Disruption of the normal rheological properties of blood is considered an independent risk factor for cardiovascular disease and plays a significant role in the aetiology of atherothrombogenesis. The acute increase in whole blood viscosity may unfavourably affect the microcirculatory blood flow and oxygen delivery to the tissues. It is universally accepted that exercise and physical activity performed on a regular basis has health benefits. However, the effects of exercise on the rheological properties of blood have not received much research attention. Recent, limited evidence indicates that the viscosities of whole blood and plasma increase in response to a variety of exercise protocols. The increase in whole blood viscosity is mainly attributed to an increase in haematocrit and plasma viscosity, whereas the deformability and aggregability of red blood cells remain unaltered. The increases in plasma viscosity and haematocrit have been ascribed to exercise-induced haemoconcentration as a result of fluid transfer from the blood to the interstitial spaces. The haemorheological changes associated with strenuous exercise appear to be linked with enhanced oxidative stress and depletion of antioxidant capacity, and that may affect oxygen delivery and availability to the tissues. Although significant advances have been made in many areas of exercise haematology, the long-term effects of endurance training on blood rheology have been very briefly examined and the exact effect of training has not as yet been determined. Available cross-sectional and longitudinal studies indicate that the blood of endurance athletes is more dilute and this has been attributed to an expansion of blood volume, particularly plasma volume as a result of training. The low haematocrit values in trained athletes represent a hydration condition rather than iron stores deficiency. It has been suggested that this hypervolaemia and blood dilutional effect of endurance training may be advantageous for heat dissipation and greater cardiac stroke volume and lower heart rates during exercise. Enhanced blood fluidity also facilitates oxygen delivery to the exercising muscles because of a reduced resistance to blood flow within the microcirculation. Furthermore, the increase in plasma volume may contribute to the body water pool and help offset dehydration. The influence of strength and power training on blood rheology is not known. The physiological mechanisms responsible for and the functional consequences of the haemorheological changes associated with exercise to a large extent remain speculative. The paradox of haematocrit and blood rheology in exercise and training warrants additional studies. Likewise, further investigations are necessary to determine the possible link between overtraining and blood rheological profiles.

In recent years, the dysfunction of the haemostatic system in relation to the clinical complications from arterioscleroses and cardiovascular diseases has become more recognised. Blood coagulation and fibrinolysis comprise two important physiological systems, which are regulated by a balance between activators and inhibitors. Activation of blood coagulation is associated with accelerated clot formation, whereas activation of blood fibrinolysis enhances the breakdown of the blood clot. Available evidence suggests that strenuous exercise induces activation of blood coagulation with simultaneous enhancement of blood fibrinolysis. Although the responses of blood coagulation and fibrinolysis appear to be related to the exercise intensity and its duration, recent reports suggest that moderate exercise intensity is followed by activation of blood fibrinolysis without concomitant hyper-coagulability, while very intense exercise is associated with concurrent activation of blood coagulation and fibrinolysis. Similar to blood coagulation and fibrinolysis, systemic platelet-related thrombogenic factors have been shown to be involved in the initiation and progression of atherogenesis and plaque growth. Although exercise effects on platelet aggregation and function in healthy individuals have been examined, the results reported have been conflicting. However, for patients with coronary heart disease, the balance of evidence available would strongly suggest that platelet aggregation and functions are increased with exercise. Few studies are available concerning the influence of training on blood coagulation and fibrinolysis and the exact effects of exercise training on the equilibrium between blood coagulation and fibrinolysis is not as yet known. Although the effects of physical training on platelets have been briefly investigated, available meagre evidence suggests that exercise training is associated with favourable effects on platelet aggregation and activation in both men and women.

This article presents an overview of the progress that has been made in recent years in our understanding of the interaction between exercise and platelets in health and disease. Although platelets are important in normal haemostasis, recent evidence emphasises the pivotal role of abnormal platelet function in acute coronary artery diseases, myocardial infarction, unstable angina and stroke. In light of the positive health benefits of exercise, interest has been heightened on the association between exercise and platelet aggregation and function, not only in normal healthy subjects but also in patients. However, the study of exercise effects on blood platelets are highly contentious because of the fact that the analytical methods employed to study platelets are bedevilled by numerous methodological problems. While exercise effects on platelet aggregation and function in healthy individuals have been extensively examined, the evidence reported has been conflicting. Somewhat less contradictory are the results generated from studies in patients with coronary heart disease, as the preponderance of evidence available would strongly suggest that platelet aggregation and function are increased with exercise. Several drugs are known to influence platelet aggregation and function, the most examined among these medications is aspirin (acetylsalicylic acid). However, aspirin appears to be ineffective to attenuate exercise-induced increases in platelet aggregation and activation. Few studies are available on the effect of training on blood platelets and the exact effects of exercise training on platelet activation and function is not as yet known. This lack of information makes further studies particularly important, in order to clarify whether there are favourable effects of exercise training on platelet aggregation and function in health and disease.

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Alcohol use, particularly excessive alcohol consumption is one of the most serious health risks in the world. A relationship between sport, exercise and alcohol consumption is clear and long-standing. Alcohol continues to be the most frequently consumed drug among athletes and habitual exercisers and alcohol-related problems appear to be more common in these individuals. Alcohol use is directly linked to the rate of injury sustained in sport events and appears to evoke detrimental effects on exercise performance capacity. The model of alcohol consumption in human experimental studies has either been acute (single dose) or chronic (repeated doses over a period). These studies suggested that alcohol consumption decreases the use of glucose and amino acids by skeletal muscles, adversely affects energy supply and impairs the metabolic process during exercise. In addition, chronic alcohol use is associated with increased citrate synthase activity and decreased cross-sectional area of type I, IIa and IIb fibres. There is evidence to suggest that exercise may attenuate the ethanol-induced decline in hepatic mitochondria and accelerates ethanol metabolism by the liver. Exercise training seems to reduce the extent of the oxidative damage caused by ethanol. Evidence generated from in vitro experiments and animal studies have also suggested that ethanol administration decreased skeletal muscle capillarity and increased pyruvate kinase and lactate dehydrogenase activities. Substantial epidemiological evidence has been accrued showing that moderate ingestion of alcohol may reduce the incidence of cardiovascular diseases. Although the existing evidence is often confusing and disparate, one of the mechanisms by which alcohol may reduce the incidence of mortality of cardiovascular diseases is through raising levels of high-density lipoprotein cholesterol. Available evidence suggests that exercise and moderate alcohol consumption may have favourable effects on blood coagulation and fibrinolysis; however, compelling experimental evidence is lacking to endorse this notion. Occasional and chronic alcohol consumption is usually linked with unfavourable alterations in platelet aggregation and function and may be associated with platelet-related thrombus formation. Although the effects of alcohol consumption on the rheological properties of the blood are not known, recent experimental evidence suggests that alcohol use following exercise is associated with unfavourable changes in the main determinants of blood viscosity. It is well documented that alcohol use modulates the immune system and impairs host defence. Compelling evidence is also mounting to suggest that chronic alcohol use is linked with adverse effects on the body systems and organs including the brain, the cardiovascular system and the liver.