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Exercise response after rapid intravenous infusion of saline in healthy humans
1 Department of Medicine, University of Washington, Seattle, Washington 98195-6522; 2 Centro di Fisiopatologia Respiratoria e di Studio della Dispnea, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo; 3 Centro Cardiologico Monzino IRCCS, Istituto di Cardiologia, Università di Milano, 20138 Milano;...
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Published in: | Journal of applied physiology (1985) 2004-08, Vol.97 (2), p.697-703 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
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Summary: | 1 Department of Medicine, University of Washington, Seattle, Washington 98195-6522; 2 Centro di Fisiopatologia Respiratoria e di Studio della Dispnea, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo; 3 Centro Cardiologico Monzino IRCCS, Istituto di Cardiologia, Università di Milano, 20138 Milano; and 4 Servizio 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 (V T ), increased alveolar ventilation, and elevated physiological dead space (V D /V T ). 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 / CO 2 slope increased from 24.9 ± 2.4 to 28.0 ± 2.9 l/l, ( P < 0.0002), associated with a small decrease in arterial P CO 2 , but without changes in V T , V D /V T , or alveolar-arterial O 2 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 O 2 pulse. Therefore, infusion of saline to normal subjects before exercise failed to reproduce either the increase in V D /V T or the smaller exercise V T 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 O 2 uptake, and heart rate after saline infusion may be linked to accumulation of edema fluid in exercising muscle, impairing the diffusion of O 2 to muscle mitochondria.
edema; tidal volume; physiological dead space; exercise ventilation; maximal O 2 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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ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/japplphysiol.00108.2004 |