Patients with chronic heart failure have an abnormal pattern of exercise ventilation (VE), characterized by small tidal volumes (VT), increased alveolar ventilation, and elevated physiological dead space (VD/VT). To investigate whether increased lung water in isolation could reproduce this pattern of exercise ventilation, 30 ml/kg of saline were rapidly infused into nine normal subjects, immediately before a symptom-limited incremental exercise test. Saline infusion significantly reduced forced vital capacity, 1-s forced expiratory volume, and alveolar volume (P <0.01 for all). After saline, exercise ventilation assessed by the V̇E/V̇O2 slope increased from 24.9 ± 2.4 to 28.0 ± 2.9 1/1, (P <0.0002), associated with a small decrease in arterial PCO2, but without changes in VT, VD/VT, or alveolar-arterial O2 difference. A reduction in maximal O 2 uptake of 175 ± 184 ml/min (P <0.02) was observed in the postsaline infusion exercise studies, associated with a consistent reduction in maximal exercise heart rate (8.1 ± 5.9 beats/min, P <0.01), but without a change in the 02 pulse. Therefore, infusion of saline to normal subjects before exercise failed to reproduce either the increase in VD/VT or the smaller exercise VT described in heart failure patients. The observed increase in V̇E can be attributed to dilution acidosis from infusion of the bicarbonate-free fluid and/or to afferent signals from lung and exercising muscles. The reduction in maximal power output, maximal O2 uptake, and heart rate after saline infusion may be linked to accumulation of edema fluid in exercising muscle, impairing the diffusion of O2 to muscle mitochondria.
- Exercise ventilation
- Maximal O uptake
- Physiological dead space
- Tidal volume
ASJC Scopus subject areas
- Orthopedics and Sports Medicine
- Physical Therapy, Sports Therapy and Rehabilitation