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00005768-200005000-0000700005768_2000_32_918_sayed_hemostasis_5review< 187_0_12_0 >Medicine & Science in Sports & Exercise©2000The American College of Sports MedicineVolume 32(5)May 2000pp 918-925Blood hemostasis in exercise and training[BASIC SCIENCES: Reviews]EL-SAYED, MAHMOUD S.; SALE, CRAIG; JONES, PETER G. W.; CHESTER, MICHAELResearch Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, ENGLAND; and Cardiothoracic Centre, Broadgreen Hospital, Broadgreen, Liverpool, ENGLANDSubmitted for publication December 1998.Accepted for publication May 1999.Address for correspondence: Prof. Mahmoud. S. El-Sayed, The Research Institute for Sport and Exercise Sciences, School of Human Sciences, Liverpool John Moores University, The Henry Cotton Campus, Webster Street, Liverpool, L3 2ET, England. E-mail: M.ElSAYED@LIVJM.ac.uk.AbstractEL-SAYED, M. S., C. SALE, P. G. W. JONES, and M. CHESTER. Blood hemostasis in exercise and training. Med. Sci. Sports Exerc., Vol. 32, No. 5, pp. 918–925, 2000. Formation of the blood clot is a slow but normal physiological process occurring as a result of the activation of blood coagulation pathways. Nature’s 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.Although blood is hypercoagulable after strenuous exercise, probably due to an increase in Factor VIII (FVIII) (3,37,50), the level of other clotting factors does not appear to be altered. Exercise-induced shortening of whole-blood clotting times and activated partial thromboplastin time (APTT) is well documented (3,5,7,37,48,52,73). However, results reported on prothrombin time (PT) and thrombin time (TT) in response to exercise have been controversial. Research has shown both a significant shortening (39) and no significant difference in PT (37,73,91) after exercise. More recently, El-Sayed et al. (37) have demonstrated that exercise significantly shortens TT. Changes in APTT and PT persist from 1 to 24 h postexercise (3,91).EFFECTS OF ACUTE EXERCISE ON BLOOD COAGULATION, FIBRINOLYSIS, AND PLATELET FUNCTIONSBlood coagulation changes in response to acute exercise.Exercise bouts of varied intensity and duration have all induced significant increases in FVIII coagulant activity (3,37,50). Additionally, increases in FVIII coagulant activity and antigen have been positively associated with exercise intensity (2), and this increase persists into recovery (3,50). Significant increases in FVIII activity were also observed after resistance exercise, and these increases were positively correlated to the volume of weight lifted (32).The mechanism by which exercise increases FVIII is not fully understood. It may either be due to activation within the circulation or to the release of stored or freshly synthesized FVIII (32). In vitro exposure of FVIII to catalytic concentrations of thrombin induced a significant increase in FVIII (55), suggesting that this increase might also be associated with thrombin formation. The stimulus responsible for exercise-induced increases in FVIII seems to be mediated via the β-adrenergic receptor pathway because β blockade blunts this increase (19).Studies investigating the effects of acute exercise on plasma fibrinogen concentration have produced conflicting results (36). A number of these studies have shown that exercise using different protocols had no significant effects on plasma fibrinogen (24,37,52,67,89,119). However, others have either reported significant increases (3,59,104) or significant decreases (5,84). Differences in exercise protocol, training status, subject health, and the analytical methods used for the assessment of plasma fibrinogen are probably responsible for the reported inconsistencies.Exercise causes an activation of blood coagulation, although it is disputable whether this leads to significant in vivo thrombin generation and fibrin formation. Weiss et al. (120) examined the relationship between exercise intensity and the activation of coagulation and fibrinolysis. They showed that exercise at ∼68% V̇O2max increased plasmin formation without corresponding increases in the markers of blood coagulation activation. Similarly, exercise at ∼83% V̇O2max was associated with an increase in plasmin formation, although this was accompanied by a concomitant increase in markers of blood coagulation. Thus, moderate exercise appears to enhance in vivo blood fibrinolysis, whereas very heavy exercise activates blood fibrinolysis and blood coagulation simultaneously. Long-term exercise such as marathon running was followed by an activation of blood coagulation, as indicated by the formation of thrombin and cross-linked fibrin (96). It should be noted, however, that the acceleration of blood coagulation was smaller than the activation of blood fibrinolysis. Patients with peripheral arterial occlusive disease exhibited increased thrombin formation postsubmaximal exercise, although no such increase was shown in healthy controls (76). These recent results would suggest that markers of the activation of blood coagulation and indicators of enhanced fibrinolysis are related to exercise intensity and the health of the populations studied.Thrombin-antithrombin complex (TAT) and prothrombin fragments 1+2 (PTF1+2) have been utilized as markers of blood coagulation activation in exercise. Significantly increased TAT has been observed after long-distance running (5,84) and postmaximal incremental cycling (29). This coincided with a significant increase in PTF1+2 concentration (7,12,52,84,85).In vivo hypercoagulability may also be linked with the formation of fibrinopeptide A (FPA). However, exercise studies on this marker of hypercoagulability have produced conflicting results. A significant increase of FPA was found after exhaustive exercise (7,85), although other studies have demonstrated no significant change (5,52). These discrepancies may be attributed to differences in exercise protocol, training status, and the analytical methods used. Therefore, evidence suggesting that acute physical exercise in healthy subjects leads to increased thrombin generation and fibrin formation in vivo remains debatable.Mandalaki et al. (69) studied blood coagulation inhibitors and reported a significant decrease in antithrombin III activity postmarathon run. Huisveld et al. (56) confirmed this reduction in antithrombin III postexercise and further reported a reduction in the blood fibrinolysis inhibitors α2-antiplasmin and C1-inactivator. Other studies have reported no significant change in antithrombin III concentrations after exhaustive exercise (3,5,24,52). Research evidence regarding the effects of exercise on these markers of blood coagulation and fibrinolysis are insufficient to draw a valid conclusion.Blood fibrinolytic changes in response to acute exercise.It is generally accepted that intense exercise induces significant activation of fibrinolysis as a consequence of tissue plasminogen activator (tPA) release from the vascular endothelial cells (37). Evidence is also available to suggest that plasma levels of urinary-type plasminogen activator (uPA) increase significantly postexercise (27,111). It should be noted, however, that peak levels of uPA and tPA do not coincide in time or magnitude in response to maximal exercise (111). This may signify independent mechanisms regulating exercise-induced increases in the level of uPA and tPA. Large increases (75–250%) in fibrinolytic activity are not apparent until heart rate reaches 50% of maximum (2), with the greatest increase occurring between 70% and 90% of maximal workload (2,21). Although this hyperfibrinolysis is transient, reports have been conflicting concerning its return to baseline levels postexercise with a time course of 45 to 60 min after intense exercise (6,39), 2 h after long distance running (50), and 24 h postmarathon (84).Tissue-type plasminogen activity and antigen levels have been shown to increase significantly following several different exercise protocols (3,24,45,48,73,84,89,91,96,105), and this increase seems to be intensity dependent (73,89,105). Similar to endurance exercise, resistance exercise increased plasminogen activator activity (32,113), and this increase was again intensity dependent (32).Research has indicated the presence of “poor responders” among groups of healthy subjects, although more often among patients (49,58,92). These individuals demonstrate a diminished fibrinolytic response to exercise (32). It is suggested that the ability to respond adequately to physical exercise represents the capacity of fibrinolytic potential. Consequently, poor responders are probably at greater risk of atherosclerotic vascular disease when challenged with exercise.The mechanism responsible for and the biological significance of exercise-induced hyperfibrinolysis is not entirely understood. Adrenoreceptor stimulation was suggested as a possible pathway for the release of plasminogen activator (35) because β blocking with propranolol partially decreases the normal fibrinolytic response to exhaustive exercise (31). This explanation seems unlikely because, during exercise, tPA release occurs before an increase in adrenaline, suggesting that the main release of tPA is mediated by some other nonadrenergic mechanism, possibly vasopressin (30).Studies have demonstrated a significant reduction of plasminogen activator inhibitor (PAI-1) activity after aerobic and anaerobic exercise (25,37,45,89,105). Maximal treadmill exercise in normoxemic and hypoxemic conditions significantly decreased PAI-1 activity (102). Resistance exercise also produced a similar reduction (32). Other studies have failed to detect any change in PAI-1 after exhaustive aerobic (84) and isometric (113) exercise protocols. As it is the case with tPA response, the PAI-1 response to exercise is related to the training status of the individual (106).Attempts have been made to relate the activation of fibrinolysis with changes in fibrinogen concentration measured in vitro and with alterations of the markers of fibrinogen and/or fibrin degradation in vivo. Significant increases in fibrin/fibrinogen degradation products (Fb/FgDP) have been demonstrated following various exhaustive exercise protocols (39,84). The plasma Fb/FgDP response appears to be related to exercise intensity and the training status of the individual (24,25).An increased level of another in vivo marker of hyperfibrinolysis, D-dimer, was observed when submaximal exercise was followed by short-term maximal exercise (73), and after endurance exercise (3,5,84,91). These results suggest that strenuous exercise results in hyperfibrinolysis in vivo. This is not a uniformly reported finding because other studies (12,70) have failed to demonstrate changes in Fb/FgDP in response to exercise. Therefore, the actual effect of exercise on Fb/FgDP has yet to be resolved.Platelet functions in response to acute exercise.Strenuous exercise results in an increased platelet count (thrombocytosis) ranging from 18% to 80% (4,7,18,43,116). This increase has been ascribed to a fresh release of platelets from the vascular beds of the spleen, the bone marrow, and from intravascular pools found in the pulmonary circulation and lungs (13,94).Although physical activity is widely recognized as being beneficial to health, attempts to relate the effects of exercise to changes in platelet aggregation and functions have produced conflicting results. Strenuous exercise increases platelet aggregation in response to various aggregatory agents such as adenosine diphosphate (ADP) (8,42,77,82,110), collagen (18,61,93,110), and adrenaline (94). In addition, Winther and Reine (121) observed a postexercise increase in platelet aggregability in stable angina patients.Research has demonstrated significant increases in plasma β-thromboglobulin (βTG) (7,17,41,52,77,80,107,110,116) and platelet factor 4 (PF4) (45,116), indicating enhanced platelet aggregation. Enhancement of in vivo platelet release, occurring in response to exercise, if it occurs, is considered minimal because the reported changes in βTG have remained within the physiological range (110). Furthermore, Lemne et al. (65) reported that, in response to strenuous exercise, βTG was higher in hypertensives than in sedentary age-matched controls, possibly due to the greater synthesis postexercise of antiaggregatory prostanoid prostacyclin. Maximal cycling (8,42,116) and maximal treadmill running (18) have also resulted in significant platelet activation, as indicated by an increased sensitivity to ADP-induced aggregation. Other markers pertinent to platelet activation such as alpha-granule membrane protein (GMP-140) (80) and thromboxane B2 (TXB2) (80,107) were also increased postexercise.Exercise-induced activation of platelets might be linked with anaerobic metabolism (18) because activation of blood platelets seems to be more pronounced in exercise above, but not below, the anaerobic threshold (18,43,116). It has been proposed that exercise-mediated elevation of catecholamines is the common pathway for enhanced platelet aggregation (14,108). In support of this theory, selective β blockade has resulted in inhibition of platelet activation postexercise (53,121). In contrast, Wallen et al. (114) reported no effect of β blockade on platelet function in exercising stable angina patients and hypertensives. Furthermore, an increased catecholamine response to static exercise has been observed without a detectable change in ADP-induced platelet aggregation, PF4, or βTG. Therefore, the influence of increased catecholamines is questionable, although it might be that the mechanism mediating platelet activation in static exercise is different from that operating during dynamic exercise. During exercise, the preaggregatory release of catecholamines is concomitant with an enhanced release of the antiaggregatory prostanoid prostacyclin. This has been found in healthy subjects (82) and diabetics (62,75).Increased platelet aggregation may be mediated by internal calcium stores because attenuated platelet aggregability has been reported in response to high doses of calcium-channel blockers (64,87,99,114). This may have implications for exercise, particularly resistance exercise, because of the importance of calcium in muscle function.Significantly decreased adrenaline-, ADP-, and collagen-induced platelet aggregation have been reported postmarathon (90). Decreases in platelet aggregation have also been reported in young healthy subjects in response to strenuous cycling (20) and submaximal exercise (15), although not in patients with stable angina pectoris (116). However, Gleerup et al. (41) observed lower βTG and PF4 concentrations in borderline hypertensives postexercise. The mechanism responsible for this exercise-induced reduction of platelet aggregability is not fully understood. However, it might be linked with the release of antiaggregatory prostanoid prostacyclin, which inhibits platelet aggregation (10,82), or to the release of tPA, which desegregates platelets (68).In contrast, aerobic exercise has been reported to produce no significant alterations in platelet aggregability, as indicated by unaltered TXB2 and βTG concentrations (18,28,107) or by a monoclonal antibodies binding technique (60). Similarly, exhaustive isometric exercise had no effect on ADP-induced platelet aggregation or on the release of βTG and PF4 (113). Furthermore, no significant changes in GMP-140 and TXA2 were observed after treadmill exercise in normal healthy subjects, although changes were reported in coronary heart disease (CHD) patients (80).Exercise studies addressing female populations have reported no exercise-induced changes in βTG- and ADP-induced aggregation (1,51), possibly because menstrual phase was not accounted for. Mixed-gender studies have also failed to consider the menstrual phase of female participants (43,60,109). Wang et al. (118) reported variations in platelet adhesiveness and ADP-induced platelet aggregation during midfollicular and midluteal phases, although submaximal exercise suppressed these markers. Currently, no published research exists investigating the effect of exercise on platelet functions in postmenopausal women or the transition with menopause.It is currently unclear whether platelet functions are altered in older individuals with exercise. Gonzales et al. (44) reported no effect of age on platelet count or βTG in sedentary individuals postexercise. Likewise, Todd et al. (107) observed no significant differences in βTG between young and middle-aged men after treadmill running. However, TXB2 was significantly higher in the middle-aged group 30 min into recovery, suggesting that older men may exhibit enhanced platelet activation postexercise. In contrast, Gleerup et al. (41) reported significantly decreased in vivo platelet aggregability postexercise in healthy young but not in middle-aged healthy males.Discrepancies in results pertaining to platelet functions may be explained by methodological variations, such as exercise protocol, analysis techniques, dietary effects, the inability to analyze measurements across time, and the use of different populations. As a result, it is not possible to draw conclusions regarding the influence of acute exercise on platelet aggregation and functions. However, some investigators believe that the enhancement of platelet functions during strenuous exercise in sedentary individuals may precipitate thrombosis in the coronary microcirculation and thus augment the risk of primary cardiac arrest (100).TRAINING EFFECTS OF EXERCISE ON BLOOD COAGULATION, FIBRINOLYSIS, AND PLATELET AGGREGATIONPhysical training and blood coagulation.Little information seems to be available regarding the effects of exercise training on blood coagulability. Cross-sectional data of PT and APTT as overall measures of blood coagulability showed no difference among sedentary individuals, joggers, or marathon runners, either at rest or postexercise (39). These results are in agreement with those reported in athletes and nonathletes who exhibited similar TT at rest (119). Likewise, a longitudinal study (37) demonstrated no significant change in TT or PT after 3 months of endurance training. When physical activity level was assessed by a questionnaire, a lower APTT, but not TT, was found in active compared with nonactive individuals (63). Physical training in postmyocardial infarction patients seems to suppress blood coagulability because APTT at rest is significantly longer after training in these patients (104).Resting levels of FVIII activity and FVIII antigen do not change with training in sedentary individuals (11,83,88,112) or endurance-trained athletes (119). However, postmyocardial patients lowered their resting levels of FVIII activity and FVIII antigen after 4 wk of physical training (104). The normal increase in FVIII activity postexercise also seems to be unaltered after 12 wk of standardized aerobic training (37). These meager results suggest that FVIII activity and FVIII antigen levels at rest or after exercise remain unchanged in response to training in normal healthy subjects, although not in cardiac patients.Plasma fibrinogen level is one of the main determinants of whole-blood viscosity and plays a pivotal role in the blood clotting mechanism (37). High levels of plasma fibrinogen are usually found in patients suffering from CHD (16,72). The relationship between plasma fibrinogen and exercise training has been recently reviewed (33) and will only be briefly discussed here. Epidemiological studies have implicated a favorable association between physical training and plasma fibrinogen levels (34,49). However, available longitudinal evidence is conflicting, with some research suggesting that physical training may reduce plasma fibrinogen concentration in patients (122) and in elderly males but not in young males (103). Surprisingly, and in contrast to these results, plasma fibrinogen concentration increased significantly in elderly males postintensive training, and this coincided with a significant rise in C-reactive protein. It was concluded that vigorous training in elderly males might cause a chronic increase in acute-phase reactant proteins such as fibrinogen (97). Unlike elderly males, recent evidence suggested that the training effects on plasma fibrinogen in elderly females appears to be negligible (26). No valid conclusion regarding the effect of training on plasma fibrinogen could be drawn from the above reports, and further investigations are required.Physical training and blood fibrinolysis.Thrombosis plays a significant role in the pathogenesis of acute myocardial infarction, unstable angina, and sudden cardiac death (47). Although the reduction in cardiovascular risk associated with regular physical activity has been repeatedly reported (66,71,98), the pathway(s) via which this occurs is not fully understood and remain speculative. It is suggested that this may be linked with exercise-induced favorable effects on blood fibrinolysis (9,37,50,91). However, it is important to note that the effect of physical training on parameters pertinent to blood fibrinolysis have produced inconsistent results. For example, no relationship between physical training status and resting fibrinolytic activity has been reported when blood fibrinolysis was assessed by global methods such as euglobulin clot lysis time and fibrin plate methods (39,63). However, when more specific techniques were used, higher resting tPA activity and tPA antigen levels were found in inactive compared with active individuals (24,106). Comparable results were reported in which PAI activity was decreased after 8 months of training, but this decrease failed to reach the designated level of significance (P > 0.05) due to large group variances and seasonal variations (23).Higher PAI values were found in postmyocardial infarction patients compared with the elderly, and also in athletes compared with age-matched sedentary individuals and elderly sportsmen (101). Evidence is also available to suggest that exercise rehabilitation programs are associated with significant reductions in PAI levels in cardiac patients but not in healthy controls (38,104). Three months of detraining seems to reverse the favorable reduction in PAI activity observed posttraining (46). Two studies on the effect of exercise training on blood fibrinolysis in non–insulin-dependent diabetics have produced varying results. An increase in the resting level of blood fibrinolysis was demonstrated after training in one study (95) but not in the other, in which blood fibrinolysis was unaltered at rest or in response to exercise (54).Enhanced fibrinolysis in response to exercise seems to be related to the training status of the individual (39). This concept was confirmed by recent evidence (24,106), which showed higher tPA release and lower tPA/PAI complex after exercise in physically trained subjects compared with untrained individuals. Diminished fibrinolytic activity, due to an increase in PAI, is often seen in patients with myocardial ischemia, although this diminishes after exercise rehabilitation (81,101). However, Estelles et al. (38) showed no significant effect of training on PAI activity in cardiac patients. This discrepancy may be attributed to methodological differences, particularly the exercise intensity and duration as well as the analytical techniques used for the measurement of PAI activity. It is interesting to note that the subjects who did not participate in the exercise rehabilitation program and acted as controls exhibited increased PAI activity (38). The increase in PAI activity after training in the control group is intriguing, and the exact mechanism responsible for this was not adequately explained. Therefore, rehabilitative exercise programs may prevent further disturbances in blood fibrinolysis in cardiac patients.Earlier studies suggested that the favorable effects of training on blood fibrinolysis appear to be age related because higher fibrinolytic potential was observed posttraining in older but not in younger subjects. For example, elderly subjects exhibited an increase in tPA and a decrease in PAI activity (103) and PAI antigen (97) after different training programs. In contrast to data reported in elderly subjects (103), recent evidence suggests that physical training can also favorably affect blood fibrinolysis in the young (112).No valid conclusion can be reached regarding the exact effects of physical training on blood coagulation and fibrinolysis. This is undoubtedly due to variations in the training programs used, the populations studied, and the analytical methods used.Physical training and platelet functions.Clinical studies have indicated that platelets play an important role in the pathogenesis and progression of cardiovascular diseases (78,123). Epidemiological research has suggested that physical conditioning may play a role in the prevention of cardiovascular diseases (40,57,74,79,86). However, the effects of exercise training on platelet aggregation and function have not been adequately studied, and the results reported are either controversial or incomplete (22,44,83,115,117)Exercise training in healthy individuals could reduce the risk of cardiovascular disease via suppressing platelet adhesiveness and aggregation. Indeed, 8 wk of endurance exercise increases aerobic capacity, and this was associated with a decrease in resting and postexercise platelet adhesiveness and aggregation (117). These results are in agreement with earlier reports that showed a significant decrease in platelet responsiveness with exercise training (22). Nevertheless, these favorable effects of training on platelet aggregability are transient and may disappear with detraining (117).Although the etiology of impaired platelet function with age is complex, physical training may curtail the detrimental effects of age on platelet function (44). Studies on the effect of training on markers pertinent to platelet activation in vivo, such as PF4 and βTG, have produced conflicting results. During the course of endurance training for 9 months PF4 concentration, but not βTG, increased progressively in both male and female subjects (83). These data indicate that training may be associated with undesirable in vivo platelet activation, probably due to an increased younger platelet population. In contrast, individuals who exercise regularly or who are physically fit exhibited lower βTG levels at rest compared with sedentary controls (22,44). Reduced platelet aggregation at rest and in response to exercise was also reported in previously sedentary women after training (115). These favorable changes in platelet aggregation with training occurred simultaneously with an increase in plasma nitric oxide level, leading the authors to suggest that platelet aggregation may be mediated via the nitric oxide pathway.After consideration of the meager results reported above, it is not possible to draw a valid conclusion on the exact effects of physical training on platelet aggregation and function, and future experimental trials are needed.CONCLUSIONAbnormal hemostatic profiles are known to have clinical and prognostic relevance in cardiovascular disease. Previous research on blood hemostasis is based on the assumption that exercise may favorably affect the hemostatic and fibrinolytic systems. Available evidence suggests that acute exercise causes activation of blood coagulation, acceleration of blood fibrinolysis, and induces alterations in platelet functions. However, information regarding the effects of physical training on blood hemostasis is incomplete and mostly fragmented. In addition, the mechanisms via which these changes occur remain to be elucidated, and the results reported should be viewed as preliminary research findings. This is undoubtedly due to differences in training programs, populations studied, and the analytical methods used. The hypothesis regarding the favorable influence of training on blood hemostasis should be further examined, and available studies should be replicated. Several questions related to exercise and blood hemostasis, particularly platelet aggregation and functions, remain unanswered and warrant future investigation. For example, it would be of interest to assess the possible impact of exercise training on blood hemostasis in relation to the incidence of ischemic heart disease. 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