***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: 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 A reduction in number and function of endothelial progenitor cells ( EPCs ) occurs in both physiologic aging and chronic heart failure ( CHF ) . We assessed whether disease and aging have additive effects on EPCs or whether beneficial effects of exercise training are diminished in old age . Methods We r and omized 60 patients with stable CHF and 60 referent controls to a training or a control group . To detect possible aging effects we included subjects below 55 ( young ) and above 65 years ( older ) . Subjects in the training group exercised four times daily at 60 % to 70 % of VO2max for four weeks under supervision . At baseline and after the intervention the number and function of EPCs were assessed . Results As compared with young referent controls , older referent controls showed at baseline a reduced EPC number ( young : 190 ± 37 CD34/KDR positive cells/ml blood ; older : 131 ± 26 CD34/KDR positive cells/ml blood ; p < 0.05 ) and function ( young : 230 ± 41 migrated cells/1000 plated cells ; older : 185 ± 28 cells/1000 plated cells ; p < 0.05 ) . In young and older CHF patients EPC-number ( young : 85 ± 21 CD34/KDR positive cells/ml blood ; older : 78 ± 20 CD34/KDR positive cells/ml blood ) and EPC-function ( young : 113 ± 26 cells/1000 plated cells ; older : 120 ± 27 cells/1000 plated cells ) were impaired . As a result of exercise training , EPC function improved by 24 % in older referent controls ( p < 0.05 ) , while it remained unchanged in young training referent controls and controls respectively . In young and older patients with CHF four weeks of exercise training result ed in a significant improvement in EPC numbers and EPC function ( young : number + 66 % function + 43 % ; p < 0.05 ; older : number + 69 % function + 36 % ; p < 0.05 ) . These results were accompanied by a significant increase in flow mediated dilatation in the training groups of young/older CHF patients and in older referent controls . Conclusions Four weeks of exercise training are effective in improving EPC number and EPC function in CHF patients . These training effects were not impaired among older patients , emphasizing the potentials of rehabilitation interventions in a patient group where CHF has a high prevalence 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 —Endothelial dysfunction plays a key role in atherogenesis . We prospect ively investigated the impact of noninvasive measurement of endothelial function on cardiovascular risk in peripheral arterial disease ( PAD ) . The study was specially aim ed at assessing whether brachial artery flow-mediated dilation ( FMD ) added to the predictive value of  ankle-brachial pressure index  ( ABPI ) . Methods and Results —Of 131 patients monitored for a mean of 23±10 months , 18 had a coronary event , 12 a cerebrovascular event , and 9 a peripheral event .  The median FMD was lower in patients with an event than in those without ( 5.8 % versus 7.6 % , P < 0.05 ) , whereas vasodilation to nitroglycerin was similar in the two groups . The cardiovascular event rate was higher in patients with FMD below the median versus those with FMD above the median ( P < 0.001 by log-rank test ) . In a Cox proportion hazard model , independent predictors of events were FMD below the median ( P < 0.01 ) , ABPI below the median ( P < 0.01 ) , and previous stroke ( P < 0.02 ) . Similar results were obtained when peripheral events were excluded from the analysis . Below-median ABPI and FMD combined was more accurate in predicting risk ( relative risk [ RR ] 13.0 ; 95 % CI , 3.0 to 56.2 ; P < 0.01 ) than ABPI ( RR , 6.4 ; 95 % CI , 1.4 to 29.1 ; P < 0.02 ) and FMD ( RR , 4.8 ; 95 % CI , 1.1 to 23.3 ; P < 0.05 ) alone . Conclusions —A low brachial artery FMD is an independent predictor of cardiovascular risk in patients with PAD and adds to the prognostic value of ABPI , which is currently the most powerful prognostic indicator in PAD AIMS Endothelial function is impaired in advanced chronic heart failure ( ACHF ) patients . We explored a possible association between endothelial function and subsequent mortality risk in ACHF . METHODS AND RESULTS We prospect ively assessed brachial flow-mediated dilation ( FMD ) in 82 consecutive New York Heart Association class IV ischaemic ACHF patients with a mean left ventricular ejection fraction ( LVEF ) of 22 + /- 3 % . Following overnight fasting and discontinuation of all medications for > or = 12 h ,  percent increase in FMD ( % FMD ) and nitroglycerin-mediated vasodilation were assessed using linear array ultrasound . All patients were followed for 14 + /- 2 months for adverse cardiovascular events , including death , hospitalization for CHF exacerbation , or myocardial infa rct ion . Patients were divided into two groups : those with an FMD lesser than or equal to the median % FMD of 4.6 % ( n = 41 ) and those with an FMD above the median ( n = 41 ) . Both groups were comparable regarding cardiovascular risk factors , LVEF , and concomitant medications . During follow-up , 22 ( 53.6 % ) patients with FMD lesser than or equal to the median had composite adverse cardiovascular events compared with only eight patients ( 19.5 % ) with FMD above the median ( P < 0. 
    Output:
    
This meta- analysis indicates that exercise training may be a therapeutic option to improve EPC levels and potentially to enhance endothelial function and repair in patients with heart failure