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.

In an attempt to better identify and inform the energy requirements of elite soccer players, we quantified the energy expenditure (EE) of players from the English Premier League (n = 6) via the doubly labeled water method (DLW) over a 7-day in-season period. Energy intake (EI) was also assessed using food diaries, supported by the remote food photographic method and 24 hr recalls. The 7-day period consisted of 5 training days (TD) and 2 match days (MD). Although mean daily EI (3186 ± 367 kcals) was not different from (p > .05) daily EE (3566 ± 585 kcals), EI was greater (p < .05) on MD (3789 ± 532 kcal; 61.1 ± 11.4 kcal.kg -1 LBM) compared with TD (2956 ± 374 kcal; 45.2 ± 9.3 kcal.kg -1 LBM, respectively). Differences in EI were reflective of greater (p < .05) daily CHO intake on MD (6.4 ± 2.2 g.kg -1 ) compared with TD (4.2 ± 1.4 g.kg -1 ). Exogenous CHO intake was also different (p < .01) during training sessions (3.1 ± 4.4 g.h -1 ) versus matches (32.3 ± 21.9 g.h -1 ). In contrast, daily protein (205 ± 30 g.kg -1 , p = .29) and fat intake (101 ± 20 g, p = .16) did not display any evidence of daily periodization as opposed to g.kg -1 , Although players readily achieve current guidelines for daily protein and fat intake, data suggest that CHO intake on the day before and in recovery from match play was not in accordance with guidelines to promote muscle glycogen storage.

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.

Purpose To investigate the effect of early evening exercise training at different intensities on nocturnal sleep and cardiac autonomic activity in endurance-trained runners. Methods Eight runners completed three experimental trials in a randomised, counterbalanced order. In the early evening (end of exercise 3.5 h before bedtime), participants performed either: (i) a 1 h high-intensity interval running session (HIGH, 6 × 5 min at 90% VO 2peak interspersed with 5 min recovery); (ii) a 1 h low-intensity running session (LOW, 60 min at 45% VO 2peak) or (iii) no exercise (CON). Subsequent nocturnal sleep was assessed using polysomnography, wristwatch actigraphy, and subjective sleep quality. A two-lead electrocardiogram recorded nocturnal cardiac autonomic activity. Results Total sleep time increased after HIGH (477.4 ± 17.7 min, p = 0.022) and LOW (479.6 ± 15.6 min, p = 0.006) compared with CON (462.9 ± 19.0 min). Time awake was lower after HIGH (31.8 ± 18.5 min, p = 0.047) and LOW (30.4 ± 15.7 min, p = 0.008) compared with CON (46.6 ± 20.0 min). There were no differences between conditions for actigraphy and subjective sleep quality (p > 0.05). Nocturnal heart rate variability was not different between conditions, but average nocturnal heart rate increased after HIGH (50 ± 5 beats min −1) compared with LOW (47 ± 5 beats min −1 , p = 0.02) and CON (47 ± 5 beats min −1 , p = 0.028). Conclusion When performed in the early evening, high-intensity exercise does not disrupt and may even improve subsequent nocturnal sleep in endurance-trained runners, despite increased cardiac autonomic activity. Additionally, low-intensity exercise induced positive changes in sleep behaviour that are comparable to those obtained following high-intensity exercise.