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.

Using an amalgamation of previously studied “train‐low” paradigms, we tested the effects of reduced carbohydrate (CHO) but high leucine availability on cell‐signaling responses associated with exercise‐induced regulation of mitochondrial biogenesis and muscle protein synthesis (MPS). In a repeated‐measures crossover design, 11 males completed an exhaustive cycling protocol with high CHO availability before, during, and after exercise (HIGH) or alternatively, low CHO but high protein (leucine enriched) availability (LOW + LEU). Muscle glycogen was different (P < 0.05) pre‐exercise (HIGH: 583 ± 158, LOW + LEU: 271 ± 85 mmol kg−1 dw) but decreased (P < 0.05) to comparable levels at exhaustion (≈100 mmol kg−1 dw). Despite differences (P < 0.05) in exercise capacity (HIGH: 158 ± 29, LOW + LEU: 100 ± 17 min), exercise induced (P < 0.05) comparable AMPK α2 (3–4‐fold) activity, PGC‐1α (13‐fold), p53 (2‐fold), Tfam (1.5‐fold), SIRT1 (1.5‐fold), Atrogin 1 (2‐fold), and MuRF1 (5‐fold) gene expression at 3 h post‐exercise. Exhaustive exercise suppressed p70S6K activity to comparable levels immediately post‐exercise (≈20 fmol min−1 mg−1). Despite elevated leucine availability post‐exercise, p70S6K activity remained suppressed (P < 0.05) 3 h post‐exercise in LOW + LEU (28 ± 14 fmol min−1 mg−1), whereas muscle glycogen resynthesis (40 mmol kg−1 dw h−1) was associated with elevated (P < 0.05) p70S6K activity in HIGH (53 ± 30 fmol min−1 mg−1). We conclude: (1) CHO restriction before and during exercise induces “work‐efficient” mitochondrial‐related cell signaling but; (2) post‐exercise CHO and energy restriction maintains p70S6K activity at basal levels despite feeding leucine‐enriched protein. Our data support the practical concept of “fuelling for the work required” as a potential strategy for which to amalgamate train‐low paradigms into periodized training programs.

Given that the enhanced oxidative adaptations observed when training in carbohydrate (CHO)-restricted states is potentially regulated through free fatty acid (FFA)-mediated signalling and that leucine-rich protein elevates muscle protein synthesis, the present study aimed to test the hypothesis that leucine-enriched protein feeding enhances circulating leucine concentration but does not impair FFA availability or whole body lipid oxidation during exercise. Nine males cycled for 2 h at 70% VO2peak when fasted (PLACEBO) or having consumed a whey protein solution (WHEY) or a leucine-enriched whey protein gel (GEL), administered as 22 g 1 h pre-exercise, 11 g/h during and 22 g 30 min post-exercise. Total leucine administration was 14.4 g and 6.3 in GEL and WHEY, respectively. Mean plasma leucine concentrations were elevated in GEL (P = 0.001) compared with WHEY and PLACEBO (375 ± 100, 272 ± 51, 146 ± 14 µmol L(-1), respectively). No differences (P = 0.153) in plasma FFA (WHEY 0.53 ± 0.30, GEL 0.45 ± 0.25, PLACEBO 0.65 ± 0.30, mmol L(-1)) or whole body lipid oxidation during exercise (WHEY 0.37 ± 0.26, GEL 0.36 ± 0.24, PLACEBO 0.34 ± 0.24 g/min) were apparent between trials, despite elevated (P = 0.001) insulin in WHEY and GEL compared with PLACEBO (38 ± 16, 35 ± 16, 22 ± 11 pmol L(-1), respectively). We conclude that leucine-enriched protein feeding does not impair FFA availability or whole body lipid oxidation during exercise, thus having practical applications for athletes who deliberately train in CHO-restricted states to promote skeletal muscle adaptations

Purpose To investigate the effects of high-intensity interval (HIIT) running on markers of gastrointestinal (GI) damage and permeability alongside subjective symptoms of GI discomfort. Methods Eleven male runners completed an acute bout of HIIT (eighteen 400 m runs at 120% O2max ) where markers of GI permeability, intestinal damage and GI discomfort symptoms were assessed and compared with resting significantly increased (p < 0.001) during and in the recovery period from HIIT whereas no changes were observed during rest. Mild-symptoms of GI discomfort, were reported immediately-and 24 h post-HIIT, although these symptoms did not correlate to GI permeability or I-FABP. Conclusion Acute HIIT increased GI permeability and intestinal I-FABP release, although these do not correlate with symptoms of GI discomfort. Furthermore, by using serum sampling, we provide data showing that it is possible to detect changes in intestinal permeability that is not observed using urinary sampling over a shorter timeperiod.

IntroductionPhysical endurance can be limited by muscle glycogen stores, in that glycogen depletion markedly reduces external work. During carbohydrate restriction, the liver synthesizes the ketone bodies, d-β-hydroxybutyrate, and acetoacetate from fatty acids. In animals and in the presence of glucose, d-β-hydroxybutyrate promotes insulin secretion and increases glycogen synthesis. Here we determined whether a dietary ketone ester, combined with plentiful glucose, can increase postexercise glycogen synthesis in human skeletal muscle.MethodsAfter an interval-based glycogen depletion exercise protocol, 12 well-trained male athletes completed a randomized, three-arm, blinded crossover recovery study that consisted of consumption of either a taste-matched, zero-calorie control or a ketone monoester drink, followed by a 10-mM glucose clamp or saline infusion for 2 h. The three postexercise conditions were control drink then saline infusion, control drink then hyperglycemic clamp, or ketone ester drink then hyperglycemic clamp. Skeletal muscle glycogen content was determined in muscle biopsies of vastus lateralis taken before and after the 2-h clamps.ResultsThe ketone ester drink increased blood d-β-hydroxybutyrate concentrations to a maximum of 5.3 versus 0.7 mM for the control drink (P < 0.0001). During the 2-h glucose clamps, insulin levels were twofold higher (31 vs 16 mU·L−1, P < 0.01) and glucose uptake 32% faster (1.66 vs 1.26 g·kg−1, P < 0.001). The ketone drink increased by 61 g, the total glucose infused for 2 h, from 197 to 258 g, and muscle glycogen was 50% higher (246 vs 164 mmol glycosyl units per kilogram dry weight, P < 0.05) than after the control drink.ConclusionIn the presence of constant high glucose concentrations, a ketone ester drink increased endogenous insulin levels, glucose uptake, and muscle glycogen synthesis.