Convertino V A
Physiology Research Branch, Clinical Sciences Division, Brooks Air Force Base, TX 78235, USA.
Med Sci Sports Exerc. 1997 Feb;29(2):191-6. doi: 10.1097/00005768-199702000-00005.
Maximal oxygen uptake (VO2max) is reduced in healthy individuals confined to bed rest, suggesting it is independent of any disease state. The magnitude of reduction in VO2max is dependent on duration of bed rest 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 cardiac beta-receptor sensitivity. Despite the elevation in heart rate, VO2max is reduced primarily from decreased maximal stroke volume and cardiac output. An elevated ejection fraction during exercise following bed rest suggests that the lower stroke volume is not caused by ventricular dysfunction but is primarily the result of decreased venous return associated with lower circulating blood volume, reduced central venous pressure, and higher venous compliance in the lower extremities. VO2max, stroke volume, and cardiac output are further compromised by exercise in the upright posture. The contribution of hypovolemia to reduced cardiac output during exercise following bed rest is supported by the 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 maintenance of VO2max after bed rest. Arteriovenous oxygen difference during maximal exercise is not altered by bed rest, suggesting that peripheral mechanisms may not contribute significantly to the decreased VO2max. However reduction in baseline and maximal muscle blood flow, red blood cell volume, and capillarization in working muscles represent peripheral mechanisms that may contribute to limited oxygen delivery and, subsequently, lowered VO2max. Thus, alterations in cardiac and vascular functions induced by prolonged confinement to bed rest contribute to diminution of maximal oxygen uptake and reserve capacity to perform physical work.
健康个体卧床休息时最大摄氧量（VO2max）会降低，这表明其与任何疾病状态无关。VO2max的降低幅度取决于卧床休息的持续时间和有氧适能的初始水平（VO2max），但似乎与年龄或性别无关。卧床休息会导致最大心率升高，进而与心脏迷走神经张力降低、交感儿茶酚胺分泌增加以及心脏β受体敏感性增强有关。尽管心率升高，但VO2max主要因最大心搏量和心输出量降低而减少。卧床休息后运动期间射血分数升高表明，较低的心搏量并非由心室功能障碍引起，而是主要由于与循环血量降低、中心静脉压降低以及下肢静脉顺应性增加相关的静脉回流减少所致。VO2max、心搏量和心输出量在直立姿势运动时会进一步受损。血容量相对变化幅度（%变化）与卧床休息期间血容量和VO2max变化的时间进程之间的密切关系，以及血浆容量的保留与卧床休息后VO2max的维持相关这一事实，均支持血容量减少对卧床休息后运动期间心输出量降低的影响。最大运动时动静脉氧差不受卧床休息影响，这表明外周机制可能对VO2max降低的贡献不大。然而，基线和最大肌肉血流量、红细胞体积以及工作肌肉中毛细血管密度的降低代表了外周机制，这些机制可能导致氧输送受限，进而降低VO2max。因此，长期卧床休息引起的心脏和血管功能改变会导致最大摄氧量和进行体力活动的储备能力下降。
