Fractional mixed skeletal muscle protein synthesis (FMPS) was estimated in 10 postabsorptive healthy men by determining the increment in the abundance of [13C]-leucine in quadriceps muscle protein during an intravenous infusion of L-[1-13C]leucine. FMPS in our subjects was 0.046 +/- 0.003%/h. Whole-body muscle protein synthesis (MPS) was calculated based on the estimation of muscle mass from creatinine excretion and compared with whole-body protein synthesis (WBPS) calculated from the nonoxidative portion of leucine flux. A significant correlation (r2 = 0.73, P less than 0.05) was found between MPS (44.7 +/- 3.4 mg.kg-1.h-1) and WBPS (167.8 +/- 8.5 mg.kg-1.h-1). The contribution of MPS to WBPS was 27 +/- 1%, which is comparable to the reports in other species. Morphometric analyses of adjacent muscle samples in eight subjects demonstrated that the biopsy specimens consisted of 86.5 +/- 2% muscular as opposed to other tissues. Because fiber type composition varies between biopsies, we examined the relationship between proportions of each fiber type and FMPS. Variation in the composition of biopsies and in fiber-type proportion did not affect the estimation of muscle protein synthesis rate. We conclude that stable isotope techniques using serial needle biopsies permit the direct measurement of FMPS in humans and that this estimation is correlated with an indirect estimation of WBPS.

Six male volunteers exercised on a cycle ergometer at 65% of maximal work load for 120 min on six occasions while ingesting water (W) only, four doses of maltodextrin (M) [0.92, 1.85, 2.77, and 3.70 g/kg body wt (4, 8, 12, and 16% M, respectively)], and sucrose (S) [1.85 g/kg body wt (8% S)]. Drinks were given during warm-up (8 ml/kg body wt) and each 15 min during exercise (2 ml/kg body wt). M and S were of high 13C natural abundance. Total carbohydrate (CHO) and fat oxidations were calculated from the nonprotein respiratory exchange ratio. M and S increased total CHO oxidation compared with W; no difference was observed between CHO solutions. Total CHO oxidation decreased continuously with time and more rapidly after W than after M or S. Fat oxidation increased continuously in all treatments. Oxidation rates of ingested CHO were 52 +/- 19, 76 +/- 12, 86 +/- 10, and 91 +/- 9 g/2 h for 4, 8, 12, and 16% M, respectively. The oxidation rate of S was 81 +/- 10 g/2 h (not different from 8% M), which indicated that the glucose polymer had no advantage over S. Oxidation rates of M and S increased to a plateau after 90-120 min of exercise. For all solutions except 4% M, the plateau oxidation rate was close to 1.0 g/min. Differences between 8, 12, and 16% M and 8% S were minimal such that ingestion of 8% M or S may well have had an optimal ergogenic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Leucine catabolism is regulated by either of the first two degradative steps: (reversible) transamination to the keto acid or subsequent decarboxylation. A method is described to measure rates of leucine transamination, reamination, and keto acid oxidation. The method is applied directly to humans by infusing the nonradioactive tracer, L-[15N,1-13C]leucine. Leucine transamination was found to be operating several times faster than the keto acid decarboxylation and to be of equal magnitude in adult human males under two different dietary conditions, postabsorptive and fed. These results indicate that decarboxylation, not transamination, is the rate-limiting step in normal human leucine metabolism.

Total body water was measured in 26 children and adolescents using the stable isotope H2O18. Body resistance was measured using a tetrapolar technique with a constant 50Khz, 800 microA alternating current. Total body water was highly correlated (r = 0.97; P less than 0.001) with height2/body resistance. Measurements of body resistance are non-invasive, rapid and readily acceptable to children. For these reasons the measurement of body resistance requires further investigation, including cross validation studies and is a potentially valuable technique for assessing body composition in the paediatric population.

Ten adult men were infused with L-[1-13C]leucine for 9 h commencing in the postabsorptive state (PA, 0-3 h), during the half-hourly feeding of low-protein meals (LP, protein = 2% calories, 3-6 h), and during feeding isoenergetic high-protein meals (HP, protein = 14% calories, 6-9 h). Leucine oxidation and turnover (protein synthesis and degradation) were determined from plasma alpha-[1-13C]ketoisocaproate enrichment and expired 13CO2 excretion measured during the third hour of each 3-h period. Plasma insulin increased markedly with feeding to a level that was maintained with both diets. The negative postabsorptive leucine balance became less negative during the LP meals (P < 0.01) and was positive with the HP meals (P < 0.01). The significant responses to feeding (all P < 0.01) were for oxidation -13% (PA-LP), +50% (LP-HP), and +29% (PA-HP); for degradation -24% (PA-LP), -30% (LP-HP), and -47% (PA-HP); and for synthesis -14% (PA-LP), +29% (LP-HP), and +11% (PA-HP). These data support a feeding mechanism involving both an insulin-mediated, protein-conserving influence of dietary energy that inhibits degradation, lowers amino acid levels, and reduces oxidation, and amino acid-mediated augmentation of the inhibition of degradation, a stimulation of synthesis, and an increase in oxidation when leucine dietary supply exceeds the capacity for its net deposition.