Key result
Myofibrillar protein degradation in premature infants with respiratory distress varied from 0.92 to 1.58 g/day/kg, with higher rates noted during acute illness and rapid growth.
Observational (n=12)
Premature infants with respiratory distress show a trend toward higher rates of myofibrillar protein degradation during acute illness and rapid growth phases.
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Higher degradation during illness may inform protein dosing in preterm infants; leaves open optimal targets and outcome impact.
The skeletal muscle content of 3-methylhistidine has been measured in two fetuses and four infants of 15 to 38 wk of gestation. The average concentration of skeletal muscle 3-methylhistidine is 1.11, 2.64, and 3.28 (mumol/mixed protein) for fetuses of 15 to 18 of gestation and infants of 26 to 32 and 37 to 38 wk of gestation, respectively. Myofibrillar protein degradation has been measured by the rate of 3-methylhistidine excretion in premature infants suffering from respiratory distress and weighing between 1310 and 2420 g. In 26 balance studies in six infants, total muscle protein breakdown varied from 0.92 to 1.58 g day-1 kg-1 body weight. Calculated fractional catabolism of myofibrillar protein varied from 0.38 to 1.07% per day. A trend toward a higher rate of myofibrillar protein degradation is noted during the infants' acute illness and during their rapid growing phase.
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Lunyong et al. (1982) conducted an observational in Premature infants with respiratory distress (n=12). Acute illness and rapid growth phase was evaluated on Myofibrillar protein degradation (total muscle protein breakdown and fractional catabolism). Myofibrillar protein degradation in premature infants with respiratory distress varied from 0.92 to 1.58 g/day/kg, with higher rates noted during acute illness and rapid growth.
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