***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Acute vigorous exercise , associated with increased release of plasma catecholamines , transiently increases the risk of primary cardiac arrest . We tested the effect of acute submaximal exercise on vasoactive substances and their combined result on platelet function . Methods Healthy volunteers , hypertensive patients and patients with coronary artery disease ( CAD ) performed a modified treadmill exercise test .  We determined plasma catecholamines , thromboxane A2 , prostacyclin , endothelin-1 and platelet aggregation induced by adenosine diphosphate ( ADP ) and collagen at rest and during exercise . Results Our results during exercise showed a ) platelet activation ( increased thromboxane B2 , TXB2 ) , b ) increased prostacyclin release from endothelium and c ) decreased platelet aggregation in all groups , significantly more in healthy volunteers than in patients with CAD ( with hypertensives lying in between these two groups ) . Conclusion Despite the pronounced activation of Sympathetic Nervous System ( SNS ) and increased TXB2 levels during acute exercise platelet aggregation decreases , possibly to counterbalance the prothrombotic state . Since this effect seems to be mediated by the normal endothelium ( through prostacyclin and nitric oxide ) , in conditions characterized by endothelial dysfunction ( hypertension , CAD ) reduced platelet aggregation is attenuated , thus posing such patients in increased risk for thrombotic complications It has been postulated that platelet function plays an important role in the initiation of atherosclerosis . Currently there are no definitive data on the longer-term effects of regular physical exercise on platelet function in humans . We assessed the influence of regular moderate-intensity physical exercise ( brisk walking to slow jogging ) on platelet aggregation in a population -based sample of middle-aged , overweight , mildly hypertensive men in eastern Finl and . In this controlled study , we evaluated the net effect of exercise on platelet aggregation by study ing changes in optical density and ATP release in platelet-rich plasma . A significant inhibition of secondary platelet aggregation from 27 % to 36 % was observed in the men taking regular exercise .  These findings give new insight into the possible protective effects of exercise against the risk of ischemic heart disease Background —Platelet reactivity is increased by exercise in patients with obstructive coronary artery disease ( CAD ) but not in patients with syndrome X. In this study , we prospect ively investigated whether the platelet response to exercise might help distinguish , among patients with angina , those with obstructive CAD from those with normal coronary arteries ( NCAs ) . Methods and Results —Venous blood sample s were collected before and 5 minutes after exercise from 194 consecutive patients with stable angina .  Platelet reactivity was measured by the platelet function analyzer (PFA)-100 system as the time for flowing whole blood to occlude a collagen-adenosine diphosphate ring ( closure time ) . Coronary angiography showed CAD in 163 patients ( 84 % ) and NCA in 31 patients ( 16 % ) . Baseline closure time was shorter in NCA patients ( 78.0±16 versus 95.5±23 seconds , P < 0.0001 ) . With exercise  , closure time decreased in CAD patients ( −15.5 seconds ; 95 % confidence limits [ CL ] , −13.0 to −18.0 seconds;P < 0.0001 ) , but increased in NCA patients ( 12.5 seconds ; 95 % CL , 7.4 to 17.7 seconds;P = 0.0004 ) . An increase in closure time  with exercise ≥10 seconds had 100 % specificity and positive predictive value for NCAs . Similarly , a decrease ≥10 seconds had 100 % specificity and positive predictive value for CAD . A closure time change ( increase or decrease ) ≥10 seconds allowed a correct classification of 55 % of all patients . Conclusions —Among patients with stable angina , the response of platelet reactivity to exercise was predictive of normal or stenosed coronary arteries at angiography . Specifically , an increase in closure time  with exercise ≥10 seconds was invariably associated with the presence of NCA To investigate the effects of chronic exercise and deconditioning on  platelet function in women , 16 healthy sedentary women were divided into control and exercise groups . The exercise group cycled on an ergometer at 50 % maximal oxygen consumption for 30 min/day , 5 days/wk , for two consecutive menstrual cycles and then were deconditioned for three menstrual cycles . During this period , platelet adhesiveness on a fibrinogen-coated surface , ADP-induced platelet aggregation and intracellular calcium concentration elevation , guanosine 3',5'-cyclic monophosphate ( cGMP ) content in platelets , and plasma nitric oxide metabolite levels were measured before and immediately after a progressive exercise test in the midfollicular phase . Our results indicated that , after exercise training , 1 ) resting heart rates and blood pressures were reduced , and exercise performance was improved ; 2 ) resting platelet function was decreased , whereas plasma nitrite and nitrate levels and platelet cGMP contents were enhanced ; and 3 ) the potentiation of platelet function by acute strenuous exercise was decreased , whereas the increases in plasma nitrite and nitrate levels and platelet cGMP contents were enhanced by acute exercise . Furthermore , deconditioning reversed these training effects . This implies that training-induced platelet functional changes in women in the midfollicular phase may be mediated by nitric oxide Moderate and strenuous exercise is known to enhance platelet aggregability in patients with obstructive coronary artery disease ( CAD ) , but the effect of low- grade exercise is not known . We assessed shear-induced platelet aggregability before and after mild exercise ( less than or equal to stage III of the modified Bruce protocol ) in 27 patients with documented CAD who were receiving aspirin and in 12 subjects without CAD ( controls ) .  Ex vivo platelet aggregability was assessed in flowing whole blood as the time to occlude a collagen and adenosine diphosphate-coated ring ; shorter times indicated greater aggregability . Aggregability , plasma von Willebr and factor ( vWF ) antigen , platelet and white cell counts , and hematocrit were measured at baseline , immediately after exercise ( peak ) , and at 30 and 180 minutes after exercise . Exercise of similar workloads induced myocardial ischemia in 14 patients ( group 1 ) , but not in the other 13 ( group 2 ) nor in controls . Both patient groups showed a reduction in aggregation time at peak exercise compared with baseline ( group 1 : 84+/-17 seconds at peak vs 96+/-22 seconds at baseline ; group 2 : 84+/-20 seconds at peak vs 99+/-20 seconds at baseline ; p < 0.03 for both comparisons ) , with a return to baseline values within 180 minutes . No significant variation occurred in controls ( 89+/-18 seconds at peak vs 85+/-21 second at baseline ) . Changes in vWF antigen did not differ significantly among groups . Aggregation times did not correlate with hematocrit or platelet and white cell counts . Thus , even low- grade exercise transiently enhances whole blood platelet aggregability in patients with obstructive CAD , but not in controls . The effect is independent of myocardial ischemia , occurs despite aspirin , and is likely dependent on hemodynamic factors interacting with coronary obstructions or dysfunctional endothelium Platelet activation induced by shear forces occurring in a stenosed coronary artery is one of the mechanisms of coronary thrombosis . We evaluated the shear-induced platelet aggregation ( SIPA ) dynamics in patients with effort angina during treadmill exercise .  SIPA was measured by a rotational cone-plate aggregometer .  SIPA was markedly increased by exercise from 71.2 + /- 8.9 % to 81.9 + /- 7.6 % ( p < 0.01 ) in the patient group . Although epinephrine concentrations were elevated , its rate of increase was not correlated with that of SIPA . Yohimbine partially inhibited the exercise-induced increase in SIPA . In contrast , a significant correlation between the changing rate of plasma von Willebr and factor ( vWF ) larger multimers and that of SIPA ( r = 0.74 , p < 0.05 ) was observed . Exercise-augmented SIPA is probably dependent on an increase in vWF larger multimers rather than platelet alpha2-receptor activation . Prevention of the interaction between vWF and its platelet receptors may play some role in decreasing the risk of coronary thrombosis during exercise To examine the risk of primary cardiac arrest during vigorous exercise , we interviewed the wives of 133 men without known prior heart disease who had had primary cardiac arrest . Cases were classified according to their activity at the time of cardiac arrest and the amount of their habitual vigorous activity . From interviews with wives of a r and om sample of healthy men , we estimated the amount of time members of the community spent in vigorous activity . Among men with low levels of habitual activity , the relative risk of cardiac arrest during exercise compared with that at other times was 56 ( 95 per cent confidence limits , 23 to 131 ) . The risk during exercise  among men at the highest level of habitual activity was also elevated , but only by a factor of 5 ( 95 per cent confidence limits , 2 to 14 ) . However , among the habitually vigorous men , the overall risk of cardiac arrest -- i.e . , during and not during vigorous activity -- was only 40 per cent that of the sedentary men ( 95 per cent confidence limits , 0.23 to 0.67 ) . Although the risk of primary cardiac arrest is transiently increased during vigorous exercise , habitual vigorous exercise is associated with an overall decreased risk of primary cardiac arrest BACKGROUND It is controversial whether the onset of myocardial infa rct ion occurs r and omly or is precipitated by identifiable stimuli . Previous studies have suggested a higher risk of cardiac events in association with exertion . METHODS Consecutive patients with acute myocardial infa rct ion were identified by recording all admissions to our hospital in Berlin and by monitoring a general population of 330,000 residents in Augsburg , Germany . Information on the circumstances of each infa rct ion was obtained by means of st and ardized interviews . The data analysis included a comparison of patients with matched controls and a case-crossover comparison ( one in which each patient serves as his or her own control ) of the patient 's usual frequency of exertion with the last episode of exertion before the onset of myocardial infa rct ion . RESULTS From January 1989 through December 1991 , 1194 patients ( 74 percent of whom were men ; mean age [ + /- SD ] , 61 + /- 9 years ) completed the interview 13 + /- 6 days after infa rct ion . We found that 7.1 percent of the case patients had engaged in physical exertion ( > or = 6 metabolic equivalents ) at the onset of infa rct ion , as compared with 3.9 percent of the controls at the onset of the control event . For the patients as compared with the matched controls , the adjusted relative risk of having engaged in strenuous physical activity at the onset of infa rct ion or the control event was 2.1 ( 95 percent confidence interval , 1.1 to 3.6 ) . The case-crossover comparison yielded a similar relative risk of 2.1 ( 95 percent confidence interval , 1.6 to 3.1 ) for having engaged in strenuous physical activity within one hour before myocardial infa rct ion . Patients whose frequency of regular exercise was less than four and four or more times per week had relative risks of 6.9 and 1.3 , respectively ( P < 0.01 ) . CONCLUSIONS A period of strenuous physical activity is associated with a temporary increase in the risk of having a myocardial infa rct ion , particularly among patients who exercise infrequently . These findings should aid in the identification of the triggering mechanisms for myocardial infa rct ion and improve prevention of this common and serious disorder Platelets play an important role in the pathogenesis of cardiovascular disease . It has also been noticed that regular exercise can reduce the risk of cardiovascular disease . This is the first study to demonstrate that endurance exercise training may suppress platelet adhesiveness and aggregation and that deconditioning may reverse the training effects . Healthy male sedentary subjects were r and omly divided into control and training groups . The trained men were trained on a bicycle ergometer at about 60 % of maximal oxygen consumption for 30 minutes per day , 5 days per week for 8 weeks , then deconditioned for 12 weeks . During the experimental period , blood sample s of the trained subjects were collected before and immediately after a progressive exercise test every 4 weeks . The same experiments were applied to the controls at the beginning of this study and 8 weeks thereafter . A tapered parallel-plate chamber was used to assess platelet adhesiveness . Platelet aggregation induced by ADP was evaluated by the percentage of reduction in single platelet count . Our results showed that ( 1 ) platelet adhesiveness and aggregability were increased by short-term strenuous exercise in both control and trained groups , but the enhancement of platelet aggregability was decreased after exercise training in the trained subjects ; ( 2 ) at rest and immediately after strenuous exercise , platelet adhesiveness and aggregability were decreased by training , whereas they were unchanged in the control group ; and ( 3 ) deconditioning reversed the training effects on resting and postexercise platelet adhesiveness and aggregability back to the pretraining state . These results suggest that platelet adhesiveness and aggregability may be depressed by exercise training but be reversed back to the pretraining state after deconditioning INTRODUCTION Coronary artery disease ( CAD ) is associated with higher platelet activation sometimes despite aspirin use . There are conflicting data concerning platelet activation course during physical exercise in patients on aspirin with CAD . AIM To assess platelet activation pattern during physical exercise in patients with CAD . M 
    Output:
    
Overall , patients did not differ from healthy controls in platelet aggregation or activation prior to exercise .
After exercise , conflicting results were reported with some studies reporting intensified platelet aggregation and /or platelet activation , some studies found no difference , whereas a few studies reported a reduction in platelet aggregation after exercise when compared with controls .
Exercise seemed to impair the effect of aspirin during or shortly after exercise .
However , this review indicates that strenuous short‐term exercise induces increased platelet activation also implying a reduced effect of aspirin during short‐term exercise .