***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 Exercise may activate platelets and leukocytes and promote thrombosis . The effects of aspirin treatment on the prothrombotic effects of exercise have not been established . METHODS AND RESULTS A total of 15 healthy men performed exhaustive exercise without and with 1 week of pretreatment with aspirin ( 500 mg/day ) . Before and immediately after exercise , platelet aggregability ex vivo was measured by filtragometry , and venous blood sample s were obtained . Whole-blood flow cytometry was used to determine platelet and leukocyte activation and platelet-leukocyte aggregates . Exercise increased platelet P-selectin expression , CD11b expression in neutrophils and lymphocytes , and platelet and leukocyte responses to thrombin , ADP , platelet activating factor , and N-formyl-methionyl-leucyl-phenylalanine ( fMLP ) in vitro . Consistent with enhanced platelet and leukocyte activation , more circulating platelet-platelet and platelet-leukocyte aggregates were detected after exercise ( P<0.001 for both ) . Filtragometry readings were shortened , and plasma soluble P-selectin and prothrombin fragment 1 + 2 were elevated . Aspirin markedly reduced the urinary excretion of 11-dehydrothromboxane B(2 ) , decreased P-selectin expression in single platelets at rest ( P<0.05 ) , and inhibited fMLP-induced neutrophil CD11b expression , but it did not attenuate exercise-induced increases in platelet aggregability , platelet P-selectin expression , leukocyte CD11b expression , platelet-leukocyte aggregate formation , soluble P-selectin , or prothrombin fragment 1 + 2 . CONCLUSIONS Exercise induced platelet and leukocyte activation and platelet-leukocyte aggregation in vivo , and it increased platelet and leukocyte responsiveness to in vitro stimulation . Aspirin treatment attenuated certain signs of platelet activity in vivo at rest and fMLP-induced neutrophil activation in vitro , but it did not attenuate the prothrombotic effects of exercise Diabetes increases the risk of coronary artery disease . We examined the effects of lifestyle modification on key contributing factors to atherogenesis , including oxidative stress , inflammation and cell adhesion . Diabetic men ( N=13 ) were placed on a high-fiber , low-fat diet in a 3-week residential program where food was provided ad libitum and daily aerobic exercise was performed . In each subject , pre- and post-intervention fasting blood was drawn for circulating levels of serum lipids , glucose and insulin , oxidative stress marker 8-isoprostagl and in F2alpha ( 8-iso-PGF2alpha ) , the inflammatory protein C-reactive protein ( CRP ) , and soluble intracellular adhesion molecule (sICAM)-1 and sE-selectin as indicators of endothelial activation . Using subject sera and human aortic endothelial cell ( HAEC ) culture systems , serum-induced monocyte adhesion , ICAM-1 , vascular cell adhesion molecule-1 ( VCAM-1 ) and cell surface abundance , and monocyte chemotactic protein-1 ( MCP-1 ) production were determined . Nitric oxide ( NO ) , superoxide , and hydrogen peroxide production were measured in vitro by fluorometric detection . After 3 weeks , significant reductions ( p<0.05 ) in BMI , all serum lipids including total cholesterol ( pre : 188.9+/-10.1 mg/dL versus post : 146.3+/-3.8 mg/dL ) and low-density lipoprotein ( 103.1+/-10.2 mg/dL versus 76.4+/-4.3 mg/dL ) , fasting serum glucose ( 157.5+/-10.1 mg/dL versus 126.7+/-8.7 mg/dL ) , insulin ( 33.8+/-4.0 microU/ml versus 23.8+/-3.4 microU/ml ) , homeostasis model assessment for insulin resistance , 8-iso-PGF2alpha , CRP , sICAM-1 , and sE-selectin were noted . In vitro , serum-stimulated monocyte adhesion , cellular ICAM-1 and VCAM-1 expression ( p<0.05 ) , and fluorometric detection of superoxide and hydrogen peroxide production decreased , while a concomitant increase in NO production was noted ( all p<0.01 ) . A combination of diet and exercise ameliorates oxidative stress , inflammation , and monocyte-endothelial interaction . Intensive lifestyle modification may improve novel CAD risk factors in men with diabetes AIMS Previous studies have shown an abnormal expression of cellular adhesion molecules and cytokines in chronic heart failure , which may be related to endothelial dysfunction characterizing this syndrome . Our study investigates the effects of physical training on serum activity of some peripheral inflammatory markers associated with endothelial dysfunction , such as granulocyte-macrophage colony-stimulating factor ( GM-CSF ) , macrophage chemoattractant protein-1 ( MCP-1 ) , soluble intercellular adhesion molecule-1 ( sICAM-1 ) and soluble vascular cell adhesion molecule-1 ( sVCAM-1 ) in patients with chronic heart failure . METHODS AND RESULTS Serum levels of GM-CSF , MCP-1 , sICAM-1 and sVCAM-1 were determined in 12 patients with stable chronic heart failure ( ischaemic heart failure : 6/12 , dilated cardiomyopathy : 6/12 , New York Heart Association : II-III , ejection fraction : 24+/-2 % ) before and after a 12-week programme of physical training in a r and omized crossover design . In addition , the functional status of chronic heart failure patients was evaluated by using a cardiorespiratory exercise stress test to measure peak oxygen consumption .  Physical training produced a significant reduction in serum GM-CSF ( 28+/-2 vs 21+/-2 pg . ml(-1 ) , P<0.001 ) , MCP-1 ( 192+/-5 vs 174+/-6 pg . ml(-1 ) , P<0.001 ) , sICAM-1 ( 367+/-31 vs 314+/-29 ng . ml(-1 ) , P<0.01 ) and sVCAM-1 ( 1247+/-103 vs 1095+/-100 ng . ml(-1 ) , P<0.01 ) as well as a significant increase in peak oxygen consumption ( 14.6+/-0.5 vs 16.5+/-0.5 ml . kg(-1)min(-1 ) , P<0.005 ) . A significant correlation was found between the training-induced improvement in peak oxygen consumption and percentage reduction in soluble adhesion molecules sICAM-1 ( r=-0.72 , P<0.01 ) and sVCAM-1 ( r=-0.67 , P<0.02 ) . CONCLUSION Physical training affects beneficially peripheral inflammatory markers reflecting monocyte/macrophage-endothelial cell interaction . Training-induced improvement in exercise tolerance is correlated with the attenuation of the inflammatory process , indicating that inflammation may contribute significantly to the impaired exercise capacity seen in chronic heart failure Abstract This study examined the effects of intensive , moderate and downhill treadmill running  on blood lymphocyte expression of adhesion/activation ( AA ) molecules .  Trained subjects completed three treadmill-running protocol s of identical duration : ( 1 ) an intensive protocol at 80 % $ $ \ifmmode\exp and after\dot\else\exp and after\.\fi{V}_{{{\text{O}}_{{2\max } } } } $ $ to volitional exhaustion , ( 2 ) a moderate protocol at 60 % $ $ \ifmmode\exp and after\dot\else\exp and after\.\fi{V}_{{{\text{O}}_{{2\max } } } } $ $ and ( 3 ) a −10 % downhill ( eccentric ) protocol at 80 % $ $ \ifmmode\exp and after\dot\else\exp and after\.\fi{V}_{{{\text{O}}_{{2\max } } } } $ $ . Blood sample s were taken before , immediately after , 1 and 24 h after exercise . Isolated lymphocytes were assessed for expression of the AA molecules CD54 , CD18 and CD53 by flow cytometry . Lymphocyte counts increased immediately after all running protocol s. Lymphocytopenia was observed 1 h after the intensive and eccentric protocol s only . Plasma creatine kinase increased 24 h after the downhill protocol only . Increases in the number and percentage of CD54 + , CD18bright and CD53bright lymphocytes were observed immediately after the intensive and eccentric protocol s , with the numbers falling below pre-exercise values at 1 h post-exercise for all protocol s. No differences were found between the intensive protocol and the eccentric protocol at the same relative intensity . Analysis of lymphocyte subsets showed that the total number of CD3 + , CD4 + , CD8 + and CD56 + lymphocytes increased after the intensive protocol before falling below pre-exercise values at 1 h post-exercise . A relatively greater mobilisation of CD56 + and CD8 + cells accounts for the changes in CD54 + , CD18bright and CD53bright cell population s. Lymphocytes that enter and exit the circulation following exercise express high levels of AA molecules , which may mediate extravasation and post-exercise lymphocytopenia . This effect appears to be influenced by exercise intensity and not muscle damage Patients with T2DM have an increased risk of CVD . Prevention of CVD represents the major goal of all treatment of T2DM , and early intervention in those patients at particularly high risk is important . We measured the insulin sensitivity and plasma biomarkers of CVD to determine whether a home-based exercise training program improves biomarker levels and insulin sensitivity . Patients with T2DM ( n=12 ) , IGT ( n=4 ) and healthy control subjects ( n=9 ) were studied before and after eight weeks of exercise training by rowing ergometry at 65—70 % of peak oxygen uptake . Conclusions : 1 ) patients with T2DM have elevated plasma concentrations of CVD biomarkers compared to the matched control and IGT groups ; 2 ) a moderate to vigorous intensity home-based training program did not reduce plasma concentrations of these CVD markers ; 3 ) insulin sensitivity improved as a result of exercise training in the control group , but not in the T2DM group Objective Abnormal expression of cellular adhesion molecules may be related to endothelial dysfunction , a key feature in chronic heart failure . This study compares the effects of 10-wk supervised moderate-intensity continuous aerobic exercise ( CAE ) and intermittent aerobic exercise ( IAE ) programs on markers of endothelial damage , disease severity , functional and metabolic status , and quality -of-life in chronic heart failure patients . Design Fifty-seven patients between 41 and 81 yrs with New York Heart Association class II – III chronic heart failure and with a left ventricular ejection fraction of 35%–55 % were r and omized into three groups : nonexercising control , CAE , and IAE , which exercised three times a week for 10 wks . Endothelial damage was assessed by serum markers of vascular cell adhesion molecule-1 , serum intercellular adhesion molecule-1 , and nitric oxide ; disease severity was measured by left ventricular ejection fraction and N-terminal probrain natriuretic peptide ; metabolic status was evaluated by body composition analysis and lipid profile levels ; functional status was evaluated by cardiorespiratory exercise stress test and 6-min walking distance ; quality -of-life was assessed with Left Ventricular Dysfunction-36 and Short-Form 36 question naires at the baseline and at the end of the 10th week . Results Significant decreases in serum vascular cell adhesion molecule-1 or serum intercellular adhesion molecule-1 in IAE and CAE groups after training were found , respectively . Resting systolic and diastolic blood pressure , peak systolic and diastolic blood pressure , 6-min walking distance , and the mental health and vitality components of Short-Form 36 improved in the CAE group , whereas left ventricular ejection fraction and 6-min walking distance improved in the IAE group compared with the control group . Conclusions Both moderate-intensity CAE and IAE programs significantly reduced serum markers of adhesion molecules and prevented the change in VO2 in patients with chronic heart failure Based on previous studies showing an increase in circulating soluble intercellular adhesion molecule-1 ( sICAM-1 ) after exercise , we hypothesized that exercise may also increase serum levels of the vascular cell adhesion molecule-1 ( sVCAM-1 ) and sE- selection . In a prospect i ve controlled clinical trial , serum levels of sE-selectin , sICAM-1 and sVAM-1  were measured before and after two different exercise protocol s in healthy untrained men .  Lactate levels increased up to 12.7 mmol/L ( 95 % confidence interval : 10.1 - 15.9 ) and 3.6 mmol/L ( CI : 2.4 - 4.7 ) after ergometry and 
    Output:
    
Results Low-to-moderate intensity aerobic exercise favorably decreased CAMs in a variety of subject population s , while CAMs momentarily increased immediately following high-intensity aerobic exercise , which then returned to the pre-exercise level within several hours post-exercise .
Resistance exercise , regardless of its intensity , did not significantly influence CAMs .
Conclusion It is evident that the responses of CAMs are dependent upon the type and intensity of exercise performed .
The most common , favorable outcome was a decrease in CAMs following low-to-moderate intensity aerobic exercise , while high-intensity aerobic exercise showed a short-lived , momentary increase in CAMs , which returned to the pre-exercise level within a few hours post-exercise .
Resistance exercise , regardless of its intensity , neither significantly increased nor decreased CAMs .