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
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.