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Divisions of 1 Physiology and 2 Nephrology, Department of Medicine, University of California, San Diego, La Jolla, California 92093
After acclimatization to high
altitude, maximal exercise cardiac output (
T) is
reduced. Possible contributing factors include 1) blood
volume depletion, 2) increased blood viscosity,
3) myocardial hypoxia, 4) altered autonomic
nervous system (ANS) function affecting maximal heart rate (HR), and
5) reduced flow demand from reduced muscle work capability.
We tested the role of the ANS reduction of HR in this phenomenon in
five normal subjects by separately blocking the sympathetic and
parasympathetic arms of the ANS during maximal exercise after 2-wk
acclimatization at 3,800 m to alter maximal HR. We used intravenous
doses of 8.0 mg of propranolol and 0.8 mg of glycopyrrolate,
respectively. At altitude, peak HR was 170 ± 6 beats/min, reduced
from 186 ± 3 beats/min (P = 0.012) at sea level.
Propranolol further reduced peak HR to 139 ± 2 beats/min
(P = 0.001), whereas glycopyrrolate increased peak HR
to sea level values, 184 ± 3 beats/min, confirming adequate dosing with each drug. In contrast, peak O2 consumption,
work rate, and
T were similar at altitude under
all drug treatments [peak
T = 16.2 ± 1.2 (control), 15.5 ± 1.3 (propranolol), and 16.2 ± 1.1 l/min
(glycopyrrolate)]. All
T results at altitude were
lower than those at sea level (20.0 ± 1.8 l/min in air). Therefore, this study suggests that, whereas the ANS may affect HR at
altitude, peak
T is unaffected by ANS blockade.
We conclude that the effect of altered ANS function on HR is not the
cause of the reduced maximal
T at altitude.
altitude acclimatization; maximal exercise; autonomous nervous system; heart rate; propranolol; glycopyrrolate; oxygen uptake; acetylene uptake
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