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The present study compared the effects of postexercise carbohydrate plus protein (CHO+PROT) and carbohydrate (CHO)-only supplementation on muscle glycogen metabolism, anabolic cell signaling, and subsequent exercise performance. Nine endurance-trained males cycled twice to exhaustion (muscle glycogen decreased from ~495 to ~125 mmol/kg dry wt) and received either CHO only (1.2 g·kg-1·h-1) or CHO+PROT (0.8/0.4 g·kg-1·h-1) during the first 90 min of recovery. Glycogen content was similar before the performance test after 5 h of recovery. Glycogen synthase (GS) fractional activity increased after exhaustive exercise and remained activated 5 h after, despite substantial glycogen synthesis (176.1 ± 19.1 and 204.6 ± 27.0 mmol/kg dry wt in CHO and CHO+PROT, respectively; P = 0.15). Phosphorylation of GS at site 3 and site 2+2a remained low during recovery. After the 5-h recovery, cycling time to exhaustion was improved by CHO+PROT supplementation compared with CHO supplementation (54.6 ± 11.0 vs. 46.1 ± 9.8 min; P = 0.009). After the performance test, muscle glycogen was equally reduced in CHO+PROT and CHO. Akt Ser473 and p70s6k Thr389 phosphorylation was elevated after 5 h of recovery. There were no differences in Akt Ser473, p70s6k Thr389, or TSC2 Thr1462 phosphorylation between treatments. Nitrogen balance was positive in CHO+PROT (19.6 ± 7.6 mg nitrogen/kg; P = 0.04) and higher than CHO (-10.7 ± 6.3 mg nitrogen/kg; P = 0.009). CHO+PROT supplementation during exercise recovery improved subsequent endurance performance relative to consuming CHO only. This improved performance after CHO+PROT supplementation could not be accounted for by differences in glycogen metabolism or anabolic cell signaling, but may have been related to differences in nitrogen balance.NEW & NOTEWORTHY Endurance athletes competing consecutive days need optimal dietary intake during the recovery period. We report that coingestion of protein and carbohydrate soon after exhaustive exercise, compared with carbohydrate only, resulted in better performance the following day. The better performance after coingestion of protein and carbohydrate was not associated with a higher rate of glycogen synthesis or activation of anabolic signaling compared with carbohydrate only. Importantly, nitrogen balance was positive after coingestion of protein and carbohydrate, which was not the case after intake of carbohydrate only, suggesting that protein synthesis contributes to the better performance the following day.

Purpose: We determined the effect of suppressing lipolysis via administration of Nicotinic acid (NA) and pre-exercise feeding on rates of whole-body substrate utilisation and cycling time trial (TT) performance. Methods: In a randomised, single-blind, crossover design, eight trained male cyclists/triathletes completed two series of TTs in which they performed a predetermined amount of work calculated to last ~60, 90 and 120 min. TTs were undertaken after a standardised breakfast (2 g kg−1 BM of carbohydrate (CHO)) and ingestion of capsules containing either NA or placebo (PL). Results: Plasma [free fatty acids] were suppressed with NA, but increased in the later stages of TT90 and TT120 with PL (p < 0.05). There was no treatment effect on time to complete TT60 (60.4 ± 4.1 vs. 59.3 ± 3.4 min) or TT90 (90.4 ± 9.1 vs. 89.5 ± 6.6 min) for NA and PL, respectively. However, TT120 was slower with NA (123.1 ± 5.7 vs. 120.1 ± 8.7 min, p < 0.001), which coincided with a decline in plasma [glucose] during the later stages of this ride (p < 0.05). For TTs of the same duration, the rates of whole-body CHO oxidation were unaffected by NA, but decreased with increasing TT time (p < 0.05). CHO was the predominant substrate for all TTs contributing between 83 and 94 % to total energy expenditure, although there was a small use of lipid-based fuels for all rides. Conclusion: (1) NA impaired cycling TT performance lasting 120 min, (2) cycling TTs lasting from 60 to 120 min are CHO dependent, and (3) there is an obligatory use of lipid-based fuels in TTs lasting 1–2 h.

Skeletal muscle glycogen is an important energy source for muscle contraction and a key regulator of metabolic responses to exercise. Manipulation of muscle glycogen is therefore a strategy to improve performance in competitions and potentially adaptation to training. However, assessing muscle glycogen in the field is impractical, and there are no normative values for glycogen concentration at rest and during exercise. The objective of this study was to meta-analyse the effects of fitness, acute dietary carbohydrate (CHO) availability and other factors on muscle glycogen concentration at rest and during exercise of different durations and intensities. PubMed was used to search for original articles in English published up until February 2018. Search terms included muscle glycogen and exercise, filtered for humans. The analysis incorporated 181 studies of continuous or intermittent cycling and running by healthy participants, with muscle glycogen at rest and during exercise determined by biochemical analysis of biopsies. Resting muscle glycogen was determined with a meta-regression mixed model that included fixed effects for fitness status [linear, as maximal oxygen uptake ( $$\dot{V}$$ O2max) in mL·kg−1·min−1] and CHO availability (three levels: high, ≥ 6 g·kg−1 of CHO per day for ≥ 3 days or ≥ 7 g·kg−1 CHO per day for ≥ 2 days; low, glycogen depletion and low-CHO diet; and normal, neither high nor low, or not specified in study). Muscle glycogen during exercise was determined with a meta-regression mixed model that included fixed effects for fitness status, resting glycogen [linear, in mmol·kg−1 of dry mass (DM)], exercise duration (five levels, with means of 5, 23, 53 and 116 min, and time to fatigue), and exercise intensity (linear, as percentage of $$\dot{V}$$ O2max); intensity, fitness and resting glycogen were interacted with duration, and there were also fixed effects for exercise modes, CHO ingestion, sex and muscle type. Random effects in both models accounted for between-study variance and within-study repeated measurement. Inferences about differences and changes in glycogen were based on acceptable uncertainty in standardised magnitudes, with thresholds for small, moderate, large and very large of 25, 75, 150 and 250 mmol·kg−1 of DM, respectively. The resting glycogen concentration in the vastus lateralis of males with normal CHO availability and $$\dot{V}$$ O2max (mean ± standard deviation, 53 ± 8 mL·kg−1·min−1) was 462 ± 132 mmol·kg−1. High CHO availability was associated with a moderate increase in resting glycogen (102, ± 47 mmol·kg−1; mean ± 90% confidence limits), whereas low availability was associated with a very large decrease (− 253, ± 30 mmol·kg−1). An increase in $$\dot{V}$$ O2max of 10 mL·kg−1·min−1 had small effects with low and normal CHO availability (29, ± 44 and 67, ± 15 mmol·kg-1, respectively) and a moderate effect with high CHO availability (80, ± 40 mmol·kg−1). There were small clear increases in females and the gastrocnemius muscle. Clear modifying effects on glycogen utilisation during exercise were as follows: a 30% $$\dot{V}$$ O2max increase in intensity, small (41, ± 20 mmol·kg−1) at 5 min and moderate (87–134 mmol·kg−1) at all other timepoints; an increase in baseline glycogen of 200 mmol·kg−1, small at 5–23 min (28–59 mmol·kg−1), moderate at 116 min (104, ± 15 mmol·kg−1) and moderate at fatigue (143, ± 33 mmol·kg−1); an increase in $$\dot{V}$$ O2max of 10 mL·kg−1·min−1, mainly clear trivial effects; exercise mode (intermittent vs. continuous) and CHO ingestion, clear trivial effects. Small decreases in utilisation were observed in females (vs. males: − 30, ± 29 mmol·kg−1), gastrocnemius muscle (vs. vastus lateralis: − 31, ± 46 mmol·kg−1) and running (vs. cycling: − 70, ± 32 mmol·kg−1). Dietary CHO availability and fitness are important factors for resting muscle glycogen. Exercise intensity and baseline muscle glycogen are important factors determining glycogen use during exercise, especially with longer exercise duration. The meta-analysed effects may be useful normative values for prescription of endurance exercise.

Leucine is a key amino acid for initiating translation in muscle cells, but the dose-dependent effects of leucine on intracellular signaling are poorly characterized. This study examined the effect that increasing doses of leucine would have on changes in mechanistic target of rapamycin (mTOR)–mediated signaling, rates of protein synthesis, and cell size in C2C12 cells. We hypothesized that a leucine “threshold” exists, which represents the minimum stimulus required to initiate mTOR signaling in muscle cells. Acute exposure to 1.5, 3.2, 5.0, and 16.1 mM leucine increased phosphorylation of mTORSer2448 (~1.4-fold; P < .04), 4E-BP1 Thr37/46 (~1.9-fold; P < .001), and rpS6Ser235/6 (~2.3-fold; P < .001). However, only p70S6kThr389 exhibited a dose-dependent response to leucine with all treatments higher than control (~4-fold; P < .001) and at least 5 mM higher than the 1.5-mM concentration (1.2-fold; P < .02). Rates of protein synthesis were not altered by any treatment. Seven days of exposure to 0.5, 1.5, 5.0, and 16.5 mM leucine resulted in an increase in cell size in at least 5 mM treatments (~1.6-fold, P < .001 vs control). Our findings indicate that even at low leucine concentrations, phosphorylation of proteins regulating translation initiation signaling is enhanced. The phosphorylation of p70S6kThr389 follows a leucine dose-response relationship, although this was not reflected by the acute protein synthetic response. Nevertheless, under the conditions of the present study, it appears that leucine concentrations of at least 5 mM are necessary to enhance cell growth.

The myofibrillar protein synthesis (MPS) response to resistance exercise (REX) and protein ingestion during energy deficit (ED) is unknown. In young men ( n = 8) and women ( n = 7), we determined protein signaling and resting postabsorptive MPS during energy balance [EB; 45 kcal·kg fat-free mass (FFM)−1·day−1] and after 5 days of ED (30 kcal·kg FFM−1·day−1) as well as MPS while in ED after acute REX in the fasted state and with the ingestion of whey protein (15 and 30 g). Postabsorptive rates of MPS were 27% lower in ED than EB ( P < 0.001), but REX stimulated MPS to rates equal to EB. Ingestion of 15 and 30 g of protein after REX in ED increased MPS ∼16 and ∼34% above resting EB ( P < 0.02). p70 S6K Thr389 phosphorylation increased above EB only with combined exercise and protein intake (∼2–7 fold, P < 0.05). In conclusion, short-term ED reduces postabsorptive MPS; however, a bout of REX in ED restores MPS to values observed at rest in EB. The ingestion of protein after REX further increases MPS above resting EB in a dose-dependent manner. We conclude that combining REX with increased protein availability after exercise enhances rates of skeletal muscle protein synthesis during short-term ED and could in the long term preserve muscle mass.

Quantity and timing of protein ingestion are major factors regulating myofibrillar protein synthesis (MPS). However, the effect of specific ingestion patterns on MPS throughout a 12 h period is unknown. We determined how different distributions of protein feeding during 12 h recovery after resistance exercise affects anabolic responses in skeletal muscle. Twenty-four healthy trained males were assigned to three groups (n = 8/group) and undertook a bout of resistance exercise followed by ingestion of 80 g of whey protein throughout 12 h recovery in one of the following protocols: 8 × 10 g every 1.5 h (PULSE); 4 × 20 g every 3 h (intermediate: INT); or 2 × 40 g every 6 h (BOLUS). Muscle biopsies were obtained at rest and after 1, 4, 6, 7 and 12 h post exercise. Resting and post-exercise MPS (l-[ring-(13)C6] phenylalanine), and muscle mRNA abundance and cell signalling were assessed. All ingestion protocols increased MPS above rest throughout 1-12 h recovery (88-148%, P INT>PULSE hierarchy in magnitude of phosphorylation. MuRF-1 and SLC38A2 mRNA were differentially expressed with BOLUS. In conclusion, 20 g of whey protein consumed every 3 h was superior to either PULSE or BOLUS feeding patterns for stimulating MPS throughout the day. This study provides novel information on the effect of modulating the distribution of protein intake on anabolic responses in skeletal muscle and has the potential to maximize outcomes of resistance training for attaining peak muscle mass.

Autophagy contributes to remodeling of skeletal muscle and is sensitive to contractile activity and prevailing energy availability. We investigated changes in targeted genes and proteins with roles in autophagy following 5 days of energy balance (EB), energy deficit (ED), and resistance exercise (REX) after ED. Muscle biopsies from 15 subjects (8 males, 7 females) were taken at rest following 5 days of EB [45 kcal·kg fat free mass (FFM)−1·day−1] and 5 days of ED (30 kcal·kg FFM−1·day−1). After ED, subjects completed a bout of REX and consumed either placebo (PLA) or 30 g whey protein (PRO) immediately postexercise. Muscle biopsies were obtained at 1 and 4 h into recovery in each trial. Resting protein levels of autophagy-related gene protein 5 (Atg5) decreased after ED compared with EB (∼23%, P < 0.001) and remained below EB from 1 to 4 h postexercise in PLA (∼17%) and at 1 h in PRO (∼18%, P < 0.05). In addition, conjugated Atg5 (cAtg12) decreased below EB in PLA at 4 h (∼20, P < 0.05); however, its values were increased above this time point in PRO at 4 h alongside increases in FOXO1 above EB (∼22–26%, P < 0.05). Notably, these changes were subsequent to increases in unc-51-like kinase 1Ser757phosphorylation (∼60%) 1 h postexercise in PRO. No significant changes in gene expression of selected autophagy markers were found, but EGR-1 increased above ED and EB in PLA (∼417–864%) and PRO (∼1,417–2,731%) trials 1 h postexercise ( P < 0.001). Postexercise protein availability, compared with placebo, can selectively promote autophagic responses to REX in ED.

We determined the effects of “periodized nutrition” on skeletal muscle and whole body responses to a bout of prolonged exercise the following morning. Seven cyclists completed two trials receiving isoenergetic diets differing in the timing of ingestion: they consumed either 8 g/kg body mass (BM) of carbohydrate (CHO) before undertaking an evening session of high-intensity training (HIT) and slept without eating (FASTED), or consumed 4 g/kg BM of CHO before HIT, then 4 g/kg BM of CHO before sleeping (FED). The next morning subjects completed 2 h of cycling (120SS) while overnight fasted. Muscle biopsies were taken on day 1 (D1) before and 2 h after HIT and on day 2 (D2) pre-, post-, and 4 h after 120SS. Muscle [glycogen] was higher in FED at all times post-HIT ( P < 0.001). The cycling bouts increased PGC1α mRNA and PDK4 mRNA ( P < 0.01) in both trials, with PDK4 mRNA being elevated to a greater extent in FASTED ( P < 0.05). Resting phosphorylation of AMPKThr172, p38MAPKThr180/Tyr182, and p-ACCSer79 (D2) was greater in FASTED ( P < 0.05). Fat oxidation during 120SS was higher in FASTED ( P = 0.01), coinciding with increases in ACCSer79 and CPT1 as well as mRNA expression of CD36 and FABP3 ( P < 0.05). Methylation on the gene promoter for COX4I1 and FABP3 increased 4 h after 120SS in both trials, whereas methylation of the PPARδ promoter increased only in FASTED. We provide evidence for shifts in DNA methylation that correspond with inverse changes in transcription for metabolically adaptive genes, although delaying postexercise feeding failed to augment markers of mitochondrial biogenesis.

Recovery from the demands of daily training is an essential element of a scientifically based periodized program whose twin goals are to maximize training adaptation and enhance performance. Prolonged endurance training sessions induce substantial metabolic perturbations in skeletal muscle, including the depletion of endogenous fuels and damage/disruption to muscle and body proteins. Therefore, increasing nutrient availability (i.e., carbohydrate and protein) in the post-training recovery period is important to replenish substrate stores and facilitate repair and remodelling of skeletal muscle. It is well accepted that protein ingestion following resistance-based exercise increases rates of skeletal muscle protein synthesis and potentiates gains in muscle mass and strength. To date, however, little attention has focused on the ability of dietary protein to enhance skeletal muscle remodelling and stimulate adaptations that promote an endurance phenotype. The purpose of this review is to critically discuss the results of recent studies that have examined the role of dietary protein for the endurance athlete. Our primary aim is to consider the results from contemporary investigations that have advanced our knowledge of how the manipulation of dietary protein (i.e., amount, type, and timing of ingestion) can facilitate muscle remodelling by promoting muscle protein synthesis. We focus on the role of protein in facilitating optimal recovery from, and promoting adaptations to strenuous endurance-based training.

IntroductionThe culture in many team sports involves consumption of large amounts of alcohol after training/competition. The effect of such a practice on recovery processes underlying protein turnover in human skeletal muscle are unknown. We determined the effect of alcohol intake on rates of myofibrillar protein synthesis (MPS) following strenuous exercise with carbohydrate (CHO) or protein ingestion.MethodsIn a randomized cross-over design, 8 physically active males completed three experimental trials comprising resistance exercise (8×5 reps leg extension, 80% 1 repetition maximum) followed by continuous (30 min, 63% peak power output (PPO)) and high intensity interval (10×30 s, 110% PPO) cycling. Immediately, and 4 h post-exercise, subjects consumed either 500 mL of whey protein (25 g; PRO), alcohol (1.5 g·kg body mass⁻¹), 12±2 standard drinks) co-ingested with protein (ALC-PRO), or an energy-matched quantity of carbohydrate also with alcohol (25 g maltodextrin; ALC-CHO). Subjects also consumed a CHO meal (1.5 g CHO·kg body mass⁻¹) 2 h post-exercise. Muscle biopsies were taken at rest, 2 and 8 h post-exercise.ResultsBlood alcohol concentration was elevated above baseline with ALC-CHO and ALC-PRO throughout recovery (PConclusionWe provide novel data demonstrating that alcohol consumption reduces rates of MPS following a bout of concurrent exercise, even when co-ingested with protein. We conclude that alcohol ingestion suppresses the anabolic response in skeletal muscle and may therefore impair recovery and adaptation to training and/or subsequent performance.

NEW FINDINGS What is the central question of this study? Does achieving energy balance mainly with ingested fat in a 'sleep-low' model of training with low muscle glycogen affect the early training adaptive response during recovery? What is the main finding and its importance? Replenishing the energy expended during exercise mainly from ingested fat to achieve energy balance in a 'sleep-low' model does not enhance the response of skeletal muscle markers of early adaptation to training and impairs glycaemic control the morning after compared to training with low energy availability. These findings are important for optimizing post-training dietary recommendations in relation to energy balance and macronutrient intake. ABSTRACT Training with low carbohydrate availability (LCHO) has been shown to acutely enhance endurance training skeletal muscle response, but the concomitant energy deficit (ED) in LCHO interventions has represented a confounding factor in past research. This study aimed at determining if achieving energy balance with high fat (EB-HF) acutely enhances the adaptive response in LCHO compared to ED with low fat (ED-LF). In a crossover design, nine well-trained males completed a 'sleep-low' protocol: on day 1 they cycled to deplete muscle glycogen while reaching a set energy expenditure (30 kcal (kg of fat free mass (FFM))-1 ). Post-exercise, low carbohydrate, protein-matched meals completely (EB-HF, 30 kcal (kg FFM)-1 ) or partially (ED-LF, 9 kcal (kg FFM)-1 ) replaced the energy expended, with the majority of energy derived from fat in EB-HF. In the morning of day 2, participants exercised fasted, and skeletal muscle and blood samples were collected and a carbohydrate-protein drink was ingested at 0.5 h recovery. Muscle glycogen showed no treatment effect (P

Background The pattern of protein intake following exercise may impact whole-body protein turnover and net protein retention. We determined the effects of different protein feeding strategies on protein metabolism in resistance-trained young men. Methods Participants were randomly assigned to ingest either 80g of whey protein as 8x10g every 1.5h (PULSE; n=8), 4x20g every 3h (intermediate, INT; n=7), or 2x40g every 6h (BOLUS; n=8) after an acute bout of bilateral knee extension exercise (4x10 repetitions at 80% maximal strength). Whole-body protein turnover (Q), synthesis (S), breakdown (B), and net balance (NB) were measured throughout 12h of recovery by a bolus ingestion of [15N]glycine with urinary [15N]ammonia enrichment as the collected end-product. Results PULSE Q rates were greater than BOLUS (~19%, P Conclusion We conclude that the pattern of ingested protein, and not only the total daily amount, can impact whole-body protein metabolism. Individuals aiming to maximize NB would likely benefit from repeated ingestion of moderate amounts of protein (~20g) at regular intervals (~3h) throughout the day.