Augmentation of circulating noradrenaline concentration stimulates ventilation during the initial stages of exercise and this is accompanied by an increased sensation of dyspnoea and exertion. This previous study [Clark, Galloway, MacFarlane, Henderson, Aitchison and McMurray (1997) Eur. Heart J. 18, 1829–1833] suggested a link between dyspnoea, which commonly limits exercise tolerance in heart failure patients, and high circulating noradrenaline concentration in these patients. The present study investigated this relationship further using sympathetic inhibition. Ten healthy normotensive males performed 10 min of submaximal cycling exercise at approx. 70% of maximal oxygen uptake per min (VċO2max) on three occasions one week apart. The first of these sessions was a familiarization session and the other two were experimental study days. On each of the study days, subjects attended the laboratory in the morning after an overnight fast and, following a resting blood sample, were administered placebo or moxonidine (0.4 mg) in a double blind cross-over design. After a 90-min absorption period, subjects undertook the exercise task. Blood was drawn, expired gas was analysed breath by breath, blood pressure, heart rate and ratings of perceived dyspnoea and exertion were obtained. Moxonidine treatment significantly reduced plasma noradrenaline concentration (P < 0.01), mean arterial pressure (P < 0.01), and blood glycerol concentration (P < 0.05), but no differences were observed in heart rate, the ventilatory response to exercise or subjective ratings of dyspnoea and exertion. This study indicates that reducing sympathetic activity does not affect ventilation, perceived dyspnoea or perceived exertion in normotensive males. Therefore it can be concluded that reducing sympathetic activity may not be an appropriate strategy to help reduce perceived dyspnoea.
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August 16 2000
Effects of sympathetic inhibition on exertional dyspnoea, ventilatory and metabolic responses to exercise in normotensive humans
Stuart D. R. GALLOWAY;
*Department of Cardiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, U.K.
Correspondence: Dr Stuart Galloway (e-mail [email protected]).
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Giuseppe DE VITO;
Giuseppe DE VITO
†Scottish School of Sport Studies, University of Strathclyde, Glasgow G13 1PP, Scotland, U.K.
*Department of Cardiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, U.K.
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Sam McCLURE;
Sam McCLURE
*Department of Sports Studies, University of Stirling, Stirling FK9 4LA, Scotland, U.K.
*Department of Cardiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, U.K.
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Myra A. NIMMO;
Myra A. NIMMO
†Scottish School of Sport Studies, University of Strathclyde, Glasgow G13 1PP, Scotland, U.K.
*Department of Cardiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, U.K.
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John J. V. McMURRAY
John J. V. McMURRAY
*Department of Sports Studies, University of Stirling, Stirling FK9 4LA, Scotland, U.K.
*Department of Cardiology, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, Scotland, U.K.
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Publisher: Portland Press Ltd
Received:
October 29 1999
Revision Received:
April 28 2000
Accepted:
May 12 2000
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2000
2000
Clin Sci (Lond) (2000) 99 (3): 223–230.
Article history
Received:
October 29 1999
Revision Received:
April 28 2000
Accepted:
May 12 2000
Citation
Stuart D. R. GALLOWAY, Giuseppe DE VITO, Sam McCLURE, Myra A. NIMMO, John J. V. McMURRAY; Effects of sympathetic inhibition on exertional dyspnoea, ventilatory and metabolic responses to exercise in normotensive humans. Clin Sci (Lond) 1 September 2000; 99 (3): 223–230. doi: https://doi.org/10.1042/cs0990223
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