Mahmoud S. El-Sayed

Effects of Exercise on Blood Coagulation, Fibrinolysis and Platelet Aggregation

SummaryDisturbances of the haemostatic balance may result in thrombosis or bleeding tendency. There have been abundant reports on the effects of exercise on blood haemostasis, but the results reported have been conflicting and difficult to interpret. This review outlines and critically evaluates the relevant literature on the effects of short term exercise and physical training on the 3 systems of blood haemostasis i.e. blood coagulation, fibrinolysis and platelet aggregation.Short term exercise is usually associated with a significant shortening of activated partial thromboplastin time (APTT) and a marked increase in factor VIII (FVIII). The rise in FVIII is directly related to exercise intensity and the individuals’ training status. Exercise also induces a significant increase in blood fibrinolysis which is dependent on exercise intensity, duration and training condition. The rise in blood fibrinolysis is mainly due to an increase in tissue-type plasminogen activator (t-PA) and a decrease in its main inhibitor plasminogen activator inhibitor (PAI-1) which are released from the endothelial cells of the vessel wall.Platelet count increases in exercise and this is probably due to a fresh release of platelets from the spleen, bone marrow and lungs. Studies on the effects of exercise on platelet aggregation and markers of platelet activation have produced conflicting results, and the exact effects of exercise remain as yet undetermined. It is suggested that short term exercise activates blood coagulation and enhances blood fibrinolysis and the delicate balance between clot formation and clot dissolution is maintained in normal populations. No valid conclusion could be reached regarding the actual effects of physical training on blood coagulation, fibrinolysis and platelet aggregation. This is undoubtedly due to variations in training programmes employed, populations studied, and the analytical methods used.

Blood hemostasis in exercise and training

Formation of the blood clot is a slow but normal physiological process occurring as a result of the activation of blood coagulation pathways. Natures guard against unwanted blood clots is the fibrinolytic enzyme system. In healthy people, there is a delicate dynamic balance between blood clot formation and blood clot dissolution. Available evidence suggests that exercise and physical training evoke multiple effects on blood hemostasis in normal healthy subjects and in patients. A single bout of exercise is usually associated with a transient increase in blood coagulation as evidenced by a shortening of activated partial thromboplastin time (APTT) and increased Factor VIII (FVIII). The rise in FVIII is intensity dependent and continues into recovery. The effects of acute exercise on plasma fibrinogen have yielded conflicting results. Thus, the issue of whether exercise-induced blood hypercoagulability in vitro mirrors an in vivo thrombin generation and fibrin formation remains disputable. Exercise-induced enhancement of fibrinolysis has been repeatedly demonstrated using a wide range of exercise protocols incorporating various exercise intensities and durations. Moderate exercise appears to enhance blood fibrinolytic activity without a concomitant activation of blood coagulation mechanisms, whereas, very heavy exercise induces simultaneous activation of blood fibrinolysis and coagulation. The increase in fibrinolysis is due to a rise in tissue-type plasminogen activator (tPA) and decrease in plasminogen activator inhibitor (PAI). The mechanism of exercise-induced hyperfibrinolysis is poorly understood, and the physiological utility of such activation remains unresolved. Strenuous exercise elicits a transient increase in platelet count, but there are conflicting results concerning the effect of exercise on platelet aggregation and activation. Few comprehensive studies exist concerning the influence of exercise training on blood hemostasis, making future investigation necessary to identify whether there are favorable effects of exercise training on blood coagulation, fibrinolysis, and platelet functions.

Haemorheology in Exercise and Training

AbstractDisruption 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.

Exercise and training effects on blood haemostasis in health and disease an update

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.

The acute effects of resistance exercise on the main determinants of blood rheology

The aim of this study was to examine short-term changes in blood rheological variables after a single bout of resistance exercise. Twenty-one healthy males completed three sets of 5 – 7 repetitions of six exercises at an intensity corresponding to 80% of one-repetition maximum (1-RM). The average duration of the exercise bout was 35 min. Venous blood samples were obtained before exercise, immediately after exercise and after 30 min of recovery and analysed for lactate, red blood cell count, haematocrit, haemoglobin, plasma viscosity, fibrinogen, total protein and albumin concentration. Plasma volume decreased 10.1% following resistance exercise. This occurred in parallel with an increase of 5.6%, 5.4% and 6.2% in red blood cell count, haemoglobin and haematocrit; respectively. Plasma viscosity increased from 1.55 ± 0.01 to 1.64 ± 0.01 mPa · s immediately after resistance exercise before decreasing to 1.57 ± 0.01 mPa · s at the end of the recovery period. Similarly, fibrinogen, albumin and total protein increased significantly following resistance exercise. However, the rises in all these rheological parameters were transient and returned to pre-exercise values by the end of recovery. We conclude that a single session of heavy resistance exercise performed by normal healthy individuals alters blood rheological variables and that these changes are transient and could be attributed to exercise-induced haemoconcentration.

Aggregation and Activation of Blood Platelets in Exercise and Training

AbstractThis 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.

THE EFFECTS OF GRADED RESISTANCE EXERCISE ON PLATELET AGGREGATION AND ACTIVATION

PURPOSE The purpose of this study was to examine the effects of resistance exercise with varying intensity but with similar volume on platelet aggregation and activation. METHODS Thirteen healthy male subjects randomly completed three resistance exercise test trials at an intensity corresponding to 40%, 60%, and 80% of one repetition maximum (1-RM) in which the subjects performed six exercises including upper- and lower-body parts. Venous blood samples were obtained before and immediately after each exercise trial and analyzed for platelet count (PLT), plateletcrit (PCT), mean platelet volume (MPV), platelet aggregation, and beta-thromboglobulin (B-TG). Plasma volume changes were estimated from hemoglobin and hematocrit readings before and after each exercise trial. RESULTS Although all exercise trials were followed by a significant (P < 0.05) increase in PLT (thrombocytosis), PCT, and MPV, this rise was not related to the exercise intensity (P > 0.05). Exercise was also followed by a significant increase (P < 0.05) in platelet aggregation, but this only occurred with the high but not with the low concentrations of adenosine diphosphate (ADP). Although ANOVA showed a significant overall increase (P < 0.05) in the concentration of B-TG after exercise, this rise only reached the assigned level of significance (P < 0.05) after 80% exercise trial. CONCLUSION It was concluded therefore that resistance exercise is followed by an increase in PLT, PCT, and MPV, and this occurred in parallel with an in vivo activation of platelet as manifested by an increase in platelet aggregation and a rise in B-TG.

Effects of Exercise and Training on Blood Rheology

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.Although the long term effects of endurance training on blood rheology have been very briefly examined, the exact effect of training has not as yet been determined. However, 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 plasma volume as a result of training. It has been suggested that this blood dilutional effect of endurance training may be advantageous in delivering oxygen to the exercising muscles because of a reduced resistance to blood flow. The increase in plasma volume may also contribute to the body water pool and help offset dehydration. The influence of strength and power training on blood rheology is not known.

Blood coagulation and fibrinolysis at rest and in response to maximal exercise before and after a physical conditioning programme

Twenty-five young subjects were divided into experimental (n = 13) and control (n = 12) groups in order to examine the acute and chronic effects of exercise on blood coagulation and fibrinolysis. Blood coagulation and fibrinolysis variables were ascertained in both groups before and after a physical conditioning programme both at rest and following maximal exercise. The experimental group exercised for 12 weeks [30 min, 3 × week at 70% (6 weeks) and 80% (6 weeks) of maximum heart rate]. The control group maintained normal activity patterns. Significant activation (P > 0.05) of blood coagulation was observed in response to maximal exercise before and after the conditioning programme in both groups in activated partial thromboplastin time (APTT), thrombin clotting time (TCT), factor VIII procoagulant activity (FVIII PA) and factor VIII antigen (FVIII A). Likewise, blood plasminogen activator showed a significant increase (P < 0.05) in response to maximal exercise before and after conditioning in both groups. Although VO2 max following the conditioning programme was significantly increased in the exercise group versus control, no significant changes (P > 0.05) were observed in either group in blood coagulation and fibrinolysis parameters at rest or in response to maximal exercise. It is concluded that maximal exercise transiently accelerates blood coagulation and activates blood fibrinolytic activity, however physical conditioning appears not to influence the haemostatic and fibrinolytic systems at rest or in response to maximal exercise.

Interaction between alcohol and exercise: physiological and haematological implications.

AbstractAlcohol 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.