title: Preventive Effects of 10-Day Supplementation With Saffron and Indomethacin on the Delayed-Onset Muscle Soreness A double-blind, placebo-controlled study of acetylsalicylic acid (ASA) in trained runners. Effects of Caffeine and Aspirin on Light Resistance Training Performance, Perceived Exertion, and Pain Perception Effects of low-dose ibuprofen supplementation and resistance training on bone and muscle in postmenopausal women: A randomized controlled trial Influence of acetaminophen and ibuprofen on skeletal muscle adaptations to resistance exercise in older adults. Nonsteroidal anti-inflammatory drug use and endurance during running in male long-distance runners. Nonsteroidal anti-inflammatory therapy after eccentric exercise in healthy older individuals. A Randomized Controlled Trial of the Effect of Naproxen on Delayed Onset Muscle Soreness and Muscle Strength The COX-2 specific inhibitor Valdecoxib versus tramadol in acute ankle sprain: a multicenter randomized, controlled trial. Indomethacin does not influence natural cell-mediated cytotoxic response to endurance exercise. The isolated and combined effects of selected physical activity and ibuprofen on delayed-onset muscle soreness Effects of ibuprofen on exercise-induced muscle soreness and indices of muscle damage. The Effects of Ibuprofen on Delayed Muscle Soreness and Muscular Performance After Eccentric Exercise Non-steroidal anti-inflammatory drugs and renal response to exercise: a comparison of indomethacin and nabumetone. Ibuprofen versus placebo effect on acute kidney injury in ultramarathons: a randomised controlled trial The effect of a prophylactic dose of flurbiprofen on muscle soreness and sprinting performance in trained subjects. Prophylactic misuse and recommended use of non-steroidal anti-inflammatory drugs by athletes Effect of ibuprofen use on muscle soreness, damage, and performance: a preliminary investigation. Aspirin does not affect exercise performance. The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training. A Systematic Examination of the Citation of Prior Research in Reports of Randomized, Controlled Trials
abstract: Objective :  Delayed-onset muscle soreness ( DOMS )  often occurs after unaccustomed eccentric exercise and reduces exercise performance . We aim ed to study the preventive effects of saffron and indomethacin on the biochemical and functional indicators of DOMS after 1-session eccentric exercise . Design : A 10-day , r and omized , double-blind , placebo-controlled , pretest – posttest design . Setting : Controlled research laboratory . Participants : Thirty-nine nonactive male university students r and omly divided into  saffron ( n = 12 ) , indomethacin ( n = 12 ) , and control ( n = 15 ) groups . Interventions : Saffron group received 1 capsule containing dried saffron powder ( n = 12 , 300 mg/d ) , indomethacin group received 75 mg indomethacin ( n = 12 , 25 mg thrice a day ) , and control group ( n = 15 ) received placebo capsules , 1 week before and 3 days after eccentric exercise . Ten days before and 24 , 48 , and 72 hours after muscle soreness protocol , the maximum isometric and isotonic forces , plasma creatine kinase ( CK ) , plasma lactate dehydrogenase ( LDH ) , perceived pain , knee range of movement , and thigh circumference were measured . Muscle soreness protocol was performed with a weight load equal to 80 % of the maximum isotonic force in 4 sessions with 20 repetitions and 3-minute rest in between . Main Outcome Measures : This study shows that 10-day supplementation with 300 mg saffron significantly decreased the CK and LDH concentrations ( P < 0.0001 ) . In the saffron group , there was no decline in maximum isometric and isotonic forces after eccentric exercise , but a significant decline in the isometric force was observed in the control group ( P < 0.0001 ) . No pain was reported in the saffron group , whereas the indomethacin group experienced pain before 72 hours ( P < 0.001 ) . Conclusions : Results obtained from the current novel research indicate a strong preventive effect of 10-day supplementation with saffron on the DOMS . Clinical Relevance : The saffron can be used to prevent DOMS and alleviate the DOMS symptoms Acetylsalicylic acid ( ASA ) is a short-acting oral inhibitor of the cyclooxygenase enzyme . Ingestion of ASA is associated with a decrease in prostagl and ins , including those of the E2 series , as well as prostacyclin , and thromboxane . Consumption of therapeutic doses is associated with decreased pain and inflammation and is therefore used in a variety of inflammatory conditions . Platelet aggregation is also inhibited . Because of these observations , and the fact that platelet aggregation has been noted to be altered during exercise , the effects of ASA on exercise tolerance was of interest . We studied 17 healthy male volunteers who regularly ran as a source of exercise . During the study they ingested either 650 mg of ASA or placebo 30 min before running 2 miles ( 3.2 km ) . Outcome of the double-blind crossover study was measured by the time required to run a 2-mile distance . No differences between ASA or placebo were noted in the subjects . These data suggest that 650 mg of ASA as a premedication has little effect on exercise performance in normal endurance runners . However , whether ASA may affect pain after exercise or whether other dosage intervals would be more beneficial needs further study Hudson , GM , Green , JM , Bishop , PA , and Richardson , MT . Effects of caffeine and aspirin on light resistance training  performance , RPE , and pain perception . J Strength Cond Res 22(6 ) : 1950 - 1957 , 2008-This study compared independent effects of caffeine and aspirin on muscular endurance ( repetitions ) , heart rate ( HR ) , perceived exertion ( RPE ) , and perceived pain index ( PPI ) during light resistance training bouts performed to volitional failure . It was hypothesized that the hypoalgesic properties of these ergogenic aids would decrease pain perception and potentially result in enhanced performance . College-aged men ( n = 15 ) participated in a within-subjects , double-blind study with three independent , counterbalanced sessions wherein aspirin ( 10 mg·kg−1 ) , caffeine ( 6 mg·kg−1 ) , or matched placebo were ingested 1 hour before exercise , and  RPE , HR , PPI , and repetitions  ( per set and total per exercise ) were recorded at 100 % of individual , predetermined , 12-repetition maximum for leg extensions ( LE ) and seated arm curls ( AC ) . Repeated- measures analyses of variance were used for between-trial comparisons . Caffeine result ed in significantly greater ( p < 0.05 ) HR ( LE and AC ) , total repetitions ( LE ) , and repetitions in set 1 ( LE and AC ) compared with aspirin and placebo . Aspirin result ed in significantly higher PPI in set 1 ( LE ) . In LE , 47 % of participants ' performance exceeded the predetermined effect size ( ≥ 5 repetitions ) for total repetitions , with 53 % exceeding the effect size ( ≥ 2 repetitions ) for repetitions in set 1 with caffeine ( vs. placebo ) . In AC , 53 % ( total repetitions ) and 47 % ( set 1 repetitions ) of participants exceeded effect sizes with caffeine ( vs. placebo ) , with only 13 % experiencing decrements in performance ( total repetitions ) . Aspirin also produced a higher PPI and RPE overall and in set 1 ( vs. placebo ) . This study demonstrates that caffeine significantly enhanced resistance training performance in LE and AC , whereas aspirin did not . Athletes may improve their resistance training performance by acute ingestion of caffeine . As with most ergogenic aids , our analyses indicate that individual responses vary greatly Purpose To compare the effects of nine months of exercise training and ibuprofen supplementation ( given immeditately after exercise sessions ) on bone and muscle in postmenopausal women . Methods In a double-blind r and omized trial , participants ( females : n = 90 , mean age 64.8 , SD 4.3 years ) were assigned ( computer generated , double blind ) to receive supervised resistance training or stretching 3 days/week , and ibuprofen ( 400 mg , post-exercise ) or placebo ( i.e. 4 groups ) for 9 months . In this proof-of-concept study the sample size was halved from required 200 identified via 90 % power calculation . Baseline and post-intervention testing included : Dual energy x-ray absorptiometry ( DXA ) for lumbar spine , femoral neck , and total body areal bone mineral density ( aBMD ) ; geometry of proximal femur ; total body lean tissue and fat mass ; predicted 1-repetition maximum muscle strength testing ( 1RM ; biceps curl , hack squat ) . Results Exercise training or ibuprofen supplementation had no effects on aBMD of the lumbar spine , femoral neck , and total body . There was a significant exercise × supplement × time interaction for aBMD of Ward 's region of the femoral neck ( p = 0.015 ) with post hoc comparison showing a 6 % decrease for stretching with placebo vs. a 3 % increase for stretching with ibuprofen ( p = 0.017 ) . Resistance training increased biceps curl and hack squat strength vs. stretching ( 22 % vs. 4 % and 114 % vs. 12 % , respectively ) ( p < 0.01 ) and decreased percent body fat compared to stretching ( 2 % vs. 0 % ) ( p < 0.05 ) . Conclusions Ibuprofen supplementation provided some benefits to bone when taken independent of exercise training in postmenopausal women . This study provides evidence towards a novel , easily accessible stimulus for enhancing bone health [ i.e. ibuprofen ] Evidence suggests that consumption of over-the-counter cyclooxygenase ( COX ) inhibitors may interfere with the positive effects that resistance exercise training has on reversing sarcopenia in older adults . This study examined the influence of acetaminophen or ibuprofen consumption on muscle mass and strength during 12 wk of knee extensor progressive resistance exercise training in older adults . Thirty-six individuals were r and omly assigned to one of three groups and consumed the COX-inhibiting drugs in double-blind placebo-controlled fashion : placebo ( 67 ± 2 yr ; n = 12 ) , acetaminophen ( 64 ± 1 yr ; n = 11 ; 4 g/day ) , and ibuprofen ( 64 ± 1 yr ; n = 13 ; 1.2 g/day ) . Compliance with the resistance training program ( 100 % ) and drug consumption ( via digital video observation , 94 % ) , and resistance training intensity were similar ( P > 0.05 ) for all three groups . Drug consumption unexpectedly increased muscle volume  ( acetaminophen : 109 ± 14 cm(3 ) , 12.5 % ; ibuprofen : 84 ± 10 cm(3 ) , 10.9 % ) and muscle strength  ( acetaminophen : 19 ± 2 kg ; ibuprofen : 19 ± 2 kg ) to a greater extent ( P < 0.05 ) than placebo ( muscle volume : 69 ± 12 cm(3 ) , 8.6 % ; muscle strength : 15 ± 2 kg ) , when controlling for initial muscle size and strength . Follow-up analysis of muscle biopsies taken from the vastus lateralis before and after training showed muscle protein content , muscle water content , and myosin heavy chain distribution were not influenced ( P > 0.05 ) by drug consumption . Similarly , muscle content of the two known enzymes potentially targeted by the drugs , COX-1 and -2 , was not influenced ( P > 0.05 ) by drug consumption , although resistance training did result in a drug-independent increase in COX-1 ( 32 ± 8 % ; P < 0.05 ) . Drug consumption did not influence the size of the nonresistance-trained hamstring muscles ( P > 0.05 ) . Over-the-counter doses of acetaminophen or ibuprofen , when consumed in combination with resistance training , do not inhibit and appear to enhance muscle hypertrophy and strength gains in older adults . The present findings coupled with previous short-term exercise studies provide convincing evidence that the COX pathway(s ) are involved in the regulation of muscle protein turnover and muscle mass in humans CONTEXT The effect of ibuprofen on pain tolerance during exercise is controversial , and its effects on endurance performance have been poorly investigated . OBJECTIVE To investigate the effect of prophylactic administration of the nonsteroidal anti-inflammatory drug ibuprofen on the time until the self-report of fatigue ( tlim ) in runners with exercise-induced muscle damage . DESIGN R and omized controlled clinical trial . SETTING Laboratory . PATIENTS OR OTHER PARTICIPANTS Twenty healthy male long-distance runners ( age = 18.8 ± 0.4 years , maximal oxygen consumption = 55.5 ± 5.9 mL·kg(-1)·min(-1 ) ) . INTERVENTION(S ) Participants were assigned to 2 groups ( ibuprofen group = 10 , placebo group = 10 ) to perform tlim trials ( speed corresponded to their previously determined secondventilatory thresholds ) 48 hours before and 48 hours after the induction of a lower limb muscle-damage protocol ( isokinetic dynamometry ) . One hour before the second tlim trial , the ibuprofen group received 1.2 g ibuprofen , and the placebo group received lactose orally . MAIN OUTCOME MEASURE(S ) Time until self-reported fatigue , heart rate , respiratory quotient , oxygen consumption , and perceived exertion were recorded during each tlim test . RESULTS Both groups reported increases in muscle pain in the knee extensors and flexors 48 hours after the muscle-damage protocol . We observed a reduction in the endurance performance of both groups ( P < .01 ) but no difference between groups ( P = .55 ) . CONCLUSIONS Ibuprofen did not reduce the effect of muscle damage and pain on performance . Prophylactic use of nonsteroidal anti-inflammatory drugs did not have an ergogenic effect on running performance after exercise-induced muscle damage in male long-distance runners BACKGROUND Aging is associated with greater susceptibility to muscle injury and soreness after exercise . Although elderly persons regularly consume nonsteroidal anti-inflammatory drugs ( NSAIDs ) , it is not clear that NSAIDs alleviate muscle dysfunction and /or inflammation following injurious exercise . METHODS In this double-blind crossover study , 10 men and 5 women ( aged 60 + /- 2 years , mean + /- SE ) consumed naproxen sodium or placebo for 10 days after performing 64 unilateral eccentric ( ECC ) knee extensions using 75 % of the ECC 1-repetition maximum .  Strength was measured before , 3 days after , and 10 days after each bout . Injury and soreness were assessed using magnetic resonance images of m. quadriceps femoris ( QF ) and a visual analog scale . RESULTS Three days after exercise , concentric strength loss was greater for placebo ( -32 + /- 9 % ) than NSAID ( -6 + /- 8 % ; p = .0064 ) . Likewise , isometric strength declined less for NSAID than placebo ( -12 + /- 7 % vs -24 + /- 4 % ; p = .0213 ) , and thigh soreness while rising from a chair was greater for placebo ( p < or = .0393 ) than NSAID ( 43 + /- 7 mm vs 26 + /- 7 mm ) . QF cross-sectional area ( cm(2 ) ) showing elevated T(2 ) was 27 % and 35 % greater ( p < or = .0096 ) for placebo on Days 3 and 10 , respectively . CONCLUSIONS Naproxen sodium attenuated muscle injury , strength loss , and soreness following ECC exercise in older individuals and may be beneficial during the early stages of increased physical activity Objective To determine the effect of naproxen in attenuating the symptoms ( muscle soreness level ) and signs ( plasma creatine kinase [ CK ] activity and muscular strength decrement ) of delayed onset muscle soreness ( DOMS ) induced by repeated bouts of eccentric exercise . Design The design was a r and omized , double-blind , placebo-controlled , crossover trial with two testing phases of 8 days ' duration that were separated by a “ washout ” period of 7 days . Setting University-based sports science center . Participants Twenty healthy male volunteers who responded to a notice in the university 's athletic complex . Interventions Eccentric single-leg exercises were performed on days 1 , 3 , and 4 to induce DOMS in the quadriceps muscles . Naproxen or placebo tablets ( 500 mg ) were taken orally twice per day beginning on day 2 and continuing until the end of the testing phase . Main Outcome Measures Perception of muscle soreness and knee extensor torque were evaluated daily throughout each phase . Plasma CK levels were evaluated on days 1 , 3 , 6 , and 8 of each phase . Results After the eccentric exercise , plasma CK levels were similarly elevated in both naproxen and placebo conditions ( F = 1.42 ; p = 0.25 ) . After DOMS developed , naproxen reduced the perception of soreness on day 3 , when muscle soreness was highest ( F = 2.20 ; p = 0.04 ) . After treatments with naproxen , peak quadriceps torque during leg extension at 60 ° /s was higher than that after treatment with the placebo ( F = 4.77 ; p = 0.04 ) . There were no significant differences between the naproxen and placebo conditions for leg extension at 180 ° /s ( F = 1.66 ; p = 0.21 ) and 300 ° /s ( F = 0.71 ; p = 0.41 ) . Conclusion The data indicate that therapeutic doses of naproxen do not prevent CK release into the plasma but decrease the perception of muscle soreness and positively influence quadriceps peak torque BACKGROUND The cyclooxygenase-2 specific inhibitor valdecoxib has not been approved in the United States for treatment of acute pain .  HYPOTHESIS Valdecoxib 20 mg twice daily or once daily ( both with a 40-mg loading dose ) is not clinical ly inferior to tramadol for treating the signs and symptoms of acute ankle pain . STUDY DESIGN R and omized , controlled clinical trial ; Level of evidence , 1 . METHODS Patients ( N = 829 ) with acute first- or second-degree ankle sprain received 7 days ' treatment with valdecoxib 20 mg either twice daily or once daily ( both with 40-mg loading dose ) , tramadol 50 mg 4 times daily , or placebo . The primary end point was Patient 's Assessment of Ankle Pain visual analog scale on day 4 ; a test of noninferiority compared valdecoxib with tramadol . RESULTS On day 4 , both valdecoxib doses were significantly better versus placebo and were comparable with tramadol in relieving ankle pain . On day 7 , valdecoxib , but not tramadol , significantly reduced pain versus placebo . On days 4 and 7 , more patients resumed normal walking with valdecoxib ( 45%-47 % and 73%-79 % , respectively ) than with placebo ( 35 % and 64 % , respectively ) or tramadol ( 38 % and 67 % , respectively ) . In contrast to valdecoxib , the number of withdrawals due to adverse events was significantly higher in the tramadol group ( 12.2 % vs 3.4 % ; P = .0005 ) . CONCLUSIONS Valdecoxib was comparable with tramadol and was significantly better than placebo in treating acute ankle sprain , and it enabled more patients to resume normal walking on days 4 and 7 . Both valdecoxib and tramadol were well tolerated Natural cell-mediated cytotoxicity ( NCMC ) has been shown to be attenuated during recovery from high-intensity or prolonged exercise . Two theories have been proposed to explain the transient suppression of NCMC : prostagl and in-induced inhibition of natural killer ( NK ) cell activity or a numerical redistribution of NK cells . This study was design ed to examine the effects of oral indomethacin ( a prostagl and in inhibitor ) on NCMC before and after 1 h of high-intensity running ( 85 % maximal oxygen uptake ) . A secondary purpose was to compare whole blood and isolated peripheral blood mononuclear cell assay procedures for assessing NCMC . Ten male distance runners completed two trials that were preceded by either 48 h of indomethacin ( Indo ; 150 mg/day ) or no treatment ( control ) . NK ( CD3(-)/CD16(+)/CD56(+ ) ) cell concentrations were significantly elevated postexercise but were not affected by Indo . NCMC was significantly suppressed at 1.5 h of recovery relative to preexercise only with the whole blood assay procedure . Indo was not found to influence NCMC , leukocyte , or lymphocyte subset concentrations . Mean cytotoxic response was significantly greater with the whole blood method Delayed-onset  muscle soreness  refers to the skeletal muscle pain that is experienced following eccentric exercise . The aim of the present study was to examine the physiological effects of physical activity with or without ibuprofen on delayed onset muscle soreness . Forty-four non-athletic male volunteers ( age 24.3 ± 2.4 years ) were r and omly assigned to one of four groups : physical activity ( n = 11 ) , ibuprofen ( n = 11 ) , physical activity and ibuprofen ( combination , n = 11 ) , or control ( n = 11 ) . The physical activity programme comprised 5 min of walking and jogging , 10 min of static stretching of the h and s and shoulder girdle , and 5 min of concentric movements with sub-maximal contractions . The total amount of ibuprofen consumed by a single individual was 2800 mg ; this was taken from 1 h before the eccentric actions up to 48 h after it . Delayed onset muscle soreness was induced by performing 70 eccentric contractions of the biceps muscle of the non-dominant side on a modified arm curl machine . Perceived muscle soreness , maximal eccentric contraction , creatine kinase enzyme activity and elbow range of motion were assessed 1 h before and 1 , 24 and 48 h after the eccentric actions . The results indicated that , after the eccentric actions , soreness increased ( P < 0.001 ) across time in all groups , with the highest values being recorded at 24 h. At 24 and 48 h , greater soreness ( P < 0.001 ) was observed in the control group than in the physical activity and combination groups . After the eccentric actions , creatine kinase increased and was elevated ( P < 0.001 ) compared with baseline in all groups , with values returning to baseline in the physical activity and combination groups by 48 h. However , creatine kinase in the control and ibuprofen groups was still significantly higher than at baseline after 48 h. Creatine kinase was higher ( P < 0.001 ) in the control group than in physical activity and combination groups at 24 and 48 h. There was also a reduction ( P < 0.001 ) in elbow range of motion across time . This reduction in elbow range of motion was greater ( P < 0.001 ) in the control and ibuprofen groups than in the physical activity and combination groups at 1 , 24 and 48 h. The reduction in maximum eccentric contraction was greater ( P < 0.001 ) in the control and ibuprofen groups than in the physical activity group at 24 and 48 h and the combination group at 48 h. In conclusion , the results add to our underst and ing of the effects of physical activity and the combination of physical activity and ibuprofen in reducing the severity of muscle soreness induced by eccentric exercise . Physical activity conducted before eccentric exercise alleviates muscle soreness . Our results indicate that physical activity with or without ibuprofen helps to prevent delayed-onset muscle soreness Thirty-two volunteers participated in a two-period crossover study in which ibuprofen was tested against an identical placebo for its effectiveness in reducing  muscle soreness and damage  after two bouts of downhill running .  Subjective soreness , quadriceps isometric strength and isometric endurance time at 50 percent of maximum strength , serum activities of creatine kinase , lactate dehydrogenase and aspartate transaminase and serum levels of creatinine and urea were recorded at intervals up to 72 hours after exercise . Each downhill run produced muscle soreness , and a decline in muscle strength and 50 percent endurance time , although these parameters were unaffected by ibuprofen treatment . All serum parameters measured increased after both runs , but for the three enzymes this increase was smaller after the second run . Serum creatine kinase and urea levels were higher in the ibuprofen group after both runs . These results indicate that ibuprofen is not an appropriate treatment for delayed onset muscle soreness and damage The purpose of this study was to examine the effects of ibuprofen on  delayed onset muscle soreness ( DOMS ) , indirect markers of muscle damage and muscular performance . Nineteen subjects ( their mean [ ± SD]age , height , and weight was 24.6 ± 3.9 years , 176.2 ± 11.1 cm , 77.3 ± 18.7 kg ) performed the eccentric leg curl exercise to induce muscle soreness in the hamstrings . Nine subjects took an ibuprofen pill of 400 mg every 8 hours within a period of 48 hours , whereas 10 subjects received a placebo r and omly ( double blind ) . White blood cells ( WBCs ) and creatine kinase ( CK ) were measured at pre-exercise , 4–6 , 24 , and 48 hours after exercise and maximal strength ( 1 repetition maximum ) . Vertical jump performance and knee flexion range of motion ( ROM ) were measured at pre-exercise , 24 and 48 hours after exercise . Muscle soreness increased ( p < 0.05 ) in both groups after 24 and 48 hours , although the ibuprofen group yielded a significantly lower value ( p < 0.05 ) after 24 hours . The WBC levels were significantly ( p < 0.05 ) increased 4–6 hours post-exercise in both groups with no significant difference ( p > 0.05 ) between the 2 groups . The CK values increased ( p < 0.05 ) in the placebo group at 24 and 48 hours postexercise , whereas no significant differences ( p > 0.05 ) were observed in the ibuprofen group . The CK values of the ibuprofen group were lower ( p < 0.05 ) after 48 hours compared with the placebo group . Maximal strength , vertical jump performance , and knee ROM decreased significantly ( p < 0.05 ) after exercise and at 24 and 48 hours postexercise in both the placebo and the ibuprofen groups with no differences being observed ( p > 0.05 ) between the 2 groups . The results of this study reveal that intake of ibuprofen can decrease muscle soreness induced after eccentric exercise but can not assist in restoring muscle function Nabumetone , a newer non-steroidal anti-inflammatory drug ( NSAID ) which preferentially blocks cyclo-oxygenase-2 activity , may be less nephrotoxic than indomethacin . This study tested whether nabumetone has effects different from those of indomethacin on exercise-induced changes in renal function and the renin-aldosterone system . In a r and omized fashion , ten subjects were studied after indomethacin ( 100 mg ) , nabumetone ( 1 g ) or no medication  ( control ) administered orally at 22.00 hours on the day before each study day , and again at 8.00 hours upon arrival at the laboratory . Renal function was studied at baseline , during grade d 20-min exercise sessions at 25 % , 50 % and 75 % of the maximal oxygen uptake rate , and subsequently during two 1-h recovery periods . Heart rate , arterial blood pressure , cardiac output and plasma catecholamines at rest and during exercise were not altered by indomethacin or nabumetone . Indomethacin decreased urinary rates of excretion of 6-oxo-prostagl and in F(1alpha ) ( 6-oxo-PGF(1alpha ) ) and thromboxane B(2 ) in all study periods . Nabumetone decreased 6-oxo-PGF(1alpha ) excretion during and after exercise . Excretion rates for PGE(2 ) did not change . Neither indomethacin nor nabumetone changed baseline values or exercise-induced decreases in renal plasma flow or glomerular filtration rate . Indomethacin , but not nabumetone , decreased sodium excretion , urine flow rate and free water clearance . The renal response to exercise , however , remained unchanged . In contrast with nabumatone , indomethacin decreased the plasma renin concentration . Thus , during exercise , nabumetone may decrease the excretion of 6-oxo-PGF(1alpha ) by inhibition of cyclo-oxygenase-1 or by inhibition of specific exercise-induced activation of cyclo-oxygenase-2 , or both . None of the drugs changed the renal response to exercise . Inhibition by indomethacin of angiotensin II and thromboxane A(2 ) synthesis may , during exercise , counterbalance renal vasoconstriction caused by blockade of vasodilatory prostagl and ins Background Despite concerns that non-steroidal anti-inflammatory drugs ( NSAIDs ) contribute to acute kidney injury ( AKI ) , up to 75 % of ultramarathon runners ingest these during competition . The effect of NSAID on AKI incidence in ultramarathon runners is unclear . Methods Multisite r and omised double-blind placebo-controlled trial in the Gobi , Atacama , Ecuador and Sri Lankan deserts to determine whether ibuprofen ( 400 mg every 4 hours ) would be non-inferior to placebo during a 50-mile ( 80 km ) foot race . The primary outcome was incidence of AKI defined as severity categories of ‘ risk ’ of injury of 1.5 × baseline creatinine ( Cr ) or ‘ injury ’ as 2 × Cr , combined to calculate total incidence at the finish line . Non-inferiority margin for difference in AKI rates was defined as 15 % . Results Eighty-nine participants ( 47 % ibuprofen and 53 % placebo ) were enrolled with similar demographics between groups .  The overall incidence of AKI was 44 % . Intent-to-treat analysis found 22 ( 52 % ) ibuprofen versus 16 ( 34 % ) placebo users developed AKI ( 18 % difference , 95 % CI –4 % to 41 % ; OR 2.1 , 95 % CI 0.9 to 5.1 ) with a number needed to harm of 5.5 . Greater severity of AKI was seen with ibuprofen compared with placebo ( risk=38 % vs 26 % ; 95 % CI –9 % to 34 % ; injury=14 % vs 9 % ; 95 % CI –10 % to 21 % ) . Slower finishers were less likely to encounter AKI ( OR 0.67 , 95 % CI 0.47 to 0.98 ) and greater weight loss ( −1.3 % ) increased AKI ( OR 1.24 , 95 % CI 1.00 to 1.63 ) . Conclusion There were increased rates of AKI in those who took ibuprofen , and although not statistically inferior to placebo by a small margin , there was a number needed to harm of 5.5 people to cause 1 case of AKI . Consideration should therefore be taken before ingesting NSAID during endurance running as it could exacerbate renal injury . Trial registration number NCT02272725 The aim of this study was to examine the effects of a prophylactic dose of a local , transcutaneously administered , non-steroidal anti-inflammatory drug on muscle soreness , muscle damage and sprinting performance in young trained males . Twenty-five subjects aged 19+/-3 years , actively participating in rugby union and field hockey , were familiarized with the test procedure and then divided at r and om into an experimental group ( n = 13 ) and a control group ( n = 12 ) . The experimental group received two patches , each containing 40 mg flurbiprofen ( TransAct LAT ) , 12 h before an exercise bout design ed to produce delayed-onset soreness ( DOMS ) . The control group received identical non-medicated placebo patches at the same time . Delayed-onset muscle soreness was induced by an exercise protocol consisting of drop jumps ( seven sets of 10 repetitions ) . Serum creatine kinase activity , muscle soreness , muscle girth and acceleration in a maximal sprint over 30 m were measured before the induction of DOMS and at 12 , 24 , 48 and 72 h thereafter . Plasma lactate concentration was measured 3 min after the 30-m sprint tests . Subjects in both groups had significantly more pain at 24 and 48 h compared with at 12 and 72 h ( P < 0.05 ; Friedman two-way analysis of variance ) . Thigh girth and serum creatine kinase did not change throughout the experiment . Although plasma lactate concentrations were elevated after the 30-m sprint , there were no differences between groups or as a result of DOMS . The greatest acceleration occurred between 5 and 10 m. This was not affected by the anti-inflammatory drug or DOMS . In conclusion , the aetiology of the DOMS induced in the trained subjects in this study seems to be independent of inflammatory processes or , more specifically , of increases in prostagl and in synthesis in the muscles Superstitions and rituals are commonplace in sports and range from simple activities such as each player touching a special inanimate object before entering the field of play to more extreme behaviours such as not washing a uniform or wearing the same underwear during a winning streak . These practice s are relatively harmless and may reduce precompetition anxiety , but a concerning ritual that has recently developed in sports is the prophylactic use of non-steroidal anti-inflammatory drugs ( NSAIDs ) . Athletes have relatively unrestricted access to NSAIDs , as they are readily available over-the-counter preparations and not considered as performance-enhancing drugs by the World Anti-Doping Agency.1 It has been known for some years that athletes are frequent users of NSAIDS,2 with approximately a quarter of athletes competing at the Sydney 2000 Olympic Games reporting NSAID use in the 3 days before r and om drug testing.3 Such prevalent NSAID use may reflect the physical rigors of elite athletic endeavours , but more recent data suggest athletes misuse their open access to NSAIDs . Tscholl and colleagues4 recently reported in this journal that 23 % of top-level male football players  used NSAIDs  in two out of three matches during the 2002 and 2006 Twenty subjects were r and omly assigned to : 1 ) prophylactic ibuprofen ( N = 5 ) [ 400 mg TID initiated 4 h before collection of baseline data and strenuous eccentric exercise bout ] , 2 ) therapeutic ibuprofen ( N = 5 ) [ 400 mg TID initiated 24 h after baseline ] , 3 ) placebo ( N = 5 ) , or 4 ) control ( N = 5 ) . Muscle soreness perception , plasma creatine kinase , knee extensor torque , and EMG of the quadriceps were evaluated at baseline , 24 , and 48 h. The prophylactic ibuprofen group had between 40 and 50 % less muscle soreness perception and significantly less decline in isometric , concentric , and eccentric torque at 24 h compared with the other three groups ( P < 0.05 ) . At 48 h both prophylactic and therapeutic ibuprofen had significantly less muscle soreness perception and decline in torque than the placebo and control groups ( P < 0.05 ) . There was no difference between the amount of muscle damage between the four groups at 24 and 48 h. Vastus medialis and lateralis EMG magnitude decreased across time . Vastus lateralis EMG magnitude had significantly less decline from baseline for prophylactic ibuprofen compared with the other three treatments at 24 h , while both prophylactic and therapeutic ibuprofen had significantly less decline at 48 h. These data indicate that a prophylactic dosage of ibuprofen does not prevent CK release from muscle , but does decrease muscle soreness perception and may assist in restoring muscle function A single-blind , cross-over study was carried out to evaluate the effects of acetylsalicylic acid ( ASA ) on cardiorespiratory performance during exercise . Eighteen young men , 9 athletes and 9 untrained but active subjects , performed a progressive maximal exercise test on a cycle ergometer ( 30 watt , 3 min steps , starting at 60 watt ) on three different occasions , after a single administration of plain aspirin ( 1000 mg of ASA ) , chewable buffered aspirin ( 1000 mg of ASA and 600 mg of calcium carbonate ) and placebo . Continuous measurement of breath-by-breath ventilation , oxygen consumption , carbon dioxide output , respiratory frequency and heart rate was carried-out at rest and during the exercise test . Blood lactate concentration was measured just before the start of exercise and at the third minute of each step in order to detect the anaerobic threshold . The pharmacokinetics of aspirin  during exercise was also investigated in ten of the eighteen participants . The analysis of all investigated variables did not show any statistically significant difference between treatments , suggesting that a single dose of 1000 mg of aspirin does not affect physical performance during submaximal and maximal exercise High doses of ibuprofen have been shown to inhibit muscle protein synthesis after a bout of resistance exercise . We determined the effect of a moderate dose of ibuprofen ( 400 mg x d(-1 ) ) consumed on a daily basis after resistance training on muscle hypertrophy and strength . Twelve males and 6 females ( approximately 24 years of age ) trained their right and left biceps on alternate days ( 6 sets of 4 - 10 repetitions ) , 5 d x week(-1 ) , for 6 weeks . In a counter-balanced , double-blind design , they were r and omized to receive 400 mg x d(-1 ) ibuprofen immediately after training their left or right arm , and a placebo after training the opposite arm the following day . Before- and after-training muscle thickness of both biceps was measured using ultrasound and 1 repetition maximum ( 1 RM ) arm curl strength was determined on both arms . Subjects rated their muscle soreness daily . There were time main effects for muscle thickness and strength ( p < 0.01 ) . Ibuprofen consumption had no effect on muscle hypertrophy ( muscle thickness of biceps for arm receiving ibuprofen : pre 3.63 + /- 0.14 , post 3.92 + /- 0.15 cm ; and placebo : pre 3.62 + /- 0.15 , post 3.90 + /- 0.15 cm ) and strength ( 1 RM of arm receiving ibuprofen : pre 18.6 + /- 2.8 , post 23.4 + /- 3.5 kg ; and placebo : pre 18.8 + /- 2.8 , post 22.8 + /- 3.4 kg ) . Muscle soreness was elevated during the first week of training only , but was not different between the ibuprofen and placebo arm . We conclude that a moderate dose of ibuprofen ingested after repeated resistance training sessions does not impair muscle hypertrophy or strength and does not affect ratings of muscle soreness BACKGROUND A r and omized , controlled trial ( RCT ) should not be started or interpreted without accounting for evidence from preceding RCTs addressing the same question . Research has suggested that evidence from prior trials is often not accounted for in reports of subsequent RCTs . OBJECTIVE To assess the extent to which reports of RCTs cite prior trials study ing the same interventions . DESIGN Meta-analyses published in 2004 that combined 4 or more trials were identified ; within each meta- analysis , the extent to which each trial report cited the trials that preceded it by more than 1 year was assessed . MEASUREMENTS The proportion of prior trials that were cited  ( prior research citation index ) , the proportion of the total participants from prior trials that were in the cited trials  ( sample size citation index ) , and the absolute number of trials cited were calculated . RESULTS 227 meta-analyses were identified , comprising 1523 trials published from 1963 to 2004 . The median prior research citation index was 0.21 ( 95 % CI , 0.18 to 0.24 ) , meaning that less than one quarter of relevant reports were cited . The median sample size citation index ( 0.24 [ CI , 0.21 to 0.27 ] ) was similar , suggesting that larger trials were not selectively cited . Of the 1101 RCTs that had 5 or more prior trials to cite , 254 ( 23 % ) cited no prior RCTs and 257 ( 23 % ) cited only 1 . The median number of prior cited trials was 2 , which did not change as the number of citable trials increased . The mean number of preceding trials cited by trials published after 2000 was 2.4 , compared with 1.5 for those published before 2000 ( P < 0.001 ) . LIMITATION The investigators could not ascertain why prior trials were not cited , and noncited trials may have been taken into account in the trial design and proposal stages . CONCLUSION In reports of RCTs published over 4 decades , fewer than 25 % of preceding trials were cited , comprising fewer than 25 % of the participants enrolled in all relevant prior trials . A median of 2 trials was cited , regardless of the number of prior trials that had been conducted . Research is needed to explore the explanations for and consequences of this phenomenon . Potential implication s include ethically unjustifiable trials , wasted re sources , incorrect conclusions , and unnecessary risks for trial participants . PRIMARY FUNDING SOURCE None
target: There was neither significant difference in the maximum performance between NSAIDs and control groups nor in the time until exhaustion nor in self-perceived pain .
background: Non-steroidal anti-inflammatory drugs ( NSAIDs ) are medications that are frequently used by athletes .
  There may also be some abuse of these substances , although it is unclear whether NSAIDs in fact enhance performance .
  We performed a systematic review and meta- analysis to evaluate the effect of NSAIDs on sport performance indices .