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Hatter Institute and
Centre for Cardiology, UCL Hospitals and Medical School, Grafton Way,
London WC1E 6DB, UK
Correspondence to: Professor Yellon hatter-institute{at}ucl.ac.uk
Accepted 8 November
2000
OBJECTIVE
To determine whether
exercise is capable of protecting the myocardium from experimental
infarction and to explore the involvement of protein kinase C, a key
signalling protein, in the development of any protection observed.
METHODSRats were exercised on a
treadmill for 30 minutes at 23-27 m/min. Sham treated animals were
placed on the stationary treadmill but not exercised. Twenty four hours
later, hearts were Langendorff perfused and subjected to 35 minute left
main coronary artery occlusion followed by 120 minute reperfusion.
Infarct size was determined by tetrazolium staining and expressed as a
percentage of the risk zone (I/R%). To examine the potential
signalling pathway, animals were treated with either the selective
protein kinase C inhibitor chelerythrine, 5 mg/kg intraperitoneally,
or with vehicle 10 minutes before the exercise or sham treadmill period.
RESULTSIn the non-exercised group,
mean (SEM) I/R was 48.4 (3.0)%. In the exercised group, infarct size
was reduced to 17.3 (3.0)% (p < 0.01). Infarct size limitation
induced by exercise was abolished by chelerythrine (I/R 45.0 (6.0)%).
Chelerythrine pretreatment alone did not have any effect on infarct
size (I/R 51.1 (3.9)%). Differences in infarct size were independent
of risk zone size and myocardial contractile function during
ischaemia-reperfusion.
CONCLUSIONSExperimental moderate
exercise induces protection against myocardial infarction 24 hours
later. Protein kinase C activation during exercise appears to be an
important signal mediator of this protective response.
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