Ornithine supplementation and insulin release in bodybuilders.

Ornithine supplementation has gained popularity with athletes because of its alleged potential to release anabolic hormones, factors governing skeletal muscle hypertrophy. Three female and nine male bodybuilders served as subjects in a study to test the effectiveness of oral ornithine in bringing about the release of insulin, an anabolic hormone. After an overnight fast, subjects were administered 40, 100, or 170 mg.kg-1 L-ornithine.HCl by mouth in a random fashion on three consecutive Saturday mornings. Blood samples were drawn at baseline (T = 0), 45, and 90 min afterward. Serum ornithine levels were elevated (p < 0.01) at T = 45 and 90 min for all three dosage levels. However, serum insulin did not change from baseline levels at any dose of ornithine. The present findings show that ornithine is not an insulin secretagogue.

Nutrition and the precontest preparations of a male bodybuilder.

A 27-year-old male bodybuilder was studied during a 30-day precontest period when his goal was to lose fat and retain muscle mass. Weighted dietary intakes were obtained for each day of the study. The subject trained 6 days per week with weights and included an aerobic component on most days. Ergogenic drugs and a diuretic were self-administered. At the contest, the subject placed in the top three for his weight division. The strict diet enabled the subject to lose fat weight predictably in preparation for the contest. However, some weight lost was lean body tissue, suggesting the rate of loss was too fast. Blood chemistry studies revealed abnormalities, including hemoconcentration and alterations in cholesterol metabolism, which could have placed the subject at risk for thromboembolic phenomena because of increased blood viscosity. Those abnormalities could reflect the use of ergogenic drugs. For this subject, bodybuilding included diet, exercise, and drug regimens, which are common among competitive athletes.

Urinary 3-methylhistidine excretion increases with repeated weight training exercise.

This investigation examines the effect of progressive resistance weight training exercise on urinary 3-methylhistidine (3-MH) excretions in untrained subjects. For 19 consecutive days, 11 males were fed a weight maintenance, lactovegetarian diet which contained the Recommended Dietary Allowance (0.8g.kg-1.d-1) for protein. No exercise was performed for the first 7 d of the study. Subjects were strength tested on day 8 and performed upper and lower body weight training exercises from days 9-19. Complete, 24-h urine collections were obtained from each subject on a daily basis. Samples were assayed for creatinine and 3-MH. Stable baseline 3-MH values were present during the pre-exercise control period. Significant increases in 3-MH occurred by study day 11, which was the third day of weight training exercise. This was true regardless of whether the data were expressed by daily excretions (microM.d-1; P less than 0.01), per unit of body weight (microM.kg-1.d-1; P less than 0.005), or per unit of creatinine excretion (microM.g Creat-1.d-1; P less than 0.001). Since urinary 3-MH is an index of actin and myosin catabolism, these data support the hypothesis that the rate of skeletal muscle degradation is increased during strength building exercises.

Iron deficiency in female athletes: its prevalence and impact on performance.

The prevalence of iron deficiency and its impact on performance have not been adequately investigated in non-endurance athletes. This study evaluated these factors in 100 female intercollegiate athletes in various sports, and in 66 non-athletes. All subjects had determinations of hemoglobin, ferritin, and transferrin saturation. Athletes reported on diet, menses, and symptoms. Athletes and coaches described mood and performance. Iron-deficient athletes were treated with iron; others received placebo. The same data were collected at season's end. Initially 31/100 (31%) athletes had iron deficiency (ferritin less than 12 ng.ml-1; transferrin saturation less than 16%, or both) compared to 30/66 (45.5%) controls (not statistically significant). Compared to normal athletes, iron-deficient athletes did not have more symptoms of iron deficiency or differences in mood state, but they considered their performance to be worse (P less than 0.05). Their total iron intakes were similar, as were menstrual blood losses. At re-evaluation, 7/45 (15.6%) initially normal athletes were iron-deficient; 14/22 (63.6%) initially iron-deficient athletes were normal. Athletes receiving an iron supplement and their coaches did not report a greater improvement in performance or mood than athletes receiving a placebo. Female college athletes frequently had iron deficiency that could be successfully treated during the season, while some untreated normal athletes became iron-deficient. Iron deficiency and its treatment had no significant impact on symptoms or mood, but affected subjective assessment of performance.

Nutritional intake from food sources of high school football athletes.

Male high school football athletes served as subjects (no. = 134; age = 15.0 +/- 1.2 years, range = 12 to 18 years; weight = 67.7 +/- 13.9 kg) (mean +/- standard deviation) in a dietary survey project to characterize nutritional intake from food sources. Dietary intake data were collected using the recall method for 1 weekday during the summer when athletes participated in unsupervised, informal conditioning. Subjects were grouped by age as junior high (JR-HI: 12 to 14 years) or senior high (SR-HI: 15 to 18 years) students. Absolute mean energy and nutrient intakes, except for vitamin A, were statistically greater for SR-HI relative to JR-HI (p less than .02). These findings are consistent with age-related growth on nutritional intake. Mean nutritional intakes from food sources for SR-HI met or exceeded the RDAs. For JR-HI, mean intakes met or exceeded the RDAs except for energy (94% RDA) and zinc (87% RDA). Mean intakes exceeded those of a representative sample of same-age boys in the larger American population.

Failure of weight training to affect urinary indices of protein metabolism in men.

It is commonly believed by some athletes that strength building exercise "tears down" skeletal muscle tissue, thereby enhancing the dietary need for protein, but this has not been demonstrated. Ten college-age males served as subjects in a 15-d, controlled feeding study. The men were 23.1 +/- 2.2 yr old (mean +/- SD), 177 +/- 5 cm in height, and 71.7 +/- 9.1 kg in body weight (study days = 1 to 15). The lacto-ovo-vegetarian diet provided 0.9 g/kg protein and 15.1 +/- 0.4 MJ (3,604 +/- 104 kcal) . d-1 energy (study days = 6 to 15). On days 8 and 12, subjects participated in a standardized strength building, weight training exercise regimen. Post-exercise days 9 to 11 and 13 to 15 were designated for recovery. Daily (24-h) urine collections were analyzed for ammonia, creatinine, 3-methylhistidine, total nitrogen, and urea. There was no acute (24-h) effect of weight training exercise on any excretion levels. In particular, urinary 3-methylhistidine excretion data indicate that skeletal muscle protein catabolism was not changed by isolated bouts of weight training exercise.

Effect of short-term energy intake level and exercise on oxygen consumption in men.

The influence of short-term energy intake and cycle exercise on oxygen consumption in response to a 1.5 MJ test meal was investigated in ten young, adult men. On the morning after a previous day's "low-energy" intake (LE regimen) of 4.5 MJ, the mean resting oxygen consumption increased by 0.7 ml X kg-1 X min-1 after the test meal (P less than 0.025). After a "high-energy" intake (HE regimen) of 18.1 MJ, the resting measurement was unchanged (+0.4 ml X kg-1 X min-1) after the meal (n.s.). These trends are the reverse of what would be expected if oxygen consumption in response to feeding is a factor in the acute control of body weight. The mean fasting oxygen consumption during cycle exercise at 56% of VO2max (constant work) for both LE and HE prior intakes was not different at 31.1 ml X kg-1 X min-1. Oxygen consumption during exercise increased after feeding by 0.5 ml X kg-1 X min-1 on the LE regimen (n.s.) and decreased by 1.2 ml X kg-1 X min-1 on the HE regimen (n.s.). These results are also the reverse of what would be expected if oxygen consumption in response to exercise is related to short-term energy intake.

Exercise and protein intake effects on urinary 3-methylhistidine excretion.

A 28-day study was conducted with 13 adult men to determine the effect of weight lifting exercise and protein intake level on urinary 3-methylhistidine (3MH) excretion. Subjects were fed the RDA for protein [0.8 g/(kg BW X d)] or 3 X RDA; there were no-exercise and exercise groups at each intake. Comparisons of last 14-day, least-squares means among groups did not reveal differences in data treated by lean body weight [3MH/(kg LBW X d)] or by urinary creatinine excretion [3MH/(kg UCE X d)], but 3MH/(kg LBW X d) excretions were higher for exercise than no-exercise subjects. Regression analyses revealed linear, increasing trends in the 3MH/(kg LBW X d) data for RDA-exercise (p less than 0.03), 3 X RDA-exercise (p less than 0.01), and 3 X RDA-no-exercise (p less than 0.01) groups; 3MH/(g UCE X d) group data plots overlapped. Our findings for 3MH/(kg LBW X d) indicate that a weight lifting program was associated with increased 3MH excretions from adult males. As an index of skeletal muscle catabolism, an increase in 3HM excretion represents an increase in tissue catabolism. No significant effect of 3 X RDA protein intake on last 14-day 3MH excretions was observed; however, linear increases in 3MH/(kg LBW X d) for 3 X RDA-no-exercise subjects suggests a relationship. Trends of exercise- or protein intake-enhanced 3MH excretion could be masked by data as 3MH/(g UCE X d) if exercise or 3 X RDA protein intake can expand the body creatine pool independent of skeletal muscle mass.