***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: OBJECTIVES To investigate the effect of 12 weeks of strength training in combination with a nonsteroidal anti-inflammatory drug ( NSAID ) , glucosamine , or placebo on muscle cross-sectional area ( CSA ) , strength ( primary outcome parameters ) , and function , power , pain , and satellite cell number ( secondary outcome parameters ) in patients with knee osteoarthritis ( OA ) . DESIGN Double-blinded , r and omized controlled trial . SETTING Hospital . PARTICIPANTS Patients ( N=36 ; 20 women , 16 men ; age range , 50 - 70y ) with bilateral tibiofemoral knee OA . A total of 181 patients were approached , and 145 were excluded . INTERVENTIONS Patients were r and omly assigned to treatment with the NSAID ibuprofen ( n=12 ) , glucosamine ( n=12 ) , or placebo ( n=12 ) during 12 weeks of quadriceps muscle strength training . MAIN OUTCOME MEASURES Muscle CSA and strength . RESULTS No differences between groups were observed in gains in muscle CSA . Training combined with ibuprofen increased maximal isometric strength by an additional .22Nm/kg ( 95 % confidence interval [ CI ] , .01-.42 ; P=.04 ) , maximal eccentric muscle strength by .38Nm/kg ( 95 % CI , .05-.70 ; P=.02 ) , and eccentric muscle work by .27J/kg ( 95 % CI , .01-.53 ; P=.04 ) in comparison with placebo . Training combined with glucosamine increased maximal concentric muscle work by an additional .24J/kg versus placebo ( 95 % CI , .06-.42 ; P=.01 ) . CONCLUSIONS In patients with knee OA , NSAID or glucosamine administration during a 12-week strength-training program did not improve muscle mass gain , but improved maximal muscle strength gain in comparison with treatment with placebo . However , we do not find that the benefits are large enough to justify taking NSAIDs or glucosamine Background Inflammation is the main cause of disease-associated muscle wasting . In a previous single blind study we have demonstrated improved recovery of muscle endurance following celecoxib treatment in hospitalized geriatric patients with acute infection . Here we further evaluate NSAID treatment with piroxicam in a double blind RCT and investigate the role of cytokines and heat shock proteins ( Hsp ) with respect to muscle performance . We hypothesized that NSAID treatment would preserve muscle performance better than antibiotic treatment alone , by reducing infection-associated inflammation and by increasing expression of cytoprotective Hsp . Methods Consecutive admissions to the geriatric ward were screened . 30 Caucasian patients , median age 84.5 years , with acute infection-induced inflammation and serum levels of CRP > 10 mg/L were included and r and omized to active treatment with 10 mg piroxicam daily or placebo . Assessment comprised general clinical and biochemical parameters , 25 cytokines in serum , intra- and extracellular Hsp27 and Hsp70 , Elderly Mobility Scale ( EMS ) scores , grip strength ( GS ) , fatigue resistance ( FR ) and lean body mass ( LBM ) . Patients were evaluated until discharge with a maximum of 3 weeks after treatment allocation . Results EMS scores , FR and grip work ( GW ) , a measure taking into account GS and FR , significantly improved with piroxicam , but not with placebo . Early decreases in IL-6 serum levels with piroxicam correlated with better muscle performance at week 2 . Basal expression of Hsp27 in monocytes without heat challenge ( WHC ) was positively correlated with FR at baseline and significantly increased by treatment with piroxicam compared to placebo . Profound modifications in the relationships between cytokines or Hsp and changes in muscle parameters were observed in the piroxicam group . Conclusions Piroxicam improves clinical ly relevant measures of muscle performance and mobility in geriatric patients hospitalized with acute infection-induced inflammation . Underlying mechanisms may include modifications in the cytokine network and increases in monocytic expression of cytoprotective Hsp27.Trial registration numberIS RCT N : IS RCT CONTEXT Plasma levels of the inflammatory biomarker C-reactive protein ( CRP ) predict cardiovascular risk , and retrospective studies suggest that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ( statins ) may lower CRP in a manner largely independent of low-density lipoprotein cholesterol ( LDL-C ) . However , prospect i ve trial data directly evaluating this anti-inflammatory effect of statins are not available . OBJECTIVE To test the hypothesis that pravastatin has anti-inflammatory effects as evidence d by CRP reduction . DESIGN , SETTING , AND PARTICIPANTS Community-based , prospect i ve , r and omized , double-blind trial including 1702 men and women with no prior history of cardiovascular disease ( primary prevention cohort ) and open-label study including 1182 patients with known cardiovascular disease ( secondary prevention cohort ) who provided at least baseline and 12-week blood sample s. The study was conducted in US office-based practice s from February to December 2000 . INTERVENTIONS Participants in the double-blind primary prevention trial were r and omly assigned to receive 40 mg/d of pravastatin ( n = 865 ) or placebo ( n = 837 ) for 24 weeks . Participants in the secondary prevention cohort received 40 mg/d of open-label pravastatin for 24 weeks . MAIN OUTCOME MEASURE Change in CRP levels from baseline to 24 weeks . RESULTS In the primary prevention trial , compared with placebo , pravastatin reduced median CRP levels by 16.9 % ( P<.001 ) at 24 weeks , reflecting a decrease of 0.02 mg/dL in the pravastatin group while no change in CRP levels was observed in the placebo group . This effect was seen as early as 12 weeks ( median reduction in CRP with pravastatin , 14.7 % ; P<.001 ) and was present among all prespecified subgroups according to sex , age , smoking status , body mass index , baseline lipid levels , presence of diabetes , and use of aspirin or hormone replacement therapy . No significant association was observed between baseline CRP and baseline LDL-C levels , end-of- study CRP and end-of- study LDL-C levels , or change in CRP and change in LDL-C levels over time . In linear regression analyses , the only significant predictors of change in CRP on a log scale were r and omized pravastatin allocation and baseline CRP levels ( P<.001 for both ) . Similar reductions in CRP levels were observed at 12 weeks ( -14.3 % ) and 24 weeks ( -13.1 % ) in the secondary prevention cohort treated with pravastatin ( P<.005 for both ) . CONCLUSIONS In this prospect i ve trial , pravastatin reduced CRP levels at both 12 and 24 weeks in a largely LDL-C-independent manner . These data provide evidence that statins may have anti-inflammatory effects in addition to lipid-lowering effects BACKGROUND Acute inflammation has a negative effect on the muscular system in elderly patients , compromising the outcome of the underlying disease . OBJECTIVE The aim of this study was to evaluate the effect of cyclooxygenase-2 ( COX-2 ) inhibition on muscle performance and mobility in hospitalized elderly patients with acute inflammation of infectious origin . METHODS In this single-blind , controlled trial , consecutively hospitalized elderly patients ( age > or = 70 years ) with inflammation ( C-reactive protein [ CRP ] levels > or = 10 mg/L ) due to acute infection were r and omly assigned to receive 2 weeks of treatment with the COX-2-selective inhibitor celecoxib , acetaminophen , or no supplementary medication ( control ) . The following variables were assessed at baseline and at 1 and 2 weeks ' follow-up : muscle fatigue resistance ( primary outcome measure ) ; grip strength and mobility ( secondary outcome measures ) ; and levels of the acute-phase markers CRP , interleukin (IL)-1beta , IL-6 , IL-10 , tumor necrosis factor-alpha ( TNF-alpha ) , and transforming growth factor-beta ( TGF-beta ) as explanatory variables . RESULTS Forty-three consecutively hospitalized elderly patients ( 31 women , 12 men ; mean [ SD ] age , 84 [ 6 ] years ) were enrolled . Fourteen patients received celecoxib , 14 received acetaminophen , and 15 received no supplementary medication . The change in fatigue resistance was significantly different between groups ( P = 0.021 , Kruskal-Wallis chi-square test ) , with significantly greater improvement in patients receiving celecoxib compared with the acetaminophen and control groups ( 63 % increase from baseline ; P < 0.05 ) . There were no significant between-group differences in changes in grip strength , mobility , IL-1beta , IL-6 , TNF-alpha , or TGF-beta . The changes in levels of IL-10 differed significantly between groups ( P = 0.020 , Kruskal-Wallis chi-square test ) , with greater improvement in the celecoxib group compared with the acetaminophen group ( P = 0.032 ) . CONCLUSION The results of this study suggest that COX-2-selective inhibition has a beneficial effect on muscle fatigue resistance in hospitalized elderly patients with acute inflammation of infectious origin . However , until further trials are conducted , the use of COX-2-selective inhibitors for this indication is not recommended Purpose Suppressing inflammaging at an early stage in life via exercise might prevent chronic diseases later in life . The aim was to investigate the influence of resistance training at different external loads on inflammatory markers in healthy young adults . Methods Serum was collected for basal levels of cytokines ( IL-1beta , IL-6 , IL-8 , sTNFR1 , IL-1RA , IL-10 and GM-CSF ) before and after 9 weeks exercise from 36 young ( 22 ± 2 years ) healthy subjects who were r and omized to  three times weekly supervised resistance training at either HImax ( n = 12 , 1 × 10–12 repetitions at 80 % 1RM ) , LO ( n = 12 , 1 × 10–12 repetitions at 40 % 1RM ) , or LOmax ( n = 12 , 1 × 10–12 repetitions at 40 % 1RM preceded by 60 repetitions at 20–25 % 1RM ) respectively . Results Overall , IL-8 increased ( p < 0.001 ) and IL-6 decreased ( p = 0.001 ) after training , but no significant time*group interaction was found ( respectively , p = 0.283 and p = 0.058 for IL-8 and IL-6 ) . When analyzed separately , IL-8 increased significantly in HImax ( p = 0.022 ) and LOmax ( p = 0.024 ) ; and IL-6 decreased significantly in LOmax ( p = 0.009 ) and LO ( p = 0.013 ) . No significant overall time effect was observed for sTNFR1 and IL-1RA ; however , in HImax sTNFR1 ( p = 0.031 ) and IL-1RA ( p = 0.014 ) increased significantly , but remained unchanged in LOmax and LO . IL-1beta , IL-10 and GM-CSF levels remained undetectable in most participants . Conclusions Nine weeks of resistance training — irrespective of the external load — have beneficial effects on circulating IL-8 and IL-6 . In addition , training at high external load increases the anti-inflammatory cytokines sTNFR1 and IL-1RA . The results of this study show that resistance training  has anti-inflammatory effects in healthy young persons and that the response of the different inflammatory mediators depends on the magnitude of the external load Background : Physical function and exercise capacity decline with age and are a major source of disability in older people . Recent evidence suggests a potential role for the renin – angiotensin system in modulating muscle function . We sought to examine the effect of the angiotensin-converting-enzyme ( ACE ) inhibitor perindopril on physical function in elderly people with functional impairment who had no heart failure or left ventricular systolic dysfunction . Methods : In this double-blind r and omized controlled trial , participants aged 65 years and older who had problems with mobility or functional impairment were r and omly assigned to receive either perindopril or placebo for 20 weeks . The primary outcome was the change in the 6-minute walking distance over the 20 weeks . Secondary outcomes were changes in muscle function , daily activity levels , self-reported function and health-related quality of life . Results : A total of 130 participants were enrolled in the study ( mean age 78.7 , st and ard deviation 7.7 years ) ; 95 completed the trial . At 20 weeks , the mean 6-minute walking distance was significantly improved in the perindopril group relative to the placebo group ( mean between-group difference 31.4 m , 95 % confidence interval [ CI ] 10.8 to 51.9 m ; p = 0.003 ) . There was a significant impact on health-related quality of life : although the mean score for part 1 of the EQ-5D question naire deteriorated over time in the 
    Output:
    
Articles on older humans with acute inflammation showed evidence that celecoxib and piroxicam could reduce inflammation and improve performance and that ibuprofen improves exercise‐induced muscle hypertrophy and gains in strength .
In younger humans , only the effects of AIDs combined with exercise were investigated ; no significant benefits of non‐selective COX‐inhibitors were reported , but improved strength gains with etanercept and reduced muscle soreness with celecoxib were noted .
Indomethacin  increased acute exercise‐induced inflammation and reduced satellite cell differentiation in exercising muscle .
Conclusions : Although AIDs showed significant reduction in inflammation‐induced muscle weakness in older hospitalised patients with acute inflammation , robust evidence is still lacking .
When combined with exercise , AIDs presented a protective effect against age‐related loss of muscle mass , thus enhancing muscle mass and performance .
The mechanism regulating muscle strength and its mass seems to differ between individuals of old and young age .
However , the effects seem drug‐specific and dose‐dependent and appear to be influenced by subjects ' trainability and the clinical context .