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: Despite distinct differences between walking and running , the two types of human locomotion are likely to be controlled by shared pattern-generating networks . However , the differences between their kinematics and kinetics imply that corresponding muscle activations may also be quite different . We examined the differences between walking and running by recording kinematics and electromyographic ( EMG ) activity  in 32 ipsilateral limb and trunk muscles during human locomotion  , and compared the effects of speed ( 3 - 12 km/h ) and gait . We found that the timing of muscle activation was accounted for by five basic temporal activation components during running as we previously found for walking . Each component was loaded on similar sets of leg muscles in both gaits but generally on different sets of upper trunk and shoulder muscles . The major difference between walking and running was that one temporal component , occurring during stance , was shifted to an earlier phase in the step cycle during running . These muscle activation differences between gaits did not simply depend on locomotion speed as shown by recordings during each gait over the same range of speeds ( 5 - 9 km/h ) . The results are consistent with an organization of locomotion motor programs having two parts , one that organizes muscle activation during swing and another during stance and the transition to swing . The timing shift between walking and running reflects therefore the difference in the relative duration of the stance phase in the two gaits This study determined the decline in oxidative capacity per volume of human vastus lateralis muscle between nine adult ( mean age 38.8 years ) and 40 elderly ( mean age 68.8 years ) human subjects ( age range 25 - 80 years ) . We based our oxidative capacity estimates on the kinetics of changes in creatine phosphate content ( [ PCr ] ) during recovery from exercise as measured by (31)P magnetic resonance ( MR ) spectroscopy . A matched muscle biopsy sample permitted determination of mitochondrial volume density and the contribution of the loss of mitochondrial content to the decline in oxidative capacity with age . The maximal oxidative phosphorylation rate or oxidative capacity was estimated from the PCr recovery rate constant ( k(PCr ) ) and the [ PCr ] in accordance with a simple electrical circuit model of mitochondrial respiratory control . Oxidative capacity was 50 % lower in the elderly vs. the adult group ( 0.61 + /- 0.04 vs. 1.16 + /- 0.147 mM ATP s(-1 ) ) . Mitochondrial volume density was significantly lower in elderly compared with adult muscle ( 2.9 + /- 0.15 vs. 3.6 + /- 0.11 % ) . In addition , the oxidative capacity per mitochondrial volume ( 0.22 + /- 0.042 vs. 0.32 + /- 0.015 mM ATP ( s % ) ( -1 ) ) was reduced in elderly vs. adult subjects . This study showed that elderly subjects had nearly 50 % lower oxidative capacity per volume of muscle than adult subjects . The cellular basis of this drop was a reduction in mitochondrial content , as well as a lower oxidative capacity of the mitochondria with age Using (31)P magnetic resonance spectroscopy , creatine kinase ( CK ) reaction kinetics was assessed in the forearm flexor digitorum profundus muscle of healthy young ( n = 11 , age 34.7 + /- 5 yr ) and older ( n = 20 , age 73.5 + /- 8 yr ) subjects at rest , intermittent exercise at 20 % maximum voluntary contraction ( MVC ) , and 40 % MVC . Exercise result ed in a significant increase in the average ratio of inorganic phosphate ( P(i ) ) to phosphocreatine ( PCr ) from resting values of 0.073 + /- 0.031 ( young ) and 0.082 + /- 0.037 ( older ) to 0 . 268 + /- 0.140 ( young , P < 0.01 ) and 0.452 + /- 0.387 ( older , P < 0 . 01 ) at 40 % MVC . At 40 % MVC , intracellular pH decreased significantly , from resting values of 7.08 + /- 0.08 ( young ) and 7.08 + /- 0.11 ( older ) to 6.84 + /- 0.19 ( young , P < 0.05 ) and to 6.75 + /- 0.25 ( older , P < 0.05 ) . Average values of the pseudo-first-order reaction rate k((PCr-->ATP ) ) at rest were 0.07 + /- 0.04 s(-1 ) in the young and 0.07 + /- 0.03 s(-1 ) in the older group . At both exercise levels , the reaction rate constant increased compared with the resting value , but only the difference between the resting value and the 20 % MVC value , which showed an 86 % higher reaction rate constant in both groups , reached statistical significance ( P < 0.05 ) . No difference in the reaction rate constant between the young and older groups was observed at either exercise level . As with k((PCr-->ATP ) ) , the average phosphorus flux through the CK reaction increased during exercise at 20 % MVC ( P < 0.05 in the older group ) but decreased toward resting values at 40 % MVC in both groups . The data in our study suggest that normal aging does not significantly affect the metabolic processes associated with the CK reaction BACKGROUND The decline in muscle mass ( sarcopenia ) with aging may be related to a decline in mitochondrial function . However , investigators have yet to reach a consensus as to whether a decline in mitochondrial function can be attenuated by physical activity has yet to reach a consensus . METHODS Using dynamic 31PMRS to measure mitochondrial function , we measured baseline Phosphocreatine ( PCr ) , inorganic phosphate ( Pi ) , phosphodiester ( PDE ) , [ ADP ] , pH and recovery times ( t(1/2 ) ) for PCr and [ ADP ] following exercise , in 45 older ( 73+/-4 years , SD ) , and 20 younger subjects ( 25+/-4 years , SD ) who were matched for body mass across high and low activity levels and within age and sex groupings . RESULTS Baseline PCr , and Pi , were lower , and PDE higher in the older subjects compared to younger subjects ( all P<0.01 ) . The t(1/2)(ADP ) was longer in older subjects ( P<0.001 ) controlling for age and sex in the low activity group ( P=0.02 ) . In the older low activity groups , t(1/2)(PCr ) was longer than high activity groups . Higher PDE levels were positively correlated with longer t(1/2)(PCr ) in the older low activity females ( both P<0.05 ) . CONCLUSIONS Our data suggests that mitochondrial function declines with age in healthy , exercising elderly adults and that the decline appears to be influenced by the level of physical activity 
    Output:
    
agent
This analysis indicates that the current body of literature does not support a de facto decrease of in vivo muscle oxidative capacity in old age .
The heterogeneity of study results and identification of significant moderators provide clarity regarding apparent discrepancies in the literature , and indicate the importance of accounting for these variables when examining purported age-related differences in muscle oxidative capacity
***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: Despite distinct differences between walking and running , the two types of human locomotion are likely to be controlled by shared pattern-generating networks . However , the differences between their kinematics and kinetics imply that corresponding muscle activations may also be quite different . We examined the differences between walking and running by recording kinematics and electromyographic ( EMG ) activity  in 32 ipsilateral limb and trunk muscles during human locomotion  , and compared the effects of speed ( 3 - 12 km/h ) and gait . We found that the timing of muscle activation was accounted for by five basic temporal activation components during running as we previously found for walking . Each component was loaded on similar sets of leg muscles in both gaits but generally on different sets of upper trunk and shoulder muscles . The major difference between walking and running was that one temporal component , occurring during stance , was shifted to an earlier phase in the step cycle during running . These muscle activation differences between gaits did not simply depend on locomotion speed as shown by recordings during each gait over the same range of speeds ( 5 - 9 km/h ) . The results are consistent with an organization of locomotion motor programs having two parts , one that organizes muscle activation during swing and another during stance and the transition to swing . The timing shift between walking and running reflects therefore the difference in the relative duration of the stance phase in the two gaits This study determined the decline in oxidative capacity per volume of human vastus lateralis muscle between nine adult ( mean age 38.8 years ) and 40 elderly ( mean age 68.8 years ) human subjects ( age range 25 - 80 years ) . We based our oxidative capacity estimates on the kinetics of changes in creatine phosphate content ( [ PCr ] ) during recovery from exercise as measured by (31)P magnetic resonance ( MR ) spectroscopy . A matched muscle biopsy sample permitted determination of mitochondrial volume density and the contribution of the loss of mitochondrial content to the decline in oxidative capacity with age . The maximal oxidative phosphorylation rate or oxidative capacity was estimated from the PCr recovery rate constant ( k(PCr ) ) and the [ PCr ] in accordance with a simple electrical circuit model of mitochondrial respiratory control . Oxidative capacity was 50 % lower in the elderly vs. the adult group ( 0.61 + /- 0.04 vs. 1.16 + /- 0.147 mM ATP s(-1 ) ) . Mitochondrial volume density was significantly lower in elderly compared with adult muscle ( 2.9 + /- 0.15 vs. 3.6 + /- 0.11 % ) . In addition , the oxidative capacity per mitochondrial volume ( 0.22 + /- 0.042 vs. 0.32 + /- 0.015 mM ATP ( s % ) ( -1 ) ) was reduced in elderly vs. adult subjects . This study showed that elderly subjects had nearly 50 % lower oxidative capacity per volume of muscle than adult subjects . The cellular basis of this drop was a reduction in mitochondrial content , as well as a lower oxidative capacity of the mitochondria with age Using (31)P magnetic resonance spectroscopy , creatine kinase ( CK ) reaction kinetics was assessed in the forearm flexor digitorum profundus muscle of healthy young ( n = 11 , age 34.7 + /- 5 yr ) and older ( n = 20 , age 73.5 + /- 8 yr ) subjects at rest , intermittent exercise at 20 % maximum voluntary contraction ( MVC ) , and 40 % MVC . Exercise result ed in a significant increase in the average ratio of inorganic phosphate ( P(i ) ) to phosphocreatine ( PCr ) from resting values of 0.073 + /- 0.031 ( young ) and 0.082 + /- 0.037 ( older ) to 0 . 268 + /- 0.140 ( young , P < 0.01 ) and 0.452 + /- 0.387 ( older , P < 0 . 01 ) at 40 % MVC . At 40 % MVC , intracellular pH decreased significantly , from resting values of 7.08 + /- 0.08 ( young ) and 7.08 + /- 0.11 ( older ) to 6.84 + /- 0.19 ( young , P < 0.05 ) and to 6.75 + /- 0.25 ( older , P < 0.05 ) . Average values of the pseudo-first-order reaction rate k((PCr-->ATP ) ) at rest were 0.07 + /- 0.04 s(-1 ) in the young and 0.07 + /- 0.03 s(-1 ) in the older group . At both exercise levels , the reaction rate constant increased compared with the resting value , but only the difference between the resting value and the 20 % MVC value , which showed an 86 % higher reaction rate constant in both groups , reached statistical significance ( P < 0.05 ) . No difference in the reaction rate constant between the young and older groups was observed at either exercise level . As with k((PCr-->ATP ) ) , the average phosphorus flux through the CK reaction increased during exercise at 20 % MVC ( P < 0.05 in the older group ) but decreased toward resting values at 40 % MVC in both groups . The data in our study suggest that normal aging does not significantly affect the metabolic processes associated with the CK reaction BACKGROUND The decline in muscle mass ( sarcopenia ) with aging may be related to a decline in mitochondrial function . However , investigators have yet to reach a consensus as to whether a decline in mitochondrial function can be attenuated by physical activity has yet to reach a consensus . METHODS Using dynamic 31PMRS to measure mitochondrial function , we measured baseline Phosphocreatine ( PCr ) , inorganic phosphate ( Pi ) , phosphodiester ( PDE ) , [ ADP ] , pH and recovery times ( t(1/2 ) ) for PCr and [ ADP ] following exercise , in 45 older ( 73+/-4 years , SD ) , and 20 younger subjects ( 25+/-4 years , SD ) who were matched for body mass across high and low activity levels and within age and sex groupings . RESULTS Baseline PCr , and Pi , were lower , and PDE higher in the older subjects compared to younger subjects ( all P<0.01 ) . The t(1/2)(ADP ) was longer in older subjects ( P<0.001 ) controlling for age and sex in the low activity group ( P=0.02 ) . In the older low activity groups , t(1/2)(PCr ) was longer than high activity groups . Higher PDE levels were positively correlated with longer t(1/2)(PCr ) in the older low activity females ( both P<0.05 ) . CONCLUSIONS Our data suggests that mitochondrial function declines with age in healthy , exercising elderly adults and that the decline appears to be influenced by the level of physical activity 
    Output:
    