTAKE

Authors
Citation
Va. Convertino, CARDIOVASCULAR CONSEQUENCES OF BED REST - EFFECT ON MAXIMAL OXYGEN-UPTAKE, Medicine and science in sports and exercise, 29(2), 1997, pp. 191-196
Citations number
48
Categorie Soggetti
Sport Sciences
ISSN journal
01959131
Volume
29
Issue
2
Year of publication
1997
Pages
191 - 196
Database
ISI
SICI code
0195-9131(1997)29:2<191:CCOBR->2.0.ZU;2-Q
Abstract
Maximal oxygen uptake (VO2max) is reduced in healthy individuals confi ned to bed rest, suggesting it is independent of any disease state. Th e magnitude of reduction in VO2max is dependent on duration of bed res t and the initial level of aerobic fitness (VO2max), but it appears to be independent of age or gender. Bed rest induces an elevated maximal heart rate which, in turn, is associated with decreased cardiac vagal tone, increased sympathetic catecholamine secretion, and greater card iac beta-receptor sensitivity. Despite the elevation in heart rate, VO 2max is reduced primarily from decreased maximal stroke volume and car diac output. An elevated ejection fraction during exercise following b ed rest suggests that the lower stroke volume is not caused by ventric ular dysfunction but is primarily the result of decreased venous retur n associated with lower circulating blood volume, reduced central veno us pressure, and higher venous compliance in the lower extremities. VO 2max, stroke volume, and cardiac output are further compromised by exe rcise in the upright posture. The contribution of hypovolemia to reduc ed cardiac output during exercise following bed rest is supported by t he close relationship between the relative magnitude (%Delta) and time course of change in blood volume and VO2max during bed rest, and also by the fact that retention of plasma volume is associated with mainte nance of VO2max after bed rest. Arteriovenous oxygen difference during maximal exercise is not altered by bed rest, suggesting that peripher al mechanisms may not contribute significantly to the decreased VO2max . However, reduction in baseline and maximal muscle blood flow, red bl ood cell volume, and capillarization in working muscles represent peri pheral mechanisms that may contribute to limited oxygen delivery and, subsequently, lowered VO2max. Thus, alterations in cardiac and vascula r functions induced by prolonged confinement to bed rest contribute to diminution of maximal oxygen uptake and reserve capacity to perform p hysical work.