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  • Recovery of Gas Exchange Variables and Heart Rate: DISCUSSION

Heart Rate

The mechanism of ventilatory impairment at maxi­mal exercise in COPD cannot be stated with certainty, although the preponderance of evidence indicates that diaphragmatic fatigue is not the major limiting factor. In the present study the lack of a tachypneic response during recovery suggests that diaphragmatic fatigue was not present, which is consistent with the findings of Gallagher and Younes. In contrast, Bye et al reported electromyographic evidence of diaphrag­matic fatigue during exhaustive exercise in five of eight patients with COPD. It is possible that changes in frequency content of the diaphragmatic electromyo- gram with exercise in patients with COPD represent a response to loading, rather than the development of muscle fatigue.

In addition to marked reduction of work capacity, patients with COPD had prolonged relative hyper- pnea, hypermetabolism, and tachycardia after exer­cise when compared to control subjects. It is important to note that although the absolute values for gas exchange variables were lower in the patients both at maximal exercise and during recovery, the relative recovery rates were significantly slower in the patients than in the control subjects. Nevertheless, the extent of recovery at eight to ten minutes after exercise was similar between the two groups.

After maximal exercise, carbon dioxide is eliminated rapidly from muscle, resulting in increased femoral venous Pco2, and is transported to the lungs for excretion in respired air. The rate of elimination of increased body stores of carbon dioxide depends on carbon dioxide chemosensitivity and ventilatory ca­pacity. It is unlikely that the delayed elimination of carbon dioxide in the group with COPD was due to impaired transport of carbon dioxide from muscle to blood, in view of the high solubility and rapid diffusion of carbon dioxide across biologic membranes. The bottleneck to carbon dioxide elimination in patients with airway disease most likely resides at the level of excretion in respired air, resulting from mechanical limitation to the attainment of adequate alveolar ventilation to rapidly restore body stores of carbon dioxide to resting levels.
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The delayed elimination of excess carbon dioxide in COPD may contribute to impairment of exercise tolerance by both heightening and prolonging the perception of respiratory loads. The importance of carbon dioxide elimination in limiting exercise per­formance in COPD has been confirmed by the obser­vation that a large carbohydrate load resulted in increased resting Vco2 and reduced 12-min walking distance. The central role of respiratory load percep­tion in limitation of exercise in patients with COPD is supported by reports of enhanced exercise perform­ance after administration of anxiolytic drugs and opiates; for example, administration of oral morphine (0.8 mg/kg) to a group of patients with COPD resulted in improvements in Vo, and maximal workload, probably on the basis of reduced ventilatory drive (reduced ventilation for the same Vco2) or altered central perception of breathlessness (or both).

Delayed elimination of excess carbon dioxide in patients with obstructive airway disease has important implications for adaptations to changes in body stores of carbon dioxide. In normal subjects the rate of elimination of carbon dioxide after an acute increase in body stores of carbon dioxide induced by rebreath- ing was correlated with the slope of the ventilatory response to carbon dioxide, but not with the magni­tude of hypercapnia; however, in patients with air­flow limitation, delayed elimination of excess carbon dioxide is most likely attributable to reduced ventila­tory capacity.

The prolonged requirement for increased ventila­tion and oxygen uptake must be considered in the total metabolic demand for the performance of work in these patients. In particular, work-rest intervals in COPD exercise rehabilitation programs must be ad­justed to allow complete restoration of basal stores of carbon dioxide in order to avoid progressive hypercap­nia. From our data, excess elimination of carbon dioxide may persist for more than ten minutes after maximal exercise.
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Several considerations underscore the importance of measurement of recovery of gas exchange variables in patients with COPD. Such measurements may give further insight into the training response in these individuals; because patients with COPD have not shown significant cardiovascular or skeletal muscle adaptations to exercise training, and improved kinet­ics of recovery of gas exchange variables have been described in response to training, the period after exercise warrants further attention in this group of patients. In addition, exercise performed early during recovery from prior exercise has been shown to require higher oxygen uptake per workload than exercise performed under basal conditions; therefore, de­layed recovery of ventilation and oxygen uptake confer an added metabolic cost to performance of repeated tasks and reduce maximal workload.

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