Pulmonary gas exchange and exercise capacity in patients with systemic lupus erythematosus

Objective. Exercise tolerance is often reduced in patients with systemic lu pus erythematosus (SLE). Mechanisms have been proposed but the underlying c auses have not yet been elucidated. The study of pulmonary gas exchange dur ing exercise may be helpful in revealing circulatory, ventilatory, and meta bolic abnormalities. We hypothesized that in SLE, exercise aerobic capacity would be reduced due to chronic inactivity and poor muscle energetics. Methods. Thirteen women with SLE and low disease activity were studied; 5 a ge matched subjects served as controls. Clinical examination, chest radiogr aphy, electrocardiogram, and pulmonary function test were all normal. Subje cts underwent 1 min incremental cycle egometer exercise to exhaustion. Oxyg en uptake (VO2), CO2 output (VCO2), minute ventilation (V-E), heart rate (H R), and arterial O-2 saturation were monitored. Anaerobic threshold (AT), V O2/HR, Delta VO2/Delta Watt, respiratory rate (RR), T-i/T-tot, V-E/VCO2, an d breathing reserve (BR) were computed. Results. At rest, patients exhibited high V-E, respiratory alkalosis, and a wide alveolar-arterial O-2 gradient [(A - a)O-2] during 50% O-2 breathing. Other indexes of respiratory function were within the normal range. In the 6 patients with SLE where pulmonary artery systolic pressure at Doppler ec hocardiography was measurable, mean level was in the upper limits of normal . During exercise, maximal aerobic capacity was reduced in all patients (VO 2 peak, 1098 +/- 74 vs 2150 +/- 160 ml/min, p < 0.01; AT, 36 +/- 3 vs 48 +/ - 3% predicted VO2 max, p < 0.05). Ventilation adjusted for the metabolic d emand (V-E/VCO2 at AT) was increased (31 +/- 1 vs 24 +/- 1; p < 0.05). A no rmal breathing pattern was observed during all tests. No patient stopped ex ercising because of ventilatory limitation (i.e., they had normal breathing reserve). Conclusion, Reduced muscle aerobic capacity is common in SLE and is most li kely because of peripheral muscle deconditioning. Increased ventilatory dem and, secondary to diffuse interstitial lung disease, is not a significant c ontributor to the reduction in exercise tolerance.