***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: INTRODUCTION Heart rate recovery , defined as the fall in heart rate during the first minute after exercise , is an indicator of autonomic function , and has been found to be an independent predictor of mortality after acute myocardial infa rct ion . Exercise training has several well-known benefits in terms of cardiorespiratory fitness , modifiable cardiovascular risk factors and prognosis after acute coronary events . However , there are no r and omized controlled studies in the literature evaluating the effects of exercise training per se , controlling for changes in medication and diet , on heart rate recovery . Thus , this study aims to assess the effects of exercise training on autonomic function in coronary artery disease patients recovering from acute myocardial infa rct ion . METHODS Thirty-eight patients following a first acute myocardial infa rct ion participated in this prospect i ve r and omized clinical trial . Patients were r and omized into two groups : exercise training or control . The exercise group participated in an 8-week aerobic exercise program , while the control received st and ard medical care and follow-up . Changes in hemodynamics at rest and at peak exercise ( heart rate , systolic and diastolic blood pressure , and rate pressure product ) , dietary intake , cardiorespiratory fitness , and heart rate recovery were assessed . RESULTS Medication and diet remained unchanged in both groups during the study period . The exercise-training group improved resting hemodynamics , particularly resting heart rate ( from 68.0 ± 9.2 to 62.6 ± 8.7 bpm , p=0.030 ) and systolic blood pressure ( from 135 ± 7.1 to 125.6 ± 11.3 mm Hg , p=0.012 ) , cardiorespiratory fitness ( from 30.8 ± 7.8 to 33.9 ± 8.3 ml/min/kg , p=0.016 ) , and heart rate recovery ( from 20 ± 6 to 24 ± 5 bpm , p=0.007 ) . No significant changes were observed in the control group . CONCLUSIONS Exercise training improved autonomic function , assessed by heart rate recovery , resting heart rate and systolic blood pressure , in the absence of changes in diet or medication Alterations in circulating angiogenic cells ( CAC ) and endothelial progenitor cells ( EPC ) , known to contribute to endothelial repair , could explain the reversal of endothelial function in response to exercise training . Moreover , training-induced vascular remodeling might affect the acute response of EPC and CAC following a single exercise bout . We studied the impact of exercise training on CAC function and numbers of CD34+/KDR+ EPC in patients with chronic heart failure ( CHF ) and we assessed the effect of acute exercise on CAC and EPC in sedentary and trained patients . Twenty-one sedentary CHF patients underwent 6-month exercise training  and were compared to a non-trained control group ( n = 17 ) and 10 healthy age-matched subjects . At baseline and follow-up , flow-mediated dilation was assessed and grade d exercise testing ( GXT ) was performed . Before and immediately after GXT , CAC migratory capacity was assessed in vitro and circulating CD34+/KDR+ EPC were quantified using flow cytometry . At baseline , CAC migration was significantly impaired in sedentary CHF patients but normalized acutely after GXT . Training corrected endothelial dysfunction , which coincided with a 77 % increase in CAC migration ( P = 0.0001 ) . Moreover , the GXT-induced improvement detected at baseline was no longer observed after training . Numbers of CD34+/KDR+ EPC increased following 6-month exercise training ( P = 0.021 ) , but were not affected by GXT , either prior or post-training . In conclusion , the present findings demonstrate for the first time that exercise training in CHF reverses CAC dysfunction and increases numbers of CD34+/KDR+ EPC , which is accompanied by improvement of peripheral endothelial function . The acute exercise-induced changes in CAC function wane with exercise training , suggesting that repetitive exercise bouts progressively lead to functional endothelial repair OBJECTIVE Muscle resistance training is often combined with aerobic endurance training during rehabilitation of patients with coronary artery disease . However , the clinical effects of additional lower-extremity low-intensity muscle resistance training during early rehabilitation ( within the first month after coronary revascularization ) in patients with coronary artery disease remain unclear . DESIGN Prospect i ve r and omized controlled trial . SUBJECTS Sixty patients with coronary artery disease . METHODS Subjects were r and omly assigned to early aerobic endurance training ( n = 30 ) or combined aerobic endurance and resistance muscle training ( n = 30 ) . Subjects performed 18 ( st and ard deviation 2 ) exercise sessions ( at 65 % VO(2peak ) , for 40 mins/session ) . In resistance muscle training , additional low-intensity ( 12 - 20 repetition maximum ) resistance muscle exercises were performed . The following parameters were evaluated : exercise capacity , body composition , blood lipid profile , glycaemic control , blood endothelial progenitor cell and cytokine content , and muscle performance . RESULTS A total of 47 patients with coronary artery disease completed the intervention . Total body lean tissue mass tended to increase with greater magnitude ( p = 0.07 ) , and blood high-density lipid cholesterol content increased with significantly greater magnitude in resistance muscle training ( p < 0.05 ) , compared with aerobic endurance training . Maximal exercise capacity , ventilatory threshold , and muscle performance increased , and steady-state exercise respiratory exchange ratio , and adipose tissue mass reduced significantly ( p < 0.05 ) , without differences between groups ( p < 0.05 ) . CONCLUSION In early aerobic endurance training intervention in patients with coronary artery disease , additional low-intensity resistance muscle training contributes to a greater increase in blood high-density lipid cholesterol content , and tends to affect lean tissue mass Background —In stable coronary artery disease ( CAD ) , exercise training has well-documented positive effects on arterial endothelial function . NO derived from endothelial NO synthase ( eNOS ) is regarded as a protective factor against atherosclerosis . The aim of the present study was to investigate the effects of exercise training on the endothelial function in relation to the expression of eNOS and Akt-dependent eNOS phosphorylation in the left internal mammary artery ( LIMA ) of patients with stable CAD . Methods and Results —In 17 training patients ( T ) and 18 control patients ( C ) , endothelium-dependent vasodilation and average peak flow velocity ( APV ) in response to  acetylcholine  were measured invasively at study beginning and after 4 weeks in the LIMA . In LIMA tissue sample d during bypass surgery , eNOS expression and content of pospho-eNOS-Ser1177 , Akt , and phospho-Akt were determined by Western blot and quantitative reverse transcriptase – polymerase chain reaction . After exercise training , LIMA APV in response to acetylcholine was increased by 56±8 % ( from + 48±8 % at beginning to + 104±11 % after 4 weeks , P < 0.001 ) . Patients in T had a 2-fold higher eNOS protein expression ( T 1.0±0.7 versus C 0.5±0.3 arbitrary units , P < 0.05 ) and 4-fold higher eNOS Ser1177-phosphorylation levels in LIMA-endothelium ( 1.2±0.9 versus 0.3±0.2 arbitrary units , P < 0.01 ) . A linear correlation was confirmed between Akt phosphorylation and phospho-eNOS levels ( R = 0.80 , P < 0.05 ) and between phospho-eNOS and & Dgr ; APV ( R = 0.59 , P < 0.05 ) . Conclusions —Exercise training in stable CAD leads to an improved agonist-mediated endothelium-dependent vasodilatory capacity . The change in acetylcholine-induced vasodilatation was closely related to a shear stress – induced/Akt-dependent phosphorylation of eNOS on Ser1177 BACKGROUND The molecular mechanisms by which physical training improves peripheral and coronary artery disease are poorly understood . Bone marrow-derived endothelial progenitor cells ( EPCs ) are thought to exert beneficial effects on atherosclerosis , angiogenesis , and vascular repair . METHODS AND RESULTS To study the effect of physical activity on the bone marrow , EPCs were quantified by fluorescence-activated cell sorter analysis in mice r and omized to running wheels ( 5.1+/-0.8 km/d , n=12 to 16 per group ) or no running wheel .  Numbers of EPCs circulating in the peripheral blood of trained mice were enhanced to 267+/-19 % , 289+/-22 % , and 280+/-25 % of control levels after 7 , 14 , and 28 days , respectively , accompanied by a similar increase of EPCs in the bone marrow and EPCs exp and ed from spleen-derived mononuclear cells . eNOS-/- mice and wild-type mice treated with N(G)-nitro-l-arginine methyl ester showed lower EPC numbers at baseline and a significantly attenuated increase of EPC in response to physical activity . Exercise NO dependently increased serum levels of vascular endothelial growth factor and reduced the rate of apoptosis in spleen-derived EPCs . Running inhibited neointima formation after carotid artery injury by 22+/-2 % . Neoangiogenesis , as assessed in a subcutaneous disc model , was increased by 41+/-16 % compared with controls . In patients with stable coronary artery disease ( n=19 ) , moderate exercise training for 28 days led to a significant increase in circulating EPCs and reduced EPC apoptosis . CONCLUSIONS Physical activity increases the production and circulating numbers of EPCs via a partially NO-dependent , antiapoptotic effect that could potentially underlie exercise-related beneficial effects on cardiovascular diseases Background —Exercise training ( ET ) has been shown to improve regional perfusion in ischemic syndromes . This might be partially related to a regeneration of diseased endothelium by circulating progenitor cells ( CPCs ) or CPC-derived vasculogenesis . The aim of the present study was to determine whether ischemic stimuli during ET are required to promote CPC mobilization in patients with cardiovascular diseases . Methods and Results — Patients with peripheral arterial occlusive disease ( PAOD ) were r and omized to 4 weeks of daily ischemic ET or control ( group A ) . Successfully revascularized patients with PAOD were r and omized to 4 weeks of daily nonischemic ET or control ( group B ) . Patients with stable coronary artery disease were subjected to 4 weeks of subischemic ET or control ( group C ) . At baseline and after 4 weeks , the number of KDR+/CD34 + CPCs was determined by fluorescence-activated cell sorting analysis . Levels of vascular endothelial growth factor ( VEGF ) were measured by ELISA . A Matrigel assay was used to quantify CPC integration into vascular structures . Expression of the homing factor CXCR4 was determined by reverse transcription-polymerase chain reaction . In group A only , ischemic ET increased VEGF levels by 310 % ( P<0.05 versus control ) associated with an increase in CPCs by 440 % ( P<0.05 versus control ) , increased CXCR4 expression , and enhanced integration of CPCs into endothelial networks . In contrast , subischemic ET in groups B and C increased CXCR4 expression and CPC integration . Conclusions —In training programs , symptomatic tissue ischemia seems to be a prerequisite for CPC mobilization . However , ischemic and subischemic ET programs affect CXCR4 expression of CPCs , which might lead to an improved CPC integration into endothelial networks Background In cardiac rehabilitation , 40 - 60-min exercise training sessions are advised . However , because of the increasing coronary artery disease ( CAD ) prevalence and higher workload for cardiac rehabilitation centres , it remains unclear whether 40-min exercise training sessions are equally effective as 60-min exercise training sessions . Design Prospect i ve r and omized clinical trial . Methods One hundred and thirty-four CAD patients were included in a 7-week rehabilitation programme . All patients exercised 3 days per week , at a heart rate corresponding to 65 % of baseline peak oxygen uptake ( VO2peak ) . Patients were r and omized in two groups : 40 versus 60-min exercise training sessions .  Changes of body anthropometrics , resting haemodynamics , exercise capacity and ventilatory threshold , blood plasma lipid profile and C-reactive protein level were assessed . Results As a result of rehabilitation , exercise capacity , ventilatory threshold , and blood plasma lipid profile improved significantly in the total population ( P < 0.05 ) , without differences between subgroups ( P > 0.05 ) . Body weight and waist circumference decreased significantly in total population ( P < 0.01 ) , but with a greater magnitude in the 40 versus 60-min exercise session group ( P < 0.05 ) . Conclusions In the early rehabilitation of CAD patients , 40-min exercise training sessions seem to be at least as effective for improving body anthropometrics , blood plasma lipid profile and exercise capacity , as compared with 60 
    Output:
    
In summary , exercise training seems to increase the number of circulating EPCs , which could contribute to vascular regeneration and angiogenesis .
These positive effects of chronic exercise seem to be closely related to the bioavailability of nitric oxide , including increased activity of endothelial nitric oxide synthase and antioxidant enzymes , and activation of matrix metalloproteinase 9