Carbohydrate (CHO) ingestion during exercise lasting less than three hours improves endurance exercise performance but there is still debate about the optimal dose. We utilised stable isotopes and blood metabolite profiles to further examine metabolic responses to CHO (glucose only) ingestion in the 20–64 g·h⁻¹ range, and to determine the association with performance outcome. In a double-blind, randomized cross-over design, male cyclists (n = 20, mean ± SD, age 34 ± 10 years, mass 75.8 ± 9 kg, peak power output 394 ± 36 W, VO_2max 62 ± 9 mL·kg⁻¹·min⁻¹) completed four main experimental trials. Each trial involved a two-hour constant load ride (185 ± 25 W) followed by a time trial, where one of three CHO beverages, or a control (water), were administered every 15 min, providing 0, 20, 39 or 64 g CHO·h⁻¹. Dual glucose tracer techniques, indirect calorimetry and blood analyses were used to determine glucose kinetics, exogenous CHO oxidation (EXO), endogenous CHO and fat oxidation; and metabolite responses. Regression analysis revealed that total exogenous CHO oxidised in the second hour of exercise, and suppression of serum NEFA concentration provided the best prediction model of performance outcome. However, the model could only explain ~19% of the variance in performance outcome. The present data demonstrate that consuming ~40 g·h⁻¹ of CHO appears to be the minimum ingestion rate required to induce metabolic effects that are sufficient to impact upon performance outcome. These data highlight a lack of performance benefit and few changes in metabolic outcomes beyond an ingestion rate of 39 g·h⁻¹. Further work is required to explore dose-response effects of CHO feeding and associations between multiple metabolic parameters and subsequent performance outcome.

We have little understanding of interactions between CHO dosage and neuromuscular regulation following fatiguing endurance exercise. Fifteen well‐trained male cyclists completed 4 experimental trials of 120 min submaximal cycling (95% lactate threshold) during which water (0 g CHO·h^‐1) or CHO beverages (20, 39, or 64 g CHO·h^‐1) were consumed every 15 min, at a rate of 1 L·h^‐1, followed by a work matched time trial ~30 mins. Maximal voluntary contraction (MVC), M‐wave twitch potentiation and torque, motor unit recruitment and firing rate were recorded pre‐ and post‐cycling. Time trial performance improved following 39 and 64 vs. 0 and 20 g CHO·h^‐1, but no effect of CHO dose on any pre‐to‐post neuromuscular function measures. Pre‐to‐post cycling exercise: 1) MVC, and M‐wave amplitude and duration declined by ‐21.5 Nm, and ‐4.9 mV and ‐7.1 ms respectively; 2) peak evoked torque remained unchanged; 3) Firing rate of early‐ and mid‐recruited motor units increased by 0.93 pps and 0.74 pps respectively, with no change in later recruited motor units. Thus, central drive to early‐ and mid‐recruited motor units increases as a result of endurance cycling, due to a likely fatigue compensatory mechanism. However, CHO availability does not appear to influence increased neuromuscular drive.

Purpose: Hypohydration of ≥ 2% body mass loss (BML) can impair cycling performance in the heat; however, it remains unclear whether this is primarily due to the body water deficit itself or the concomitant, typically observed increase in serum sodium concentration (S _[Na ⁺ _] ). To disentangle these effects, we examined the performance effects of 60% (60FR) vs. 80% (80FR) fluid replacement, designed to achieve > 2% vs < 2% BML, with personalised sodium prescription targeting condition-matched S _[Na ⁺ _] . Methods: Eleven male cyclists (35 ± 6 years, VȮ _2max 58 ± 5 ml·kg ⁻¹ ·min ⁻¹ ) completed two trials, consisting of 180 min cycling (90% LT ₁ , 32 °C, 50% humidity), followed by a work-matched time-trial (TT). Participants received either 60% or 80% of projected fluid losses, along with sodium supplementation aiming to maintain S _[Na ⁺ _] where dilution of S _[Na ⁺ _] was predicted. Outcomes included BML, S _[Na ⁺ _] , plasma volume change (∆PV), rectal (T _re ) and skin (T _sk ) temperatures, whole-body sweat rate (WBSR), and TT performance. Results: BML was greater in 60FR at all time-points (P < 0.01), whereas S _[[Na ⁺ _] remained stable across both trials (P = 0.07). In 80FR, ∆PV was smaller during the preload, T _re was lower from 120 min onwards and T _sk and WBSR were higher during the TT compared to 60FR (all P < 0.05). TT completion time was 8 ± 10% faster in 80FR (1793 ± 174 vs 1968 ± 246 s, P = 0.02). Conclusion: Fluid replacement resulting in BML > 2% impairs thermoregulation and cycling performance in the heat, compared to maintaining BML < 2%, despite no differences in S _[Na ⁺ _] .

Purpose : Glycemic variability is a potential risk factor for cardiometabolic disease. As adolescence is a critical period for establishing metabolic health, this study examined associations between daily physical activity (PA) levels, sedentary time, and glycemic variability in healthy adolescents under free-living conditions. Methods : Eighty-seven adolescents (53 girls; mean age: 12.9 [0.8] y) wore a continuous glucose monitor (FreeStyle Libre) and an accelerometer (ActiGraph) concurrently over 8 days. Generalized estimating equations examined daily associations in participants with ≥3 days of concurrent accelerometer/continuous glucose monitor data, after adjusting for key confounders. Results : Vigorous PA was consistently associated with a lower glucose coefficient of variation (exponentiated beta coefficient [exp β] = 0.898; 95% CI, 0.828–0.974; P = .010), mean amplitude of glycemic excursion (exp β = 0.889; 95% CI, 0.804–0.983; P = .022), and SD of glucose (exp β = 0.914; 95% CI, 0.845–0.988; P = .023) and a greater percentage in the 3.9 to 7.8 mmol·L ⁻¹ glucose range (exp β = 1.020; 95% CI, 1.003–1.038; P = .019). Moderate-to-vigorous PA was also inversely associated with coefficient of variation and SD of glucose ( P ≤ .018). Yet, sedentary time, light PA, moderate PA, and total PA were not significantly associated with any glycemic metric ( P ≥ .145). Conclusion : PA at moderate-to-vigorous, and especially vigorous, intensities was associated with lower glycemic variability in healthy adolescents.