Share this article on:

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. 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. Although blood coagulation and fibrinolysis are strongly related mechanisms, training effects could be different in different populations. The combined influence of diet and exercise on blood hemostasis is another topic that warrants further investigation.REFERENCES1. Agren, J. J., H. Pekkarinen, H. Litmanen, and O. Hanninen. Fish diet and physical-fitness in relation to membrane and serum-lipids, prostanoid metabolism and platelet-aggregation in female students. Eur. J. Appl. Physiol. 63:393–398, 1991. [CrossRef] [Medline Link] [Context Link]2. Andrew, M., C. Carter, H. O’Brodovich, and G. Heigenhauser. Increases in factor VIII complex and fibrinolytic activity are dependent on exercise intensity. J. Appl. Physiol. 60:1917–1922, 1986. [Medline Link] [Context Link]3. Arai, M., H. Yorifuji, S. Ikematsu, et al. Influences of strenuous exercise on blood coagulation and fibrinolytic system. Thromb. Res. 57:465–471, 1990. [CrossRef] [Medline Link] [Context Link]4. Banfi, G., M. Marinelli, G. S. Roi, and M. Giacometti. Platelet indices in athletes performing a race in altitude environment. J. Clin. Lab. Anal. 9:34–36, 1995. [Context Link]5. Bartsch, P., A. Haeberli, and P. W. Straub. Blood coagulation after long distance running: antithrombin III prevents fibrin formation. Thromb. Hemost. 63:430–434, 1990. [Medline Link] [Context Link]6. Bartsch, P., E. K. Schmidt, and P. W. Straub. Fibrinopeptide A after strenuous exercise at high altitude. J. Appl. Physiol. 53:40–43, 1982. [Medline Link] [Context Link]7. Bartsch, P., B. Welsch, M. Albert, B. Friedman, M. Levi, and E. K. O. Kruithof. Balanced activation of coagulation and fibrinolysis after a 2-h triathlon. Med. Sci. Sports Exerc. 27:1465–1470, 1995. [CrossRef] [Full Text] [Medline Link] [Context Link]8. Beisiegel, B., N. Treese, G. Hafner, J. Meyer, and H. Darius. Increase in endogenous fibrinolysis and platelet activity during exercise in young volunteers. Agents Actions 37:(Suppl.)S183–S189, 1992. [Context Link]9. Biggs, R., R. G. Macfarlane, and J. Pilling. Observations on fibrinolysis: experimental activity produced by exercise or adrenaline. Lancet 1:402–405, 1947. [Context Link]10. Boger, R. H., S. M. Bodeboger, E. P. Schroder, D. Tsikas, and J. C. Frolich. Increased prostacyclin production during exercise in untrained and trained men: effect of low-dose aspirin. J. Appl. Physiol. 78:1832–1838, 1995. [Medline Link] [Context Link]11. Boman, K., G. Hellsten, A. Bruce, G. Hallmans, and T. K. Nilsson. Endurance physical activity, diet and fibrinolysis. Atherosclerosis 106:65–74, 1994. [CrossRef] [Medline Link] [Context Link]12. Bounameaux, H., A. Righetti, P. D. Moerloose, O. Bongard, G. Reber. Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia. Thromb. Res. 65:27–32, 1992. [CrossRef] [Medline Link] [Context Link]13. Bourey, R. E., and S. A. Santoro. Interactions of exercise, coagulation, platelets, and fibrinolysis: a brief review. Med. Sci. Sports Exerc. 20:439–446, 1988. [Context Link]14. Brezinski, D. A., G. H. Tolfer, J. E. Muller, et al. Morning increase in platelet aggregability association with assumption and the upright posture. Circulation 78:35–40, 1988. [CrossRef] [Full Text] [Medline Link] [Context Link]15. Buczynski, A., J. Kedziora, W. Tkaczewski, B. Wachowicz. Effect of submaximal physical exercise on antioxidative protection of human blood platelets. Int. J. Sports Med. 12:52–54, 1991. [Context Link]16. Ceriello, A., M. Pirisi, R. Giacomello, et al. Fibrinogen plasma levels as a marker of thrombin activation: new insights on the role of fibrinogen as a cardiovascular risk factor. Thromob. Hemost. 71:593–595, 1994. [Context Link]17. Chen M.-F., H.-C. Hsu, and Y.-T. Lee. Effects of acute exercise on the changes of lipid profiles and peroxides, prostanoids, and platelet activation in hypercholesterolemic patients before and after treatment. Postaglandins 48:157–174, 1994. [Context Link]18. Chicharro, J. L., O. Sanchez, F. Bandres, et al. Platelet aggregability in relation to the anaerobic threshold. Thromb. Res. 75:251–257, 1994. [CrossRef] [Medline Link] [Context Link]19. Cohen, R. J., S. E. Epstein, L. S. Cohen, and L. H. Dennis. Alterations in blood fibrinolysis, and blood coagulation induced by exercise and the role of beta-adrenergic receptor stimulation. Lancet 2:1264–1266, 1968. [Context Link]20. Dag, B., G. Gleerup, A. M. Bak, I. Hindberg, J. Mehlsen, and K. Winter. Effect of supine exercise on platelet aggregation and fibrinolytic activity. Clin. Physiol. 14:181–186, 1994. [CrossRef] [Medline Link] [Context Link]21. Davis, G. L., C. T. Abildgaard, E. M. Bernauer, and M. Britton. Fibrinolytic and hemostatic changes during and after maximal exercise in males. J. Appl. Physiol. 40:287–292, 1976. [Medline Link] [Context Link]22. Davis, R. B., D. G. Boyd, M. E. McKinney, and C. C. Jones. Clinical chemistry: effects of exercise and exercise conditioning on blood platelet function. Med. Sci. Sports Exerc. 22:49–53, 1990. [CrossRef] [Full Text] [Medline Link] [Context Link]23. De Geus, E. J. C., C. Kluft, A. C. W. De Bart, and J. P. Van Doornen. Effects of exercise training on plasminogen activator inhibitor activity. Med. Sci. Sports Exerc. 24:1210–1219, 1992. [CrossRef] [Full Text] [Medline Link] [Context Link]24. De Paz, J. A., J. Lasierra, J. G. Villa, E. Vilades, M. A. Martin-Nuno, J. Gonzalez-Gallego. Changes in the fibrinolytic system associated with physical conditioning. Eur. J. Appl. Physiol. 65:388–393, 1992. [CrossRef] [Medline Link] [Context Link]25. De Paz, J. A., J. G. Villa, E. Vilades, M. A. Martin-Nuno, and J. Gonzalez-Gallego. Effects of oral contraceptives on fibrinolytic response to exercise. Med. Sci. Sports Exerc. 27:961–966, 1995. [CrossRef] [Full Text] [Medline Link] [Context Link]26. Desouza, C. A., P. Paker-Jones, and D. R. Seals. Physical activity status and adverse age-related differences in coagulation and fibrinolytic factors in women. Arterioscler. Thromb. Vasc. Biol. 18:362–368, 1998. [CrossRef] [Full Text] [Medline Link] [Context Link]27. Dooijewaard, G., A. D. Deboer, P. N. C. Turion, Cohen, A., F. Breimer, D. D., and C. Kluft. Physical exercise induces enhancement of urokinase-type plasminogen activator (uPA) levels in plasma. Thromb. Hemost. 65:82–86, 1991. [Context Link]28. Drygas, W. K. Changes in blood platelet function, coagulation, and fibrinolytic activity in response to moderate, exhaustive, and prolonged exercise. Int. J. Sports Med. 9:67–72, 1988. [CrossRef] [Medline Link] [Context Link]29. Dufaux, B., U. Order, and H. Liesen. Effect of a short maximal physical exercise on coagulation, fibrinolysis, and complement system. Int. J. Sports Med. 12:S38–S42, 1991. [CrossRef] [Medline Link] [Context Link]30. El-Sayed, M. S. Exercise intensity-related responses of fibrinolytic activity and vasopressin in man. Med. Sci. Sports Exerc. 22:494–500, 1990. [Context Link]31. El-Sayed, M. S. Extrinsic plasminogen activator response to exercise after a single dose of propanolol. Med. Sci. Sports Exerc. 24:327–332, 1992. [CrossRef] [Full Text] [Medline Link] [Context Link]32. El-Sayed, M. S. Fibrinolytic and hemostatic parameters response after resistance exercise. Med. Sci. Sports Exerc. 25:597–602, 1993. [CrossRef] [Full Text] [Medline Link] [Context Link]33. El-Sayed, M. S. Effects of exercise on blood coagulation, fibrinolysis and platelet aggregation. Sports Med. 22:282–298, 1996. [CrossRef] [Full Text] [Medline Link] [Context Link]34. El-Sayed, M. S. Effects of high and low intensity aerobic conditioning programs on blood fibrinolysis and lipid profile. Blood Coagul. Fibrinol. 7:484–490, 1996. [Context Link]35. El-Sayed, M. S., and B. A. Davies. Effect of two formulations of beta blocker on fibrinolytic response to maximum exercise. Med. Sci. Sports Exerc. 21:369–373, 1989. [Context Link]36. El-Sayed, M. S., and B. A. Davies. Physical conditioning program does not alter fibrinogen concentration in young healthy subjects. Med. Sci. Sports Exerc. 27:485–489, 1995. [CrossRef] [Full Text] [Medline Link] [Context Link]37. El-Sayed M. S., X. Lin, and A. J. M. Rattu. Blood coagulation and fibrinolysis at rest and in response to maximal exercise before and after a physical conditioning programme. Blood Coagul. Fibrinol. 6:747–752, 1996. [Context Link]38. Estelles, A., J. Aznar, G. Tormo, P. Sapena, V. Tormo, and F. Espana. Influence of a rehabilitation sports programme on the fibrinolytic activity of patients after myocardial infarction. Thromb. Res. 55:203–212, 1989. [CrossRef] [Medline Link] [Context Link]39. Ferguson, E. W., L. L. Bernier, G. R. Banta, J. Yu-Yahiro, and E. B. Schoomaker. Effects of exercise and conditioning on clotting and fibrinolytic activity in men. J. Appl. Physiol. 62:1416–1421, 1987. [Medline Link] [Context Link]40. Folsom, A. R., D. K. Arnett, R. G. Hutchinson, F. Liao, L. X. Clegg, and L. S. Cooper. Physical activity and incidence of CHD in middle-aged women and men. Med. Sci. Sports Exerc. 29:901–909, 1997. [Context Link]41. Gleerup, G., J. Vind, and K. Winther. Platelet function and fibrinolytic activity during rest and exercise in borderline hypertensive patients. Eur. J. Clin. Invest. 25:266–270, 1995. [CrossRef] [Medline Link] [Context Link]42. Gleerup, G., and K. Winther. The effect of ageing on platelet function and fibrinolytic activity. Angiology 46:715–718, 1995. [CrossRef] [Medline Link] [Context Link]43. Gleeson, M., A. K. Blannin, D. A. Sewell, and R. Cave. Short-term changes in the blood leukocyte and platelet count following different durations of high-intensity treadmill running. J. Sports Sci. 13:115–123, 1995. [CrossRef] [Medline Link] [Context Link]44. Gonzales F, M. Manas, I. Seiquer, et al. Blood platelet function in healthy individuals of different ages: effects of exercise and exercise Conditioning. J. Sports Med. Phys. Fitness 36:112–116, 1996. [Medline Link] [Context Link]45. Gough, S. C. L., S. Whitworth, P. J. S. Rice, and P. Grant. The effect of exercise and heart rate on fibrinolytic activity. Blood Coagul. Fibrinol. 3:179–182, 1992. [CrossRef] [Full Text] [Medline Link] [Context Link]46. Gris, J. C., J. F. Schved, O. Feugeas, et al. Impact of smoking, physical training and weight reduction on FVIII, PAI-1and hemostatic markers in sedentary men. Thromb. Res. 64:516–520, 1990. [Context Link]47. Hamsten, A. The hemostatic system and CHD. Thromb. Res. 70:1–38, 1993. [CrossRef] [Medline Link] [Context Link]48. Handa, K., Y. Terao, T. Mori, et al. Different coagulability and fibrinolytic activity during exercise depending on exercise intensities. Thromb. Res. 66:613–616, 1992. [CrossRef] [Medline Link] [Context Link]49. Hansen, J. B., B. Svensson, C. L. Zhang, V. Llyngmo, A. Nordoy. Basal plasma concentration of tissue plasminogen activator (tPA) and the adaptation to strenuous exercise in familial hypercholesterolemia (FH). Blood Coagul. Fibrinol. 5:781–787, 1994. [CrossRef] [Full Text] [Medline Link] [Context Link]50. Hansen, J. B., L. Wilsgard, J. O. Olsen, and B. Osterud. Formation and persistence of procoagulant and fibrinolytic activities in circulation after strenuous physical exercise. Thromb. Hemost. 64:385–389, 1990. [Medline Link] [Context Link]51. Held, C., P. Hjemdahl, N. Rehnquist, et al. Hemostatic markers, inflammatory parameters, and lipids in male, and female patients in the Angina Prognosis Study in Stockholm (APSIS): a comparison with healthy controls. J. Intern. Med. 241:59–69, 1997. [CrossRef] [Full Text] [Medline Link] [Context Link]52. Herren, T., P. Bartsch, A. Haeberli, and P. W. Straub. Increased thrombin-antithrombin III complexes after 1 h of physical exercise. J. Appl. Physiol. 73:499–504, 1992. [Context Link]53. Homuth, V. Treatment of arterial-hypertension with the selective beta-adrenergic-receptor blocker Talinolol. Perfusion 8:402–418, 1995. [Medline Link] [Context Link]54. Hornsby, W. G., K. A. Boggess, T. J. Lyons, W. H. Barnwell, J. Lazarchick, and J. A. Coldwell. Hemostatic alterations with exercise conditioning in NIDDM. Diabetes Care 13:87–92, 1990. [CrossRef] [Medline Link] [Context Link]55. Hoyer, L. W., and N. C. Trabold. The effect of thrombin on human factor VIII: cleavage of the factor VIII procoagulant protein during activation. J. Lab. Clin. Med. 97:50–64, 1981. [Medline Link] [Context Link]56. Huisveld, I. A., A. J. H. Hospers, M. J. E. Bernink, M. W. A. Biersteker, W. B. M. Erich, and B. N. Bouma. Oral contraceptives and fibrinolysis among female cyclists before and after exercise. J. Appl. Physiol. 53:330–334, 1982. [Medline Link] [Context Link]57. Hunter, G. R., T. Kekes-Szabo, S. W. Snyder, C. Nicholson, I. Nyikos, and L. Berland. Fat distribution, physical activity, and cardiovascular risk factors. Med. Sci. Sports Exerc. 29:362–369, 1997. [CrossRef] [Full Text] [Medline Link] [Context Link]58. Jansson, J. H., B. Johansson, K. Boman, and T. K. Nilsson. Hypofibrinolysis in patients with hypertension and elevated cholesterol. J. Inter. Med. 229:309–316, 1991. [Context Link]59. Jootar, S., W. Chaisiripoomkere, O. Thaikla, and M. Kaewborworn. Effect of running exercise on haematological changes, hematopoietic cells (CFU-GM) and fibrinolytic system in humans. J. Med. Assoc. Thai. 75:94–8, 1992. [Context Link]60. Kestin A. S., A. Patricia, M. R. Barnard, A. Errichetti, B. A. Rosner, and A. D. Michelson. Effect of strenuous exercise on platelet activation state and reactivity. Circulation 88:1502–1511, 1993. [CrossRef] [Full Text] [Medline Link] [Context Link]61. Kishi, Y., T. Ashikaga, and F. Numano. Inhibition of platelet-aggregation by prostacyclin is attenuated after exercise in patients with angina-pectoris. Am. Heart J. 123:291–297, 1992. [CrossRef] [Medline Link] [Context Link]62. Koivisto, V. A., M. Jantunen, T. Sane, et al. Stimulation of prostacyclin synthesis by physical exercise in type I diabetes. Diabetes Care 12:609–614, 1989. [CrossRef] [Medline Link] [Context Link]63. Korsan-Bengsten, K., L. Wilhelmsen, and G. Tibblin. Blood coagulation and fibrinolysis in relation to degree of physical activity during work and leisure time. Acta Med. Scand. 193:73–77, 1973. [Medline Link] [Context Link]64. Lacoste, L. L. J. Y., T. Lam, J. Jung, and D. Waters. Oral verapamil inhibits platelet thrombus formation in humans. Circulation 89:630–634, 1994. [CrossRef] [Full Text] [Medline Link] [Context Link]65. Lemne, C., O. Vesterqvist, N. Egberg, K. Green, T. Jogestrand, and U. Defaire. Platelet activation and prostacyclin release in essential hypertension. Prostaglandins 44:219–235, 1992. [CrossRef] [Medline Link] [Context Link]66. Leon, A. S., M. J. Myers, and J. Connett. Leisure-time physical activity and the 16-year risk of mortality from CHD and all-causes in the Multiple Risk Factor Intervention Trial (MRFIT). Int. J. Sports Med. 18:S208–S215, 1997. [CrossRef] [Medline Link] [Context Link]67. Loon, B. J., E. Briet, and L. Heere. Fibrinolytic system during long-distance running in IDDM patients and in health subjects. Diabetes Care 15:991–996, 1992. [CrossRef] [Medline Link] [Context Link]68. Loscalzo, J., and D. E. Vaughan. Tissue plasminogen activator promotes platelet disaggregation in plasma. J. Clin. Invest. 79:1749–1755, 1987. [CrossRef] [Medline Link] [Context Link]69. Mandalaki, T., A. Dessypris, C. Louizou, C. P. Boulou, and C. Dimitriadou. Marathon run: I. effects on coagulation, fibrinolysis, platelet aggregation and serum cortisol levels. Thromb. Hemost. 43:49–52, 1980. [Medline Link] [Context Link]70. Marsh, N. A., and P. J. Gafney. Exercise-induced fibrinolysis- fact or fiction? Thromb. Hemost. 48:201–203, 1982. [Medline Link] [Context Link]71. McMurray, R. G., B. E. Ainsworth, J. S. Harrell, T. R. Griggs, and O. D. Williams. Is physical activity or aerobic power more influential on reducing cardiovascular disease risk factors? Med. Sci. Sports Exerc. 30:1521–1529, 1998. [CrossRef] [Full Text] [Medline Link] [Context Link]72. Meade, T. W. Fibrinogen in ischaemic heart disease. Eur. Heart J. 16(Suppl. A):31–35, 1995. [CrossRef] [Medline Link] [Context Link]73. Molz, A. B., B. Heyduck, H. Lill, E. Spanuth, and L. Rocker. The effect of different exercise intensities on the fibrinolytic system. Eur. J. Appl. Physiol. 67:298–304, 1993. [CrossRef] [Medline Link] [Context Link]74. Morris, J. N., D. G. Clayton, M. G. Everitt, A. M. Semmence, and E. H. Burgess. Exercise in leisure time: coronary attack and death rates. Br. Heart J. 63:325–334, 1990. [Medline Link] [Context Link]75. Mourits-Anderson, T., I. W. Jensen, P. Nohr Jensen, J. Ditzel, and J. Dyerberg. Plasma-6-keto PGF1α, thromboxane B2a, thromboxane B2 and PGF2 in type 1 (insulin dependent) diabetic patients during exercise. Diabetologica 30:460–463, 1987. [Context Link]76. Mustonen, P., M. Lepantalo, and R. Lassila. Physical exertion induces thrombin formation and fibrin degradation in patients with peripheral atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 18:244–249, 1998. [CrossRef] [Full Text] [Medline Link] [Context Link]77. Naesh, O., I. Hindberg, J. Trap-Jensen, and J. O. Lund. Post-exercise platelet activation-aggregation and release in relation to dynamic exercise. Clin. Physiol. 10:221–230, 1990. [CrossRef] [Medline Link] [Context Link]78. Olgun, N., K. M. Uysal, G. Irken, et al. Platelet activation in congenital heart diseases. Acta Paediatrica Japonica 39:566–569, 1997. [Medline Link] [Context Link]79. Paffenberger, R. S., R. T. Hyde, A. L. Wing, and C. H. Steinmetz. A natural history of athleticism and cardiovascular health. JAMA 252:491–495, 1984. [Context Link]80. Pan, Y.-Z., B.-M. Wu, X.-S. Hong, et al. The clinical significance of platelet activation during exercise-induced myocardial ischemia. Zhong Hua Nei Ke Zha Zhi 33:106–108, 1994. [Context Link]81. Paramo, J. A., I. Olavide, J. Barba, et al. Long-term rehabilitation program favorably influences fibrinolysis and lipid concentrations in acute myocardial infarction. Haematologica 83:519–524, 1998. [Medline Link] [Context Link]82. Piret, A., G. Niset, E. Depiesse, et al. Increased platelet aggregability and prostacyclin biosynthesis induced by physical exercise. Thromb. Res. 57:685–695, 1990. [CrossRef] [Medline Link] [Context Link]83. Ponjee, G. A. E., G. M. E. Janssen, and W. J. Wersch. Prolonged endurance exercise and blood coagulation: a 9 month prospective study. Blood Coagul. Fibrinol. 4:21–25, 1993. [CrossRef] [Full Text] [Medline Link] [Context Link]84. Prisco, D., R. Paniccia, B. Bandinelli, et al. Evaluation of clotting and fibrinolytic activation after protracted exercise. Thromb. Res. 89:73–78, 1998. [CrossRef] [Medline Link] [Context Link]85. Prisco, D., R. Paniccia, V. Guarnaccia, et al. Thrombin generation after physical exercise. Thromb. Res. 69:159–164, 1993. [CrossRef] [Medline Link] [Context Link]86. Raitakari O. T., S. Taimela, K. V. K. Porkka, et al. Associations between physical activity and risk factors for CHD: the cardiovascular risk in young Finns study. Med. Sci. Sports Exerc. 29:1055–1061, 1997. [CrossRef] [Full Text] [Medline Link] [Context Link]87. Ranieri, G., V. Filitti, A. Andriani, et al. Effects of isradipine sustained-release on platelet-function and fibrinolysis in essential hypertensives with or without other risk factors. Cardiovasc. Drugs Ther. 10:119–123, 1996. [CrossRef] [Medline Link] [Context Link]88. Rankinen, T., R. Vaisanen, S. P. Halonen, and I. M. Penttila. Blood coagulation and fibrinolytic factors are unchanged by aerobic exercise or fat modified diet. Fibrinolysis 8:48–53, 1994. [CrossRef] [Medline Link] [Context Link]89. Rankinen, T., S. Vaisanen, I. Penttila, and R. Rauramaa. Acute dynamic exercise increases fibrinolytic activity. Thromb. Hemost. 73:281–286, 1995. [Medline Link] [Context Link]90. Rock, G., P. Tittely, and A. Pipe. Coagulation factor changes following endurance exercise. Clin. J. Sports Med. 7:94–99, 1997. [Context Link]91. Rocker, L., M. Taenzer, W. K. Drygas, H. Lill, B. Heyduck, and H. U. Altenkirch. Effect of prolonged physical exercise on the fibrinolytic system. Eur. J. Appl. Physiol. 60:478–481, 1990. [CrossRef] [Medline Link] [Context Link]92. Rydzewski, A., K. Sakata, A. Kobayashi, et al. Changes in plasminogen activator inhibitor 1 and tissue-type plasminogen activator during exercise in patients with coronary artery disease. Hemostasis 20:305–312, 1990. [Context Link]93. Sakita, S.-Y., Y. Kishi, and F. Numano. Acute vigorous exercise attenuates sensitivity of platelets to nitric oxide. Thromb. Res. 87:5461–471, 1997. [Context Link]94. Schmidt, K. G., and J. W. Rasmussen. Are young platelets released in excess from the spleen in response to short-term physical exercise. Scand. J. Haematol. 32:207–214, 1984. [Medline Link] [Context Link]95. Schneider S. H., H. C. Kim, A. K. Khachadurian, and N. B. Roderman. Impaired fibrinolytic response to exercise in type II diabetes: effects of exercise and physical training. Metabolism 37:924–929, 1988. [CrossRef] [Medline Link] [Context Link]96. Schobersberger, W., B. Wirleitner, B. Puschendorf, et al. Influence of an ultramarathon race at moderate altitude on coagulation and fibrinolysis. Fibrinolysis 10:37–42, 1996. [CrossRef] [Medline Link] [Context Link]97. Schuit, A. J., E. G. Schouten, C. Kluft, M. de Maat, P. P. C. A. Menheere, and F. J. Kok. Effect of strenuous exercise on fibrinogen and fibrinolysis in healthy elderly men and women. Thromb. Hemost. 78:845–851, 1997. [Medline Link] [Context Link]98. Shaper, A. G., and G. Wannamethee. Physical activity and ischaemic heart disease in middle-aged men. Br. Heart J. 66:384–389, 1991. [Medline Link] [Context Link]99. Sinzinger, H., I. Virgolini, F. Rauscha, P. Fitscha, and J. O’Grady. Isredipine improves platelet-function in hypertensives. Eur. J. Clin. Pharmacol. 42:43–46, 1992. [CrossRef] [Medline Link] [Context Link]100. Siscovic, D. S., N. S. Weiss, R. H. Fletcher, and T. Laskty. The incidence of primary cardiac arrest during vigorous exercise. N. Engl. J. Med. 311:874–877, 1984. [Context Link]101. Speiser, W., W. Langer, A. Pschaick, et al. Increased blood fibrinolytic activity after physical exercise: comparative study in individuals with different sporting activities and in patients after myocardial infarction taking part in a rehabilitation sports program. Thromb. Res. 51:543–55, 1988. [CrossRef] [Medline Link] [Context Link]102. Stegnar, M., P. Paeternel, and J. P. Chen. Acute hypoxia does not increase blood fibrinolytic activity in man. Thromb. Res. 45:333–343, 1987. [CrossRef] [Medline Link] [Context Link]103. Stratton, J. R., W. L. Chandler, R. S. Schwartz, et al. Effects of physical conditioning on fibrinolytic variables and fibrinogen in young and old healthy adults. Circulation 83:1692–97, 1991. [CrossRef] [Full Text] [Medline Link] [Context Link]104. Suzuki, T., K. Yamauchi, Y. Yamada, et al. Blood coagulability and fibrinolytic activity before and after physical training during the recovery phase of acute myocardial infarction. Clin. Cardiol. 15:358–364, 1992. [CrossRef] [Medline Link] [Context Link]105. Szymanski, L. M., and R. R. Pate. Effect of exercise intensity, duration, and time of day on fibrinolytic activity in physically active men. Med. Sci. Sports Exerc. 26:1102–8, 1994. [CrossRef] [Full Text] [Medline Link] [Context Link]106. Szymanski, L. M., R. R. Pate, and J. L. Durstine. Effects of maximal exercise and venous occlusion on fibrinolytic activity in physically active and inactive men. J. Appl. Physiol. 77:2305–2310, 1994. [Medline Link] [Context Link]107. Todd, M. K., A. H. Goldfarb, R. D. Kauffman, and C. Burleson. Combined effects of age and exercise on thromboxane B2 and platelet activation. J. Appl. Physiol. 76:1548–52, 1994. [Context Link]108. Tofler, G. H., D. A. Brezinski, A. L. Schafer, et al. Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death. N. Engl. J. Med. 316:1514–1518, 1987. [CrossRef] [Medline Link] [Context Link]109. Tokuue, J., J. Hayashi, Y. Hata, K. Nakahara, and Y. Ikeda. Enhanced platelet aggregability under high shear stress after treadmill exercise in patients with effort angina. Thromb. Hemost. 75:833–837, 1996. [Medline Link] [Context Link]110. Trovati, M., E. Milaroni, S. Bruzacca, et al. Moderate exercise increases platelet function in type 1 diabetic patients without severe angiopathy and in good control. Diabetic Care 15:1742–1746, 1992. [CrossRef] [Medline Link] [Context Link]111. Van den Burg, P. J. M., G. Dooijewaard, M. Van Vliet, W. L. Mosterd, C. Kluft, and I. A. Huisveld. Differences in uPA and tPA increase during acute exercise: relation with exercise parameters. Thromb. Hemost. 71:236–239, 1994. [Medline Link] [Context Link]112. Van den Burg P. J. M., J. E. Hospers, M. van Vliet, W. L. Mosterd, B. N. Bouma, and I. A. Huisveld. Effect of endurance training and seasonal fluctuation on coagulation and fibrinolysis in young sedentary men. J. Appl. Physiol. 82:613–20, 1997. [Medline Link] [Context Link]113. Vind, J., G. Gleerup, P. T. Nielsen, and K. Winter. The impact of static work on fibrinolysis and platelet function. Thromb. Res. 72:441–461, 1993. [CrossRef] [Medline Link] [Context Link]114. Wallen, N. H., C. Held, N. Rehnqvist, and P. Hjemdahl. Platelet aggregability in vivo is attenuated by verapamil but not by metoprolol in patients with stable angina pectoris. Am. J. Cardiol. 75:1–6, 1995. [CrossRef] [Full Text] [Medline Link] [Context Link]115. Wang, J.-S., C. J. Jen, and H.-I. Chen. Effects of chronic exercise and deconditioning on platelet function in women. J. Appl. Physiol. 83:2080–2085, 1997. [Medline Link] [Context Link]116. Wang, J.-S., C. J. Jen, H.-C. Kung, L.-J. Lin, T.-R. Hsiue, and H.-I. Chen. Different effects of strenuous exercise and moderate exercise on platelet function in men. Circulation 90:2877–2885, 1994. [CrossRef] [Full Text] [Medline Link] [Context Link]117. Wang, J.-S., C. J. Jen, H.-C. Kung, L.-J. Lin, T.-R. Hsiue, and H.-I. Chen. Effects of exercise training and deconditioning on platelet function in men. Arterioscler. Thromb. Vasc. Biol. 15:1668–1674, 1995. [CrossRef] [Full Text] [Medline Link] [Context Link]118. Wang, J.-S. C. J., H. L. Lee, and H.-I. Chen. Effects of short-term exercise on female platelet function during different phases of the menstrual cycle. Arterioscler. Thromb. Vasc. Biol. 17:1682–1686, 1997. [CrossRef] [Full Text] [Medline Link] [Context Link]119. Watts E. J. Hemostatic changes in long-distance runners and their relevance to the prevention of ischemic heart disease. Blood Coagul. Fibrinol. 2:221–225, 1991. [Context Link]120. Weiss, C., G. Seitel, and P. Bartsch. Coagulation and fibrinolysis after moderate and very heavy exercise in healthy male subjects. Med. Sci. Sports Exerc. 30:246–251, 1998. [CrossRef] [Full Text] [Medline Link] [Context Link]121. Winther, K., and E. Reine. Exercise-induced platelet aggregation in angina, and its possible prevention by β1-selective blockade. Eur. Heart J. 11:819–823, 1990. [Medline Link] [Context Link]122. Worsornu, D., W. Allardyce, D. Ballantyne, and P. Tansey. Influence of power and aerobic exercise training on haemostatic factors after coronary artery surgery. Br. Heart J. 68:181–186, 1992. [Context Link]123. Wu, K. K. Hemostatic tests in the prediction of atherothrombotic disease. Int. J. Clin. Lab. Res. 27:145–152, 1997. [Context Link] COAGULATION; FIBRINOLYSIS; PLATELET FUNCTION; ACUTE EXERCISE; PHYSICAL|00005768-200005000-00007#xpointer(id(R1-7))|11065213||ovftdb|SL0000364719916339311065213P63[CrossRef]|00005768-200005000-00007#xpointer(id(R1-7))|11065405||ovftdb|SL0000364719916339311065405P63[Medline Link]|00005768-200005000-00007#xpointer(id(R2-7))|11065405||ovftdb|SL00004560198660191711065405P64[Medline Link]|00005768-200005000-00007#xpointer(id(R3-7))|11065213||ovftdb|SL0000778819905746511065213P65[CrossRef]|00005768-200005000-00007#xpointer(id(R3-7))|11065405||ovftdb|SL0000778819905746511065405P65[Medline Link]|00005768-200005000-00007#xpointer(id(R5-7))|11065405||ovftdb|SL0000777719906343011065405P67[Medline Link]|00005768-200005000-00007#xpointer(id(R6-7))|11065405||ovftdb|SL000045601982534011065405P68[Medline Link]|00005768-200005000-00007#xpointer(id(R7-7))|11065213||ovftdb|00005768-199511000-00001SL00005768199527146511065213P69[CrossRef]|00005768-200005000-00007#xpointer(id(R7-7))|11065404||ovftdb|00005768-199511000-00001SL00005768199527146511065404P69[Full Text]|00005768-200005000-00007#xpointer(id(R7-7))|11065405||ovftdb|00005768-199511000-00001SL00005768199527146511065405P69[Medline Link]|00005768-200005000-00007#xpointer(id(R10-7))|11065405||ovftdb|SL00004560199578183211065405P72[Medline Link]|00005768-200005000-00007#xpointer(id(R11-7))|11065213||ovftdb|SL0000089819941066511065213P73[CrossRef]|00005768-200005000-00007#xpointer(id(R11-7))|11065405||ovftdb|SL0000089819941066511065405P73[Medline Link]|00005768-200005000-00007#xpointer(id(R12-7))|11065213||ovftdb|SL000077881992652711065213P74[CrossRef]|00005768-200005000-00007#xpointer(id(R12-7))|11065405||ovftdb|SL000077881992652711065405P74[Medline Link]|00005768-200005000-00007#xpointer(id(R14-7))|11065213||ovftdb|00003017-198807000-00005SL000030171988783511065213P76[CrossRef]|00005768-200005000-00007#xpointer(id(R14-7))|11065404||ovftdb|00003017-198807000-00005SL000030171988783511065404P76[Full Text]|00005768-200005000-00007#xpointer(id(R14-7))|11065405||ovftdb|00003017-198807000-00005SL000030171988783511065405P76[Medline Link]|00005768-200005000-00007#xpointer(id(R18-7))|11065213||ovftdb|SL0000778819947525111065213P80[CrossRef]|00005768-200005000-00007#xpointer(id(R18-7))|11065405||ovftdb|SL0000778819947525111065405P80[Medline Link]|00005768-200005000-00007#xpointer(id(R20-7))|11065213||ovftdb|SL0000312019941418111065213P82[CrossRef]|00005768-200005000-00007#xpointer(id(R20-7))|11065405||ovftdb|SL0000312019941418111065405P82[Medline Link]|00005768-200005000-00007#xpointer(id(R21-7))|11065405||ovftdb|SL0000456019764028711065405P83[Medline Link]|00005768-200005000-00007#xpointer(id(R22-7))|11065213||ovftdb|00005768-199002000-00008SL000057681990224911065213P84[CrossRef]|00005768-200005000-00007#xpointer(id(R22-7))|11065404||ovftdb|00005768-199002000-00008SL000057681990224911065404P84[Full Text]|00005768-200005000-00007#xpointer(id(R22-7))|11065405||ovftdb|00005768-199002000-00008SL000057681990224911065405P84[Medline Link]|00005768-200005000-00007#xpointer(id(R23-7))|11065213||ovftdb|00005768-199211000-00004SL00005768199224121011065213P85[CrossRef]|00005768-200005000-00007#xpointer(id(R23-7))|11065404||ovftdb|00005768-199211000-00004SL00005768199224121011065404P85[Full Text]|00005768-200005000-00007#xpointer(id(R23-7))|11065405||ovftdb|00005768-199211000-00004SL00005768199224121011065405P85[Medline Link]|00005768-200005000-00007#xpointer(id(R24-7))|11065213||ovftdb|SL0000364719926538811065213P86[CrossRef]|00005768-200005000-00007#xpointer(id(R24-7))|11065405||ovftdb|SL0000364719926538811065405P86[Medline Link]|00005768-200005000-00007#xpointer(id(R25-7))|11065213||ovftdb|00005768-199507000-00003SL0000576819952796111065213P87[CrossRef]|00005768-200005000-00007#xpointer(id(R25-7))|11065404||ovftdb|00005768-199507000-00003SL0000576819952796111065404P87[Full Text]|00005768-200005000-00007#xpointer(id(R25-7))|11065405||ovftdb|00005768-199507000-00003SL0000576819952796111065405P87[Medline Link]|00005768-200005000-00007#xpointer(id(R26-7))|11065213||ovftdb|00043605-199803000-00006SL0004360519981836211065213P88[CrossRef]|00005768-200005000-00007#xpointer(id(R26-7))|11065404||ovftdb|00043605-199803000-00006SL0004360519981836211065404P88[Full Text]|00005768-200005000-00007#xpointer(id(R26-7))|11065405||ovftdb|00043605-199803000-00006SL0004360519981836211065405P88[Medline Link]|00005768-200005000-00007#xpointer(id(R28-7))|11065213||ovftdb|SL00004355198896711065213P90[CrossRef]|00005768-200005000-00007#xpointer(id(R28-7))|11065405||ovftdb|SL00004355198896711065405P90[Medline Link]|00005768-200005000-00007#xpointer(id(R29-7))|11065213||ovftdb|SL00004355199112s3811065213P91[CrossRef]|00005768-200005000-00007#xpointer(id(R29-7))|11065405||ovftdb|SL00004355199112s3811065405P91[Medline Link]|00005768-200005000-00007#xpointer(id(R31-7))|11065213||ovftdb|00005768-199203000-00008SL0000576819922432711065213P93[CrossRef]|00005768-200005000-00007#xpointer(id(R31-7))|11065404||ovftdb|00005768-199203000-00008SL0000576819922432711065404P93[Full Text]|00005768-200005000-00007#xpointer(id(R31-7))|11065405||ovftdb|00005768-199203000-00008SL0000576819922432711065405P93[Medline Link]|00005768-200005000-00007#xpointer(id(R32-7))|11065213||ovftdb|00005768-199305000-00011SL0000576819932559711065213P94[CrossRef]|00005768-200005000-00007#xpointer(id(R32-7))|11065404||ovftdb|00005768-199305000-00011SL0000576819932559711065404P94[Full Text]|00005768-200005000-00007#xpointer(id(R32-7))|11065405||ovftdb|00005768-199305000-00011SL0000576819932559711065405P94[Medline Link]|00005768-200005000-00007#xpointer(id(R33-7))|11065213||ovftdb|00007256-199622050-00002SL0000725619962228211065213P95[CrossRef]|00005768-200005000-00007#xpointer(id(R33-7))|11065404||ovftdb|00007256-199622050-00002SL0000725619962228211065404P95[Full Text]|00005768-200005000-00007#xpointer(id(R33-7))|11065405||ovftdb|00007256-199622050-00002SL0000725619962228211065405P95[Medline Link]|00005768-200005000-00007#xpointer(id(R36-7))|11065213||ovftdb|00005768-199504000-00004SL0000576819952748511065213P98[CrossRef]|00005768-200005000-00007#xpointer(id(R36-7))|11065404||ovftdb|00005768-199504000-00004SL0000576819952748511065404P98[Full Text]|00005768-200005000-00007#xpointer(id(R36-7))|11065405||ovftdb|00005768-199504000-00004SL0000576819952748511065405P98[Medline Link]|00005768-200005000-00007#xpointer(id(R38-7))|11065213||ovftdb|SL0000778819895520311065213P100[CrossRef]|00005768-200005000-00007#xpointer(id(R38-7))|11065405||ovftdb|SL0000778819895520311065405P100[Medline Link]|00005768-200005000-00007#xpointer(id(R39-7))|11065405||ovftdb|SL00004560198762141611065405P101[Medline Link]|00005768-200005000-00007#xpointer(id(R41-7))|11065213||ovftdb|SL0000365319952526611065213P103[CrossRef]|00005768-200005000-00007#xpointer(id(R41-7))|11065405||ovftdb|SL0000365319952526611065405P103[Medline Link]|00005768-200005000-00007#xpointer(id(R42-7))|11065213||ovftdb|SL0000055019954671511065213P104[CrossRef]|00005768-200005000-00007#xpointer(id(R42-7))|11065405||ovftdb|SL0000055019954671511065405P104[Medline Link]|00005768-200005000-00007#xpointer(id(R43-7))|11065213||ovftdb|SL0000539019951311511065213P105[CrossRef]|00005768-200005000-00007#xpointer(id(R43-7))|11065405||ovftdb|SL0000539019951311511065405P105[Medline Link]|00005768-200005000-00007#xpointer(id(R44-7))|11065405||ovftdb|SL0000533719963611211065405P106[Medline Link]|00005768-200005000-00007#xpointer(id(R45-7))|11065213||ovftdb|00001721-199204000-00006SL000017211992317911065213P107[CrossRef]|00005768-200005000-00007#xpointer(id(R45-7))|11065404||ovftdb|00001721-199204000-00006SL000017211992317911065404P107[Full Text]|00005768-200005000-00007#xpointer(id(R45-7))|11065405||ovftdb|00001721-199204000-00006SL000017211992317911065405P107[Medline Link]|00005768-200005000-00007#xpointer(id(R47-7))|11065213||ovftdb|SL00007788199370111065213P109[CrossRef]|00005768-200005000-00007#xpointer(id(R47-7))|11065405||ovftdb|SL00007788199370111065405P109[Medline Link]|00005768-200005000-00007#xpointer(id(R48-7))|11065213||ovftdb|SL0000778819926661311065213P110[CrossRef]|00005768-200005000-00007#xpointer(id(R48-7))|11065405||ovftdb|SL0000778819926661311065405P110[Medline Link]|00005768-200005000-00007#xpointer(id(R49-7))|11065213||ovftdb|00001721-199410000-00016SL000017211994578111065213P111[CrossRef]|00005768-200005000-00007#xpointer(id(R49-7))|11065404||ovftdb|00001721-199410000-00016SL000017211994578111065404P111[Full Text]|00005768-200005000-00007#xpointer(id(R49-7))|11065405||ovftdb|00001721-199410000-00016SL000017211994578111065405P111[Medline Link]|00005768-200005000-00007#xpointer(id(R50-7))|11065405||ovftdb|SL0000777719906438511065405P112[Medline Link]|00005768-200005000-00007#xpointer(id(R51-7))|11065213||ovftdb|00004777-199701000-00010SL0000477719972415911065213P113[CrossRef]|00005768-200005000-00007#xpointer(id(R51-7))|11065404||ovftdb|00004777-199701000-00010SL0000477719972415911065404P113[Full Text]|00005768-200005000-00007#xpointer(id(R51-7))|11065405||ovftdb|00004777-199701000-00010SL0000477719972415911065405P113[Medline Link]|00005768-200005000-00007#xpointer(id(R53-7))|11065405||ovftdb|SL000104201995840211065405P115[Medline Link]|00005768-200005000-00007#xpointer(id(R54-7))|11065213||ovftdb|SL000034581990138711065213P116[CrossRef]|00005768-200005000-00007#xpointer(id(R54-7))|11065405||ovftdb|SL000034581990138711065405P116[Medline Link]|00005768-200005000-00007#xpointer(id(R55-7))|11065405||ovftdb|SL000049651981975011065405P117[Medline Link]|00005768-200005000-00007#xpointer(id(R56-7))|11065405||ovftdb|SL0000456019825333011065405P118[Medline Link]|00005768-200005000-00007#xpointer(id(R57-7))|11065213||ovftdb|00005768-199703000-00011SL0000576819972936211065213P119[CrossRef]|00005768-200005000-00007#xpointer(id(R57-7))|11065404||ovftdb|00005768-199703000-00011SL0000576819972936211065404P119[Full Text]|00005768-200005000-00007#xpointer(id(R57-7))|11065405||ovftdb|00005768-199703000-00011SL0000576819972936211065405P119[Medline Link]|00005768-200005000-00007#xpointer(id(R60-7))|11065213||ovftdb|00003017-199310000-00014SL00003017199388150211065213P122[CrossRef]|00005768-200005000-00007#xpointer(id(R60-7))|11065404||ovftdb|00003017-199310000-00014SL00003017199388150211065404P122[Full Text]|00005768-200005000-00007#xpointer(id(R60-7))|11065405||ovftdb|00003017-199310000-00014SL00003017199388150211065405P122[Medline Link]|00005768-200005000-00007#xpointer(id(R61-7))|11065213||ovftdb|SL00000406199212329111065213P123[CrossRef]|00005768-200005000-00007#xpointer(id(R61-7))|11065405||ovftdb|SL00000406199212329111065405P123[Medline Link]|00005768-200005000-00007#xpointer(id(R62-7))|11065213||ovftdb|SL0000345819891260911065213P124[CrossRef]|00005768-200005000-00007#xpointer(id(R62-7))|11065405||ovftdb|SL0000345819891260911065405P124[Medline Link]|00005768-200005000-00007#xpointer(id(R63-7))|11065405||ovftdb|SL0000010919731937311065405P125[Medline Link]|00005768-200005000-00007#xpointer(id(R64-7))|11065213||ovftdb|00003017-199402000-00014SL0000301719948963011065213P126[CrossRef]|00005768-200005000-00007#xpointer(id(R64-7))|11065404||ovftdb|00003017-199402000-00014SL0000301719948963011065404P126[Full Text]|00005768-200005000-00007#xpointer(id(R64-7))|11065405||ovftdb|00003017-199402000-00014SL0000301719948963011065405P126[Medline Link]|00005768-200005000-00007#xpointer(id(R65-7))|11065213||ovftdb|SL0000677419924421911065213P127[CrossRef]|00005768-200005000-00007#xpointer(id(R65-7))|11065405||ovftdb|SL0000677419924421911065405P127[Medline Link]|00005768-200005000-00007#xpointer(id(R66-7))|11065213||ovftdb|SL00004355199718s20811065213P128[CrossRef]|00005768-200005000-00007#xpointer(id(R66-7))|11065405||ovftdb|SL00004355199718s20811065405P128[Medline Link]|00005768-200005000-00007#xpointer(id(R67-7))|11065213||ovftdb|SL0000345819921599111065213P129[CrossRef]|00005768-200005000-00007#xpointer(id(R67-7))|11065405||ovftdb|SL0000345819921599111065405P129[Medline Link]|00005768-200005000-00007#xpointer(id(R68-7))|11065213||ovftdb|SL00004686198779174911065213P130[CrossRef]|00005768-200005000-00007#xpointer(id(R68-7))|11065405||ovftdb|SL00004686198779174911065405P130[Medline Link]|00005768-200005000-00007#xpointer(id(R69-7))|11065405||ovftdb|SL000077771980434911065405P131[Medline Link]|00005768-200005000-00007#xpointer(id(R70-7))|11065405||ovftdb|SL0000777719824820111065405P132[Medline Link]|00005768-200005000-00007#xpointer(id(R71-7))|11065213||ovftdb|00005768-199810000-00009SL00005768199830152111065213P133[CrossRef]|00005768-200005000-00007#xpointer(id(R71-7))|11065404||ovftdb|00005768-199810000-00009SL00005768199830152111065404P133[Full Text]|00005768-200005000-00007#xpointer(id(R71-7))|11065405||ovftdb|00005768-199810000-00009SL00005768199830152111065405P133[Medline Link]|00005768-200005000-00007#xpointer(id(R72-7))|11065213||ovftdb|SL000036281995163111065213P134[CrossRef]|00005768-200005000-00007#xpointer(id(R72-7))|11065405||ovftdb|SL000036281995163111065405P134[Medline Link]|00005768-200005000-00007#xpointer(id(R73-7))|11065213||ovftdb|SL0000364719936729811065213P135[CrossRef]|00005768-200005000-00007#xpointer(id(R73-7))|11065405||ovftdb|SL0000364719936729811065405P135[Medline Link]|00005768-200005000-00007#xpointer(id(R74-7))|11065405||ovftdb|SL0000224319906332511065405P136[Medline Link]|00005768-200005000-00007#xpointer(id(R76-7))|11065213||ovftdb|00043605-199802000-00013SL0004360519981824411065213P138[CrossRef]|00005768-200005000-00007#xpointer(id(R76-7))|11065404||ovftdb|00043605-199802000-00013SL0004360519981824411065404P138[Full Text]|00005768-200005000-00007#xpointer(id(R76-7))|11065405||ovftdb|00043605-199802000-00013SL0004360519981824411065405P138[Medline Link]|00005768-200005000-00007#xpointer(id(R77-7))|11065213||ovftdb|SL0000312019901022111065213P139[CrossRef]|00005768-200005000-00007#xpointer(id(R77-7))|11065405||ovftdb|SL0000312019901022111065405P139[Medline Link]|00005768-200005000-00007#xpointer(id(R78-7))|11065405||ovftdb|SL0000016019973956611065405P140[Medline Link]|00005768-200005000-00007#xpointer(id(R81-7))|11065405||ovftdb|SL0000398919988351911065405P143[Medline Link]|00005768-200005000-00007#xpointer(id(R82-7))|11065213||ovftdb|SL0000778819905768511065213P144[CrossRef]|00005768-200005000-00007#xpointer(id(R82-7))|11065405||ovftdb|SL0000778819905768511065405P144[Medline Link]|00005768-200005000-00007#xpointer(id(R83-7))|11065213||ovftdb|00001721-199304010-00004SL00001721199342111065213P145[CrossRef]|00005768-200005000-00007#xpointer(id(R83-7))|11065404||ovftdb|00001721-199304010-00004SL00001721199342111065404P145[Full Text]|00005768-200005000-00007#xpointer(id(R83-7))|11065405||ovftdb|00001721-199304010-00004SL00001721199342111065405P145[Medline Link]|00005768-200005000-00007#xpointer(id(R84-7))|11065213||ovftdb|SL000077881998897311065213P146[CrossRef]|00005768-200005000-00007#xpointer(id(R84-7))|11065405||ovftdb|SL000077881998897311065405P146[Medline Link]|00005768-200005000-00007#xpointer(id(R85-7))|11065213||ovftdb|SL0000778819936915911065213P147[CrossRef]|00005768-200005000-00007#xpointer(id(R85-7))|11065405||ovftdb|SL0000778819936915911065405P147[Medline Link]|00005768-200005000-00007#xpointer(id(R86-7))|11065213||ovftdb|00005768-199708000-00011SL00005768199729105511065213P148[CrossRef]|00005768-200005000-00007#xpointer(id(R86-7))|11065404||ovftdb|00005768-199708000-00011SL00005768199729105511065404P148[Full Text]|00005768-200005000-00007#xpointer(id(R86-7))|11065405||ovftdb|00005768-199708000-00011SL00005768199729105511065405P148[Medline Link]|00005768-200005000-00007#xpointer(id(R87-7))|11065213||ovftdb|SL0000235319961011911065213P149[CrossRef]|00005768-200005000-00007#xpointer(id(R87-7))|11065405||ovftdb|SL0000235319961011911065405P149[Medline Link]|00005768-200005000-00007#xpointer(id(R88-7))|11065213||ovftdb|SL00009307199484811065213P150[CrossRef]|00005768-200005000-00007#xpointer(id(R88-7))|11065405||ovftdb|SL00009307199484811065405P150[Medline Link]|00005768-200005000-00007#xpointer(id(R89-7))|11065405||ovftdb|SL0000777719957328111065405P151[Medline Link]|00005768-200005000-00007#xpointer(id(R91-7))|11065213||ovftdb|SL0000364719906047811065213P153[CrossRef]|00005768-200005000-00007#xpointer(id(R91-7))|11065405||ovftdb|SL0000364719906047811065405P153[Medline Link]|00005768-200005000-00007#xpointer(id(R94-7))|11065405||ovftdb|SL0000746719843220711065405P156[Medline Link]|00005768-200005000-00007#xpointer(id(R95-7))|11065213||ovftdb|SL0000582219883792411065213P157[CrossRef]|00005768-200005000-00007#xpointer(id(R95-7))|11065405||ovftdb|SL0000582219883792411065405P157[Medline Link]|00005768-200005000-00007#xpointer(id(R96-7))|11065213||ovftdb|SL000093071996103711065213P158[CrossRef]|00005768-200005000-00007#xpointer(id(R96-7))|11065405||ovftdb|SL000093071996103711065405P158[Medline Link]|00005768-200005000-00007#xpointer(id(R97-7))|11065405||ovftdb|SL0000777719977884511065405P159[Medline Link]|00005768-200005000-00007#xpointer(id(R98-7))|11065405||ovftdb|SL0000224319916638411065405P160[Medline Link]|00005768-200005000-00007#xpointer(id(R99-7))|11065213||ovftdb|SL000036541992424311065213P161[CrossRef]|00005768-200005000-00007#xpointer(id(R99-7))|11065405||ovftdb|SL000036541992424311065405P161[Medline Link]|00005768-200005000-00007#xpointer(id(R101-7))|11065213||ovftdb|SL0000778819885154311065213P163[CrossRef]|00005768-200005000-00007#xpointer(id(R101-7))|11065405||ovftdb|SL0000778819885154311065405P163[Medline Link]|00005768-200005000-00007#xpointer(id(R102-7))|11065213||ovftdb|SL0000778819874533311065213P164[CrossRef]|00005768-200005000-00007#xpointer(id(R102-7))|11065405||ovftdb|SL0000778819874533311065405P164[Medline Link]|00005768-200005000-00007#xpointer(id(R103-7))|11065213||ovftdb|00003017-199105000-00023SL00003017199183169211065213P165[CrossRef]|00005768-200005000-00007#xpointer(id(R103-7))|11065404||ovftdb|00003017-199105000-00023SL00003017199183169211065404P165[Full Text]|00005768-200005000-00007#xpointer(id(R103-7))|11065405||ovftdb|00003017-199105000-00023SL00003017199183169211065405P165[Medline Link]|00005768-200005000-00007#xpointer(id(R104-7))|11065213||ovftdb|SL0000305519921535811065213P166[CrossRef]|00005768-200005000-00007#xpointer(id(R104-7))|11065405||ovftdb|SL0000305519921535811065405P166[Medline Link]|00005768-200005000-00007#xpointer(id(R105-7))|11065213||ovftdb|00005768-199409000-00006SL00005768199426110211065213P167[CrossRef]|00005768-200005000-00007#xpointer(id(R105-7))|11065404||ovftdb|00005768-199409000-00006SL00005768199426110211065404P167[Full Text]|00005768-200005000-00007#xpointer(id(R105-7))|11065405||ovftdb|00005768-199409000-00006SL00005768199426110211065405P167[Medline Link]|00005768-200005000-00007#xpointer(id(R106-7))|11065405||ovftdb|SL00004560199477230511065405P168[Medline Link]|00005768-200005000-00007#xpointer(id(R108-7))|11065213||ovftdb|SL000060241987316151411065213P170[CrossRef]|00005768-200005000-00007#xpointer(id(R108-7))|11065405||ovftdb|SL000060241987316151411065405P170[Medline Link]|00005768-200005000-00007#xpointer(id(R109-7))|11065405||ovftdb|SL0000777719967583311065405P171[Medline Link]|00005768-200005000-00007#xpointer(id(R110-7))|11065213||ovftdb|SL00003458199215174211065213P172[CrossRef]|00005768-200005000-00007#xpointer(id(R110-7))|11065405||ovftdb|SL00003458199215174211065405P172[Medline Link]|00005768-200005000-00007#xpointer(id(R111-7))|11065405||ovftdb|SL0000777719947123611065405P173[Medline Link]|00005768-200005000-00007#xpointer(id(R112-7))|11065405||ovftdb|SL0000456019978261311065405P174[Medline Link]|00005768-200005000-00007#xpointer(id(R113-7))|11065213||ovftdb|SL0000778819937244111065213P175[CrossRef]|00005768-200005000-00007#xpointer(id(R113-7))|11065405||ovftdb|SL0000778819937244111065405P175[Medline Link]|00005768-200005000-00007#xpointer(id(R114-7))|11065213||ovftdb|00000416-199501010-00001SL00000416199575111065213P176[CrossRef]|00005768-200005000-00007#xpointer(id(R114-7))|11065404||ovftdb|00000416-199501010-00001SL00000416199575111065404P176[Full Text]|00005768-200005000-00007#xpointer(id(R114-7))|11065405||ovftdb|00000416-199501010-00001SL00000416199575111065405P176[Medline Link]|00005768-200005000-00007#xpointer(id(R115-7))|11065405||ovftdb|SL00004560199783208011065405P177[Medline Link]|00005768-200005000-00007#xpointer(id(R116-7))|11065213||ovftdb|00003017-199412000-00036SL00003017199490287711065213P178[CrossRef]|00005768-200005000-00007#xpointer(id(R116-7))|11065404||ovftdb|00003017-199412000-00036SL00003017199490287711065404P178[Full Text]|00005768-200005000-00007#xpointer(id(R116-7))|11065405||ovftdb|00003017-199412000-00036SL00003017199490287711065405P178[Medline Link]|00005768-200005000-00007#xpointer(id(R117-7))|11065213||ovftdb|00043605-199510000-00019SL00043605199515166811065213P179[CrossRef]|00005768-200005000-00007#xpointer(id(R117-7))|11065404||ovftdb|00043605-199510000-00019SL00043605199515166811065404P179[Full Text]|00005768-200005000-00007#xpointer(id(R117-7))|11065405||ovftdb|00043605-199510000-00019SL00043605199515166811065405P179[Medline Link]|00005768-200005000-00007#xpointer(id(R118-7))|11065213||ovftdb|00043605-199709000-00010SL00043605199717168211065213P180[CrossRef]|00005768-200005000-00007#xpointer(id(R118-7))|11065404||ovftdb|00043605-199709000-00010SL00043605199717168211065404P180[Full Text]|00005768-200005000-00007#xpointer(id(R118-7))|11065405||ovftdb|00043605-199709000-00010SL00043605199717168211065405P180[Medline Link]|00005768-200005000-00007#xpointer(id(R120-7))|11065213||ovftdb|00005768-199802000-00012SL0000576819983024611065213P182[CrossRef]|00005768-200005000-00007#xpointer(id(R120-7))|11065404||ovftdb|00005768-199802000-00012SL0000576819983024611065404P182[Full Text]|00005768-200005000-00007#xpointer(id(R120-7))|11065405||ovftdb|00005768-199802000-00012SL0000576819983024611065405P182[Medline Link]|00005768-200005000-00007#xpointer(id(R121-7))|11065405||ovftdb|SL0000362819901181911065405P183[Medline Link]1977586Blood hemostasis in exercise and trainingEL-SAYED, MAHMOUD S.; SALE, CRAIG; JONES, PETER G. W.; CHESTER, MICHAELBASIC SCIENCES: Reviews532InternalMedicine & Science in Sports & Exercise10.1249/mss.0b013e31802eff4b2007394587-592APR 2007Exercise Training-Induced Changes in Coagulation Factors in Older AdultsLOCKARD, MM; GOPINATHANNAIR, R; PATON, CM; PHARES, DA; HAGBERG, JM & Science in Sports & Exercise2001336S516-S520JUN 2001Dose-response and coagulation and hemostatic factorsRAURAMAA, R; LI, G; VÄISÄNEN, SB & Science in Sports & Exercise20033561026-1032JUN 2003The Effects of Graded Resistance Exercise on Platelet Aggregation and ActivationAHMADIZAD, S; EL-SAYED, MS & Science in Sports & Exercise2003353444-448MAR 2003Exercise-Induced Increases in Cardiac Troponins and Prothrombotic MarkersKOLLER, A