Search Results

L-arginine may enhance endurance performance mediated by two primary mechanisms including enhanced secretion of endogenous growth hormone (GH) and as a precursor of nitric oxide (NO); however, research in trained participants has been equivocal. The purpose was to investigate the effect of acute L-arginine ingestion on the hormonal and metabolic response during submaximal exercise in trained cyclists. Fifteen aerobically trained men (age: 28 ± 5 y; body mass: 77.4 ± 9.5 kg; height: 180.9 ± 7.9 cm; VO_2max: 59.6 ± 5.9 ml·kg^-1·min⁻¹) participated in a randomized, double-blind, crossover study. Subjects consumed L-arginine (ARG; 0.075 g·kg^-1 body mass) or a placebo (PLA) before performing an acute bout of submaximal exercise (60 min at 80% of power output achieved at ventilatory threshold). The ARG condition significantly increased plasma L-arginine concentrations (~146%), while no change was detected in the PLA condition. There were no differences between conditions for GH, nonesterified fatty acids (NEFA), lactate, glucose, VO₂, VCO₂, RER, CHO oxidation, and NO_x. There was reduced fat oxidation at the start of exercise (ARG: 0.36 ± 0.25 vs. PLA: 0.42 ± 0.23 g·min⁻¹, p < .05) and an elevated plasma glycerol concentrations at the 45-min time point (ARG: 340.3 vs. PLA: 288.5 μmol·L^-1, p < .05) after L-arginine consumption. In conclusion, the acute ingestion of L-arginine did not alter any hormonal, metabolic, or cardio-respiratory responses during submaximal exercise except for a small but significant increase in glycerol at the 45-min time point and a reduction in fat oxidation at the start of exercise.

The purpose was to investigate the effects of a controlled typical 1-day diet supplemented with two different doses of whey protein isolate on blood amino acid profiles and hormonal concentrations following the final meal. Nine males (age: 29.6 ± 6.3 yrs) completed four conditions in random order: a control (C) condition of a typical mixed diet containing ~10% protein (0.8 g·kg–1), 65% carbohydrate, and 25% fat; a placebo (P) condition calorically matched with carbohydrate to the whey protein conditions; a low-dose condition of 0.8 grams of whey protein isolate per kilogram body mass per day (g·kg–1·d–1; W1) in addition to the typical mixed diet; or a high-dose condition of 1.6 g·kg–1·d–1 (W2) of supplemental whey protein in addition to the typical mixed diet. Following the final meal, significant (p < .05) increases in total amino acids, essential amino acids (EAA), branch-chained amino acids (BCAA), and leucine were observed in plasma with whey protein supplementation while no changes were observed in the control and placebo conditions. There was no significant group difference for glucose, insulin, testosterone, cortisol, or growth hormone. In conclusion, supplementing a typical daily food intake consisting of 0.8 g of protein·kg–1·d–1 with a whey protein isolate (an additional 0.8 or 1.6 g·kg–1·d–1) significantly elevated total amino acids, EAA, BCAA, and leucine but had no effect on glucose, insulin, testosterone, cortisol, or growth hormone following the final meal. Future acute and chronic supplementation research examining the physiological and health outcomes associated with elevated amino acid profiles is warranted.

Acute resistance exercise and L-arginine have both been shown to independently elevate plasma growth hormone (GH) concentrations; however, their combined effect is controversial. The purpose was to investigate the combined effects of resistance exercise and L-arginine supplementation on plasma L-arginine, GH, GH secretagogues, and IGF-1 in strength trained participants. Fourteen strength trained males (age: 25 ± 4 y; body mass: 81.4 ± 9.0 kg; height: 179.4 ± 6.9 cm; and training experience: 6.3 ± 3.4 y) participated in a randomized double-blind crossover design (separated by ~7 days). Subjects reported to the laboratory at 08:00 in a fasted state, consumed L-arginine (ARG; 0.075 g·kg⁻¹ body mass) or a placebo (PLA) before performing an acute bout of resistance exercise (3 sets of 8 exercises, 10 repetitions at ~75% 1RM). Blood samples were collected at rest, before exercise, and at 0, 15, 30, and 60 min of rest-recovery. The ARG condition significantly increased plasma L-arginine concentrations (~120%) while no change was detected in the PLA condition. There were no differences between conditions for GH, GH-releasing hormone, ghrelin, or IGF-1 at any time point. GH-inhibiting hormone was significantly lower in the ARG condition. However, integrated area under the curve for GH was blunted in the ARG condition (L-arginine = 288.4 ± 368.7 vs. placebo = 487.9 ± 482.0 min·ng·mL⁻¹, p < .05). L-arginine ingested before resistance exercise significantly elevated plasma L-arginine concentration but attenuated plasma GH in strength trained individuals despite a lower GHIH. Furthermore our data shows that the GH suppression was not due to a GH or IGF-1 induced autonegative feedback loop.

Creatine (Cr) supplementation increases muscle mass, strength, and power. Arginine α-ketoglutarate (A-AKG) is a precursor for nitric oxide production and has the potential to improve blood flow and nutrient delivery (i.e., Cr) to muscles. This study compared a commercial dietary supplement of Cr, A-AKG, glutamine, taurine, branchedchain amino acids, and medium-chain triglycerides with Cr alone or placebo on exercise performance and body composition. Thirty-five men (~23 yr) were randomized to Cr + A-AKG (0.1 g · kg⁻¹ · d⁻¹ Cr + 0.075 g · kg⁻¹ · d⁻¹ A-AKG, n = 12), Cr (0.1 g · kg⁻¹ · d⁻¹, n = 11), or placebo (1 g · kg⁻¹ · d⁻¹ sucrose, n = 12) for 10 d. Body composition, muscle endurance (bench press), and peak and average power (Wingate tests) were measured before and after supplementation. Bench-press repetitions over 3 sets increased with Cr + A-AKG (30.9 ==6.6 → 34.9 ± 8.7 reps; p < .01) and Cr (27.6 ± 5.9 → 31.0 ± 7.6 reps; p < .01), with no change for placebo (26.8 ± 5.0 → 27.1 ± 6.3 reps). Peak power significantly increased in Cr + A-AKG (741 ± 112 → 794 ± 92 W; p < .01), with no changes in Cr (722 ± 138 → 730 ± 144 W) and placebo (696 ± 63 → 705 ± 77 W). There were no differences in average power between groups over time. Only the Cr-only group increased total body mass (79.9 ± 13.0→81.1 ± 13.8 kg; p < .01), with no significant changes in lean-tissue or fat mass. These results suggest that Cr alone and in combination with A-AKG improves upper body muscle endurance, and Cr + A-AKG supplementation improves peak power output on repeated Wingate tests.

The purpose of this study was to determine the effects of Red Bull energy drink on Wingate cycle performance and muscle endurance. Healthy young adults (N = 15, 11 men, 4 women, 21 ± 5 y old) participated in a crossover study in which they were randomized to supplement with Red Bull (2 mg/kg body mass of caffeine) or isoenergetic, isovolumetric, noncaffeinated placebo, separated by 7 d. Muscle endurance (bench press) was assessed by the maximum number of repetitions over 3 sets (separated by 1-min rest intervals) at an intensity corresponding to 70% of baseline 1-repetition maximum. Three 30-s Wingate cycling tests (load = 0.075 kp/kg body mass), with 2 min recovery between tests, were used to assess peak and average power output. Red Bull energy drink significantly increased total bench-press repetitions over 3 sets (Red Bull = 34 ± 9 vs. placebo = 32 ± 8, P < 0.05) but had no effect on Wingate peak or average power (Red Bull = 701 ± 124 W vs. placebo = 700 ± 132 W, Red Bull = 479 ± 74 W vs. placebo = 471 ± 74 W, respectively). Red Bull energy drink significantly increased upper body muscle endurance but had no effect on anaerobic peak or average power during repeated Wingate cycling tests in young healthy adults.

High-intensity interval training (HIIT) has been shown to improve cardiorespiratory fitness, performance, body composition, and insulin sensitivity. Creatine (Cr) supplementation may augment responses to HIIT, leading to even greater physiological adaptations. The purpose of this study was to determine the effects of 4 weeks of HIIT (three sessions/week) combined with Cr supplementation in recreationally active females. Seventeen females (age = 23 ± 4 yrs; BMI = 23.4 ± 2.4) were randomly assigned to either Cr (Cr; 0.3 g・kg^-1・d^-1 for 5 d followed by 0.1 g・kg^-1・d^-1 for 23 days; n = 9) or placebo (PLA; n = 8). Before and after the intervention, VO_2peak, ventilatory threshold (VT), time-trial performance, lean body mass and fat mass, and insulin sensitivity were assessed. HIIT improved VO_2peak (Cr = +10.2%; PLA = +8.8%), VT (Cr = +12.7%; PLA = +9.9%), and time-trial performance (Cr = -11.5%; PLA = -11.6%) with no differences between groups (time main effects, all p < .001). There were no changes over time for fat mass (Cr = -0.3%; PLA = +4.3%), whole-body lean mass (Cr = +0.5%; PLA = -0.9%), or insulin resistance (Cr = +3.9%; PLA = +18.7%). In conclusion, HIIT is an effective way to improve cardiorespiratory fitness, VT, and time-trial performance. The addition of Cr to HIIT did not augment improvements in cardiorespiratory fitness, performance or body composition in recreationally active females.

The purpose was to investigate the effects of CYP1A2 −163C > A polymorphism on the effects of acute caffeine (CAF) supplementation on anaerobic power in trained males. Sixteen trained males (age: 21.6 ± 7.1 years; height: 179.7 ± 5.6 cm; body mass: 72.15 ± 6.8 kg) participated in a randomized, double-blind, placebo (PLA) controlled crossover design. Participants supplemented with CAF (6 mg/kg of body mass) and an isovolumetric PLA (maltodextrin) in random order and separated by 7 days, before an all-out 30-s anaerobic cycling test to determine peak, average, and minimum power output, and fatigue index. Genomic deoxyribonucleic acid was extracted to identify each participants CYP1A2 genotype. Six participants expressed AA homozygote and 10 expressed C alleles. There was a treatment by genotype interaction for peak power output (p = .041, η² = .265, observed power = 0.552) with only those expressing AA genotype showing improvement following CAF supplementation compared with PLA (CAF: 693 ± 108 watts vs. PLA: 655 ± 97 watts; p = .039), while no difference between treatments was noted in those expressing C alleles (CAF: 614 ± 92 watts vs. PLA: 659 ± 144 watts; p = .135). There were no other interaction or main effects for average or minimum power output, or fatigue index (p > .05). In conclusion, the ingestion of 6 mg/kg of CAF improved peak power output only in participants with the AA genotype compared with PLA; however, expression of the CYP1A2 did not influence average or minimum power output or fatigue index.

Despite the abundance of research investigating the efficacy of caffeine supplementation on exercise performance, the physiological and biochemical responses to caffeine supplementation during intermittent activities are less evident. This study investigated the acute effects of caffeine supplementation on measures of exercise performance, ratings of perceived exertion, and biomarkers of oxidative stress induced by an acute bout of sprint interval training. In a randomized crossover design, 12 healthy males (age: 26 ± 4 years, height: 177.5 ± 6 cm, body mass: 80.7 ± 7.6 kg) ingested 6 mg/kg of caffeine or placebo 60 min prior to performing sprint interval training (12 × 6 s “all-out sprints” interspersed by 60 s of rest). Performance scores and ratings of perceived exertion were assessed after every sprint. Blood samples were collected before supplementation, prior to and following each sprint, and 5 and 60 min after the last sprint. Caffeine had no effect on any performance measures, ratings of perceived exertion, or biomarkers of oxidative stress (p > .05). In conclusion, caffeine supplementation does not improve performance or decrease oxidative stress after an acute bout of sprint interval training.