Exercise capacity is reduced in pulmonary arterial hypertension and in chronic left heart failure, but it is not known whether the cardiopulmonary exercise testing profile is different in the two conditions at the same severity of functional limitation.Nineteen patients with pulmonary arterial hypertension and 19 with chronic heart failure underwent a 6-min walk test and symptom-limited maximal incremental cycle ergometry.The patients with pulmonary arterial hypertension and chronic heart failure did not differ in New York Heart Association Functional Class (mean¡SEM 2.8¡0.1 versus 2.8¡0.2), 6-min walking distance (395¡30 versus 419¡20 m), peak work-rate, oxygen consumption, ventilation and cardiac frequency. However, patients with pulmonary arterial hypertension exhibited higher dyspnoea scores (5.8¡0.6 versus 3.8¡0.5) higher ventilatory equivalents for carbon dioxide (58¡3 versus 44¡3 at the anaerobic threshold) and lower peak oxygen pulse (5.9¡0.4 versus 8.7¡0.5 mL?beat -1 , or 53¡4 versus 64¡4% of the predicted value).It is concluded that the cardiopulmonary exercise testing profile in pulmonary arterial hypertension differs from that in chronic heart failure by showing more dyspnoea at comparable work-rates, related to greater reductions in ventilatory efficiency and stroke volume.

The phosphodiesterase-5 inhibitor sildenafil has been reported to improve hypoxic exercise capacity, but the mechanisms accounting for this observation remain incompletely understood. Sixteen healthy subjects were included in a randomized, double-blind, placebo-controlled, cross-over study on the effects of 50-mg sildenafil on echocardiographic indexes of the pulmonary circulation and on cardiopulmonary cycle exercise in normoxia, in acute normobaric hypoxia (fraction of inspired O2, 0.1), and then again after 2 weeks of acclimatization at 5000 m on Mount Chimborazo (Ecuador). In normoxia, sildenafil had no effect on maximum VO2 or O2 saturation. In acute hypoxia, sildenafil increased maximum VO2 from 27 +/- 5 to 32 +/- 6 mL/min/kg and O2 saturation from 62% +/- 6% to 68% +/- 9%. In chronic hypoxia, sildenafil did not affect maximum VO2 or O2 saturation. Resting mean pulmonary artery pressure increased from 16 +/- 3 mmHg in normoxia to 28 +/- 5 mmHg in normobaric hypoxia and 32 +/- 6 mmHg in hypobaric hypoxia. Sildenafil decreased pulmonary vascular resistance by 30% to 50% in these different conditions. We conclude that sildenafil increases exercise capacity in acute normobaric hypoxia and that this is explained by improved arterial oxygenation, rather than by a decrease in right ventricular afterload.

We tested the ability of exercise testing to predict not only survival, but also time to clinical worsening (TTCW) in idiopathic versus associated pulmonary arterial hypertension (PAH).136 patients with PAH (85 idiopathic and 51 with associated conditions) underwent cardiopulmonary exercise testing and a 6-min walk test. Death or transplantation, and clinical worsening events were recorded.32 patients died and four had lung transplantation. In a univariate analysis, PAH patients survival was associated with oxygen uptake (V9O 2 ) at peak exercise and at the anaerobic threshold, ventilatory equivalent for carbon dioxide (minute ventilation (V9E)/carbon dioxide production (V9CO 2 ) at the anaerobic threshold (at)), V9E/V9CO 2 slope and distance walked. TTCW was associated with peak V9O 2 and V9O 2 ,at, V9E/V9CO 2 ,at, end-tidal carbon dioxide tension measured at the anaerobic threshold, peak oxygen pulse, increase in oxygen pulse and distance walked. In a multivariable analysis, distance walked and V9E/V9CO 2 ,at predicted survival, and only peak V9O 2 predicted TTCW. The receiver operating characteristic curve-derived cut-off values were 305 m for the 6-min walk distance, 54 for V9E/V9CO 2 ,at and 11.6 mL?kg -1 ?min for peak V9O 2 . In the subgroup with associated PAH, no variable independently predicted either survival or clinical worsening. We conclude that several exercise variables predict survival and clinical stability in idiopathic PAH. Exercise variables are less accurate predictors of outcome in associated PAH.

The 6-min walk test (6MWT) is commonly used to evaluate exercise capacity in patients with pulmonary arterial hypertension (PAH). However, little is known about the corresponding metabolic stress as measured by cardiopulmonary exercise testing.The present study, therefore, measured ventilatory variables and heart rate during the 6MWT and symptom-limited incremental maximal exercise testing in 20 patients with PAH.The distance walked in 6 min was 450¡22 m (mean¡SE). During the 6MWT, ventilation, O 2 consumption, CO 2 production and heart rate increased during the first 3-4 min, and then remained stable. As compared with the maximum values measured during the cardiopulmonary exercise test, O 2 consumption tended to be higher (14.2¡0.6 versus 12.9¡0.7 mL?kg ), respiratory quotient (0.90¡0.02 versus 1.15¡0.02) and heart rate (119¡4 versus 135¡4 beats?min -1 ) remained lower.In conclusion, patients with pulmonary arterial hypertension exercise at higher aerobic capacity and lower metabolic stress during the 6MWT than during a cardiopulmonary exercise test.

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These results suggest that decreased aerobic exercise capacity after intake of beta-blockers is accompanied by decreased ventilation at any metabolic rate. However, this occurs without detectable change in the sympathetic nervous system tone or in metabo- or chemosensitivity and is therefore probably of hemodynamic origin.

In patients with CF, the intensity of systemic inflammation does not account significantly for the variance of FFM and diaphragm or limb muscle strength and bulk. Training of the diaphragm in CF occurs despite the presence of systemic inflammation.