Pharmacokinetics, safety, and effects on exercise performance of L-arginine alpha-ketoglutarate in trained adult men.

OBJECTIVE: We evaluated the pharmacokinetics, safety, and efficacy of l-arginine alpha-ketoglutarate (AAKG) in trained adult men. METHODS: Subjects participated in two studies that employed a randomized, double-blind, controlled design. In study 1, 10 healthy men (30-50 y old) fasted for 8 h and then ingested 4 g of time-released or non-timed-released AAKG. Blood samples were taken for 8 h after AAKG ingestion to assess the pharmacokinetic profile of L-arginine. After 1 wk the alternative supplement was ingested. In study 2, which was placebo controlled, 35 resistance-trained adult men (30-50 y old) were randomly assigned to ingest 4 g of AAKG (three times a day, i.e., 12 g daily, n = 20) or placebo (n = 15). Participants performed 4 d of periodized resistance training per week for 8 wk. At 0, 4, and 8 wk of supplementation the following tests were performed: clinical blood markers, one repetition maximum bench press, isokinetic quadriceps muscle endurance, anaerobic power, aerobic capacity, total body water, body composition, and psychometric parameters tests. Data were analyzed by repeated measures analysis of variance. RESULTS: In study 1, significant differences were observed in plasma arginine levels in subjects taking non-timed-release and timed-release AAKG. In study 2, significant differences were observed in the AAKG group (P < 0.05) for 1RM bench press, Wingate peak power, blood glucose, and plasma arginine. No significant differences were observed between groups in body composition, total body water, isokinetic quadriceps muscle endurance, or aerobic capacity. CONCLUSION: AAKG supplementation appeared to be safe and well tolerated, and positively influenced 1RM bench press and Wingate peak power performance. AAKG did not influence body composition or aerobic capacity.

The acute effects of the thermogenic supplement Meltdown on energy expenditure, fat oxidation, and hemodynamic responses in young, healthy males.

The purpose of this study was to evaluate the effects of a thermogenic supplement, Meltdown, on energy expenditure, fat oxidation, and hemodynamics before and after maximal treadmill exercise. In a double-blind, randomized, placebo-controlled, cross-over design, 12 male participants underwent two testing sessions after consuming either the Meltdown or placebo supplement. While in a fasted state, participants rested for one hour, orally ingested either Meltdown or placebo and rested for another hour, performed a maximal treadmill exercise test, and then rested for another hour. Throughout the testing protocol, resting energy expenditure (REE) and respiratory exchange ratio (RER) were assessed. In addition, heart rate (HR) and blood pressure (BP) were assessed before and after exercise. Meltdown increased REE significantly more than placebo at 45 min (1.44 +/- 0.25 vs. 1.28 +/- 0.23 kcal/min; p = 0.003), 60 min (1.49 +/- 0.28 vs. 1.30 +/- 0.22 kcal/min; p = 0.025), and 120 min (1.51 +/- 0.26 vs. 1.33 +/- 0.27 kcals/min; p = 0.014) post-ingestion. Meltdown significantly decreased RER at 30 min (0.84 +/- 0.03 vs. 0.91 +/- 0.04; p = 0.022) and 45 min post-ingestion (0.82 +/- 0.04 vs. 0.89 +/- 0.05; p = 0.042), and immediately post-exercise (0.83 +/- 0.05 vs. 0.90 +/- 0.07; p = 0.009). Furthermore, over the course of the evaluation period, area under the curve assessment demonstrated that REE was significantly increased with Meltdown compared to placebo (992.5 +/- 133.1 vs. 895.1 +/- 296.1 kcals; p = 0.043), while RER was significantly less than placebo (5.55 +/- 0.61 vs. 5.89 +/- 0.44; p = 0.002) following ingestion. HR and BP were not significantly affected prior to exercise with either supplement (p > 0.05) and the exercise-induced increases for HR and BP decreased into recovery and were not different between supplements (p > 0.05). These data suggest that Meltdown enhances REE and fat oxidation more than placebo for several hours after ingestion in fully rested and post-exercise states without any adverse hemodynamic responses associated with maximal exercise.

Effects of a single dose of N-Acetyl-5-methoxytryptamine (Melatonin) and resistance exercise on the growth hormone/IGF-1 axis in young males and females.

Melatonin and resistance exercise alone have been shown to increase the levels of growth hormone (GH). The purpose of this study was to determine the effects of ingestion of a single dose of melatonin and heavy resistance exercise on serum GH, somatostatin (SST), and other hormones of the GH/insulin-like growth factor 1 (IGF-1) axis. Physically active males (n = 30) and females (n = 30) were randomly assigned to ingest either a melatonin supplement at 0.5 mg or 5.0 mg, or 1.0 mg of dextrose placebo. After a baseline blood sample, participants ingested the supplement and underwent blood sampling every 15 min for 60 min, at which point they underwent a single bout of resistance exercise with the leg press for 7 sets of 7 reps at 85% 1-RM. After exercise, participants provided additional blood samples every 15 min for a total of 120 min. Serum free GH, SST, IGF-1, IGFBP-1, and IGFBP-3 were determined with ELISA. Data were evaluated as the peak pre- and post-exercise values subtracted from baseline and the delta values analyzed with separate three-way ANOVA (p < 0.05). In males, when compared to placebo, 5.0 mg melatonin caused GH to increase (p = 0.017) and SST to decrease prior to exercise (p = 0.031), whereas both 0.5 and 5.0 mg melatonin were greater than placebo after exercise (p = 0.045) and less than placebo for SST. No significant differences occurred for IGF-1; however, males were shown to have higher levels of IGFBP-1 independent of supplementation (p = 0.004). The 5.0 mg melatonin dose resulted in higher IGFBP-3 in males (p = 0.017). In conclusion, for males 5.0 mg melatonin appears to increase serum GH while concomitantly lowering SST levels; however, when combined with resistance exercise both melatonin doses positively impacts GH levels in a manner not entirely dependent on SST.

Obesity: prevalence, theories, medical consequences, management, and research directions.

Obesity and its associated disorders are a growing epidemic across the world. Many genetic, physiological, and behavioral factors play a role in the etiology of obesity. Diet and exercise are known to play a valuable role in the treatment and prevention of obesity and associated disorders such as hypertension, heart disease, and diabetes. Therefore, the purpose of this review is to examine the prevalence, etiology, consequences, and treatment of obesity.