Anti-arrhythmic mechanisms during exercise.
Paterson, David J.
University Laboratory of Physiology, Parks Road, Oxford OX1 3PT,
UK, tel 44 1865 272518, fax 44 1865 272469, email
djp@physiol.ox.ac.uk
APStracts 3:0019A, 1996.
Exercise disturbs cardiac sympatho-vagal and ionic balance. In
arterial blood, vigorous exercise can double plasma potassium,
decrease pH by 0.4 units and raise catecholamines 15 fold. If any of
these changes are experienced at rest there is an increased risk of
arrhythmia and cardiac arrest, yet in exercise they are usually
tolerated. How the heart is protected from the chemical stress caused
by exercise is not fully understood, but may be related to a
collective anti-arrhythmic effect of these chemical changes, so when
they combine there is a mutual antagonism. Catecholamines can offset
the harmful cardiac effects of hyperkalemia and acidosis in isolated
hearts and whole hearts in vivo and improve action potential
characteristics in potassium-depolarised ventricular myocytes. This
results from an increase in the inward calcium current that is
modulated by both adrenergic and non-adrenergic hormones. Conversely,
hyperkalemia can reduce or abolish the incidence of norepinephrine
-induced arrhythmias. The efficacy of the mutual antagonism is reduced
when the combination of acidosis, hyperkalemia and high levels of
norepinephrine are superimposed on a heart with regional ischemia or
a small infarct. However, the heart may be at greatest risk in the
post exercise period when plasma potassium is low and the adrenergic
tone is high. Little is known about this period, but abnormal
regulation of electrolyte and cardiac sympatho-vagal balance may
increase the incidence of arrhythmia, especially if there is
underlying ischemia. Although regular physical activity can reduce
the incidence of sudden cardiac death, recent epidemiological studies
show that vigorous exercise can trigger myocardial infarction and
sudden cardiac death, especially in habitually sedentary subjects
with coronary artery disease. This may be partly related to
disruption of the normal protective mechansim that allows the heart
to cope with the chemical stress caused exercise.
Received 21 July 1995; accepted in final form 19 December 1995.
APS Manuscript Number A1363-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96