human
***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: Young male jockeys compromise bone health by engaging in caloric restriction and high volumes of physical activity during periods of musculoskeletal growth and development . The aim of this r and omised , double-blinded , placebo-controlled trial was to establish whether calcium and vitamin D supplementation would improve bone properties of young male jockeys . We conducted a 6-month trial with two groups of weight- , height- and age-matched apprentice male jockeys ( age=20.2 ± 3.2 yrs ) . Participants were supplemented with 800 mg of calcium and 400 IU of vitamin D ( S , n=8 ) or a placebo ( cellulose ) ( P , n=9 ) daily for 6-months . Baseline calcium intake was ( 669.7 ± 274.3 ( S ) vs 790.4 ± 423.9 ( P ) and vitamin D 64.6 ± 19.5 ( S ) vs 81.2 ± 24.4 ( P ) with no statistical differences . Peripheral quantitative computed tomography ( pQCT ) measured ultra-distal ( 4 % ) and proximal ( 66 % ) tibial bone properties at baseline and 6 months . Blood-borne markers of bone turnover , P1NP and CTX and vitamin D concentration were assessed . After co-varying for height , weight and baseline bone measurements , the supplemented group displayed greater post-intervention bone properties at the 66 % proximal site with cortical content ( mgmm ) 6.6 % greater ( p<0.001 ) , cortical area ( mm(2 ) ) 5.9 % larger ( p<0.001 ) , cortical density ( mgcm(2 ) ) 1.3 % greater ( p=0.001 ) , and total area ( mm(2 ) ) 4 % larger ( p=0.003 ) . No other between group differences in bone variables were observed . Blood analysis indicated higher vitamin D levels ( 18.1 % , p=0.014 ) and lower CTx ( ng/L ) ( -24.8 % , p=0.011 ) in the supplemented group with no differences observed in P1NP . This is the first r and omised controlled trial to examine the efficacy of calcium and vitamin D supplementation in improving bone properties in a highly vulnerable , young athletic , weight-restricted population . Results using pQCT indicate beneficial effects of supplementation on bone properties in as little as six months . Although the study size is small , this intervention appears promising as a strategy for improving bone health in young athletes in weight-restricted sports Vitamin D insufficiency is common in athletes and may lower physical performance . Many cross-sectional studies associate vitamin D status with physical performance in athletes ; however , there have been few prospect i ve r and omized controlled trials with adequate statistical power to test this relationship , and none in the southern hemisphere . Thus , a prospect i ve double-blind , r and omized , placebo-controlled intervention trial was conducted involving 57 professional rugby union players in New Zeal and . Participants were r and omized to receive 50,000 IU of cholecalciferol ( equivalent to 3,570 IU/day ) or placebo once every two weeks over 11 - 12 weeks . Serum 25(OH)D concentrations and physical performance were measured at baseline , weeks 5 - 6 , and weeks 11 - 12 . Mean ( SD ) serum 25(OH)D concentrations for all participants at baseline was 94 ( 18 ) nmol/L , with all players above 50 nmol/L. Vitamin D supplementation significantly increased serum 25(OH)D concentrations compared to placebo , with a 32 nmol/L difference between groups at 11 - 12 weeks ( 95 % CI , 26 - 38 ; p < 0.001 ) . Performance in five of the six tests at study completion , including the primary outcome variable of 30-m sprint time , did not differ between the vitamin D supplemented and placebo groups ( p > 0.05 ) . Performance on the weighted reverse-grip chin up was significantly higher in players receiving vitamin D compared with placebo , by 5.5 kg ( 95 % CI , 2.0 - 8.9 ; p = 0.002 ) . Despite significantly improving vitamin D status in these professional rugby union players , vitamin D supplementation had little impact on physical performance outcomes . Thus , it is unlikely that vitamin D supplementation is an ergogenic aid in this group of athletes In all species tested , except humans , biological differences between vitamins D2 and D3 are accepted as fact . To test the presumption of equivalence in humans , we compared the ability of equal molar quantities of vitamin D2 or D3 to increase serum 25-hydroxyvitamin D [ 25(OH)D ] , the measure of vitamin D nutrition .  Subjects took 260 nmol ( approximately 4000 IU ) vitamin D2  ( n=17 ) or vitamin D3  ( n=55 ) daily for 14 d. 25(OH)D was assayed with a method that detects both the vitamin D2 and D3 forms . With vitamin D3 , mean ( + /-SD ) serum 25(OH)D increased from 41.3+/-17.7 nmol/L before to 64.6+/-17.2 nmol/L after treatment . With vitamin D2 , the 25(OH)D concentration went from 43.7+/-17.7 nmol/L before to 57.4+/-13.0 nmol/L after . The increase in 25(OH)D with vitamin D3  was 23.3+/-15.7 nmol/L , or 1.7 times the increase obtained with vitamin D2 ( 13.7+/-11.4 nmol/L ; P=0.03 ) . There was an inverse relation between the increase in 25(OH)D and the initial 25(OH)D concentration . The lowest 2 tertiles for basal 25(OH)D showed larger increases in 25(OH)D : 30.6 and 25.5 nmol/L , respectively , for the first and second tertiles . In the highest tertile [ 25(OH)D > 49 nmol/L ] the mean increase in 25(OH)D was 13.3 nmol/L ( P < 0.03 for comparison with each lower tertile ) . Although the 1.7-times greater efficacy for vitamin D3 shown here may seem small , it is more than what others have shown for 25(OH)D increases when comparing 2-fold differences in vitamin D3 dose . The assumption that vitamins D2 and D3 have equal nutritional value is probably wrong and should be reconsidered This study determined if 6-weeks vitamin D2 supplementation ( vitD2 , 3800 IU/day ) had an influence on muscle function , eccentric exercise-induced muscle damage ( EIMD ) , and delayed onset of muscle soreness ( DOMS ) in National Association for Stock Car Auto Racing ( NASCAR ) NASCAR pit crew athletes . Subjects were r and omized to vitD2 ( n = 13 ) and placebo ( n = 15 ) , and ingested supplements ( double-blind ) for six weeks . Blood sample s were collected and muscle function tests conducted pre- and post- study ( leg-back and h and grip dynamometer strength tests , body weight bench press to exhaustion , vertical jump , 30-s Wingate test ) . Post- study , subjects engaged in 90 min eccentric-based exercise , with blood sample s and DOMS ratings obtained immediately after and 1- and 2-days post-exercise . Six weeks vitD2 increased serum 25(OH)D2 456 % and decreased 25(OH)D3 21 % versus placebo ( p < 0.001 , p = 0.036 , respectively ) , with no influence on muscle function test scores . The post- study eccentric exercise bout induced EIMD and DOMS , with higher muscle damage biomarkers measured in vitD2 compared to placebo ( myoglobin 252 % , 122 % increase , respectively , p = 0.001 ; creatine phosphokinase 24 h post-exercise , 169 % , 32 % , p < 0.001 ) , with no differences for DOMS . In summary , 6-weeks vitD2 ( 3800 IU/day ) significantly increased 25(OH)D2 and decreased 25(OH)D3 , had no effect on muscle function tests , and amplified muscle damage markers in NASCAR pit crew athletes following eccentric exercise Public health recommendations do not distinguish between vitamin D2 and vitamin D3 , yet disagreement exists on whether these two forms should be considered equivalent . The objective of the present study was to evaluate the effect of a daily physiological dose of vitamin D2 or vitamin D3 on 25-hydroxyvitamin D ( 25(OH)D ) status over the winter months in healthy adults living in Dunedin , New Zeal and ( latitude 46 ° S ) . Participants aged 18 - 50 years were r and omly assigned to 25 μg ( 1000 IU ) vitamin D3 ( n 32 ) , 25 μg ( 1000 IU ) vitamin D2 ( n 31 ) or placebo ( n 32 ) daily for 25 weeks beginning at the end of summer . A per- protocol approach , which included ≥ 90 % supplement compliance , was used for all analyses . Serum 25-hydroxyvitamin D3 ( 25(OH)D3 ) , 25-hydroxyvitamin D2 ( 25(OH)D2 ) and parathyroid hormone ( PTH ) were measured at baseline and at 4 , 8 , 13 and 25 weeks . Geometric mean total serum 25(OH)D concentrations ( sum of 25(OH)D2 and 25(OH)D3 ) at baseline was 80 nmol/l . After 25 weeks , participants r and omised to D2 and placebo had a significant reduction in serum 25(OH)D3 concentrations over the winter months compared with vitamin D3-supplemented participants ( both P < 0.001 ) . Supplementation with vitamin D2  increased serum 25(OH)D2 but produced a 9 ( 95 % CI 1 , 17 ) nmol/l greater decline in the 25(OH)D3 metabolite compared with placebo ( P < 0.036 ) . Overall , total serum 25(OH)D concentrations were 21 ( 95 % CI 14 , 30 ) nmol/l lower in participants receiving vitamin D2 compared with those receiving D3 ( P < 0.001 ) , among whom total serum 25(OH)D concentrations remained unchanged . No intervention-related changes in PTH were observed . Daily supplementation of vitamin D3 was more effective than D2 ; however , the functional consequence of the differing metabolic response warrants further investigation Abstract : The first part of this study consisted of an 18 month follow-up of the vitamin D status and parathyroid function in a group of 54 French male adolescents , aged from 13 to 16 years old and all pupils of a jockey training school . During the 18 month period four samplings were made , one every 6 months . The first was during September of the first year , the second and third during March and October of the second year , and the last in March of the third year . Therefore we had two main periods : summer and winter . The summer 25-hydroxyvitamin D ( 25(OH)D ) concentrations were higher ( 71.6 ± 19.9 and 52.4 ± 16.5 nmol/l ) than the winter ones ( 20.4 ± 6.9 and 21.4 ± 6.1 nmol/l ) . Conversely , the winter intact parathyroid hormone ( iPTH ) serum levels ( 4.18 ± 1.18 and 4.11 ± 1.35 pmol/l ) were higher than the summer ones ( 2.44 ± 0.82 and 2.71 ± 0.71 pmol/l ) . At the two winter time points the 25(OH)D concentrations were lower than 25 nmol/l ( 10 ng/ml ) in 72 % ( 2nd year ) and 68 % ( 3rd year ) of the adolescents . In the second part of the study we tried a vitamin D3 supplementation procedure design ed to maintain the 25(OH)D and iPTH postsummer serum levels throughout the winter . Pairs of male adolescents matched for height , weight and Tanner pubertal stage were r and omly assigned to either vitamin D3 supplementation ( 2.5 mg , i.e. , 100 000 IU ) administered orally at three specific periods ( end of September , November and January ) or no vitamin D3 treatment ( control subjects ) . Blood was collected just before the first intake of vitamin D3 and 2 months after the last intake ( March ) . The control subjects had blood drawn at the same time points . In the vitamin D3-treated subjects , the concentrations of 25 (OH)D ( 55.3 ± 11.5 nmol/l ) and of iPTH ( 3.09 ± 1.16 pmol/l ) in March and September ( 53.8 ± 12.3 nmol/l and 2.75 ± 1.26 pmol/l ) were not 
    Output:
    
agent
Conclusion Although , serum 25(OH)D concentrations after supplementation reached sufficiency was observed , muscle strength did not significantly improve at this point of current meta- analysis .
***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: Young male jockeys compromise bone health by engaging in caloric restriction and high volumes of physical activity during periods of musculoskeletal growth and development . The aim of this r and omised , double-blinded , placebo-controlled trial was to establish whether calcium and vitamin D supplementation would improve bone properties of young male jockeys . We conducted a 6-month trial with two groups of weight- , height- and age-matched apprentice male jockeys ( age=20.2 ± 3.2 yrs ) . Participants were supplemented with 800 mg of calcium and 400 IU of vitamin D ( S , n=8 ) or a placebo ( cellulose ) ( P , n=9 ) daily for 6-months . Baseline calcium intake was ( 669.7 ± 274.3 ( S ) vs 790.4 ± 423.9 ( P ) and vitamin D 64.6 ± 19.5 ( S ) vs 81.2 ± 24.4 ( P ) with no statistical differences . Peripheral quantitative computed tomography ( pQCT ) measured ultra-distal ( 4 % ) and proximal ( 66 % ) tibial bone properties at baseline and 6 months . Blood-borne markers of bone turnover , P1NP and CTX and vitamin D concentration were assessed . After co-varying for height , weight and baseline bone measurements , the supplemented group displayed greater post-intervention bone properties at the 66 % proximal site with cortical content ( mgmm ) 6.6 % greater ( p<0.001 ) , cortical area ( mm(2 ) ) 5.9 % larger ( p<0.001 ) , cortical density ( mgcm(2 ) ) 1.3 % greater ( p=0.001 ) , and total area ( mm(2 ) ) 4 % larger ( p=0.003 ) . No other between group differences in bone variables were observed . Blood analysis indicated higher vitamin D levels ( 18.1 % , p=0.014 ) and lower CTx ( ng/L ) ( -24.8 % , p=0.011 ) in the supplemented group with no differences observed in P1NP . This is the first r and omised controlled trial to examine the efficacy of calcium and vitamin D supplementation in improving bone properties in a highly vulnerable , young athletic , weight-restricted population . Results using pQCT indicate beneficial effects of supplementation on bone properties in as little as six months . Although the study size is small , this intervention appears promising as a strategy for improving bone health in young athletes in weight-restricted sports Vitamin D insufficiency is common in athletes and may lower physical performance . Many cross-sectional studies associate vitamin D status with physical performance in athletes ; however , there have been few prospect i ve r and omized controlled trials with adequate statistical power to test this relationship , and none in the southern hemisphere . Thus , a prospect i ve double-blind , r and omized , placebo-controlled intervention trial was conducted involving 57 professional rugby union players in New Zeal and . Participants were r and omized to receive 50,000 IU of cholecalciferol ( equivalent to 3,570 IU/day ) or placebo once every two weeks over 11 - 12 weeks . Serum 25(OH)D concentrations and physical performance were measured at baseline , weeks 5 - 6 , and weeks 11 - 12 . Mean ( SD ) serum 25(OH)D concentrations for all participants at baseline was 94 ( 18 ) nmol/L , with all players above 50 nmol/L. Vitamin D supplementation significantly increased serum 25(OH)D concentrations compared to placebo , with a 32 nmol/L difference between groups at 11 - 12 weeks ( 95 % CI , 26 - 38 ; p < 0.001 ) . Performance in five of the six tests at study completion , including the primary outcome variable of 30-m sprint time , did not differ between the vitamin D supplemented and placebo groups ( p > 0.05 ) . Performance on the weighted reverse-grip chin up was significantly higher in players receiving vitamin D compared with placebo , by 5.5 kg ( 95 % CI , 2.0 - 8.9 ; p = 0.002 ) . Despite significantly improving vitamin D status in these professional rugby union players , vitamin D supplementation had little impact on physical performance outcomes . Thus , it is unlikely that vitamin D supplementation is an ergogenic aid in this group of athletes In all species tested , except humans , biological differences between vitamins D2 and D3 are accepted as fact . To test the presumption of equivalence in humans , we compared the ability of equal molar quantities of vitamin D2 or D3 to increase serum 25-hydroxyvitamin D [ 25(OH)D ] , the measure of vitamin D nutrition .  Subjects took 260 nmol ( approximately 4000 IU ) vitamin D2  ( n=17 ) or vitamin D3  ( n=55 ) daily for 14 d. 25(OH)D was assayed with a method that detects both the vitamin D2 and D3 forms . With vitamin D3 , mean ( + /-SD ) serum 25(OH)D increased from 41.3+/-17.7 nmol/L before to 64.6+/-17.2 nmol/L after treatment . With vitamin D2 , the 25(OH)D concentration went from 43.7+/-17.7 nmol/L before to 57.4+/-13.0 nmol/L after . The increase in 25(OH)D with vitamin D3  was 23.3+/-15.7 nmol/L , or 1.7 times the increase obtained with vitamin D2 ( 13.7+/-11.4 nmol/L ; P=0.03 ) . There was an inverse relation between the increase in 25(OH)D and the initial 25(OH)D concentration . The lowest 2 tertiles for basal 25(OH)D showed larger increases in 25(OH)D : 30.6 and 25.5 nmol/L , respectively , for the first and second tertiles . In the highest tertile [ 25(OH)D > 49 nmol/L ] the mean increase in 25(OH)D was 13.3 nmol/L ( P < 0.03 for comparison with each lower tertile ) . Although the 1.7-times greater efficacy for vitamin D3 shown here may seem small , it is more than what others have shown for 25(OH)D increases when comparing 2-fold differences in vitamin D3 dose . The assumption that vitamins D2 and D3 have equal nutritional value is probably wrong and should be reconsidered This study determined if 6-weeks vitamin D2 supplementation ( vitD2 , 3800 IU/day ) had an influence on muscle function , eccentric exercise-induced muscle damage ( EIMD ) , and delayed onset of muscle soreness ( DOMS ) in National Association for Stock Car Auto Racing ( NASCAR ) NASCAR pit crew athletes . Subjects were r and omized to vitD2 ( n = 13 ) and placebo ( n = 15 ) , and ingested supplements ( double-blind ) for six weeks . Blood sample s were collected and muscle function tests conducted pre- and post- study ( leg-back and h and grip dynamometer strength tests , body weight bench press to exhaustion , vertical jump , 30-s Wingate test ) . Post- study , subjects engaged in 90 min eccentric-based exercise , with blood sample s and DOMS ratings obtained immediately after and 1- and 2-days post-exercise . Six weeks vitD2 increased serum 25(OH)D2 456 % and decreased 25(OH)D3 21 % versus placebo ( p < 0.001 , p = 0.036 , respectively ) , with no influence on muscle function test scores . The post- study eccentric exercise bout induced EIMD and DOMS , with higher muscle damage biomarkers measured in vitD2 compared to placebo ( myoglobin 252 % , 122 % increase , respectively , p = 0.001 ; creatine phosphokinase 24 h post-exercise , 169 % , 32 % , p < 0.001 ) , with no differences for DOMS . In summary , 6-weeks vitD2 ( 3800 IU/day ) significantly increased 25(OH)D2 and decreased 25(OH)D3 , had no effect on muscle function tests , and amplified muscle damage markers in NASCAR pit crew athletes following eccentric exercise Public health recommendations do not distinguish between vitamin D2 and vitamin D3 , yet disagreement exists on whether these two forms should be considered equivalent . The objective of the present study was to evaluate the effect of a daily physiological dose of vitamin D2 or vitamin D3 on 25-hydroxyvitamin D ( 25(OH)D ) status over the winter months in healthy adults living in Dunedin , New Zeal and ( latitude 46 ° S ) . Participants aged 18 - 50 years were r and omly assigned to 25 μg ( 1000 IU ) vitamin D3 ( n 32 ) , 25 μg ( 1000 IU ) vitamin D2 ( n 31 ) or placebo ( n 32 ) daily for 25 weeks beginning at the end of summer . A per- protocol approach , which included ≥ 90 % supplement compliance , was used for all analyses . Serum 25-hydroxyvitamin D3 ( 25(OH)D3 ) , 25-hydroxyvitamin D2 ( 25(OH)D2 ) and parathyroid hormone ( PTH ) were measured at baseline and at 4 , 8 , 13 and 25 weeks . Geometric mean total serum 25(OH)D concentrations ( sum of 25(OH)D2 and 25(OH)D3 ) at baseline was 80 nmol/l . After 25 weeks , participants r and omised to D2 and placebo had a significant reduction in serum 25(OH)D3 concentrations over the winter months compared with vitamin D3-supplemented participants ( both P < 0.001 ) . Supplementation with vitamin D2  increased serum 25(OH)D2 but produced a 9 ( 95 % CI 1 , 17 ) nmol/l greater decline in the 25(OH)D3 metabolite compared with placebo ( P < 0.036 ) . Overall , total serum 25(OH)D concentrations were 21 ( 95 % CI 14 , 30 ) nmol/l lower in participants receiving vitamin D2 compared with those receiving D3 ( P < 0.001 ) , among whom total serum 25(OH)D concentrations remained unchanged . No intervention-related changes in PTH were observed . Daily supplementation of vitamin D3 was more effective than D2 ; however , the functional consequence of the differing metabolic response warrants further investigation Abstract : The first part of this study consisted of an 18 month follow-up of the vitamin D status and parathyroid function in a group of 54 French male adolescents , aged from 13 to 16 years old and all pupils of a jockey training school . During the 18 month period four samplings were made , one every 6 months . The first was during September of the first year , the second and third during March and October of the second year , and the last in March of the third year . Therefore we had two main periods : summer and winter . The summer 25-hydroxyvitamin D ( 25(OH)D ) concentrations were higher ( 71.6 ± 19.9 and 52.4 ± 16.5 nmol/l ) than the winter ones ( 20.4 ± 6.9 and 21.4 ± 6.1 nmol/l ) . Conversely , the winter intact parathyroid hormone ( iPTH ) serum levels ( 4.18 ± 1.18 and 4.11 ± 1.35 pmol/l ) were higher than the summer ones ( 2.44 ± 0.82 and 2.71 ± 0.71 pmol/l ) . At the two winter time points the 25(OH)D concentrations were lower than 25 nmol/l ( 10 ng/ml ) in 72 % ( 2nd year ) and 68 % ( 3rd year ) of the adolescents . In the second part of the study we tried a vitamin D3 supplementation procedure design ed to maintain the 25(OH)D and iPTH postsummer serum levels throughout the winter . Pairs of male adolescents matched for height , weight and Tanner pubertal stage were r and omly assigned to either vitamin D3 supplementation ( 2.5 mg , i.e. , 100 000 IU ) administered orally at three specific periods ( end of September , November and January ) or no vitamin D3 treatment ( control subjects ) . Blood was collected just before the first intake of vitamin D3 and 2 months after the last intake ( March ) . The control subjects had blood drawn at the same time points . In the vitamin D3-treated subjects , the concentrations of 25 (OH)D ( 55.3 ± 11.5 nmol/l ) and of iPTH ( 3.09 ± 1.16 pmol/l ) in March and September ( 53.8 ± 12.3 nmol/l and 2.75 ± 1.26 pmol/l ) were not 
    Output:
    