Circulation, Vol 88, 1502-1511, Copyright © 1993 by American Heart Association
AS Kestin, PA Ellis, MR Barnard, A Errichetti, BA Rosner and AD Michelson
BACKGROUND. It has been hypothesized that platelets are activated, or made
more activatible, by strenuous exercise and that these changes may play a
role in the genesis of exercise-induced coronary ischemia. Previous studies
have yielded conflicting results but have used assays (eg, platelet
aggregation, plasma platelet factor 4, and plasma beta- thromboglobulin)
that are subject to methodological problems. METHODS AND RESULTS. In the
present study, a whole blood flow cytometric method was used to study the
platelet activation state and reactivity of 12 physically active and 12
sedentary individuals before and after standardized treadmill exercise
testing. The peptide gly-pro-arg-pro (GPRP) was included in this assay to
prevent fibrin polymerization and platelet aggregation, thus allowing the
measurement of the reactivity to thrombin of individual platelets in the
physiological milieu of whole blood. A panel of fluorescent-labeled
monoclonal antibodies was used to monitor activation-dependent platelet
surface changes: downregulation of glycoprotein (GP) Ib (6D1) and
upregulation of GMP- 140 (S12), the GPIIb-IIIa complex (PAC1), and GPIV
(OKM5). In samples obtained before exercise, platelets not exposed to
thrombin showed no evidence of in vitro activation. In the sedentary
subjects, exercise caused a consistent and significant augmentation of the
platelet activation state and reactivity as judged by the binding of 6D1 in
the presence of thrombin 0.05 U/mL (P < .001), 0.005 U/mL (P = .001),
and 0 U/mL (P = .004) and by the binding of OKM5 in the presence of
thrombin 0.05 U/mL (P < .001), 0.005 U/mL (P = .029), and 0 U/mL (P =
.035). Exercise increased the binding of PAC1 at only a single thrombin
concentration (0.005 U/mL, P = .027) and did not alter the binding of S12
at any thrombin concentration. In contrast, in the physically active
subjects, exercise failed to cause a consistent alteration in either
platelet activation state or platelet reactivity. No significant
differences were found between the 12 male and 12 female volunteers.
CONCLUSIONS. Strenuous exercise in sedentary subjects but not physically
active subjects resulted in both platelet activation and platelet
hyperreactivity. These changes were more readily detected with monoclonal
antibodies directed against GPIb (6D1) and, to a lesser extent, GPIV (OKM5)
rather than those directed against the GPIIb-IIIa complex (PAC1) and
GMP-140 (S12). Platelet activation by thrombin, generally regarded as the
most physiologically important agonist, can be studied in whole blood in a
clinical setting through the use of the peptide GPRP.
ARTICLES
Effect of strenuous exercise on platelet activation state and reactivity
Department of Medicine, Medical Center of Central Massachusetts, Worcester.
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