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1 Department of Medical Physiology and Sports Medicine and 2 Department of Hematology, University of Utrecht, 3508 TA Utrecht, The Netherlands
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The influence of age on training-induced changes in resting and stimulated hemostatic potential was studied in three age categories (Cat I-III; 20-30 yr, 35-45 yr, and 50-60 yr, respectively) of sedentary men before and after 12 wk of training. Coagulation, fibrinolytic activity, and activation markers (reflecting fibrin formation and degradation) were determined. Physical conditioning resulted in a more pronounced increase in von Willebrand factor (vWF) and factor VIII clotting activity (FVIII:c) in Cat I and II and a more pronounced shortening of the activated partial thromboplastin time in all categories at maximal exertion and during recovery. Enhanced increases in tissue-type plasminogen activator (t-PA) antigen and activity and single-chain (sc) urokinase-type plasminogen activator (u-PA) at maximal exercise and 5 min of recovery were observed in all age groups after training. The effects on FVIII:c, vWF, and scu-PA were most pronounced in the youngest age group (Cat I). Increases in the marker of thrombin generation were highest in Cat III; no effect was seen on thrombin-antithrombin complex, plasmin-antiplasmin complex, and D-dimer in any of the age groups. We concluded that training enhances both coagulation and fibrinolytic potential during strenuous exercise. The effect on FVIII/vWF and t-PA/u-PA is most pronounced in younger individuals, whereas thrombin formation is most pronounced in older individuals.
activation markers; coagulation; fibrinolysis
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE EFFECT OF PHYSICAL CONDITIONING on various cardiovascular risk factors has been studied extensively. Beneficial effects of training have been observed on lipid profile, hypertension, and insulin resistance, factors that are linked to cardiovascular complications (11, 19, 21, 32, 33). As a result, large numbers of sedentary individuals are, irrespective of age, advised to participate in training activities.
More recently, physical inactivity has been declared an independent risk factor in the pathogenesis of cardiovascular diseases, suggesting that additional unknown risk factors are involved (5). A disturbance in the hemostatic balance associated with increased fibrin deposition and enhanced thrombogenesis might constitute such an important risk factor (3, 8). Aging is also associated with adverse changes in coagulation and fibrinolysis that are suggestive of a thrombophilic state (1, 10, 26, 30). We therefore studied the effects of regular physical exercise on the balance between two systems that play a crucial role in thrombogenic processes, i.e., coagulation and fibrinolysis, in relation to age. A decrease in thrombogenic potential would further support the concept that "regular exercise is good for heart and blood vessels."
Activation of coagulation results in the formation of thrombin, an enzyme that converts fibrinogen into (insoluble) fibrin. Activation of this system is reflected in enhanced levels of active clotting factors and of activation markers such as prothrombin activation fragment 1+2 (F1+2), which is a marker of thrombin generation, and thrombin-antithrombin complex (TAT), associated with a decrease in clotting time.
When the fibrinolytic system is activated, plasmin, which is
responsible for the degradation of fibrin, is formed. Activation of
this mechanism is reflected in increased levels of tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA) and activation products such as
plasmin-
2-antiplasmin complex (PAP) and D-dimer (a
cross-linked fibrin degradation product). Results of predominantly
cross-sectional studies are suggestive of a beneficial antithrombotic
effect of physical training on fibrinolytic components such as t-PA
and/or plasminogen activator inhibitor (PAI-1), at rest and during
acute exercise (6, 10, 14, 20, 26-28). Whether this is indeed
associated with enhanced fibrin degradation remains to be determined.
Less attention has been paid to the effect of physical conditioning on coagulation activity, and the results are scarce and far less consistent (6, 10, 14, 27).
In this study, we determined plasma levels of hemostatic variables that are known to change during acute exercise, i.e., factor VIII clotting activity (FVIII:c), von Willebrand factor (vWF), activated partial thromboplastin time (APTT), t-PA, and u-PA (6, 27, 30). Recently, sophisticated tests for the determination of activation markers and activator-inhibitor complexes that reflect in vivo activation of coagulation and fibrinolysis have become available. The influence of acute exercise and/or training on the actual in vivo thrombin formation and fibrin degradation has been determined separately and simultaneously, but the results are conflicting and not consistent (9, 13, 16, 18, 20, 23).
An important aspect that has to be taken into consideration when training studies are performed is the fact that aging is associated with a thrombophilic state that may contribute to cardiovascular complications (1, 10). Another aspect that may determine the outcome of training studies and thus requires careful attention is changes in body composition related to weight loss and changes in dietary habits (15, 30, 33). The purpose of our study was to investigate the influence of aging on training-induced adaptations in the hemostatic system, both at rest and under stimulated conditions. We designed a highly standardized testing and training program and included three well-defined age categories of sedentary men in our study.
Coagulation and fibrinolytic factors, which are activated during exercise, as well as activation markers, were determined at rest, during acute submaximal and maximal exercise, and during the subsequent recovery period, before and after a 12-wk of training period.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Participants
Sedentary men in three age categories [20-30 yr (Cat I), 35-45 (Cat II), and 50-60 yr (Cat III)] were recruited by an advertisement in a local newspaper. Respondents were asked to fill in a questionnaire providing information about their daily activity pattern and other health and lifestyle factors. Subjects were characterized as sedentary if they worked in sedentary jobs and did not participate in any form of sporting activity during leisure time. Other inclusion criteria were: no sporting activities during the previous 5 yr, apparently healthy, no medication, nonsmoking, and only moderate alcohol use. The study was approved by the Ethical Commission of the Utrecht University Hospital and participants joined the study after written informed consent was obtained.Training and Test Procedure
Training.
All subjects participated for 12 wk in the supervised training sessions
performed in the laboratory. Participants exercised twice a week for 1 h at a constant submaximal level. During each training session, the
work rate was adjusted for each individual to maintain a heart rate
corresponding with that at 60-70% maximal oxygen uptake
(
O2 max).
At this submaximal level, on the basis of advice for
recreational sporting activities, clear training-induced changes can be
expected (2). Anthropometric measurements,
O2 max test, and
exercise test (Ex-test) were performed before the start and after 12 wk
of training.
Anthropometric measurements. Height, body mass, and four skinfolds were measured as described previously (4), and body mass index (kg/m2) and fat percentage were calculated.
O2 max test.
O2 max was determined
with an increasing workload test on a cycle ergometer (Lode, Groningen,
The Netherlands). Subjects started with an initial load of 1 W/kg (60 rpm), which was increased every 2 min with 1 W/kg. After an
age-dependent threshold was reached, the load was increased 2 W/kg
every 2 min until participants reached their maximal performance. This
threshold was 150 beats/min for Cat I, 135 beats/min for Cat II, and
110 beats/min for Cat III. Maximal exercise was indicated by a
respiratory exchange ratio level >1.15, age-predicted maximal
heart rate (HRmax), or when participants were unable to
continue. Participants were encouraged to exert themselves maximally.
The total work capacity (TWC) was calculated, at each step during
O2 max
test, as the product of load (W = J/s) and time (s). The total amount
of work (in J) is expressed per kilogram body mass. Ventilatory
parameters were determined with Oxycon-
(Mijnhardt, the
Netherlands), which was calibrated before and after each test.
Electrocardiogram was monitored continuously by using three leads (CC5,
CM5, and CB5) with a megacart electrocardiograph (Siemens, The
Netherlands). In addition, HRmax and heart rate (HR) at 60 and 70% O2 max were
recorded. These parameters were used for the standardization of the
Ex-test procedure and training intensity.
Ex-test.
This standardized test, designed for the collection of blood samples at
rest, during submaximal exercise, at maximal exercise, and during
recovery, was scheduled between 8:00 and 10:00 AM. Participants
refrained from alcohol and coffee for 12 h before the test. On the day
of the test, they had a light breakfast consisting of tea and toast.
Ex-tests were performed on a cycle ergometer and comprised four
consecutive periods: 1) the initial 10 min, during which the
load was gradually increased until the HR was reached that corresponded
with the participant's HR at 70%
O2 max; 2) 15 min of exercise, during which the load was continuously adjusted to
maintain a constant HR corresponding with 70%
O2 max, representing submaximal exercise intensity; 3) a period during which the load was increased in four steps of 1 min to attain the HR
corresponding with the HR at each participant's
O2 max, representing
maximal exertion; and 4) the recovery period, which comprised
10 min of active recovery whereby participants cycled at a load of 1 W/kg followed by 15 min passive recovery during which the participants
remained upright.
Blood collection procedure.
Blood samples were drawn (without stasis) by clean venipuncture (B-D
Microlance 19 gauge) from the antecubital vein. The first 3 ml of each
blood sample were discarded. Blood was collected in tubes containing
chilled 3.8% (0.11 mmol/l) trisodium citrate and in EDTA-coated tubes.
For the determination of t-PA activity (Act), 1 ml of citrate blood was
immediately mixed with an equal amount of sodium acetate buffer (0.2 mol/l, pH 3.9). Blood for PAI-1 antigen PAI-1 antigen (Ag)
determinations was collected in tubes containing citric acid,
theophylline, adenosine, and dipyridamole (Becton-Dickinson). Within 10 min after collection, plasma was separated by centrifugation at 2,000 g for 20 min at 4°C, divided in small aliquots of 200 µl,
and snap frozen in liquid nitrogen to be stored at 
80°C.
Hematologic parameters. Samples from each individual obtained before and after 12 wk of training were tested simultaneously in one run to eliminate the intra-assay variation.
Coagulation activities of FVIII:c and vWF as well as APTT were determined, according to the manufacturer's instructions, with a laser-nephelometric centrifugal ACL 200 analyzer (Instrumentation Laboratory, IJsselstein, The Netherlands). Deficient plasmas were obtained from Organon Teknica Nederland (Boxtel). Cephalin, calcium chloride, and calcium thromboplastin were provided by Instrumentation Laboratory. Blood for the normal plasma pool was donated by 40 healthy men. F1+2 was determined with Enzygnost F1+2 (Behring). TAT was determined with Enzygnost TAT micro (Behring). t-PA Ag was measured with a commercial ELISA (Imulyse t-PA, Biopool, Umeå, Sweden), and t-PA Act was determined by using a commercially available kit (Coaset t-PA, Chromogenix). PAI-1 Ag was determined with Coaliza PAI-1 (Chromogenix). u-PA Ag and single-chain u-PA (scu-PA) Ag were determined with TintElize uPA and Chromolize uPA, respectively (Biopool). PAP was determined with EIA APP micro-ELISA (Behring), and D-dimer was determined with Innotest D-dimer (Innogenetics). Hb and hematocrit were determined with a Sysmex NE 8000 (Toa Medical Electronics) analyzer. Changes in plasma volume were calculated according to Dill and Costill (12).Statistics
Statistical analyses were performed with Superior Performing Software Systems (SPSS) version 5.01. Deviations from normality of distribution were checked for each variable. The distributions of hematologic parameters, except for vWF, were slightly skewed, and for these variables log10 transformations were performed. Multiple ANOVA repeated measures were used for analysis of each variable. Differences in time (training) and between categories were calculated. Results are expressed as means ± SE. Two-sided probability values were considered significant at P < 0.05.| |
RESULTS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Participants
Four participants withdrew before the study started, and two quit the study because of lack of motivation. Ultimately, 39 participants (Cat I: n = 13; Cat II: n = 13; Cat III: n = 13) completed the whole test and training program and were included in this study. No medical complications were observed during the 12-wk test and training program.Anthropometric Measurements
Age-related differences were observed in percent body fat and lean body mass but not in total body mass. No change in any of the anthropometric parameters was seen during the training period. The age-related differences observed before training persisted after training (see Table 1).
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Exercise Parameters
O2 max,
HRmax, and TWC were related to age, being significantly
lower in the older age groups. Training resulted in a significant increase in both O2 max
and TWC in all three age categories (see Table 1).
Hemostatic Variables and Reaction Products
Age-related effects on hemostatic variables and reaction products
before the start of the training.
Preexercise plasma level of PAI-1 Ag (Cat I-III; 43 ± 8, 61 ± 8, and 62 ± 11 IU/ml, respectively) and t-PA Ag were higher in Cat II
and III, whereas levels of F1+2 were higher in Cat III only
(Figs. 1, 2,
and 3).
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Age-related effects on coagulation parameters after training.
No effect of training was observed on basal (resting) or submaximal
exercise (70% O2 max)
plasma levels (see Fig. 1). At maximal exercise intensity and during
the entire recovery period, a more pronounced increase was observed in
FVIII:c and vWF (Cat I and Cat II only), accompanied by a more
pronounced shortening of the APTT (Cat I, Cat II, and Cat III),
compared with pretraining results.
Age-related effects on fibrinolytic parameters after training.
No changes in basal (resting) or submaximal exercise (70%
O2 max) plasma levels
were observed after training (see Fig. 2). At maximal exercise
intensity and during the initial 5 min of recovery, more pronounced
increases in t-PA Ag, t-PA Act, and scu-PA Ag were seen after training.
The magnitude of this training-induced increase in both u-PA Ag and
scu-PA Ag was significantly larger in Cat I.
Age-related effects on reaction products after training. F1+2 demonstrated an increase after 25 min of submaximal exercise in contrast to pretraining results and a more pronounced increase at maximal performance and part of the recovery period in the older age groups (Cat II and Cat III). Although TAT, PAP, and D-dimer levels tended to increase more at 12 wk of training, results did not reach significance level (see Fig. 3).
Plasma Volume
A decrease in plasma volume was observed that was maximal during maximal exercise, independent of age (see Table 1). This decrease was significantly more pronounced after training (10.7 ± 0.6 vs. 13.2 ± 0.6%) and of comparable magnitude for all three age categories. Correction applied for hemoconcentration did not significantly affect the outcome of the results.| |
DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The purpose of this study was to evaluate the influence of age on training-induced changes in resting and stimulated coagulation and fibrinolytic potential.
Our study comprised three well-defined age groups of 13 sedentary male
subjects each, who were tested before and after 12 wk of submaximal
(70% O2 max) aerobic
cycle ergometer training twice a week. Hemostatic factors representing
in vitro coagulation and fibrinolytic activity, and activation markers
reflecting thrombin and plasmin generation as well as fibrin
degradation in vivo, were determined under both resting and stimulated
conditions with the use of highly standardized test and exercise procedures.
Aging is associated with unfavorable changes in coagulation and fibrinolytic components that may play a role in the enhanced risk for thrombotic events (1, 10). In contrast, regular physical activity is generally accepted as part of a favorable lifestyle that is known to reduce the risk for cardiovascular diseases (5, 11, 21, 22, 33). Both a decrease in coagulation activity and an increase in fibrinolytic activity are associated with a reduced thrombogenic tendency. A number of authors have suggested that training-related adaptations, mainly in fibrinolytic potential, could be responsible for the reduced risk for coronary artery thrombosis (3, 7, 8, 33).
The majority of these studies have focused on the t-PA and its main inhibitor PAI-1 either at rest or under stimulated conditions (6, 20, 25-29). In contrast to fibrinolysis, the coagulation system has received little attention. The studies performed so far report no change or a slight increase in coagulation potential after training (6, 14, 20, 27, 29).
Although training-related adaptations in coagulation and fibrinolytic potential seem evident, the influence of aging (associated with an enhanced thrombogenicity) on these training-related processes has received little attention and has only been studied in a cross-sectional setting (10, 26).
It is also interesting to know whether the observed adaptations are indeed reflected in changes in the actual in vivo fibrin formation and/or degradation.
Influence of Aging on Hemostatic Variables Before the Start of the Training Program
Before the start of the training, the older participants demonstrated a less favorable hemostatic profile reflected in significantly higher constitutive (resting) F1+2, PAI-1, and t-PA levels, underscoring earlier observations (1, 10, 26).During exercise, the well-known increases in the in vitro coagulation (vWF, FVIII:c, and APTT) and fibrinolytic (t-PA and u-PA) activation were observed, comparable for all age groups. Significant changes were also seen in the activation markers TAT, PAP, and D-dimer, but not in F1+2, indicating that additional fibrin degradation in vivo did occur with only marginal or no prothrombin conversion, which support the findings in most studies (9, 13, 24) but is not supported by the results in other studies (16, 18, 23).
During recovery, the enhanced fibrinolytic activity returned to baseline levels (in contrast to the coagulation activity, which was still significantly enhanced at the end of the recovery) to a comparable extent in all three age groups. The results of exercise-induced changes in relation to age and the possible unfavorable effects of the unbalanced hemostasis have been presented and discussed previously (30).
Influence of Aging on Training-Induced Adaptations in Hemostasis
The significant increase inO2 max in all three age
categories clearly indicated that training had been equally effective in improving cardiopulmonary fitness. It is important to note that no
changes in either body mass or body fat percent were observed in any of
the three groups, given that changes in body composition per se are
closely associated with changes in coagulation and fibrinolysis (10,
15, 30).
Resting and submaximal exercise. With the exception of a significant increase in F1+2 in the elderly, reflecting additional thrombin formation, no effect of training was observed on constitutive and submaximal plasma levels of coagulation variables in either group, which underscores previous results obtained in longitudinal studies (14, 29).
No effect was seen on resting and submaximal levels of fibrinolytic parameters, which is in agreement with some but at variance with others who reported enhanced fibrinolytic activity (6, 26-28). The majority of these studies are, however, cross-sectional with the exception of that of Stratton et al. (26), who performed a longitudinal training study and observed an increase in fibrinolytic activity in elderly only but not in young subjects. Unfortunately, few authors apply corrections for changes in body mass and composition observed after conditioning or for differences in anthropometry between trained and untrained individuals. In addition, differences in experimental setup may also be responsible for the discrepant results. As mentioned before, the study of hemostatic variables requires a meticulous standardization. Differences in blood sampling procedures, e.g., clean venipuncture vs. the use of a catheter which may cause additional activation (17); intensity (strenuous vs. submaximal), or duration and type (running vs. cycling) of training could affect the outcome of the studies.Maximal exercise and recovery. The increase in clotting potential that was observed during maximal exercise varied with age. FVIII:c and vWF were significantly more pronounced in the younger age groups (Cat I and II) only, although the decrease in the clotting time (APTT) was comparable for all three age categories. An explanation for the more pronounced increase in vWF and FVIII:c in the younger men could be a greater susceptibility to endothelial triggers, e.g., higher shear stress or an enhanced capacity of the endothelium to release vWF. The F1+2 increase during maximal exercise and part of the recovery was highest in the oldest age category (Cat III). That the older men demonstrated a more pronounced increase in prothrombin activation is compatible the with diminished levels of coagulation inhibitors as reported before (30).
The training-induced effect on scu-PA was also more pronounced in the youngest participants (Cat I). In contrast, (the smaller) training-related changes in t-PA were not related to age. This finding underscores the notion that the mechanisms responsible for the increase in t-PA and scu-PA during exercise are different, scu-PA levels being closer related with workload than t-PA (30, 31). From the results of the present study we conclude 1) that aging is associated with unfavorable changes in constitutive plasma levels of hemostatic variables; 2) that the acute exercise-induced changes are superimposed on the resting levels; 3) that after 12 wk of submaximal aerobic training, no changes are observed in constitutive (resting) plasma levels of the hemostatic variables and activation products under study in either young or elderly healthy individuals; 4) that both the hypercoagulability and hyperfibrinolysis induced by (acute) exercise are enhanced after 12 wk of submaximal training and maintained at a higher level during recovery; 5) that the exercise-induced increase in hemostatic activators after training is more prominent in younger individuals, suggesting a greater plasticity and susceptibility to exercise stimuli; 6) that thrombin formation is accelerated in trained individuals in relation with age, whereas fibrin(ogen) degradation is not affected; 7) that aging seems to be associated with additional risks during maximal exertion because lower increases in FVIII:c and vWF are needed for comparable shortening of the clotting times and the fibrinolytic response of scu-PA is less pronounced; and 8) that the disparate decrease of coagulation and fibrinolysis during the recovery period seems aggravated in trained individuals. From the results, we cannot infer a direct beneficial or detrimental effect of recreational physical conditioning in healthy subjects. It would, however, be advisable for older individuals with an enhanced thrombotic tendency and at risk for cardiovascular complication to avoid extreme exertional activity. Regular submaximal exercise remains nevertheless advisable because hemostatic changes are relatively small and clear beneficial effects on hypercholesterolemia, hypertension, insulin resistance, and body composition have been reported (11, 19).| |
ACKNOWLEDGEMENTS |
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We thank Dr. E. Bol for statistical advice and J. J. H. de Wit for drawing the illustrations.
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FOOTNOTES |
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The study was supported by The Netherlands Heart Foundation Grant 90.059.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: I. A. Huisveld, Dept. of Medical Physiology and Sports Medicine, P.O. Box 80043, 3508 TA Utrecht, The Netherlands (E-mail: I.A.Huisveld{at}med.uu.nl).
Received 29 March 1999; accepted in final form 17 December 1999.
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REFERENCES |
|---|
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Abbate, R,
Prisco D,
Rostangno C,
Boddi M,
and
Gensini GF.
Age-related changes in the hemostatic system.
Int J Clin Lab Res
23:
1-3,
1993[ISI][Medline].
2.
Åstrand, P-O,
and
Rodahl K.
Textbook of Work Physiology: Physiological Bases of Exercise (3th ed.). New York: McGraw-Hill, 1986.
3.
Barold, SS,
Hannss RJ,
Ling Ong S,
Falkoff MD,
Robert Heinle A,
and
Sengupta A.
Exercise-induced myocardial infarction due to coronary thrombosis.
Am Heart J
109:
590-593,
1985[ISI][Medline].
4.
Bernink, MJE,
Erich WBM,
Peltenburg AL,
Zonderland ML,
and
Huisveld IA.
Socio-economic factors in relation to lipid profiles in young girl athletes.
Eur J Appl Physiol
54:
427-431,
1985.
5.
Bijnen, FCH,
Caspersen CJ,
and
Mosterd WL.
Physical inactivity as a risk factor for coronary heart disease: a WHO and International Society and Federation of Cardiology position statement.
Bull World Health Organ
72:
1-4,
1994[ISI][Medline].
6.
Bourey, RE,
and
Santoro SA.
Interactions of exercise, coagulation, platelets, and fibrinolysis: a brief review.
Med Sci Sports Exerc
20:
439-446,
1988[ISI][Medline].
7.
Chandrashekhar, Y,
and
Anand JS.
Exercise as a coronary protective factor.
Am Heart J
122:
1723-1739,
1991[ISI][Medline].
8.
Ciampricotti, R,
El Gamal M,
Relik T,
Taverne R,
Panis J,
de Swart J,
van Gelder B,
and
Relik-van Wely LJ.
Clinical characteristics and coronary angiographic findings of patients with unstable angina, acute myocardial infraction, and survivors of sudden ischemic death occurring during and after sport.
Am Heart J
120:
1267-1277,
1990[ISI][Medline].
9.
Collen, D,
Semeraro N,
Tricoy JP,
and
Vermylen J.
Turnover of fibrinogen, plasminogen, and prothrombin during exercise in man.
J Appl Physiol
42:
865-873,
1977
10.
DeSouza, CA,
Jones PP,
and
Seals DR.
Physical activity status and adverse age-related differences in coagulation and fibrinolytic factors in women.
Arterioscler Thromb Vasc Biol
18:
362-368,
1998
11.
Després, JP,
and
Lamarche B.
Low-intensity endurance exercise training, plasma lipoproteins and the risk of coronary heart disease (CHD).
J Intern Med
236:
7-22,
1994[ISI][Medline].
12.
Dill, DB,
and
Costill DL.
Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration.
J Appl Physiol
37:
247-248,
1974
13.
Dufaux, B,
Order U,
and
Liesen H.
Effect of a short maximal physical exercise on coagulation, fibrinolysis, and complement system.
Int J Sports Med
12, Suppl1:
S39-S42,
1991.
14.
El-Sayed, MS,
Lin X,
and
Rattu AJM
Blood coagulation and fibrinolysis at rest and in response to maximal exercise before and after a physical conditioning programme.
Blood Coagul Fibrinolysis
6:
747-752,
1995[ISI][Medline].
15.
Heinrich, J,
Wahrburg U,
Martin H,
and
Assmann G.
The effect of diets, rich in mono- or polysaturated fatty acids, on lipid metabolism and haemostasis.
Fibrinolysis
4:
76-78,
1990.
16.
Herren, T,
Bärtsch P,
Heaberli A,
and
Straub PW.
Increased thrombin-antithrombin III complexes after 1 h of physical exercise.
J Appl Physiol
73:
2499-2504,
1992
17.
Huisveld, IA,
van den Burg PJM,
Meijer P,
Hospers JEH,
van Vliet M,
Mosterd WL,
Bouma BN,
and
Kluft C.
Catheter unsuitable for the turn-over products of coagulation, fibrinolysis and platelet activation.
Fibrinolysis
6:
78-80,
1992.
18.
Hyers, TM,
Martin BJ,
Pratt DS,
Dreisin RB,
and
Franks JJ.
Enhanced thrombin and plasmin activity with exercise in man.
J Appl Physiol
48:
821-825,
1980
19.
Katzel, LI,
Bleecker ER,
Colman EG,
Rogus EM,
Sorkin JD,
and
Goldberg AP.
Effects of weight loss vs aerobic exercise training on risk factors for coronary disease in healthy, obese, middle-aged and older men: a randomized controlled trial.
JAMA
274:
1915-1921,
1995[Abstract].
20.
Kvernmo, HD,
and
Østerud B.
The effect of physical conditioning suggests adaptation in procoagulant and fibrinolytic potential.
Thromb Res
87:
559-569,
1997[ISI][Medline].
21.
Lakka, TA,
Vanäläinen JM,
Rauramaa R,
Salonen R,
Tuomilehta J,
and
Salonen JT.
Relationship of leisure-time physical activity and cardiorespiratory fitness to the risk of acute myocardial infarction in men.
N Engl J Med
330:
1549-1554,
1994
22.
Mittleman, MA,
Maclure M,
Tofler GH,
Sherwood JB,
Goldberg RJ,
and
Muller JE.
Triggering of acute myocardial infarction by heavy physical exertion-protected against triggering by regular exertion.
N Engl J Med
329:
1677-1683,
1993
23.
Prisco, D,
Paniccia R,
Guarnaccia V,
Olivo G,
Taddei T,
Boddi M,
and
Gensini GF.
Thrombin generation after physical exercise.
Thromb Res
69:
159-164,
1993[ISI][Medline].
24.
Röcker, L,
Taenzer M,
Drygas WK,
Lill H,
Heydruck B,
and
Altenkirch HU.
Effect of prolonged physical exercise on the fibrinolytic system.
Eur J Appl Physiol
60:
478-481,
1990.
25.
Speiser, W,
Langer W,
Pschaik A,
Selmayr E,
Ibe B,
Nowacki PE,
and
Müller-Berghaus G.
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:
543-555,
1988[ISI][Medline].
26.
Stratton, JR,
Chandler WL,
Schwartz RS,
Cerqueira MD,
Levy WC,
Kahn SE,
Larson VG,
Cain KC,
Beard JC,
and
Abrass IB.
Effects of physical conditioning on fibrinolytic variables and fibrinogen in young and old healthy adults.
Circulation
83:
1692-1697,
1991
27.
Streiff, M,
and
Bell WR.
Exercise and haemostasis in humans.
Semin Hematol
31:
155-165,
1994[ISI][Medline].
28.
Szymanski, LM,
Pate RR,
and
Durstine JL.
Effects of maximal exercise and venous occlusion on fibrinolytic activity in physically active and inactive men.
J Appl Physiol
77:
2305-2310,
1994
29.
Van den Burg, PJM,
Hospers JEH,
van Vliet M,
Mosterd WL,
Bouma BN,
and
Huisveld IA.
Effect of endurance training and seasonal fluctuation on coagulation and fibrinolysis in young sedentary men.
J Appl Physiol
82:
613-620,
1997
30.
Van den Burg, PJM,
Hospers JEH,
van Vliet M,
Mosterd WL,
Bouma BN,
and
Huisveld IA.
Changes in haemostatic factors and activation products after exercise in healthy subjects with different ages.
Thromb Haemost
74:
1457-1464,
1995[ISI][Medline].
31.
Van den Burg, PJM,
Hospers JEH,
van Vliet M,
Mosterd WL,
and
Huisveld IA.
Unbalanced haemostatic changes following strenuous physical exercise: a study in young sedentary males.
Eur Heart J
16:
1995-2001,
1995
32.
Willich, SN,
Lewis M,
Löwel H,
Arntz H-R,
Schubert F,
and
Schröder R.
Physical exertion as a trigger of acute myocardial infarction.
N Engl J Med
329:
1684-1690,
1993
33.
Young, DR,
Haskell WL,
Jatulis DE,
and
Fortmann SP.
Association between changes in physical activity and risk factors for coronary heart disease in a community-based sample of men and women: the Stanford Five-City Project.
Am J Epidemiol
138:
205-216,
1993
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