Evidence for Central and Peripheral Circulatory Exercise-Training Responses in COPD An impairment in peak exercise cardiac output (Qc) and stroke volume (Qs) measured during incremental exercise testing has been observed in subjects with COPD, and a relationship between severity of expiratory obstruction and the exercise-induced changes in stroke volume has been reported.41,42
There are relatively few reports of central and peripheral blood flow during steady-state submaximal exercise in COPD, and except for one study43 of hemodynamics of patients with COPD following exercise training, there are no studies investigating the effects of pulmonary rehabilitation on central and peripheral blood flow distribution. In the above-mentioned study, 12 COPD and emphysema patients were trained three times 20 minutes daily on a cycle ergome- ter at a self-selected intensity, for a total of 18 weeks. Right heart catheterization was performed before and after train- ing, cardiac output was measured by the Fick technique, and pulmonary capillary wedge, pulmonary artery, right ventric- ular, and right atrial pressures were recorded. Although a small decrease in resting and exercise VO2 was observed, the results failed to show any change in exercising cardiac index or in right or left stroke work following training, suggesting that the improved oxygen transport resulted from peripheral rather than central adaptations. However, measurements were reported only for one exercise condition, which was also not clearly described. Thus, the effects of exercise reha- bilitation on exercise cardiac output and its distribution to the periphery remain incompletely documented. A potential relationship between ventilatory mechanics and stroke vol- ume has been suggested by several authors, including Montes de Oca and colleagues,44 who observed pleural pres- sure swings during exercise to be the best predictor of O2 pulse (VO2/HR). Although significant knowledge has been gained over the last decade regarding the role of dynamic hyperinflation on dyspnea and exercise limitation in COPD,3 the extent to which exercise ventilatory mechanics may contribute to a central circulatory limitation and the effects of endurance training to reverse such a potential effect have not been examined.
Evidence for Central and Peripheral Circulatory Exercise-Training Responses in COPD An impairment in peak exercise cardiac output (Qc) and stroke volume (Qs) measured during incremental exercise testing has been observed in subjects with COPD, and a relationship between severity of expiratory obstruction and the exercise-induced changes in stroke volume has been reported.41,42
There are relatively few reports of central and peripheral blood flow during steady-state submaximal exercise in COPD, and except for one study43 of hemodynamics of patients with COPD following exercise training, there are no studies investigating the effects of pulmonary rehabilitation on central and peripheral blood flow distribution. In the above-mentioned study, 12 COPD and emphysema patients were trained three times 20 minutes daily on a cycle ergome- ter at a self-selected intensity, for a total of 18 weeks. Right heart catheterization was performed before and after train- ing, cardiac output was measured by the Fick technique, and pulmonary capillary wedge, pulmonary artery, right ventric- ular, and right atrial pressures were recorded. Although a small decrease in resting and exercise VO2 was observed, the results failed to show any change in exercising cardiac index or in right or left stroke work following training, suggesting that the improved oxygen transport resulted from peripheral rather than central adaptations. However, measurements were reported only for one exercise condition, which was also not clearly described. Thus, the effects of exercise reha- bilitation on exercise cardiac output and its distribution to the periphery remain incompletely documented. A potential relationship between ventilatory mechanics and stroke vol- ume has been suggested by several authors, including Montes de Oca and colleagues,44 who observed pleural pres- sure swings during exercise to be the best predictor of O2 pulse (VO2/HR). Although significant knowledge has been gained over the last decade regarding the role of dynamic hyperinflation on dyspnea and exercise limitation in COPD,3 the extent to which exercise ventilatory mechanics may contribute to a central circulatory limitation and the effects of endurance training to reverse such a potential effect have not been examined.
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