Patessio A, Carone M, Ioli F, Donner C F
Division of Pulmonary Disease, Clinica del Lavoro Foundation, Medical Center of Rehabilitation, Veruno, Italy.
Chest. 1992 May;101(5 Suppl):274S-278S. doi: 10.1378/chest.101.5_supplement.274s.
Patients with COPD feel better and are able to sustain a given level of activity longer after a program of exercise training, but the underlying physiologic mechanisms have not been completely elucidated. Since the physical performance of patients with COPD is limited mainly by pathophysiologic derangements of the ventilatory system, the exercise performance can be ameliorated by increasing the level of ventilation that they can sustain or by reducing the ventilatory requirement for a given level of activity. Almost all studies have yielded negative results in patients with COPD in terms of exercise training having the ability to improve VEmax. The only way to reduce the ventilatory requirement is to reduce CO2 output. Lower levels of lactate result in less nonmetabolic CO2 produced by bicarbonate buffering and this is the likely mechanism responsible for a lower ventilatory requirement for work rates above the pretraining anaerobic threshold. We specifically wished to determine whether a program of intensity, frequency, and duration known capable of producing a physiologic training effect in healthy subjects would do so in patients with COPD. Further, we sought to determine whether exercise training at a work rate associated with lactic acidosis is more effective in inducing a training effect in patients with COPD than a work rate not associated with lactic acidosis. Nineteen patients with COPD were selected and performed an incremental test as well as 2 square wave tests at a low and a high work rate. Identical tests were performed after an 8-week program of cycle ergometer training either for 45 min/day at a high work rate or for a proportionally longer time at a low work rate. For the high work rate training group, identical work rates engendered less lactate (4.5 vs 7.2 mEq/L) and less VE (48 vs 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p less than 0.01). Further, in the first group, there was an increase in exercise tolerance averaging 71% in the high constant work rate test. There was a good correlation (r = 0.73, p less than 0.005) between the decrease in blood lactate and the decrease in ventilation. The major findings of this study are that patients with COPD who experience lactic acidosis during exercise can achieve physiologic training responses from a program of endurance training and that training work rates engendering high levels of blood lactate are more effective than work rates eliciting low lactate levels.
慢性阻塞性肺疾病(COPD)患者在接受运动训练计划后感觉更好,并且能够在更长时间内维持特定水平的活动,但潜在的生理机制尚未完全阐明。由于COPD患者的身体表现主要受通气系统病理生理紊乱的限制,因此可以通过提高他们能够维持的通气水平或降低给定活动水平的通气需求来改善运动表现。几乎所有研究在COPD患者中关于运动训练提高最大通气量(VEmax)的能力都得出了阴性结果。降低通气需求的唯一方法是减少二氧化碳输出。较低水平的乳酸会减少碳酸氢盐缓冲产生的非代谢性二氧化碳,这可能是高于训练前无氧阈值的工作率通气需求降低的原因。我们特别希望确定一个已知能够在健康受试者中产生生理训练效果的强度、频率和持续时间的计划在COPD患者中是否也能如此。此外,我们试图确定与乳酸酸中毒相关的工作率下的运动训练在诱导COPD患者训练效果方面是否比与乳酸酸中毒无关的工作率更有效。选择了19名COPD患者,他们进行了递增测试以及在低工作率和高工作率下的2次方波测试。在进行为期8周的自行车测力计训练计划后,以高工作率每天训练45分钟或以低工作率按比例训练更长时间后,进行相同的测试。对于高工作率训练组,训练后相同工作率产生的乳酸较少(4.5对7.2毫当量/升),通气量(VE)也较少(48对55升/分钟);低工作率训练组的乳酸和VE降低明显较少(p小于0.01)。此外,在第一组中,高恒定工作率测试中的运动耐力平均增加了71%。血乳酸降低与通气量降低之间存在良好的相关性(r = 0.73,p小于0.005)。本研究的主要发现是,运动期间经历乳酸酸中毒的COPD患者可以从耐力训练计划中获得生理训练反应,并且产生高血乳酸水平的训练工作率比产生低乳酸水平的工作率更有效。