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The present randomized study investigated the effect of acute supplementation of 800 mg/kg of ketone monoester ingestion (KE) or placebo (PL) and 210 mg/kg of NaHCO₃ co-ingestion on cycling performance of WorldTour cyclists during a road cycling stage simulation. Twenty-eight cyclists participated in the study (27.46 ± 4.32 years; 1.80 ± 0.06 m; 69.74 ± 6.36 kg). Performance, physiological, biochemical, and metabolism outcomes, gut discomfort, and effort perceived were assessed during a road cycling simulation composed of an 8-min time-trial (TT) performance + 30-s TT + 4.5 hr of outdoor cycling + a second 8-min TT + a second 30-s TT. Greater absolute and relative mean power during the first 8-min TT (F = 5.067, p = .033, ${\mathrm{\eta }}_{\mathrm{p}}^2=.163$ , F = 5.339, p = .029, ${\mathrm{\eta }}_{\mathrm{p}}^2=.170$ , respectively) was observed after KE than after PL (KE: 389 ± 34, PL: 378 ± 44 W, p = .002, d = 0.294 and KE: 5.60 ± 0.42, PL: 5.41 ± 0.44 W/kg, p = .001, d = 0.442). Additionally, greater concentration of β-hydroxybutyrate blood concentration (F = 42.195, p < .001, ${\mathrm{\eta }}_{\mathrm{p}}^2=.619$ ) was observed after KE than after PL during the first steps of the stage (e.g., after warm-up KE: 1.223 ± 0.642, PL: 0.044 ± 0.058 mM, p < .001, d = 2.589), although the concentrations returned to near baseline after 4.5 hr of outdoor cycling. Moreover, higher values of anion gap were observed (F = 2.333, p = .026, ${\mathrm{\eta }}_{\mathrm{p}}^2=.080$ ) after KE than after PL ingestion, after the warm-up and after the first 8-min and 30-s TT. Additionally, lower concentrations of ${\mathrm{HCO}}_3^{-}$ were reported in the KE condition after warm-up and after the first 8-min and 30-s TT. During the initial phase of the stage simulation, acute supplementation with KE + NaHCO₃ co-ingestion enhanced 8-min TT cycling performance (3.1%) in WorldTour cyclists with a concomitant hyperketonaemia.

The purpose of this study was to investigate the influence of mouth rinsing and ingesting unpleasant salty or bitter solutions on cycling sprint performance and knee extensor force characteristics. Eleven male and one female trained cyclists (age: 34 ± 9 years, maximal oxygen uptake 56.9 ± 3.9 ml·kg⁻¹·min⁻¹) completed a ramp test and familiarization followed by four experimental trials. In each trial, participants completed an all-out 30-s cycling sprint with knee extensor maximal voluntary contractions before and immediately after the sprint. In a randomized, counterbalanced, cross-over order, the four main trials were: a no solution control condition, water, salty (5.8%), or bitter (2 mM quinine) solutions that were mouth rinsed (10 s) and ingested immediately before the cycling sprint. There were no significant differences between conditions in mean power (mean ± SD, no solution: 822 ± 115 W, water: 818 ± 108 W, salt: 832 ± 111 W, bitter: 818 ± 105 W); peak power (no solution: 1,184 ± 205 W, water: 1,177 ± 207 W, salt: 1,195 ± 210 W, bitter: 1,184 ± 209 W); or fatigue index (no solution: 51.5% ± 5.7%, water: 50.8% ± 7.0%, salt: 51.1% ± 5.9%, bitter: 51.2% ± 7.1%) during the sprint. Maximal force and impulse declined postexercise; however, there were no significant differences between conditions in knee extensor force characteristics. The present data do not support the use of unpleasant salty or bitter solutions as an ergogenic aid to improve sprint exercise performance.

Endurance exercise can disturb intestinal epithelial integrity, leading to increased systemic indicators of cell injury, hyperpermeability, and pathogenic translocation. However, the interaction between exercise, diet, and gastrointestinal disturbance still warrants exploration. This study examined whether a 6-day dietary intervention influenced perturbations to intestinal epithelial disruption in response to a 25-km race walk. Twenty-eight male race walkers adhered to a high carbohydrate (CHO)/energy diet (65% CHO, energy availability = 40 kcal·kg FFM⁻¹·day⁻¹) for 6 days prior to a Baseline 25-km race walk. Athletes were then split into three subgroups: high CHO/energy diet (n = 10); low-CHO, high-fat diet (LCHF: n = 8; <50 g/day CHO, energy availability = 40 kcal·kg FFM⁻¹·day⁻¹); and low energy availability (n = 10; 65% CHO, energy availability = 15 kcal·kg FFM⁻¹·day⁻¹) for a further 6-day dietary intervention period prior to a second 25-km race walk (Adaptation). During both trials, venous blood was collected pre-, post-, and 1 hr postexercise and analyzed for markers of intestinal epithelial disruption. Intestinal fatty acid-binding protein concentration was significantly higher (twofold increase) in response to exercise during Adaptation compared to Baseline in the LCHF group (p = .001). Similar findings were observed for soluble CD14 (p < .001) and lipopolysaccharide-binding protein (p = .003), where postexercise concentrations were higher (53% and 36%, respectively) during Adaptation than Baseline in LCHF. No differences in high CHO/energy diet or low energy availability were apparent for any blood markers assessed (p > .05). A short-term LCHF diet increased intestinal epithelial cell injury in response to a 25-km race walk. No effect of low energy availability on gastrointestinal injury or symptoms was observed.

Although the ergogenic effects of 3–6 mg/kg caffeine are widely accepted, the efficacy of low doses of caffeine has been discussed. However, it is unclear whether the ergogenic effects of caffeine on jump performance are dose responsive in a wide range of doses. This study aimed to examine the effect of very low (1 mg/kg) to moderate doses of caffeine, including commonly utilized ergogenic doses (i.e., 3 and 6 mg/kg), on vertical jump performance. A total of 32 well-trained collegiate sprinters and jumpers performed countermovement jumps and squat jumps three times each in a double-blind, counterbalanced, randomized, crossover design. Participants ingested a placebo or 1, 3, or 6 mg/kg caffeine 60 min before jumping. Compared with the placebo, 6 mg/kg caffeine significantly enhanced countermovement jump (p < .001) and squat jump (p = .012) heights; furthermore, 1 and 3 mg/kg of caffeine also significantly increased countermovement jump height (1 mg/kg: p = .002, 3 mg/kg: p < .001) but not squat jump height (1 mg/kg: p = .436, 3 mg/kg: p = .054). There were no significant differences among all caffeine doses in both jumps (all p > .05). In conclusion, even at a dose as low as 1 mg/kg, caffeine improved vertical jump performance in a dose-independent manner. This study provides new insight into the applicability and feasibility of 1 mg/kg caffeine as a safe and effective ergogenic strategy for jump performance.