Whey protein ingestion activates mTOR-dependent signalling after resistance exercise in young men : a double-blinded randomized controlled trial

The effect of resistance exercise with the ingestion of supplementary protein on the activation of the mTOR cascade, in human skeletal muscle has not been fully elucidated. In this study, the impact of a single bout of resistance exercise, immediately followed by a single dose of whey protein isolate (WPI) or placebo supplement, on the activation of mTOR signalling was analyzed. Young untrained men completed a maximal single-legged knee extension exercise bout and were randomized to ingest either WPI supplement (n = 7) or the placebo (n = 7). Muscle biopsies were taken from the vastus lateralis before, and 2, 4 and 24 hr post-exercise. WPI or placebo ingestion consumed immediately post-exercise had no impact on the phosphorylation of Akt (Ser⁴⁷³). However, WPI significantly enhanced phosphorylation of mTOR (Ser²⁴⁴⁸), 4E-BP1 (Thr^37/46) and p70S6K (Thr³⁸⁹) at 2 hr post-exercise. This study demonstrates that a single dose of WPI, when consumed in modest quantities, taken immediately after resistance exercise elicits an acute and transient activation of translation initiation within the exercised skeletal muscle.

Does the rate of foraging attempts predict ingestion rate for young-of-the-year brook trout (Salvelinus fontinalis) in the field?

To assess the costs and benefits of young fish adopting different behavioural tactics, field studies of juvenile salmonines have assumed that (but did not test whether) the rate of foraging attempts predicts ingestion rate. We tested this assumption by quantifying capture, ingestion, and rejection rates of potential prey items for individual young-of-the-year brook trout (Salvelinus fontinalis) in a lake. Overall, capture rate (a conservative estimate of the rate of foraging attempts) was only a fair predictor of overall ingestion rate (Kendall's 1 = 0.54) and only 46% of captured items (number/minute) were ingested. Surface capture rate was a poor predictor of surface ingestion rate (T = 0.27) and only 1% of captured items were ingested. In contrast, subsurface capture rate was an excellent predictor of subsurface ingestion rate (T = 0.75) and 93% of captured items were ingested. No benthic prey captures were observed. Fish that ingested a low proportion of captured items spent a greater proportion of time moving, moved faster, and pursued prey further than fish that ingested a higher proportion of captured items. Rejection of captured items can represent a significant and little appreciated component of the foraging cycle for young salmonid fishes.

Improved 2000-meter rowing performance in competitive oarswomen after caffeine ingestion

Eight competitive oarswomen (age, 22 ± 3 years; mass, 64.4 ± 3.8 kg) performed three simulated 2,000-m time trials on a rowing ergometer. The trials, which were preceded by a 24-hour dietary and training control and 72 hours of caffeine abstinence, were conducted 1 hour after ingesting caffeine (6 or 9 mg · kg-1 body mass) or placebo. Plasma free fatty acid concentrations before exercise were higher with caffeine than placebo (0.67 ± 0.34 vs. 0.72 ± 0.36 vs. 0.30 ± 0.10 mM for 6 and 9 mg · kg-1caffeine and placebo, respectively; p < .05). Performance time improved 0.7% (95% confidence interval [CI] 0 to 1.5%) with 6 mg · kg-1 caffeine and 1.3% (95% CI 0.5 to 2.0%) with 9 mg · kg-1 caffeine. The first 500 m of the 2,000 m was faster with the higher caffeine dose compared with placebo or the lower dose (1.53 ± 0.52 vs. 1.55 ± 0.62 and 1.56 ± 0.43 min; p = .02). We concluded that caffeine produces a worthwhile enhancement of performance in a controlled laboratory setting, primarily by improving the first 500 m of a 2,000-m row.

Self-reported risk-taking behavior during matched-frequency sessions of alcohol versus combined alcohol and energy drinks consumption: Does co-ingestion increase risk-taking?

Background: Emerging evidence indicates that consumers of alcohol mixed with energy drink (AmED) self-report lower odds of risk-taking after consuming AmED versus alcohol alone. However, these studies have been criticized for failing to control for relative frequency of AmED versus alcohol-only consumption sessions. These studies also do not account for quantity of consumption and general alcohol-related risk-taking propensity. The aims of the present study were to (i) compare rates of risk-taking in AmED versus alcohol sessions among consumers with matched frequency of use and (ii) identify consumption and person characteristics associated with risk-taking behavior in AmED sessions. Methods: Data were extracted from 2 Australian community samples and 1 New Zealand community sample of AmED consumers (n = 1,291). One-fifth (21%; n = 273) reported matched frequency of AmED and alcohol use. Results: The majority (55%) of matched-frequency participants consumed AmED and alcohol monthly or less. The matched-frequency sample reported significantly lower odds of engaging in 18 of 25 assessed risk behaviors in AmED versus alcohol sessions. Similar rates of engagement were evident across session type for the remaining behaviors, the majority of which were low prevalence (reported by <15%). Regression modeling indicated that risk-taking in AmED sessions was primarily associated with risk-taking in alcohol sessions, with increased average energy drink (ED) intake associated with certain risk behaviors (e.g., being physically hurt, not using contraception, and driving while over the legal alcohol limit). Conclusions: Bivariate analyses from a matched-frequency sample align with past research showing lower odds of risk-taking behavior after AmED versus alcohol consumption for the same individuals. Multivariate analyses showed that risk-taking in alcohol sessions had the strongest association with risk-taking in AmED sessions. However, hypotheses of increased risk-taking post-AmED consumption were partly supported: Greater ED intake was associated with increased likelihood of specific behaviors, including drink-driving, sexual behavior, and aggressive behaviors in the matched-frequency sample after controlling for alcohol intake and risk-taking in alcohol sessions. These findings highlight the need to consider both personal characteristics and beverage effects in harm reduction strategies for AmED consumers.

Soy protein ingestion results in less prolonged p70S6 kinase phosphorylation compared to whey protein after resistance exercise in older men

BACKGROUND: The phosphorylation of p70S6 Kinase (p70S6K) is an important step in the initiation of protein translation. p70S6K phosphorylation is enhanced with graded intakes of whey protein after resistance exercise. Soy protein ingestion results in lower muscle protein synthesis after exercise compared with whey; however, the underlying mechanisms responsible for this difference have not been reported. FINDINGS: 13 older men (60-75) completed an acute bout of lower body resistance exercise and ingested 30 g of soy protein or carbohydrate. Muscle biopsies were obtained in the rested and fasted state and 2 and 4 hours post exercise. Phosphorylation status of p70S6K was measured with western blot. Results were compared with previously reported data from the ingestion of 30 g of whey protein or placebo. p70S6K phosphorylation was increased 2, but not 4 hours post exercise with soy protein ingestion. p70S6K phosphorylation was not increased post exercise with carbohydrate ingestion. CONCLUSIONS: Ingesting 30 g of either whey or soy protein resulted in equivalent p70S6K phosphorylation at 2 hours post exercise, however, unlike whey, soy protein failed to promote prolonged phosphorylation of p70S6K to 4 hours post-exercise.

Co-ingestion of energy drinks with alcohol and other substances among a sample of people who regularly use ecstasy

INTRODUCTION AND AIMS: Despite the potential harms of mixing unregulated drugs with energy drinks (ED), research to date has primarily been focused on EDs co-ingested with alcohol. Consequently, the aim of the present study was to explore the rate of use, harms and correlates of EDs co-ingested with alcohol and other drugs among a sample of people who regularly use illicit stimulant drugs. DESIGN AND METHODS: In 2010, 693 Australians who regularly used ecstasy completed a 1-h interview about their past six-month ED and drug use. RESULTS: Three-quarters of the sample (77%) had recently consumed EDs with other substances, primarily alcohol (70%) and ecstasy (57%). People who consumed ED with alcohol versus those who had consumed ED with ecstasy and with alcohol (only 8% reported only consuming ED with ecstasy) had similar profiles in regards to demographics, drug use, mental health and drug-related problems. Primary motives for consuming ED with alcohol included increased alertness (59%), the taste (25%), to party for longer (23%) and to combat fatigue (16%). One-half (52%) and one-quarter (27%) of participants who consumed EDs with alcohol and with ecstasy respectively had recently experienced adverse outcomes post-consumption, primarily headaches (24% and 11%) and heart palpitations (21% and 14%). DISCUSSION AND CONCLUSIONS: Co-ingestion of EDs with licit and illicit drugs is common among people who regularly use ecstasy and related drugs. Adverse outcomes of co-ingestion suggest that targeted education regarding negative interactive drug effects is crucial for harm reduction. [Peacock A, Sindicich N, Dunn M, Whittaker E, Sutherland R, Entwistle G, Burns L, Bruno R. Co-Ingestion of Energy Drinks with Alcohol and Other Substances among a Sample of People Who Regularly Use Ecstasy. Drug Alcohol Rev 2015].

Visualization and quantitation of GLUT4 translocation in human skeletal muscle following glucose ingestion and exercise

Insulin- and contraction-stimulated increases in glucose uptake into skeletal
muscle occur in part as a result of the translocation of glucose transporter 4
(GLUT4) from intracellular stores to the plasma membrane (PM). This study
aimed to use immunofluorescence microscopy in human skeletal muscle to
quantify GLUT4 redistribution from intracellular stores to the PM in response
to glucose feeding and exercise. Percutaneous muscle biopsy samples were
taken from the m. vastus lateralis of ten insulin-sensitive men in the basal
state and following 30 min of cycling exercise (65% VO2 max). Muscle biopsy
samples were also taken from a second cohort of ten age-, BMI- and VO2 maxmatched insulin-sensitive men in the basal state and 30 and 60 min following
glucose feeding (75 g glucose). GLUT4 and dystrophin colocalization, measured
using the Pearson’s correlation coefficient, was increased following
30 min of cycling exercise (baseline r = 0.47 0.01; post exercise
r = 0.58 0.02; P < 0.001) and 30 min after glucose ingestion (baseline
r = 0.42 0.02; 30 min r = 0.46 0.02; P < 0.05). Large and small GLUT4
clusters were partially depleted following 30 min cycling exercise, but not
30 min after glucose feeding. This study has, for the first time, used immunofluorescence microscopy in human skeletal muscle to quantify increases in
GLUT4 and dystrophin colocalization and depletion of GLUT4 from large
and smaller clusters as evidence of net GLUT4 translocation to the PM.

The effect of double - blind carbohydrate ingestion during 60 km of self-paced exercise in warm ambient conditions

This study evaluated double blind ingestions of placebo (PLA) versus 6% carbohydrate (CHO) either as capsules (c) or beverage (b) during 60 km self-paced cycling in the heat (32°C and 50% relative humidity). Ten well-trained males (mean ± SD: 26±3 years; 64.5±7.7 kg and 70.7±8.8 ml.kg-1.min-1 maximal oxygen consumption) completed four separate 60 km time trials (TT) punctuated by 1 km sprints (14, 29, 44, 59 km) whilst ingesting either PLAb or PLAc or CHOb or CHOc. The TT was not different among treatments (PLAb 130.26 11.2 min, CHOb 140.5±18.1 min, PLAc 143.1±29.2 min, CHOc 137.3±20.1 min; P>0.05). Effect size (Cohen's d) for time was only moderate when comparing CHOb - PLAb (d = 0.68) and PLAb - PLA c (d = 0.57) whereas all other ES were 'trivial' to 'small'. Mean speed throughout the trial was significantly higher for PLAb only (P<0.05). Power output was only different (P<0.05) between the sprints and low intensity efforts within and across conditions. Core and mean skin temperatures were similar among trials. We conclude that CHO ingestion is of little or no benefit as a beverage compared with placebo during 60 km TT in the heat.

Ibuprofen ingestion does not affect markers of post-exercise muscle inflammation

PURPOSE: We investigated if oral ingestion of ibuprofen influenced leucocyte recruitment and infiltration following an acute bout of traditional resistance exercise Methods: Sixteen male subjects were divided into two groups that received the maximum over-the-counter dose of ibuprofen (1200mg d(-1)) or a similarly administered placebo following lower body resistance exercise. Muscle biopsies were taken from m.vastus lateralis and blood serum samples were obtained before and immediately after exercise, and at 3 and 24 h after exercise. Muscle cross-sections were stained with antibodies against neutrophils (CD66b and MPO) and macrophages (CD68). Muscle damage was assessed via creatine kinase and myoglobin in blood serum samples, and muscle soreness was rated on a ten-point pain scale.

RESULTS: The resistance exercise protocol stimulated a significant increase in the number of CD66b(+) and MPO(+) cells when measured 3 h post exercise. Serum creatine kinase, myoglobin and subjective muscle soreness all increased post-exercise. Muscle leucocyte infiltration, creatine kinase, myoglobin and subjective muscle soreness were unaffected by ibuprofen treatment when compared to placebo. There was also no association between increases in inflammatory leucocytes and any other marker of cellular muscle damage.

CONCLUSION: Ibuprofen administration had no effect on the accumulation of neutrophils, markers of muscle damage or muscle soreness during the first 24 h of post-exercise muscle recovery.

Pre-exercise nutritional strategies: effects on metabolism and performance

The goals of pre-exercise nutritional strategies are to optimise the availability of carbohydrate (CHO) and fluid. Ingestion of CHO 3-4 hr prior to exercise can increase liver and muscle glycogen stores and has been associated with enhanced endurance exercise performance. The metabolic effects of CHO ingestion persist for at least 6 hr. Although an increase in plasma insulin following CHO ingestion in the hour prior to exercise inhibits lipolysis and liver glucose output, and can lead to transient hypoglycemia during subsequent exercise, there is no convincing evidence that this is always associated with impaired exercise performance. Having said that, individual experience should inform individual practice. Interventions to increase plasma FFA availability prior to exercise have been shown to reduce CHO utilisation during exercise, but do not appear to have major ergogenic benefits. It is more difficult to hyperhydrate prior to exercise and although there has been interest in glycerol ingestion, to date research results have been equivocal. At the very least, athletes should ensure euhydration prior to exercise.

Effect of prior exercise on glucose metabolism in trained men.

Several studies have demonstrated that oral glucose tolerance is impaired in the immediate postexercise period. A double-tracer technique was used to examine glucose kinetics during a 2-h oral glucose (75 g) tolerance test (OGTT) 30 min after exercise (Ex, 55 min at 71 ± 2% of peak O₂ uptake) and 24 h after exercise (Rest) in endurance-trained men. The area under the plasma glucose curve was 71% greater in Ex than in Rest (P = 0.01). The higher glucose response occurred even though whole body rate of glucose disappearance was 24% higher after exercise (P = 0.04, main effect). Whole body rate of glucose appearance was 25% higher after exercise (P = 0.03, main effect). There were no differences in total (2 h) endogenous glucose appearance (R_aE) or the magnitude of suppression of R_aE, although R_aE was higher from 15 to 30 min during the OGTT in Ex. However, the cumulative appearance of oral glucose was 30% higher in Ex (P = 0.03, main effect). There were no differences in glucose clearance rate or plasma insulin responses between the two conditions. These results suggest that adaptations in splanchnic tissues by prior exercise facilitate greater glucose output from the splanchnic region after glucose ingestion, resulting in a greater glycemic response and, consequently, a greater rate of whole body glucose uptake.

Carbohydrate metabolism during exercise in females : effect of reduced fat availability

This study examined the effect of reduced plasma free fatty acid (FFA) availability on carbohydrate metabolism during exercise. Six untrained women cycled for 60 minutes at approximately 58% of maximum oxygen uptake after ingestion of a placebo (CON) or nicotinic acid (NA), 30 minutes before exercise (7.4 ± 0.5 mg·kg⁻¹ body weight), and at 0 minutes (3.7 ± 0.3 mg·kg⁻¹) and 30 minutes (3.7 ± 0.3 mg·kg⁻¹) of exercise. Glucose kinetics were measured using a primed, continuous infusion of [6,6-²H] glucose. Plasma FFA (CON, 0.86 ± 0.12; NA, 0.21 ± 0.11 mmol·L⁻¹ at 60 minutes, P < .05) and glycerol (CON, 0.34 ± 0.05; NA, 0.10 ± 0.04 mmol·L⁻¹ at 60 minutes, P < .05) were suppressed throughout exercise. Mean respiratory exchange ratio (RER) during exercise was higher (P < .05) in NA (0.89 ± 0.02) than CON (0.83 ± 0.02). Plasma glucose and glucose production were similar between trials. Total glucose uptake during exercise was greater (P < .05) in NA (1,876 ± 161 μmol·kg⁻¹) than in CON (1,525 ± 107 μmol·kg⁻¹). Total fat oxidation was reduced (P < .05) by approximately 32% during exercise in NA. Total carbohydrate oxidized was approximately 42% greater (P < .05) in NA (412 ± 40 mmol) than CON (290 ± 37 mmol), of which, approximately 16% (20 ± 10 mmol) could be attributed to glucose. Plasma insulin and glucagon were similar between trials. Catecholamines were higher (P < .05) during exercise in NA. In summary, during prolonged moderate exercise in untrained women, reduced FFA availability results in a compensatory increase in carbohydrate oxidation, which appears to be due predominantly to an increase in glycogen utilization, although there was a small, but significant, increase in whole body glucose uptake.

Regulation of glucose kinetics during intense exercise in humans: effects of α- and β-adrenergic blockade

This study examined the effect of combined α- and β-adrenergic blockade on glucose kinetics during intense exercise. Six endurance-trained men exercised for 20 minutes at approximately 78% of their peak oxygen consumption (V_O 2) following ingestion of a placebo (CON) or combined α- (prazosin hydrochloride) and β- (timolol maleate) adrenoceptor antagonists (BLK). Plasma glucose increased during exercise in CON (0 minutes: 5.5 ± 0.1; 20 minutes: 6.5 ± 0.3 mmol · L⁻¹, P < .05). In BLK, the exercise-induced increase in plasma glucose was abolished (0 minutes: 5.7 ± 0.3; 20 minutes: 5.7 ± 0.1 mmol · L⁻¹). Glucose kinetics were measured using a primed, continuous infusion of [6,6-²H] glucose. Glucose production was not different between trials; on average these values were 25.3 ± 3.9 and 30.9 ± 4.4 μmol · kg⁻¹ · min⁻¹ in CON and BLK, respectively. Glucose uptake during exercise was greater (P < .05) in BLK (30.6 ± 4.6 μmol · kg⁻¹ · min⁻¹) compared with CON (18.4 ± 2.5 μmol · kg⁻¹ · min⁻¹). In BLK, plasma insulin and catecholamines were higher (P < .05), while plasma glucagon was unchanged from CON. Free fatty acids (FFA) and glycerol were lower (P < .05) in BLK. These findings demonstrate that adrenergic blockade during intense exercise results in a blunted plasma glucose response that is due to enhanced glucose uptake, with no significant change in glucose production.