Plant Protein Blend Ingestion Stimulates Post-Exercise Myofibrillar Protein Synthesis Rates Equivalently to Whey in Resistance-Trained Adults.

PURPOSE: Whey protein ingestion is typically considered an optimal dietary strategy to maximize myofibrillar protein synthesis (MyoPS) following resistance exercise. While single source plant protein ingestion is typically less effective, at least partly, due to less favorable amino acid profiles, this could theoretically be overcome by blending plant-based proteins with complementary amino acid profiles. We compared the post-exercise MyoPS response following the ingestion of a novel plant-derived protein blend with an isonitrogenous bolus of whey protein. METHODS: Ten healthy, resistance trained, young adults (male/female: 8/2; age: 26 ± 6 y; BMI: 24 ± 3 kg·m-2) received a primed continuous infusion of L-[ring-2H5]-phenylalanine and completed a bout of bilateral leg resistance exercise before ingesting 32 g protein from whey (WHEY) or a plant protein blend (BLEND; 39.5% pea, 39.5% brown rice, 21.0% canola) in a randomized, double-blind crossover fashion. Blood and muscle samples were collected at rest, and 2 and 4 h after exercise and protein ingestion, to assess plasma amino acid concentrations, and postabsorptive and post-exercise MyoPS rates. RESULTS: Plasma essential amino acid availability over the 4 h postprandial post-exercise period was ~44% higher in WHEY compared with BLEND (P = 0.04). From equivalent postabsorptive values (WHEY, 0.042 ± 0.020%·h-1; BLEND, 0.043 ± 0.015%·h-1) MyoPS rates increased following exercise and protein ingestion (time effect; P < 0.001) over a 0-2 h (WHEY, 0.085 ± 0.037%·h-1; BLEND, 0.080 ± 0.037%·h-1) and 2-4 h (WHEY, 0.085 ± 0.036%·h-1; BLEND, 0.086 ± 0.034%·h-1) period, with no differences between conditions during either period or throughout the entire (0-4 h) postprandial period (time × condition interactions; all P > 0.05). CONCLUSIONS: Ingestion of a novel plant-based protein blend stimulates post-exercise MyoPS to an equivalent extent as a whey protein, demonstrating the utility of plant protein blends to optimize post-exercise skeletal muscle reconditioning.

Bridging the gap: Evidence-based practice guidelines for sports nutritionists.

Evidence-based practice is a systematic approach to decision-making developed in the 1990s to help healthcare professionals identify and use the best available evidence to guide clinical practice and patient outcomes amid a plethora of information in often challenging, time-constrained circumstances. Today's sports nutrition practitioners face similar challenges, as they must assess and judge the quality of evidence and its appropriateness to their athlete, in the often chaotic, time-pressed environment of professional sport. To this end, we present an adapted version of the evidence-based framework to support practitioners in navigating their way through the deluge of available information and guide their recommendations to athletes whilst also reflecting on their practice experience and skills as evidence-based practitioners, thus, helping to bridge the gap between science and practice in sport and exercise nutrition.

Nutritional Modulation of Sleep Latency, Duration, and Efficiency: A Randomized, Repeated-Measures, Double-Blind Deception Study.

PURPOSE: This study aimed to test the hypothesis that a novel nutritional blend composed of tryptophan, glycine, magnesium, tart cherry powder, and l -theanine enhances subjective and objective measures of sleep during free living conditions. METHODS: In a randomized, repeated-measures crossover and double-blind deception design, participants ( n = 9 males and 7 females, age = 24 ± 3 yr, body mass = 69.8 ± 11.6 kg, stature = 170.8 ± 9.1 cm) completed a 3-d familiarization period, followed by 3-d intervention and placebo trials. Subjective Pittsburgh Quality Sleep Index, Core Consensus Sleep Diary, and Karolinska Sleepiness Scale survey tools, alongside objective actigraphy measures of sleep, were assessed, with daily nutritional intake, activity, and light exposure standardized between trials. Participants provided daily urine samples for assessment of targeted and untargeted metabolomes. RESULTS: The intervention trial reduced sleep onset latency (-24 ± 25 min; P = 0.002), increased total sleep time (22 ± 32 min; P = 0.01), and increased sleep efficiency (2.4% ± 3.9%; P = 0.03), while also reducing morning sleepiness ( P = 0.02). Throughout the study, 75% of participants remained blinded to sleep assessment as a primary outcome measure, with 56% subjectively indicating improved sleep during the intervention trial. Metabolomic analysis highlighted several significantly altered metabolomes related to sleep regulation between trials, inclusive of 6-sulfatoxymelatonin, d -serine, and l -glutamic acid. CONCLUSIONS: Data demonstrate that using the proposed blend of novel nutritional ingredients during free living conditions reduced sleep onset latency, increased total sleep duration, and increased sleep efficiency, leading to reduced perceptions of morning sleepiness. These effects may be mediated by the upregulation of key metabolites involved in the neurophysiological modulation of the sleep/wake cycle.

13C-glucose-fructose labeling reveals comparable exogenous CHO oxidation during exercise when consuming 120 g/h in fluid, gel, jelly chew, or coingestion.

We examined the effects of carbohydrate (CHO) delivery form on exogenous CHO oxidation, gastrointestinal discomfort, and exercise capacity. In a randomized repeated-measures design [after 24 h of high CHO intake (8 g·kg-1) and preexercise meal (2 g·kg-1)], nine trained males ingested 120 g CHO·h-1 from fluid (DRINK), semisolid gel (GEL), solid jelly chew (CHEW), or a coingestion approach (MIX). Participants cycled for 180 min at 95% lactate threshold, followed by an exercise capacity test (150% lactate threshold). Peak rates of exogenous CHO oxidation (DRINK 1.56 ± 0.16, GEL 1.58 ± 0.13, CHEW 1.59 ± 0.08, MIX 1.66 ± 0.02 g·min-1) and oxidation efficiency (DRINK 72 ± 8%, GEL 72 ± 5%, CHEW 75 ± 5%, MIX, 75 ± 6%) were not different between trials (all P > 0.05). Despite ingesting 120 g·h-1, participants reported minimal symptoms of gastrointestinal distress across all trials. Exercise capacity was also not significantly different (all P > 0.05) between conditions (DRINK 446 ± 350, GEL 529 ± 396, CHEW 596 ± 416, MIX 469 ± 395 s). Data represent the first time that rates of exogenous CHO oxidation (via stable isotope methodology) have been simultaneously assessed with feeding strategies (i.e., preexercise CHO feeding and the different forms and combinations of CHO during exercise) commonly adopted by elite endurance athletes. We conclude that 120 g·h-1 CHO (in a 1:0.8 ratio of maltodextrin or glucose to fructose) is a practically tolerable strategy to promote high CHO availability and oxidation during exercise.NEW & NOTEWORTHY We demonstrate comparable rates of exogenous CHO oxidation from fluid, semisolid, solid, or a combination of sources. Considering the sustained high rates of total and exogenous CHO oxidation and relative lack of gastrointestinal symptoms, consuming 120 g CHO·h-1 appears to be a well-tolerated strategy to promote high CHO availability during exercise. Additionally, this is the first time that rates of exogenous CHO oxidation have been assessed with feeding strategies (e.g., coingestion of multiple CHO forms) typically reported by endurance athletes.

Carbohydrate improves exercise capacity but does not affect subcellular lipid droplet morphology, AMPK and p53 signalling in human skeletal muscle.

KEY POINTS: Muscle glycogen and intramuscular triglycerides (IMTG, stored in lipid droplets) are important energy substrates during prolonged exercise. Exercise-induced changes in lipid droplet (LD) morphology (i.e. LD size and number) have not yet been studied under nutritional conditions typically adopted by elite endurance athletes, that is, after carbohydrate (CHO) loading and CHO feeding during exercise. We report for the first time that exercise reduces IMTG content in both central and peripheral regions of type I and IIa fibres, reflective of decreased LD number in both fibre types whereas reductions in LD size were exclusive to type I fibres. Additionally, CHO feeding does not alter subcellular IMTG utilisation, LD morphology or muscle glycogen utilisation in type I or IIa/II fibres. In the absence of alterations to muscle fuel selection, CHO feeding does not attenuate cell signalling pathways with regulatory roles in mitochondrial biogenesis. ABSTRACT: We examined the effects of carbohydrate (CHO) feeding on lipid droplet (LD) morphology, muscle glycogen utilisation and exercise-induced skeletal muscle cell signalling. After a 36 h CHO loading protocol and pre-exercise meal (12 and 2 g kg-1 , respectively), eight trained males ingested 0, 45 or 90 g CHO h-1 during 180 min cycling at lactate threshold followed by an exercise capacity test (150% lactate threshold). Muscle biopsies were obtained pre- and post-completion of submaximal exercise. Exercise decreased (P < 0.01) glycogen concentration to comparable levels (∼700 to 250 mmol kg-1 DW), though utilisation was greater in type I (∼40%) versus type II fibres (∼10%) (P < 0.01). LD content decreased in type I (∼50%) and type IIa fibres (∼30%) (P < 0.01), with greater utilisation in type I fibres (P < 0.01). CHO feeding did not affect glycogen or IMTG utilisation in type I or II fibres (all P > 0.05). Exercise decreased LD number within central and peripheral regions of both type I and IIa fibres, though reduced LD size was exclusive to type I fibres. Exercise induced (all P < 0.05) comparable AMPKThr172 (∼4-fold), p53Ser15 (∼2-fold) and CaMKIIThr268 phosphorylation (∼2-fold) with no effects of CHO feeding (all P > 0.05). CHO increased exercise capacity where 90 g h-1 (233 ± 133 s) > 45 g h-1 (156 ± 66 s; P = 0.06) > 0 g h-1 (108 ± 54 s; P = 0.03). In conditions of high pre-exercise CHO availability, we conclude CHO feeding does not influence exercise-induced changes in LD morphology, glycogen utilisation or cell signalling pathways with regulatory roles in mitochondrial biogenesis.

Graded reductions in pre-exercise glycogen concentration do not augment exercise-induced nuclear AMPK and PGC-1α protein content in human muscle.

NEW FINDINGS: What is the central question of this study? What is the absolute level of pre-exercise glycogen concentration required to augment the exercise-induced signalling response regulating mitochondrial biogenesis? What is the main finding and its importance? Commencing high-intensity endurance exercise with reduced pre-exercise muscle glycogen concentrations confers no additional benefit to the early signalling responses that regulate mitochondrial biogenesis. ABSTRACT: We examined the effects of graded muscle glycogen on the subcellular location and protein content of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and mRNA expression of genes associated with the regulation of mitochondrial biogenesis and substrate utilisation in human skeletal muscle. In a repeated measures design, eight trained male cyclists completed acute high-intensity interval (HIT) cycling (8 × 5 min at 80% peak power output) with graded concentrations of pre-exercise muscle glycogen. Following initial glycogen-depleting exercise, subjects ingested  2 g kg-1  (L-CHO), 6 g kg-1 (M-CHO) or 14 g kg-1 (H-CHO) of carbohydrate during a 36 h period, such that exercise was commenced with graded (P < 0.05) muscle glycogen concentrations (mmol (kg dw)-1 : H-CHO, 531 ± 83; M-CHO, 332 ± 88; L-CHO, 208 ± 79). Exercise depleted muscle glycogen to <300 mmol (kg dw)-1 in all trials (mmol (kg dw)-1 : H-CHO, 270 ± 88; M-CHO, 173 ± 74; L-CHO, 100 ± 42) and induced comparable increases in nuclear AMPK protein content (∼2-fold) and PGC-1α (∼5-fold), p53 (∼1.5-fold) and carnitine palmitoyltransferase 1 (∼2-fold) mRNA between trials (all P < 0.05). The magnitude of increase in PGC-1α mRNA was also positively correlated with post-exercise glycogen concentration (P < 0.05). In contrast, neither exercise nor carbohydrate availability affected the subcellular location of PGC-1α protein or PPAR, SCO2, SIRT1, DRP1, MFN2 or CD36 mRNA. Using a sleep-low, train-low model with a high-intensity endurance exercise stimulus, we conclude that pre-exercise muscle glycogen does not modulate skeletal muscle cell signalling.

Graded reductions in preexercise muscle glycogen impair exercise capacity but do not augment skeletal muscle cell signaling: implications for CHO periodization.

We examined the effects of graded muscle glycogen on exercise capacity and modulation of skeletal muscle signaling pathways associated with the regulation of mitochondrial biogenesis. In a repeated-measures design, eight men completed a sleep-low, train-low model comprising an evening glycogen-depleting cycling protocol followed by an exhaustive exercise capacity test [8 × 3 min at 80% peak power output (PPO), followed by 1-min efforts at 80% PPO until exhaustion] the subsequent morning. After glycogen-depleting exercise, subjects ingested a total of 0 g/kg (L-CHO), 3.6 g/kg (M-CHO), or 7.6 g/kg (H-CHO) of carbohydrate (CHO) during a 6-h period before sleeping, such that exercise was commenced the next morning with graded (P < 0.05) muscle glycogen concentrations (means ± SD: L-CHO: 88 ± 43, M-CHO: 185 ± 62, H-CHO: 278 ± 47 mmol/kg dry wt). Despite differences (P < 0.05) in exercise capacity at 80% PPO between trials (L-CHO: 18 ± 7, M-CHO: 36 ± 3, H-CHO: 44 ± 9 min), exercise induced comparable AMPKThr172 phosphorylation (~4-fold) and PGC-1α mRNA expression (~5-fold) after exercise and 3 h after exercise, respectively. In contrast, neither exercise nor CHO availability affected the phosphorylation of p38MAPKThr180/Tyr182 or CaMKIIThr268 or mRNA expression of p53, Tfam, CPT-1, CD36, or PDK4. Data demonstrate that when exercise is commenced with muscle glycogen < 300 mmol/kg dry wt, further graded reductions of 100 mmol/kg dry weight impair exercise capacity but do not augment skeletal muscle cell signaling. NEW & NOTEWORTHY We provide novel data demonstrating that when exercise is commenced with muscle glycogen below 300 mmol/kg dry wt (as achieved with the sleep-low, train-low model) further graded reductions in preexercise muscle glycogen of 100 mmol/kg dry wt reduce exercise capacity at 80% peak power output by 20-50% but do not augment skeletal muscle cell signaling.

Regulation of Muscle Glycogen Metabolism during Exercise: Implications for Endurance Performance and Training Adaptations.

Since the introduction of the muscle biopsy technique in the late 1960s, our understanding of the regulation of muscle glycogen storage and metabolism has advanced considerably. Muscle glycogenolysis and rates of carbohydrate (CHO) oxidation are affected by factors such as exercise intensity, duration, training status and substrate availability. Such changes to the global exercise stimulus exert regulatory effects on key enzymes and transport proteins via both hormonal control and local allosteric regulation. Given the well-documented effects of high CHO availability on promoting exercise performance, elite endurance athletes are typically advised to ensure high CHO availability before, during and after high-intensity training sessions or competition. Nonetheless, in recognition that the glycogen granule is more than a simple fuel store, it is now also accepted that glycogen is a potent regulator of the molecular cell signaling pathways that regulate the oxidative phenotype. Accordingly, the concept of deliberately training with low CHO availability has now gained increased popularity amongst athletic circles. In this review, we present an overview of the regulatory control of CHO metabolism during exercise (with a specific emphasis on muscle glycogen utilization) in order to discuss the effects of both high and low CHO availability on modulating exercise performance and training adaptations, respectively.

Fuel for the Work Required: A Theoretical Framework for Carbohydrate Periodization and the Glycogen Threshold Hypothesis.

Deliberately training with reduced carbohydrate (CHO) availability to enhance endurance-training-induced metabolic adaptations of skeletal muscle (i.e. the 'train low, compete high' paradigm) is a hot topic within sport nutrition. Train-low studies involve periodically training (e.g., 30-50% of training sessions) with reduced CHO availability, where train-low models include twice per day training, fasted training, post-exercise CHO restriction and 'sleep low, train low'. When compared with high CHO availability, data suggest that augmented cell signalling (73% of 11 studies), gene expression (75% of 12 studies) and training-induced increases in oxidative enzyme activity/protein content (78% of 9 studies) associated with 'train low' are especially apparent when training sessions are commenced within a specific range of muscle glycogen concentrations. Nonetheless, such muscle adaptations do not always translate to improved exercise performance (e.g. 37 and 63% of 11 studies show improvements or no change, respectively). Herein, we present our rationale for the glycogen threshold hypothesis, a window of muscle glycogen concentrations that simultaneously permits completion of required training workloads and activation of the molecular machinery regulating training adaptations. We also present the 'fuel for the work required' paradigm (representative of an amalgamation of train-low models) whereby CHO availability is adjusted in accordance with the demands of the upcoming training session(s). In order to strategically implement train-low sessions, our challenge now is to quantify the glycogen cost of habitual training sessions (so as to inform the attainment of any potential threshold) and ensure absolute training intensity is not compromised, while also creating a metabolic milieu conducive to facilitating the endurance phenotype.