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Ventilatory and metabolic changes as a result of exercise training in COPD patients
Patessio A, Carone M, Ioli F, Donner CF
Chest 1992 May;101(5 Suppl):274S-278S
clinical trial
4/10 [Eligibility criteria: No; Random allocation: Yes; Concealed allocation: No; Baseline comparability: Yes; Blind subjects: No; Blind therapists: No; Blind assessors: No; Adequate follow-up: No; Intention-to-treat analysis: No; Between-group comparisons: Yes; Point estimates and variability: Yes. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed*

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 versus 7.2 mEq/L) and less VE (48 versus 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p < 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 < 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.

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