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.

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.

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.

Key points Reduced carbohydrate (CHO) availability before and after exercise may augment endurance training‐induced adaptations of human skeletal muscle, as mediated via modulation of cell signalling pathways. However, it is not known whether such responses are mediated by CHO restriction, energy restriction or a combination of both. In recovery from a twice per day training protocol where muscle glycogen concentration is maintained within 200–350 mmol kg−1 dry weight (dw), we demonstrate that acute post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate potent cell signalling pathways that regulate hallmark adaptations associated with endurance training. In contrast, consuming CHO before, during and after an acute training session attenuated markers of bone resorption, effects that are independent of energy availability. Whilst the enhanced muscle adaptations associated with CHO restriction may be regulated by absolute muscle glycogen concentration, the acute within‐day fluctuations in CHO availability inherent to twice per day training may have chronic implications for bone turnover. Abstract We examined the effects of post‐exercise carbohydrate (CHO) and energy availability (EA) on potent skeletal muscle cell signalling pathways (regulating mitochondrial biogenesis and lipid metabolism) and indicators of bone metabolism. In a repeated measures design, nine males completed a morning (AM) and afternoon (PM) high‐intensity interval (HIT) (8 × 5 min at 85% V̇O2 peak ) running protocol (interspersed by 3.5 h) under dietary conditions of (1) high CHO availability (HCHO: CHO ∼12 g kg−1, EA∼ 60 kcal kg−1 fat free mass (FFM)), (2) reduced CHO but high fat availability (LCHF: CHO ∼3 (−1, EA∼ 60 kcal kg−1 FFM) or (3), reduced CHO and reduced energy availability (LCAL: CHO ∼3 g kg−1, EA∼ 20 kcal kg−1 FFM). Muscle glycogen was reduced to ∼200 mmol kg−1 dw in all trials immediately post PM HIT (P < 0.01) and remained lower at 17 h (171, 194 and 316 mmol kg−1 dw) post PM HIT in LCHF and LCAL (P < 0.001) compared to HCHO. Exercise induced comparable p38MAPK phosphorylation (P < 0.05) immediately post PM HIT and similar mRNA expression (all P < 0.05) of PGC‐1α, p53 and CPT1 mRNA in HCHO, LCHF and LCAL. Post‐exercise circulating βCTX was lower in HCHO (P < 0.05) compared to LCHF and LCAL whereas exercise‐induced increases in IL‐6 were larger in LCAL (P < 0.05) compared to LCHF and HCHO. In conditions where glycogen concentration is maintained within 200–350 mmol kg−1 dw, we conclude post‐exercise CHO and energy restriction (i.e. < 24 h) does not potentiate cell signalling pathways that regulate hallmark adaptations associated with endurance training. In contrast, consuming CHO before, during and after HIT running attenuates bone resorption, effects that are independent of energy availability and circulating IL‐6.

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.