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J Appl Physiol 97: 697-703, 2004. First published April 16, 2004; doi:10.1152/japplphysiol.00108.2004
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Exercise response after rapid intravenous infusion of saline in healthy humans

H. Thomas Robertson,1 Riccardo Pellegrino,2 Daniela Pini,3 Jacopo Oreglia,3 Stefano DeVita,3 Vito Brusasco,4 and PierGiuseppe Agostoni1,3

1Department of Medicine, University of Washington, Seattle, Washington 98195-6522; 2Centro di Fisiopatologia Respiratoria e di Studio della Dispnea, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo; 3Centro Cardiologico Monzino IRCCS, Istituto di Cardiologia, Università di Milano, 20138 Milano; and 4Servizio di Fisiopatologia Respiratoria, Dipartimento di Medicina Interna, Università di Genova, 16132 Genova, Italy

Submitted 2 February 2004 ; accepted in final form 15 April 2004

Patients with chronic heart failure have an abnormal pattern of exercise ventilation (E), 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 E/CO2 slope increased from 24.9 ± 2.4 to 28.0 ± 2.9 l/l, (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 O2 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 O2 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 E 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.

edema; tidal volume; physiological dead space; exercise ventilation; maximal O2 uptake


Address for reprint requests and other correspondence: H. T. Robertson, Pulmonary and Critical Care Medicine, Box 356522, University Hospital, Seattle, WA 98195-6522 (E-mail: tomrobt{at}u.washington.edu).




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