(Circulation. 2001;104:1785.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Denmark (R.B., J.-A.L.C., G.R., H.S., B.S.), and the Department of Medicine, University of California, San Diego (P.D.W.).
Correspondence to Robert Boushel, DSc, Department of Exercise Science, Concordia University, 7141 Sherbrooke St West, Montreal, Quebec, H4B 1R6 Canada. E-mail boushel{at}alcor.concordia.ca
Background In chronic hypoxia, both heart rate (HR) and cardiac output (Q) are reduced during exercise. The role of parasympathetic neural activity in lowering HR is unresolved, and its influence on Q and oxygen transport at high altitude has never been studied.
Methods and Results HR, Q, oxygen uptake, mean arterial pressure, and leg blood flow were determined at rest and during cycle exercise with and without vagal blockade with glycopyrrolate in 7 healthy lowlanders after 9 weeks residence at
5260 m (ALT). At ALT, glycopyrrolate increased resting HR by 80 bpm (73±4 to 153±4 bpm) compared with 53 bpm (61±3 to 114±6 bpm) at sea level (SL). During exercise at ALT, glycopyrrolate increased HR by
40 bpm both at submaximal (127±4 to 170±3 bpm; 118 W) and maximal (141±6 to 180±2 bpm) exercise, whereas at SL, the increase was only by 16 bpm (137±6 to 153±4 bpm) at 118 W, with no effect at maximal exercise (181±2 bpm). Despite restoration of maximal HR to SL values, glycopyrrolate had no influence on Q, which was reduced at ALT. Breathing FIO2=0.55 at peak exercise restored Q and power output to SL values.
Conclusions Enhanced parasympathetic neural activity accounts for the lowering of HR during exercise at ALT without influencing Q. The abrupt restoration of peak exercise Q in chronic hypoxia to maximal SL values when arterial PO2 and SO2 are similarly increased suggests hypoxia-mediated attenuation of Q.
Key Words: heart rate cardiac output hypoxia nervous system, autonomic exercise
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