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Institute of Physiology- Centre for Physiology & Pharmacology, Medical University of Vienna, Schwarzspanierstra. Virtually all cardiovascular risk factors favor platelet hyperreactivity and, accordingly, also physical (in)activity affects platelet function. Within this paper, we will summarize and discuss the current knowledge on the impact of acute and habitual exercise on platelet function. Although there are apparent discrepancies regarding the reported effects of acute, strenuous exercise on platelet activation, a deeper analysis of the available literature reveals that the applied exercise intensity and the subjects' cardiorespiratory fitness represent critical determinants for the observed effects. Consideration of these factors leads to the summary that (i) acute, strenuous exercise can lead to platelet activation, (ii) regular physical activity and/or physical fitness diminish or prevent platelet activation in response to acute exercise, and (iii) habitual physical activity and/or physical fitness also favorably modulate platelet function at physical rest. Notably, these effects of exercise on platelet function show obvious similarities to the well- recognized relation between exercise and the risk for cardiovascular events where vigorous exercise transiently increases the risk for myocardial infarction and a physically active lifestyle dramatically reduces cardiovascular mortality. Introduction. A large body of evidence indicates that both acute exercise and habitual physical activity affect platelet function.
This is of special interest as the inflammatory and immunomodulatory consequences of platelet activation are increasingly recognized and platelets therefore seem to be of central importance not only to the final stages of cardiovascular disease (CVD), but also to the development of these diseases. Therefore, a modulation of platelet function by acute exercise and/or habitual physical activity might represent a mechanistic link between physical exertion and its observed effects on CVD. This would be especially interesting as a remarkable strong correlation exists between CVD- related mortality and physical activity, as we will discuss later in this review. In order to give a structured overview based on currently available literature, the first part of this review will deal with the influence of acute (mostly strenuous) exercise on platelet function. To introduce the reader to different aspects of platelet activation as well as platelet function tests (and also as interpretation of obtained results may critically depend on the applied methodologies), this will be done from a platelet- centered view where different aspects of platelet activation are treated separately. Subsequently, the impact of exercise intensity and the subjects' cardiorespiratory fitness on the effects of exercise on platelet function is summarized and discussed, including the modulating effects of cardiorespiratory fitness/physical activity on platelet function in the resting state. Introduction to Platelets and Their Function. Platelets represent the smallest formed elements of blood. They are anucleate cells with a life- span of 7–1. Activation of platelets, finally resulting in platelet degranulation and aggregation, is essential for hemostasis and can be triggered by several specific platelet- stimulating mediators (e. ADP, and elements of the extracellular matrix) as well as by shear and oxidative stress. As blood platelets are of central importance to the process of (primary) hemostasis and coagulation, abnormalities in platelet function (resulting in thrombosis or bleeding) result in severe and potentially lethal consequences. In principle, activation of platelets immediately results in platelet aggregation and subsequent thrombus formation—however, these consequences of platelet activation can to some extent be antagonized by functional endothelium, pointing to a crucial role of endothelium- derived mediators that counteract platelet activation (namely, nitric oxide and prostacyclin) in this process. However, as activated platelets compromise endothelial function, the situation is complex. The importance of platelets to the development of atherosclerotic disease is apparent from the fact that platelet activation is associated with accelerated atherosclerosis and correlates with severity of this disease in humans. An injection of activated platelets exacerbates the formation of native atherosclerotic lesions and an increase in systemic platelet activation has been described for a variety of atherosclerotic diseases including coronary artery disease . Influence of Acute Exercise on Diverse Aspects of Platelet Activation. Platelet Count and Volume. Several studies show that acute exercise results in a transient increase in platelet count. This increase is caused by hemoconcentration and by platelet release from the liver, lungs, and, importantly, the spleen . The latter contracts in response to elevated concentrations of epinephrine, as can be seen with increasing exercise intensity where epinephrine raises from preexercise plasma concentrations of 4. M to > 3. 50. 0 p. M with intense exercise . Interestingly, platelets stored in the spleen have been reported to be significantly larger than normal circulating platelets . Accordingly, some studies have reported an increase of mean platelet volume in response to exercise . Activation of Glycoprotein IIb/IIIa. Glycoprotein IIb/IIIa (GPIIb/IIIa, integrin . Upon platelet activation, this receptor undergoes a conformational change resulting in a drastically increased affinity towards fibrin(ogen), enabling the firm binding of platelets to fibrin(ogen) and thus facilitating platelet- platelet interaction, that is, platelet aggregation and the formation of stable thrombi. Only a limited number of studies found an increase in GPIIb/IIIa activation after exercise . Platelet Aggregation. Potential effects of exercise on platelet aggregation have been addressed by a multitude of studies using different techniques. The vast majority of these studies found increased platelet aggregability after exercise in response to various agonists, while a few studies found no such effect . Importantly, platelet aggregation is affected by cell density (see above); therefore, interpretation of experimental results might be difficult, as an increase in agonist- induced platelet aggregation is not necessarily related to platelet hyperreactivity when platelet count is not corrected. Nevertheless, increased platelet aggregation in response to exercise was observed by light transmission aggregometry without . Notably, this observed increase of in vitro platelet aggregation after acute exercise is not in contrast to those studies that found no effects of exercise on GPIIb/IIIa activation, as platelet aggregation rather depends on sensitivity of platelets towards agonists than on the basal activation state of glycoprotein IIb/IIIa. Another test indicative of platelet aggregate formation (following adhesion at high shear) is carried out by the Platelet Function Analyzer (PFA- 1. After exercise, shorter closure times have been reported . Decreased closure times in response to exercise were also observed with hemostatometry . Platelet Adhesion. Various platelet adhesion assays have been used in the literature to test for an effect of exercise on platelet function. These studies have yielded inconsistent results; whereas one study showed decreased platelet adhesion to fibrinogen (evoked by shear- stress with a rotational viscometer) . With this method, the authors found more adhering platelets after exhaustive exercise . Platelet Degranulation. Degranulation represents an integral consequence of platelet activation that results in the concomitant release of a variety of soluble mediators and the expression of distinct proteins on the platelet surface due to membrane fusion of the granules with the platelet membrane. 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