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We have studied the effect of a pharmacological dose of testosterone enanthate (3 mg.kg-1.wk-1 for 12 wk) on muscle mass and total-body potassium and on whole-body and muscle protein synthesis in normal male subjects. Muscle mass estimated by creatinine excretion increased in all nine subjects (20% mean increase, P less than 0.02); total body potassium mass estimated by 40K counting increased in all subjects (12% mean increase, P less than 0.0001). In four subjects, a primed continuous infusion protocol with L-[1-13C]leucine was used to determine whole-body leucine flux and oxidation. Whole-body protein synthesis was estimated from nonoxidative flux. Muscle protein synthesis rate was determined by measuring [13C]leucine incorporation into muscle samples obtained by needle biopsy. Testosterone increased muscle protein synthesis in all subjects (27% mean increase, P less than 0.05). Leucine oxidation decreased slightly (17% mean decrease, P less than 0.01), but whole-body protein synthesis did not change significantly. Muscle morphometry showed no significant increase in muscle fiber diameter. These studies suggest that testosterone increases muscle mass by increasing muscle protein synthesis.

Lean and fat compartments of the body are companions. Dietary alterations induce changes in both compartments.

In a group of 34 adult and child subjects a high correlation (r = 0.988) was found between lean body mass, as determined by potassium-40 counting, and urinary creatinine excretion. The effect of technical errors was reduced by averaging the results of two or three 40K assays on each subject, and by making consecutive 3-day collections of urine. It appears that one can make a reasonable estimate of lean body mass from urinary creatinine excretion.

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In most situations involving a significant change in body weight, both fat‐free body mass (FFM) and body fat participate, but the relative contribution of FFM and fat to the total weight change is influenced by the initial body fat content. Overfeeding: In experiments of at least 3‐weeks' duration, the weight gain of thin people comprises 60–70% lean tissues, whereas in the obese it is 30–40%. Underfeeding: In humans, there is an inverse curvilinear relationship between initial body fat content and the proportion of weight loss consisting of lean tissue. The same trend holds for animals and birds, including loss during hibernation. Another factor is the magnitude of the energy deficit: as energy intake is reduced, lean tissue makes up an increasing fraction of the total weight loss. Exercise: If individuals lose much weight with exercise, the result is usually some loss of lean tissue as well as fat, and once again the proportion of lean loss to total weight loss is greater in thin people than in those who have larger body fat burdens. Members of twin pairs often differ in weight. In thin individuals, lean accounts for about half of the intrapair weight difference, whereas in the obese it accounts for only one quarter. Body fat content must be taken into account in evaluating body composition changes induced by nutrition and exercise.

1. Thirteen adult females and two males were overfed a total of 79-1 59 MJ (1900G38 000 kcal) during a 3-week period at the Clinical Research Center, Rochester. The average energy cost of the weight gain was 28 kJ (6.7 kcal)/g, and about half the gain consisted of lean body mass (LBM) as estimated by 40K counting.2. A survey of the literature disclosed twenty-eight normal males and five females who had been overfed a total of 104362 MJ (2500&87000 kcal) under controlled conditions: twenty-five of these had assays of body composition, and three had complete nitrogen balances.3. When these values were combined with those from our subjects (total forty-eight), there was a significant correlation between weight gain and total excess energy consumed ( r 0.77, P < 0.01) and between LBM gain and excess energy (r 0.49, P < 0.01). Based on means the energy cost was 33.7 kJ (8.05 kcal)/g gain and 43.6% of the gain was LBM; from regression analysis these values were 33.7 kJ (8.05 kcal)/g gain and 38.4% of gain as LBM. 4. Individual variations in the response could not be explained on the basis of sex, initial body-weight or fat content, duration of overfeeding, type of food eaten, amount of daily food consumption or, in a subset of subjects, on smoking behaviour.5. The average energy cost of the weight gain was close to the theoretical value of 33.8 kJ (8.08 kcal)/g derived from the composition of the tissue gained.The relation of energy intake to body-weight status is a topic of current interest. When human subjects are studied under controlled conditions energy deficits lead to weight loss, and the greater the deficit the greater is the loss. Does the converse hold true for excess energy intake, and do such gains involve fat or lean, or both? Do women gain weight more easily than men? Do thin people gain weight less easily than those who are overweight?A number of short-term overfeeding studies have been done on normal human subjects during the past 50 years, ranging from the early studies of Cuthbertson et al. (1937) to the most recent one of Dallosso & James (1984a, b), and these have shown that nitrogen retention occurs as weight is gahed. However, longer-term studies (of 2 weeks or more) provide for better quantification of the energy cost of weight gain and of the induced changes in body composition. Several studies have been reported in which subjects were fed under controlled conditions and observations were made on changes in body composition for periods of 2-7 weeks (Wiley & Newburgh, 1931; Passmore et al. 1955a, b ; Miller & Mumford, 1967a, b ;Goldman et al. 1975;Norgan & Durnin, 1980; Webb & Annis, 1983). Almost all the subjFcts were males.The present report describes our studies of deliberate overfeeding of human subjects and uses these findings, together with those reported by others, to examine the questions posed previously. Overall, these studies encompass a wide range of energy intakes and of duration of overfeeding, a variety of diets, a range of initial body-weights, and include both sexes.

FFM loss is not inevitable during adulthood-at least up to age 81 y, the oldest age yet studied. The magnitude and direction of the FFM change, be it positive or negative, is strongly influenced by change in body weight.