Effects of sympathetic inhibition on exertional dyspnoea, ventilatory and metabolic responses to exercise in normotensive humans

Augmentation of circulating noradrenaline concentration stimulates ventilat ion during the initial stages of exercise and this is accompanied by an inc reased sensation of dyspnoea and exertion. This previous study [Clark, Gall oway, MacFarlane, Henderson, Aitchison and McMurray (1997) fur. Heart J. 18 , 1829-1833] suggested a link between dyspnoea, which commonly limits exerc ise tolerance in heart failure patients, and high circulating noradrenaline concentration in these patients. The present study investigated this relat ionship further using sympathetic inhibition. Ten healthy normotensive male s performed 10 min of submaximal cycling exercise at approx, 70% of maximal oxygen uptake per min ((V) over dot O-2max) On three occasions one week ap art. The first of these sessions was a familiarization session and the othe r two were experimental study days. On each of the study days, subjects att ended 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, subjec ts undertook the exercise task. Blood was drawn, expired gas was analysed b reath by breath, blood pressure, heart rate and ratings of perceived dyspno ea and exertion were obtained. Moxonidine treatment significantly reduced p lasma 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 sympat hetic activity does not affect ventilation, perceived dyspnoea or perceived exertion in normotensive males. Therefore it can be concluded that reducin g sympathetic activity may not be an appropriate strategy to help reduce pe rceived dyspnoea.