Babb T G, Long K A, Rodarte J R
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, TX 75231, USA.
Am J Respir Crit Care Med. 1997 Jul;156(1):116-21. doi: 10.1164/ajrccm.156.1.9511021.
We previously reported that patients with mild to moderate airflow limitation have a lower exercise capacity than age-matched controls with normal lung function, but the mechanism of this reduction remains unclear (1). Although the reduced exercise capacity appeared consistent with deconditioning, the patients had altered breathing mechanics during exercise, which raised the possibility that the reduced exercise capacity and the altered breathing mechanics may have been causally related. Reversal of reduced exercise capacity by an adequate exercise training program is generally accepted as evidence of deconditioning as the cause of the reduced exercise capacity. We studied 11 asymptomatic volunteer subjects (58 +/- 8 yr of age [mean +/- SD]) selected to have a range of lung function (FEV1 from 61 to 114% predicted, with a mean of 90 +/- 18% predicted). Only one subject had an FEV1 of less than 70% predicted. Gas exchange and lung mechanics were measured during both steady-state and maximal exercise before and after training for 30 min/d on 3 d/wk for 10 wk, beginning at the steady-state workload previously determined to be the maximum steady-state exercise level that subjects could sustain for 30 min without exceeding 90% of their observed maximal heart rate (HR). The training workload was increased if the subject's HR decreased during the training period. After 10 wk, subjects performed another steady-state exercise test at the initial pretraining level, and another maximal exercise test. HR decreased significantly between the first and second steady-state exercise tests (p < 0.05), and maximal oxygen uptake (VO2max) and ventilation increased significantly (p < 0.05) during the incremental test, indicating a training effect. However, the training effect did not occur in all subjects. Relationships between exercise parameters and lung function were examined by regression against FEV1 expressed as percent predicted. There was a significant positive correlation between VO2max percent predicted and FEV1 percent predicted (p < 0.02), and a negative correlation between FEV1 and end-expiratory lung volume (EELV) at maximal exercise (p < 0.03). There was no significant correlation between FEV1 and maximal HR achieved during exercise; moreover, all subjects achieved a maximal HR in excess of 80% predicted, suggesting a cardiovascular limitation to exercise. These data do not support the hypothesis that the lower initial VO2max in the subjects with a reduced FEV1 was due to deconditioning. Although increased EELV at maximal exercise, reduced VO2max and a reduced VO2max response with training are all statistically associated with a reduced FEV1, there is no direct evidence of causality.
我们之前报道过，轻度至中度气流受限患者的运动能力低于年龄匹配、肺功能正常的对照组，但这种运动能力下降的机制仍不清楚(1)。尽管运动能力下降似乎与身体机能减退一致，但患者在运动过程中呼吸力学发生了改变，这增加了运动能力下降与呼吸力学改变可能存在因果关系的可能性。通过适当的运动训练计划使降低的运动能力得到恢复，通常被认为是身体机能减退导致运动能力下降的证据。我们研究了11名无症状志愿者受试者(年龄58±8岁[平均值±标准差])，他们的肺功能范围各异(FEV1为预测值的61%至114%，平均为预测值的90±18%)。只有一名受试者的FEV1低于预测值的70%。在每周训练3天、每天训练30分钟、共训练10周之前和之后，在稳态和最大运动期间测量气体交换和肺力学，训练从之前确定的稳态工作量开始，该工作量为受试者能够持续30分钟且不超过其观察到的最大心率(HR)的90%的最大稳态运动水平。如果受试者在训练期间心率下降，则增加训练工作量。10周后，受试者在初始训练前水平进行另一次稳态运动测试，以及另一次最大运动测试。在第一次和第二次稳态运动测试之间，心率显著下降(p<0.05)，在递增测试期间，最大摄氧量(VO2max)和通气量显著增加(p<0.05)，表明有训练效果。然而，并非所有受试者都出现了训练效果。通过对以预测百分比表示的FEV1进行回归分析，研究了运动参数与肺功能之间的关系。预测的VO2max百分比与预测的FEV1百分比之间存在显著正相关(p<0.02)，在最大运动时FEV1与呼气末肺容积(EELV)之间存在负相关(p<0.03)。FEV1与运动期间达到的最大心率之间无显著相关性；此外，所有受试者的最大心率均超过预测值的80%，表明存在运动的心血管限制。这些数据不支持FEV1降低的受试者初始VO2max较低是由于身体机能减退的假设。尽管在最大运动时EELV增加、VO2max降低以及训练后VO2max反应降低在统计学上均与FEV1降低相关，但没有直接的因果关系证据。
