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We previously observed an increase in minute ventilation (V E) with resistive unloading (He-O2 breathing) in healthy elderly subjects with normal pulmonary function. To investigate the effects of resistive unloading in elderly subjects with mild chronic airflow limitation (FEV(1)/FVC: 61 +/- 4%), we studied 10 elderly men and women 70 +/- 3 yr of age. These subjects performed graded cycle ergometry to exhaustion, once breathing room air and once breathing a He-O2 gas mixture (79% He, 21% O2). V E, pulmonary mechanics, and PET(CO2) were measured during each 1-min increment in work rate. Data were analyzed by paired t test at rest, at ventilatory threshold (VTh), and during maximal exercise. V E was significantly (p0.05) increased at VTh (3.4 +/- 4.0 L/min or 12 +/- 15% increase) and maximal exercise (15.2 +/- 9.7 L/min or 22 +/- 13% increase) while breathing He-O2. Concomitant to the increase in V E, PET(CO2) was decreased at all levels (p0.01), whereas total work of breathing against the lung was not different. We concluded that V E is increased during He-O2 breathing because of resistive unloading of the airways and the maintenance of the relationship between the work of breathing and exercise work rate.

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.

Although exertional dyspnea in obesity is an important and prolific clinical concern, the underlying mechanism remains unclear.To investigate whether dyspnea on exertion in otherwise healthy obese women was associated with an increase in the oxygen cost of breathing or cardiovascular deconditioning.Obese women with and without dyspnea on exertion participated in two independent experiments (n = 16 and n = 14). All participants underwent pulmonary function testing, hydrostatic weighing, ratings of perceived breathlessness during cycling at 60 W, and determination of the oxygen cost of breathing during eucapnic voluntary hyperpnea at 40 and 60 L/min. Cardiovascular exercise capacity, fat distribution, and respiratory mechanics were determined in 14 women in experiment 2. Data were analyzed between groups by independent t test, and the relationship between the variables was determined by regression analysis.In both experiments, breathlessness during 60 W cycling was markedly increased in over 37% of the obese women (P0.01). Age, height, weight, lung function, and %body fat were not different between the groups in either experiment. In contrast, the oxygen cost of breathing was significantly (P0.01) and markedly (38-70%) greater in the obese women with dyspnea on exertion. The oxygen cost of breathing was significantly (P0.001) correlated with the rating of perceived breathlessness obtained during the 60 W exercise in experiment 1 (r(2) = 0.57) and experiment 2 (r(2) = 0.72). Peak cardiovascular exercise capacity, fat distribution, and respiratory mechanics were not different between groups in experiment 2.Dyspnea on exertion is prevalent in otherwise healthy obese women, which seems to be strongly associated with an increased oxygen cost of breathing. Exercise capacity is not reduced in obese women with dyspnea on exertion.