Convertino V A, Bloomfield S A, Greenleaf J E
Physiology Research Branch, Clinical Sciences Division, Brooks Air Force Base, TX 78235, USA.
Med Sci Sports Exerc. 1997 Feb;29(2):187-90. doi: 10.1097/00005768-199702000-00004.
Reduction of exercise capacity with confinement to bed rest is well recognized. Underlying physiological mechanisms include dramatic reductions in maximal stroke volume, cardiac output, and oxygen uptake. However, bed rest by itself does not appear to contribute to cardiac dysfunction. Increased muscle fatigue is associated with reduced muscle blood flow, red cell volume, capillarization and oxidative enzymes. Loss of muscle mass and bone density may be reflected by reduced muscle strength and higher risk for injury to bones and joints. The resultant deconditioning caused by bed rest can be independent of the primary disease and physically debilitating in patients who attempt to reambulate to normal active living and working. A challenge to clinicians and health care specialists has been the identification of appropriate and effective methods to restore physical capacity of patients during or after restricted physical activity associated with prolonged bed rest. The examination of physiological responses to bed rest deconditioning and exercise training in healthy subjects has provided significant information to develop effective rehabilitation treatments. The successful application of acute exercise to enhance orthostatic stability, daily endurance exercise to maintain aerobic capacity, or specific resistance exercises to maintain musculoskeletal integrity rather than the use of surgical, pharmacological, and other medical treatments for clinical conditions has been enhanced by investigation and understanding of underlying mechanisms that distinguish physical deconditioning from the disease. This symposium presents an overview of cardiovascular and musculoskeletal deconditioning associated with reduced physical work capacity following prolonged bed rest and exercise training regimens that have proven successful in ameliorating or reversing these adverse effects.
长期卧床休息会导致运动能力下降，这是众所周知的。潜在的生理机制包括最大心搏量、心输出量和摄氧量的显著降低。然而，卧床休息本身似乎并不会导致心脏功能障碍。肌肉疲劳增加与肌肉血流量减少、红细胞体积减少、毛细血管密度降低以及氧化酶减少有关。肌肉质量和骨密度的丧失可能表现为肌肉力量下降以及骨骼和关节受伤风险增加。卧床休息导致的身体机能下降可能与原发性疾病无关，对于试图恢复正常活动和工作的患者来说，这会使身体虚弱。临床医生和医疗保健专家面临的一个挑战是，确定在与长期卧床休息相关的身体活动受限期间或之后，恢复患者身体能力的适当有效方法。对健康受试者卧床休息导致的身体机能下降和运动训练的生理反应进行研究，为开发有效的康复治疗方法提供了重要信息。通过对区分身体机能下降和疾病的潜在机制的研究和理解，急性运动增强直立稳定性、日常耐力运动维持有氧能力或特定抗阻运动维持肌肉骨骼完整性的成功应用得到了加强，而不是使用手术、药物和其他针对临床病症的治疗方法。本次研讨会概述了与长期卧床休息后体力工作能力下降相关的心血管和肌肉骨骼机能下降，以及已被证明在改善或逆转这些不良反应方面成功的运动训练方案。
