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[English] This study determined if supplementation with pantothenic acid (PA) for 16 weeks could increase skeletal muscle coenzyme A (CoASH) content and exercise performance. Trained male cyclists (n = 14) were matched into control or PA (6 g·day1) groups. At 0, 4, 8, and 16 weeks, subjects performed an incremental time to exhaustion cycle with muscle biopsies taken prior to and following exercise. Prolonged PA supplementation did not change skeletal muscle CoASH and acetyl- CoA contents or exercise performance. Novelty: Supplementation with pantothenic acid for 16 weeks had no effect on skeletal muscle CoASH and acetyl-CoA content or exercise performance in trained male cyclists. [French] Cette étude détermine si une supplémentation en acide pantothénique (« PA ») pendant 16 semaines peut augmenter la teneur en coenzyme A (« CoASH ») du muscle squelettique et la performance à l’exercice. Les cyclistes masculins entraînés (n = 14) sont appariés dans des groupes témoins ou PA (6 g·jour−1). Aux semaines 0, 4, 8 et 16, les sujets effectuent un exercice incrémental de pédalage au cours duquel on mesure la durée jusqu’à épuisement ; des biopsies musculaires sont prélevées avant et après l’exercice. Une supplémentation prolongée en PA ne modifie pas les teneurs en CoASH et en acétyl-CoA du muscle squelettique ni la performance à l’exercice. [Traduit par la Rédaction]

This study implemented a 2-week high carbohydrate (CHO) diet intended to maximize CHO oxidation rates and examined the iron-regulatory response to a 26-km race walking effort. Twenty international-level, male race walkers were assigned to either a novel high CHO diet (MAX = 10 g/kg body mass CHO daily) inclusive of gut-training strategies, or a moderate CHO control diet (CON = 6 g/kg body mass CHO daily) for a 2-week training period. The athletes completed a 26-km race walking test protocol before and after the dietary intervention. Venous blood samples were collected pre-, post-, and 3 hr postexercise and measured for serum ferritin, interleukin-6, and hepcidin-25 concentrations. Similar decreases in serum ferritin (17–23%) occurred postintervention in MAX and CON. At the baseline, CON had a greater postexercise increase in interleukin-6 levels after 26 km of walking (20.1-fold, 95% CI [9.2, 35.7]) compared with MAX (10.2-fold, 95% CI [3.7, 18.7]). A similar finding was evident for hepcidin levels 3 hr postexercise (CON = 10.8-fold, 95% CI [4.8, 21.2]; MAX = 8.8-fold, 95% CI [3.9, 16.4]). Postintervention, there were no substantial differences in the interleukin-6 response (CON = 13.6-fold, 95% CI [9.2, 20.5]; MAX = 11.2-fold, 95% CI [6.5, 21.3]) or hepcidin levels (CON = 7.1-fold, 95% CI [2.1, 15.4]; MAX = 6.3-fold, 95% CI [1.8, 14.6]) between the dietary groups. Higher resting serum ferritin (p = .004) and hotter trial ambient temperatures (p = .014) were associated with greater hepcidin levels 3 hr postexercise. Very high CHO diets employed by endurance athletes to increase CHO oxidation have little impact on iron regulation in elite athletes. It appears that variations in serum ferritin concentration and ambient temperature, rather than dietary CHO, are associated with increased hepcidin concentrations 3 hr postexercise.

Key points Brief (5–6 days) adaptation to a low carbohydrate high fat diet in elite athletes increased exercise fat oxidation to rates previously observed with medium (3–4 weeks) or chronic (>12 months) adherence to this diet, with metabolic changes being washed out in a similar time frame.Increased fat utilisation during exercise was associated with a 5–8% increase in oxygen cost at speeds related to Olympic Programme races.Acute restoration of endogenous carbohydrate (CHO) availability (24 h high CHO diet, pre‐race CHO) only partially restored substrate utilisation during a race warm‐up. Fat oxidation continued to be elevated above baseline values although it was lower than achieved by 5–6 days’ keto adaptation; CHO oxidation only reached 61% and 78% of values previously seen at exercise intensities related to race events.Acute restoration of CHO availability failed to overturn the impairment of high‐intensity endurance performance previously associated with low carbohydrate high fat adaptation, potentially due to the blunted capacity for CHO oxidation. Abstract We investigated substrate utilisation during exercise after brief (5–6 days) adaptation to a ketogenic low‐carbohydrate (CHO), high‐fat (LCHF) diet and similar washout period. Thirteen world‐class male race walkers completed economy testing, 25 km training and a 10,000 m race (Baseline), with high CHO availability (HCHO), repeating this (Adaptation) after 5–6 days’ LCHF (n = 7; CHO: 200%) increases in exercise fat oxidation occurred in the LCHF Adaptation economy and 25 km tests, reaching mean rates of ∼1.43 g min−1. However, relative V˙O2 (ml min−1 kg−1) was higher (P, Key points Brief (5–6 days) adaptation to a low carbohydrate high fat diet in elite athletes increased exercise fat oxidation to rates previously observed with medium (3–4 weeks) or chronic (>12 months) adherence to this diet, with metabolic changes being washed out in a similar time frame.Increased fat utilisation during exercise was associated with a 5–8% increase in oxygen cost at speeds related to Olympic Programme races.Acute restoration of endogenous carbohydrate (CHO) availability (24 h high CHO diet, pre‐race CHO) only partially restored substrate utilisation during a race warm‐up. Fat oxidation continued to be elevated above baseline values although it was lower than achieved by 5–6 days’ keto adaptation; CHO oxidation only reached 61% and 78% of values previously seen at exercise intensities related to race events.Acute restoration of CHO availability failed to overturn the impairment of high‐intensity endurance performance previously associated with low carbohydrate high fat adaptation, potentially due to the blunted capacity for CHO oxidation.

Purpose:To determine the acute effects of carbohydrate (CHO) ingestion following a bout of maximal eccentric resistance exercise on key anabolic kinases of mammalian target of rapamycin and extracellular signal-regulated kinase (ERK) pathways. The authors’ hypothesis was that the activation of anabolic signaling pathways known to be upregulated by resistance exercise would be further stimulated by the physiological hyperinsulinemia resulting from CHO supplementation.Methods:Ten resistance-trained men were randomized in a crossover, double-blind, placebo (PLA)-controlled manner to ingest either a noncaloric PLA or 3 g/kg of CHO beverage throughout recovery from resistance exercise. Muscle biopsies were collected at rest, immediately after a single bout of intense lower body resistance exercise, and after 3 hr of recovery.Results:CHO ingestion elevated plasma glucose and insulin concentrations throughout recovery compared with PLA ingestion. The ERK pathway (phosphorylation of ERK1/2 [Thr202/Tyr204], RSK [Ser380], and p70S6K [Thr421/Ser424]) was markedly activated immediately after resistance exercise, without any effect of CHO supplementation. The phosphorylation state of AKT (Thr308) was unchanged postexercise in the PLA trial and increased at 3 hr of recovery above resting with ingestion of CHO compared with PLA. Despite stimulating-marked phosphorylation of AKT, CHO ingestion did not enhance resistance exercise–induced phosphorylation of p70S6K (Thr389) and rpS6 (Ser235/236 and Ser240/244).Conclusion:CHO supplementation after resistance exercise and hyperinsulinemia does not influence the ERK pathway nor the mTORC1 target p70S6K and its downstream proteins, despite the increased AKT phosphorylation.

Given the importance of exercise economy to endurance performance, we implemented two strategies purported to reduce the oxygen cost of exercise within a 4 week training camp in 21 elite male race walkers. Fourteen athletes undertook a crossover investigation with beetroot juice (BRJ) or placebo (PLA) [2 d preload, 2 h pre-exercise + 35 min during exercise] during a 26 km race walking at speeds simulating competitive events. Separately, 19 athletes undertook a parallel group investigation of a multi-pronged strategy (MAX, n = 9) involving chronic (2 w high carbohydrate [CHO] diet + gut training) and acute (CHO loading + 90 g/h CHO during exercise) strategies to promote endogenous and exogenous CHO availability, compared with strategies reflecting lower ranges of current guidelines (CON, n = 10). There were no differences between BRJ and PLA trials for rates of CHO (p = 0.203) or fat (p = 0.818) oxidation or oxygen consumption (p = 0.090). Compared with CON, MAX was associated with higher rates of CHO oxidation during exercise, with increased exogenous CHO use (CON, peak = ~0.45 g/min, MAX: peak = ~1.45 g/min, p &lt, 0.001). High rates of exogenous CHO use were achieved prior to gut training, without further improvement, suggesting that elite athletes already optimise intestinal CHO absorption via habitual practices. No differences in exercise economy were detected despite small differences in substrate use. Future studies should investigate the impact of these strategies on sub-elite athletes’ economy as well as the performance effects in elite groups.

The ingestion of quinine, a bitter tastant, improves short-term (30 s) cycling performance, but it is unclear whether this effect can be integrated into the last effort of a longer race. The purpose of this study was to determine whether midtrial quinine ingestion improves 3,000-m cycling time-trial (TT) performance. Following three familiarization TTs, 12 well-trained male cyclists (mean ± SD: mass = 76.6 ± 9.2 kg, maximal aerobic power = 390 ± 50 W, maximal oxygen uptake = 4.7 ± 0.6 L/min) performed four experimental 3,000-m TTs on consecutive days. This double-blind, crossover design study had four randomized and counterbalanced conditions: (a) Quinine 1 (25-ml solution, 2 mM of quinine); (b) Quinine 2, replicate of Quinine 1; (c) a 25-ml sweet-tasting no-carbohydrate solution (Placebo); and (d) 25 ml of water (Control) consumed at the 1,850-m point of the TT. The participants completed a series of perceptual scales at the start and completion of all TTs, and the power output was monitored continuously throughout all trials. The power output for the last 1,000 m for all four conditions was similar: mean ± SD: Quinine 1 = 360 ± 63 W, Quinine 2 = 367 ± 63 W, Placebo = 364 ± 64 W, and Control = 367 ± 58 W. There were also no differences in the 3,000-m TT power output between conditions. The small perceptual differences between trials at specific 150-m splits were not explained by quinine intake. Ingesting 2 mM of quinine during the last stage of a 3,000-m TT did not improve cycling performance.

Menthol is effective at stimulating thermosensitive neurons that evoke pleasant cooling sensations. Internal application of menthol can be ergogenic for athletes, and hence, addition of menthol to sports nutrition products may be beneficial for athletes. The aim of this study was to develop a menthol energy gel for consumption during exercise and to determine acceptability and preferences for gels with different menthol concentrations. With a randomized, crossover, and double-blind placebo-controlled design, 40 endurance athletes (20 females) ingested an energy gel with a menthol additive at a high (0.5%; HIGH) or low concentration (0.1%; LOW), or a mint-flavored placebo (CON), on separate occasions during outdoor endurance training sessions. The athletes rated the gels for cooling sensation, mint flavor intensity, sweetness, and overall experience and provided feedback. Results are reported as median (interquartile range). Both menthol gels successfully delivered a cooling sensation, with a significantly greater response for HIGH (5.0 [4.0–5.0]) compared with LOW (3.5 [3.0–4.0]; p = .022) and CON (1.0 [1.0–2.0]; p p p = .001) and CON (4.0 [3.0–4.0]; p

Purpose: Hot-water immersion (HWI) after training in temperate conditions has been shown to induce thermophysiological adaptations and improve endurance performance in the heat; however, the potential additive effects of HWI and training in hot outdoor conditions remain unknown. Therefore, this study aimed to determine the effect of repeated postexercise HWI in athletes training in a hot environment. Methods: A total of 13 (9 female) elite/preelite racewalkers completed a 15-day training program in outdoor heat (mean afternoon high temperature = 34.6°C). Athletes were divided into 2 matched groups that completed either HWI (40°C for 30–40 min) or seated rest in 21°C (CON), following 8 training sessions. Pre–post testing included a 30-minute fixed-intensity walk in heat, laboratory incremental walk to exhaustion, and 10,000-m outdoor time trial. Results: Training frequency and volume were similar between groups (P = .54). Core temperature was significantly higher during immersion in HWI (38.5 [0.3]) than CON (37.8°C [0.2°C]; P 2 uptake, or 10,000-m performance (P > .05). There were significant (P −1), sweat rate (0.34–0.55 L·h−1) and thermal comfort (1.2–1.5 arbitrary units), and 10,000-m racewalking performance time (∼3 min). Conclusions: Both groups demonstrated significant improvement in markers of heat adaptation and performance; however, the addition of HWI did not provide further enhancements. Improvements in adaptation appeared to be maximized by the training program in hot conditions.

We investigated the effects of adaptation to a ketogenic low carbohydrate (CHO), high fat diet (LCHF) during 3 weeks of intensified training on metabolism and performance of world-class endurance athletes. We controlled three isoenergetic diets in elite race walkers: high CHO availability (g kg−1 day−1: 8.6 CHO, 2.1 protein, 1.2 fat) consumed before, during and after training (HCHO, n = 9); identical macronutrient intake, periodised within or between days to alternate between low and high CHO availability (PCHO, n = 10); LCHF (< 50 g day−1 CHO; 78% energy as fat; 2.1 g kg−1 day−1 protein; LCHF, n = 10). Post-intervention, ˙V O2peak during race walking increased in all groups (P < 0.001, 90% CI: 2.55, 5.20%). LCHF was associated with markedly increased rates of whole-body fat oxidation, attaining peak rates of 1.57±0.32 gmin−1 during 2 h of walking at 80% ˙V O2peak.However, LCHFalso increased the oxygen (O2) cost of race walking at velocities relevant to real-life race performance: O2 uptake (expressed as a percentage of new ˙V O2peak) at a speed approximating 20 km race pace was reduced in HCHO and PCHO (90% CI:−7.047,−2.55 and−5.18,−0.86, respectively), but was maintained at pre-intervention levels in LCHF. HCHO and PCHO groups improved times for 10 km race walk: 6.6% (90% CI: 4.1, 9.1%) and 5.3% (3.4, 7.2%), with no improvement (−1.6% (−8.5, 5.3%)) for the LCHF group. In contrast to training with diets providing chronic or periodised high-CHO availability, and despite a significant improvement in ˙V O2peak, adaptation to the topical LCHF diet negated performance benefits in elite endurance athletes, in part due to reduced exercise economy.

Purpose: The core temperature responses during exercise and effects of different cooling strategies on endurance performance under heat stress have been investigated in recreational athletes. This investigation aimed to determine peak rectal temperatures during elite racewalking competitions and to detail any cooling strategies used. Methods: Rectal temperature was measured in 14 heat-adapted elite/preelite race walkers (9 females) via a telemetric capsule across 4 outdoor events, including the 2018 Commonwealth Games (race 1: 20 km, 25°C, 74% relative humidity [RH], n = 2) and 3 International Association of Athletics Federations–sanctioned 10-km events (race 2: 19°C, 34% RH, n = 2; race 3: 29°C, 47% RH, n = 14; and race 4: 23°C, 72% RH, n = 11). All athletes completed race 3, and a subsample completed the other events. Their use of cooling strategies and symptoms of heat illness were determined. Results: Peak rectal temperatures >40°C were observed in all events. The highest rectal temperature observed during an event was 41.2°C. These high rectal temperatures were observed without concomitant heat illness, with the exception of cramping in one athlete during race 1. The rectal temperatures tended to reach a steady state in the second half of the 20-km event, but no steady state was observed in the 10-km events. The athletes used cooling strategies in race 1 only, implementing different combinations of cold-water immersion, ice-slurry ingestion, ice-towel application, ice-vest application, and facial water spraying. Conclusions: Elite/preelite race walkers experience rectal temperatures >40°C during competition despite only moderate-warm conditions, and even when precooling and midcooling strategies are applied.

It is the position of Sports Dietitians Australia (SDA) that exercise in hot and/or humid environments, or with significant clothing and/or equipment that prevents body heat loss (i.e., exertional heat stress), provides significant challenges to an athlete’s nutritional status, health, and performance. Exertional heat stress, especially when prolonged, can perturb thermoregulatory, cardiovascular, and gastrointestinal systems. Heat acclimation or acclimatization provides beneficial adaptations and should be undertaken where possible. Athletes should aim to begin exercise euhydrated. Furthermore, preexercise hyperhydration may be desirable in some scenarios and can be achieved through acute sodium or glycerol loading protocols. The assessment of fluid balance during exercise, together with gastrointestinal tolerance to fluid intake, and the appropriateness of thirst responses provide valuable information to inform fluid replacement strategies that should be integrated with event fuel requirements. Such strategies should also consider fluid availability and opportunities to drink, to prevent significant under- or overconsumption during exercise. Postexercise beverage choices can be influenced by the required timeframe for return to euhydration and co-ingestion of meals and snacks. Ingested beverage temperature can influence core temperature, with cold/icy beverages of potential use before and during exertional heat stress, while use of menthol can alter thermal sensation. Practical challenges in supporting athletes in teams and traveling for competition require careful planning. Finally, specific athletic population groups have unique nutritional needs in the context of exertional heat stress (i.e., youth, endurance/ultra-endurance athletes, and para-sport athletes), and specific adjustments to nutrition strategies should be made for these population groups.

Objectives: To investigate diet-exercise interactions related to bone markers in elite endurance athletes after a 3.5-week ketogenic low-carbohydrate, high-fat (LCHF) diet and subsequent restoration of carbohydrate (CHO) feeding.Methods: World-class race walkers (25 male, 5 female) completed 3.5-weeks of energy-matched (220 kJ·kg·d−1) high CHO (HCHO; 8.6 g·kg·d−1 CHO, 2.1 g·kg·d−1 protein, 1.2 g·kg·d−1 fat) or LCHF (0.5 g·kg·d−1 CHO, 2.1 g·kg·d−1 protein, 75–80% of energy from fat) diet followed by acute CHO restoration. Serum markers of bone breakdown (cross-linked C-terminal telopeptide of type I collagen, CTX), formation (procollagen 1 N-terminal propeptide, P1NP) and metabolism (osteocalcin, OC) were assessed at rest (fasting and 2 h post meal) and after exercise (0 and 3 h) at Baseline, after the 3.5-week intervention (Adaptation) and after acute CHO feeding (Restoration).Results: After Adaptation, LCHF increased fasting CTX concentrations above Baseline (p = 0.007, Cohen's d = 0.69), while P1NP (p < 0.001, d = 0.99) and OC (p < 0.001, d = 1.39) levels decreased. Post-exercise, LCHF increased CTX concentrations above Baseline (p = 0.001, d = 1.67) and above HCHO (p < 0.001, d = 0.62), while P1NP (p < 0.001, d = 0.85) and OC concentrations decreased (p < 0.001, d = 0.99) during exercise. Exercise-related area under curve (AUC) for CTX was increased by LCHF after Adaptation (p = 0.001, d = 1.52), with decreases in P1NP (p < 0.001, d = 1.27) and OC (p < 0.001, d = 2.0). CHO restoration recovered post-exercise CTX and CTX exercise-related AUC, while concentrations and exercise-related AUC for P1NP and OC remained suppressed for LCHF (p = 1.000 compared to Adaptation).Conclusion: Markers of bone modeling/remodeling were impaired after short-term LCHF diet, and only a marker of resorption recovered after acute CHO restoration. Long-term studies of the effects of LCHF on bone health are warranted.

Introduction We repeated our study of intensified training on a ketogenic low-carbohydrate (CHO), high-fat diet (LCHF) in world-class endurance athletes, with further investigation of a “carryover” effect on performance after restoring CHO availability in comparison to high or periodised CHO diets. Methods After Baseline testing (10,000 m IAAF-sanctioned race, aerobic capacity and submaximal walking economy) elite male and female race walkers undertook 25 d supervised training and repeat testing (Adapt) on energy-matched diets: High CHO availability (8.6 g∙kg-1∙d-1 CHO, 2.1 g∙kg-1∙d-1 protein; 1.2 g∙kg-1∙d-1 fat) including CHO before/during/after workouts (HCHO, n = 8): similar macronutrient intake periodised within/between days to manipulate low and high CHO availability at various workouts (PCHO, n = 8); and LCHF (

Purpose: The authors investigated the potential benefit of ingesting 2 mM of quinine (bitter tastant) on a 3000-m cycling time-trial (TT) performance. Methods: Nine well-trained male cyclists (maximal aerobic power: 386 [38] W) performed a maximal incremental cycling ergometer test, three 3000-m familiarization TTs, and four 3000-m intervention TTs (∼4 min) on consecutive days. The 4 interventions were (1) 25 mL of placebo, (2) a 25-mL sweet solution, and (3) and (4) repeat 25 mL of 2-mM quinine solutions (Bitter1 and Bitter2), 30 s before each trial. Participants self-selected their gears and were only aware of distance covered. Results: Overall mean power output for the full 3000 m was similar for all 4 conditions: placebo, 348 (45) W; sweet, 355 (47) W; Bitter1, 354 (47) W; and Bitter2, 355 (48) W. However, quinine administration in Bitter1 and Bitter2 increased power output during the first kilometer by 15 ± 11 W and 21 ± 10 W (mean ± 90% confidence limits), respectively, over placebo, followed by a decay of 34 ± 32 W during Bitter1 and Bitter2 during the second kilometer. Bitter2 also induced a 11 ± 13-W increase during the first kilometer compared with the sweet condition. Conclusions: Ingesting 2 mM of quinine can improve cycling performance during the first one-third of a 3000-m TT and could be used for sporting events lasting ∼80 s to potentially improve overall performance.

Researchers and practitioners in sports nutrition would greatly benefit from a rapid, portable, and non-invasive technique to measure muscle glycogen, both in the laboratory and field. This explains the interest in MuscleSound®, the first commercial system to use high-frequency ultrasound technology and image analysis from patented cloud-based software to estimate muscle glycogen content from the echogenicity of the ultrasound image. This technique is based largely on muscle water content, which is presumed to act as a proxy for glycogen. Despite the promise of early validation studies, newer studies from independent groups reported discrepant results, with MuscleSound® scores failing to correlate with the glycogen content of biopsy-derived mixed muscle samples or to show the expected changes in muscle glycogen associated with various diet and exercise strategies. The explanation of issues related to the site of assessment do not account for these discrepancies, and there are substantial problems with the premise that the ratio of glycogen to water in the muscle is constant. Although further studies investigating this technique are warranted, current evidence that MuscleSound® technology can provide valid and actionable information around muscle glycogen stores is at best equivocal.

Purpose: The extent to which hepcidin regulation after acute bouts of exercise is influenced by baseline (resting) concentrations of key iron parameters remains uncertain. This investigation explored the influence of selected iron parameters and 25-km race walk time on 3-h post-exercise hepcidin-25 levels in international-level race walkers. Methods: Twenty-four male race walkers completed a graded exercise test and a 25-km race-walk trial. Throughout the 25-km race-walk, venous blood samples were collected pre-exercise, immediately post-exercise, and at 3-h post-exercise. Blood was analysed for serum ferritin, serum iron, Interleukin-6 (IL-6), and hepcidin-25 concentration. Results: IL-6 and hepcidin-25 increased (7.6- and 7.5-fold, respectively) in response to the 25-km race-walk trial (both p < 0.01). Significant individual relationships were evident between 3-h post-exercise hepcidin-25, baseline serum ferritin and serum iron (r > 0.62; p < 0.05). Multiple regression analysis showed that these two iron parameters, in addition to post-exercise IL-6 concentration and 25-km race-walk time, accounted for ~77% of the variance in 3-h post-exercise hepcidin-25 (p < 0.01). A median split by the cohort’s baseline serum ferritin concentration (LOW: 58.0 vs. HIGH: 101.8 µg/L; p < 0.01) showed a significant between group difference in the 3-h post-exercise hepcidin-25 (LOW: 6.0 ± 3.6 vs. 11.3 ± 5.4 nM; p = 0.01), despite no differences in baseline serum iron, post-exercise IL-6, or 25-km race-walk time (all p > 0.05). Conclusion: Despite exercise activating numerous hepcidin regulators, baseline iron status appears to play a dominant role in the regulation of hepcidin-25 in elite-level athletes subsequent to endurance exercise.

Purpose The short-term restriction of carbohydrate (CHO) can potentially influence iron regulation via modification of postexercise interleukin-6 (IL-6) and hepcidin levels. This study examined the effect of a chronic ketogenic low-CHO high-fat (LCHF) diet on iron status and iron-regulatory markers in elite athletes. Methods International-level race walkers (n = 50) were allocated to one of three dietary interventions: (i) a high-CHO diet (n = 16), (ii) a periodized CHO availability (n = 17), or (iii) an LCHF diet (n = 17) while completing a periodized training program for 3 wk. A 19- to 25-km race walking test protocol was completed at baseline and after adaptation, and changes in serum ferritin, IL-6, and hepcidin concentrations were measured. Results from high-CHO and periodized CHO were combined into one group (CHO; n = 33) for analysis. Results The decrease in serum ferritin across the intervention period was substantially greater in the CHO group (37%) compared with the LCHF (23%) group (P = 0.021). After dietary intervention, the postexercise increase in IL-6 was greater in LCHF (13.6-fold increase; 95% confidence interval [CI] = 7.1–21.4) than athletes adhering to a CHO-rich diet (7.6-fold increase; 95% CI = 5.5–10.2; P = 0.033). Although no significant differences occurred between diets, CI values indicate that 3 h postexercise hepcidin concentrations were lower after dietary intervention compared with baseline in CHO (β = −4.3; 95% CI = −6.6 to −2.0), with no differences evident in LCHF. Conclusion Athletes who adhered to a CHO-rich diet experienced favorable changes to the postexercise IL-6 and hepcidin response, relative to the LCHF group. Lower serum ferritin after 3 wk of additional dietary CHO might reflect a larger more adaptive hematological response to training.

Objectives Adhering to a low carbohydrate (CHO) high fat (LCHF) diet can alter markers of iron metabolism in endurance athletes. This investigation examined the re-introduction of CHO prior to, and during exercise on the iron-regulatory response to exercise in a homogenous (in regard to serum ferritin concentration) group of athletes adapted to a LCHF diet. Design Parallel groups design. Methods Three weeks prior to the exercise trials, twenty-three elite race walkers adhered to either a CHO-rich (n = 14) or LCHF diet (n = 9). A standardised 19–25 km race walk was performed while athletes were still adhering to their allocated dietary intervention (Adapt). A second test was performed three days later, where all athletes were placed on a high CHO diet (CHO Restoration). Venous blood samples were collected pre-, post- and 3 h post-exercise and measured for interleukin-6 (IL-6) and hepcidin-25. Results The post-exercise IL-6 increase was greater in LCHF (p < 0.001) during both the Adapt (LCHF: 13.1-fold increase; 95% CI: 5.6–23.0, CHO: 8.0-fold increase; 5.1–11.1) and CHO Restoration trials (LCHF: 18.5-fold increase; 10.9–28.9, CHO: 6.3-fold increase; 3.9–9.5); outcomes were not different between trials (p = 0.84). Hepcidin-25 concentrations increased 3 h post-exercise (p < 0.001), however, they did not differ between trials (p = 0.46) or diets (p = 0.84). Conclusions The elevated IL-6 response in athletes adapted to a LCHF diet was not attenuated by an acute increase in exogenous CHO availability. Despite diet-induced differences in IL-6 response to exercise, post-exercise hepcidin levels were similar between diets and trials, indicating CHO availability has minimal influence on post-exercise iron metabolism.

Carbohydrate (CHO) availability could alter mucosal immune responses to exercise. This study compared the effect of three dietary approaches to CHO availability on resting and post-exercise s-IgA levels. Elite race walkers (n = 26) adhered to a high CHO diet (HCHO), periodised CHO availability (PCHO) or a low CHO/high fat diet (LCHF) for 3 weeks while completing an intensified training program. HCHO and PCHO groups consumed 8.0–8.5 g.kg−1 CHO daily, with timing of ingestion manipulated to alter CHO availability around key training sessions. The LCHF diet comprised 80% fat and restricted CHO to < 50 g.day−1. A race walk test protocol (19 km females, 25 km males) was completed at baseline, after adaptation, and following CHO restoration. On each occasion, saliva samples were obtained pre- and post-exercise to quantify s-IgA levels. Resting s-IgA secretion rate substantially increased ~ two-fold post-intervention in all groups (HCHO: 2.2 ± 2.2, PCHO: 2.8 ± 3.2, LCHF: 1.6 ± 1.6; fold-change± 95% confidence limits), however, no substantial differences between dietary treatments were evident. Post-exercise, substantial 20–130% increases in s-IgA concentration and 43–64% reductions in flow rate occurred in all dietary treatments, with trivial differences evident between groups. It appears that high volume training overrides any effect of manipulating CHO availability on mucosal immunity in elite athletes.

Although short (up to 3 days) exposure to major shifts in macronutrient intake appears to alter acid–base status, the effects of sustained ( > 1 week) interventions in elite athletes has not been determined. Using a non‐randomized, parallel design, we examined the effect of adaptations to 21 days of a ketogenic low carbohydrate high fat (LCHF) or periodized carbohydrate (PCHO) diet on pre‐ and post‐exercise blood pH, and concentrations of bicarbonate (HCO3 −) and lactate (La−) in comparison to a high carbohydrate (HCHO) control. Twenty‐four (17 male and 7 female) elite‐level race walkers completed 21 days of either LCHF (n = 9), PCHO (n = 7), or HCHO (n = 8) under controlled diet and training conditions. At baseline and post‐intervention, blood pH, blood [HCO3 −], and blood [La−] were measured before and after a graded exercise test. Net endogenous acid production (NEAP) over the previous 48–72 h was also calculated from monitored dietary intake. LCHF was not associated with significant differences in blood pH, [HCO3 −], or [La−], compared with the HCHO diet pre‐ or post‐exercise, despite a significantly higher NEAP (mEq∙day−1) (95% CI = [10.44; 36.04]). Our results indicate that chronic dietary interventions are unlikely to influence acid–base status in elite athletes, which may be due to pre‐existing training adaptations, such as an enhanced buffering capacity, or the actions of respiratory and renal pathways, which have a greater influence on regulation of acid–base status than nutritional intake.

Standardizing a dual x-ray absorptiometry (DXA) protocol is thought to provide a reliable measurement of body composition.We investigated the effects of manipulating muscle glycogen and creatine content independently and additively on DXA estimates of lean mass.Eighteen well-trained male cyclists undertook a parallel group application of creatine loading (n = 9) (20 g·d for 5 d loading; 3 g·d maintenance) or placebo (n = 9) with crossover application of glycogen loading (12 v 6 g·kg BM per day for 48 h) as part of a larger study involving a glycogen-depleting exercise protocol. Body composition, total body water, muscle glycogen and creatine content were assessed via DXA, bioelectrical impedance spectroscopy and standard biopsy techniques. Changes in the mean were assessed using the following effect-size scale:0.2 small,0.6, moderate,1.2 large and compared with the threshold for the smallest worthwhile effect of the treatment.Glycogen loading, both with and without creatine loading, resulted in substantial increases in estimates of lean body mass (mean ± SD; 3.0% ± 0.7% and 2.0% ± 0.9%) and leg lean mass (3.1% ± 1.8% and 2.6% ± 1.0%) respectively. A substantial decrease in leg lean mass was observed after the glycogen depleting condition (-1.4% ± 1.6%). Total body water showed substantial increases after glycogen loading (2.3% ± 2.3%), creatine loading (1.4% ± 1.9%) and the combined treatment (2.3% ± 1.1%).Changes in muscle metabolites and water content alter DXA estimates of lean mass during periods in which minimal change in muscle protein mass is likely. This information needs to be considered in interpreting the results of DXA-derived estimates of body composition in athletes.

PURPOSE: To investigate the impact of CHO re-introduction in athletes previously adapted to a LCHF diet on subsequent inflammatory and hepcidin responses to exercise. METHODS: In the three weeks prior to the exercise trials, twenty-three elite race walkers adhered to either a CHO-rich (n=14) or LCHF diet (n=9). A 19-25 km race walking protocol was performed while the race walkers were still adhering to their allocated dietary intervention (Adapt). A second exercise test was performed three days later, where the LCHF consumed CHO 2 h prior to, and during the exercise protocol (in line with sports nutrition guidelines) for the first time in 3.5 weeks (CHO Restoration). Venous blood samples were collected pre-, post- and 3 h post-exercise and analysed for serum ferritin, interleukin-6 (IL-6) and hepcidin-25. RESULTS: Serum ferritin concentration was similar between trials (p=0.48) and dietary groups (p=0.93). The post-exercise IL-6 increase was greater in LCHF (p

Quantity and timing of protein ingestion are major factors regulating myofibrillar protein synthesis (MPS). However, the effect of specific ingestion patterns on MPS throughout a 12 h period is unknown. We determined how different distributions of protein feeding during 12 h recovery after resistance exercise affects anabolic responses in skeletal muscle. Twenty-four healthy trained males were assigned to three groups (n = 8/group) and undertook a bout of resistance exercise followed by ingestion of 80 g of whey protein throughout 12 h recovery in one of the following protocols: 8 × 10 g every 1.5 h (PULSE); 4 × 20 g every 3 h (intermediate: INT); or 2 × 40 g every 6 h (BOLUS). Muscle biopsies were obtained at rest and after 1, 4, 6, 7 and 12 h post exercise. Resting and post-exercise MPS (l-[ring-(13)C6] phenylalanine), and muscle mRNA abundance and cell signalling were assessed. All ingestion protocols increased MPS above rest throughout 1-12 h recovery (88-148%, P INT>PULSE hierarchy in magnitude of phosphorylation. MuRF-1 and SLC38A2 mRNA were differentially expressed with BOLUS. In conclusion, 20 g of whey protein consumed every 3 h was superior to either PULSE or BOLUS feeding patterns for stimulating MPS throughout the day. This study provides novel information on the effect of modulating the distribution of protein intake on anabolic responses in skeletal muscle and has the potential to maximize outcomes of resistance training for attaining peak muscle mass.

Background Musculoskeletal injuries are the most common complaint in active populations. More than 50% of all injuries in sports can be classified as sprains, strains, ruptures, or breaks of musculoskeletal tissues. Nutritional and/or exercise interventions that increase collagen synthesis and strengthen these tissues could have an important effect on injury rates. Objective This study was designed to determine whether gelatin supplementation could increase collagen synthesis. Design Eight healthy male subjects completed a randomized, double-blinded, crossover-design study in which they consumed either 5 or 15 g of vitamin C-enriched gelatin or a placebo control. After the initial drink, blood was taken every 30 min to determine amino acid content in the blood. A larger blood sample was taken before and 1 h after consumption of gelatin for treatment of engineered ligaments. One hour after the initial supplement, the subjects completed 6 min of rope-skipping to stimulate collagen synthesis. This pattern of supplementation was repeated 3 times/d with ≥6 h between exercise bouts for 3 d. Blood was drawn before and 4, 24, 48, and 72 h after the first exercise bout for determination of amino-terminal propeptide of collagen I content. Results Supplementation with increasing amounts of gelatin increased circulating glycine, proline, hydroxyproline, and hydroxylysine, peaking 1 h after the supplement was given. Engineered ligaments treated for 6 d with serum from samples collected before or 1 h after subjects consumed a placebo or 5 or 15 g gelatin showed increased collagen content and improved mechanics. Subjects who took 15 g gelatin 1 h before exercise showed double the amino-terminal propeptide of collagen I in their blood, indicating increased collagen synthesis. Conclusion These data suggest that adding gelatin to an intermittent exercise program improves collagen synthesis and could play a beneficial role in injury prevention and tissue repair. This trial was registered at the Australian New Zealand Clinical Trials Registry as ACTRN12616001092482.

We investigated the effect of pre- "race" ingestion of a 1,3-butanediol acetoacetate diester on blood ketone concentration, substrate metabolism and performance of a cycling time trial (TT) in professional cyclists. In a randomized cross-over design, 10 elite male cyclists completed a ~31 km laboratory-based TT on a cycling ergometer programmed to simulate the 2017 World Road Cycling Championships course. Cyclists consumed a standardized meal [2 g/kg body mass (BM) carbohydrate (CHO)] the evening prior to a trial day and a CHO breakfast (2 g/kg BM CHO) with 200 mg caffeine on the morning of a trial day. Cyclists were randomized to consume either the ketone diester (2 × 250 mg/kg) or a placebo drink, followed immediately by 200 mL diet cola, given ~ 30 min before and immediately prior to commencing a 20 min incremental warm-up. Blood samples were collected prior to and during the warm-up, pre- and post- TT and at regular intervals after the TT. Urine samples were collected pre- and post- warm-up, immediately post TT and 60 min post TT. Pre-exercise ingestion of the diester resulted in a 2 ± 1% impairment in TT performance that was associated with gut discomfort and higher perception of effort. Serum β-hydroxybutyrate, serum acetoacetate, and urine ketone concentrations increased from rest following ketone ingestion and were higher than placebo throughout the trial. Ketone ingestion induces hyperketonemia in elite professional cyclists when in a carbohydrate fed state, and impairs performance of a cycling TT lasting ~50 min.

Cycling is recognised as a sport in which there is a high incidence of poor bone health. Sweat calcium losses may contribute to this. Purpose To examine whether a calcium-rich pre-exercise meal attenuates exercise-induced perturbations of bone calcium homeostasis caused by maintenance of sweat calcium losses. Methods Using a randomized, counterbalanced crossover design, 32 well-trained female cyclists completed two 90 min cycling trials separated by 1 day. Exercise trials were preceded 2 hours by either a calcium-rich (1352 ± 53 mg calcium) dairy based meal (CAL) or a control meal (CON; 46 ± 7 mg calcium). Blood was sampled pre-trial; pre-exercise; and immediately, 40 min, 100 min and 190 min post-exercise. Blood was analysed for ionized calcium and biomarkers of bone resorption (Cross Linked C-Telopeptide of Type I Collagen (CTX-I), Cross Linked C-Telopeptide of Type II Collagen (CTX-II), Parathyroid Hormone (PTH), and bone formation (Procollagen I N-Terminal Propeptide (PINP)) using the established enzyme-linked immunosorbent assay technique. Results PTH and CTX-I increased from pre-exercise to post-exercise in both conditions but was attenuated in CAL (p < 0.001). PTH was 1.55 [1.20, 2.01] times lower in CAL immediately post-exercise and 1.45 [1.12, 1.88] times lower at 40 min post-exercise. CTX-I was 1.40 [1.15, 1.70] times lower in CAL at immediately post-exercise, 1.30 [1.07, 1.57] times lower at 40 min post-exercise and 1.22 [1.00, 1.48] times lower at 190 min post-exercise (p < 0.05). There was no significant interaction between pre-exercise meal condition and time point for CTX-II (p = 0.732) or PINP (p = 0.819). Conclusion This study showed that a calcium-rich pre-exercise breakfast meal containing ~1350 mg of calcium consumed ~90 min before a prolonged and high intensity bout of stationary cycling attenuates the exercise induced rise in markers of bone resorption – PTH and CTX-I. Trial Registration Australian New Zealand Clinical Trials Registry ACTRN12614000675628

Some athletes avoid dairy in the meal consumed before exercise due to fears about gastrointestinal discomfort. Regular exclusion of dairy foods may unnecessarily reduce intake of high quality proteins and calcium with possible implications for body composition and bone health. This study compared the effects of meals that included (Dairy) or excluded (Control) dairy foods on gastric comfort and subsequent cycling performance. Well-trained female cyclists (n = 32; mean ± SD; 24.3 ± 4.1 y; VO2peak 57.1 ± 4.9 ml/kg/min) completed two trials (randomized cross-over design) in which they consumed a meal (2 g/kg carbohydrate and 54 kJ/kg) 2 hr before a 90-min cycle session (80 min at 60% maximal aerobic power followed by a 10-min time trial; TT). The dairy meal contained 3 servings of dairy foods providing ~1350 mg calcium. Gut comfort and palatability were measured using questionnaires. Performance was measured as maximum mean power during the TT (MMP10min). There was no statistical or clinical evidence of an effect of meal type on MMP10min with a mean difference (Dairy – Control) of 4 W (95% CI [–2, 9]). There was no evidence of an association between pretrial gut comfort and meal type (p = .15) or between gut comfort delta scores and meal type postmeal (p = .31), preexercise (p = .17) or postexercise (p = .80). There was no statistical or clinical evidence of a difference in palatability between meal types. In summary, substantial amounts of dairy foods can be included in meals consumed before strenuous cycling without impairing either gut comfort or performance.

We have previously shown that the aminoacidemia caused by the consumption of a rapidly digested protein after resistance exercise enhances muscle protein synthesis (MPS) more than the amino acid (AA) profile associated with a slowly digested protein. Here, we investigated whether differential feeding patterns of a whey protein mixture commencing before exercise affect postexercise intracellular signaling and MPS.Twelve resistance-trained males performed leg resistance exercise 45 min after commencing each of three volume-matched nutrition protocols: placebo (PLAC, artificially sweetened water), BOLUS (25 g of whey protein + 5 g of leucine dissolved in artificially sweetened water; 1 × 500 mL), or PULSE (15 × 33-mL aliquots of BOLUS drink every 15 min).The preexercise rise in plasma AA concentration with PULSE was attenuated compared with BOLUS (P0.05); this effect was reversed after exercise, with two-fold greater leucine concentrations in PULSE compared with BOLUS (P0.05). One-hour postexercise, phosphorylation of p70 S6K(thr389) and rpS6(ser235/6) was increased above baseline with BOLUS and PULSE, but not PLAC (P0.05); furthermore, PULSEBOLUS (P0.05). MPS throughout 5 h of recovery was higher with protein ingestion compared with PLAC (0.037 ± 0.007), with no differences between BOLUS or PULSE (0.085 ± 0.013 vs. 0.095 ± 0.010%.h(-1), respectively, P = 0.56).Manipulation of aminoacidemia before resistance exercise via different patterns of intake of protein altered plasma AA profiles and postexercise intracellular signaling. However, there was no difference in the enhancement of the muscle protein synthetic response after exercise. Protein sources producing a slow AA release, when consumed before resistance exercise in sufficient amounts, are as effective as rapidly digested proteins in promoting postexercise MPS.

Background Hypohydration and hyperthermia are factors that may contribute to fatigue and impairment of endurance performance. The purpose of this study was to investigate the effectiveness of combining glycerol hyperhydration and an established precooling technique on cycling time trial performance in hot environmental conditions. Methods Twelve well-trained male cyclists performed three 46.4-km laboratory-based cycling trials that included two climbs, under hot and humid environmental conditions (33.3 ± 1.1°C; 50 ± 6% r.h.). Subjects were required to hyperhydrate with 25 g.kg-1 body mass (BM) of a 4°C beverage containing 6% carbohydrate (CON) 2.5 h prior to the time trial. On two occasions, subjects were also exposed to an established precooling technique (PC) 60 min prior to the time trial, involving 14 g.kg-1 BM ice slurry ingestion and applied iced towels over 30 min. During one PC trial, 1.2 g.kg-1 BM glycerol was added to the hyperhydration beverage in a double-blind fashion (PC+G). Statistics used in this study involve the combination of traditional probability statistics and a magnitude-based inference approach. Results Hyperhydration resulted in large reductions (−0.6 to −0.7°C) in rectal temperature. The addition of glycerol to this solution also lowered urine output (330 ml, 10%). Precooling induced further small (−0.3°C) to moderate (−0.4°C) reductions in rectal temperature with PC and PC+G treatments, respectively, when compared with CON (0.0°C, P Conclusions Despite increasing fluid intake and reducing core temperature, performance and thermoregulatory benefits of a hyperhydration strategy with and without the addition of glycerol, plus practical precooling, were not superior to hyperhydration alone. Further research is warranted to further refine preparation strategies for athletes competing in thermally stressful events to optimize health and maximize performance outcomes.

Purpose: To develop and investigate the efficacy of a new precooling strategy combining external and internal techniques on the performance of a cycling time trial (TT) in a hot and humid environment. Methods: Eleven well-trained male cyclists undertook three trials of a laboratory-based cycling TT simulating the course characteristics of the Beijing Olympic Games event in a controlled hot and humid environment (32°C-35°C at 50%-60% relative humidity). The trials, separated by 3-7 d, were undertaken in a randomized crossover design and consisted of the following: 1) CON-no treatment apart from the ad libitum consumption of cold water (4°C), 2) STD COOL-whole-body immersion in cold (10°C) water for 10 min followed by wearing a cooling jacket, or 3) NEW COOL-combination of consumption of 14 g of ice slurry ("slushie") per kilogram body mass made from a commercial sports drink while applying iced towels. Results: There was an observable effect on rectal temperature (Trec) before the commencement of the TT after both precooling techniques (STD COOL < NEW COOL < CON, P < 0.05), but pacing of the TT resulted in similar Trec, HR, and RPE throughout the cycling protocol in all trials. NEW COOL was associated with a 3.0% increase in power (~8 W) and a 1.3% improvement in performance time (~1:06 min) compared with the CON trial, with the true likely effects ranging from a trivial to a large benefit. The effect of the STD COOL trial compared with the CON trial was "unclear." Conclusions: This new precooling strategy represents a practical and effective technique that could be used by athletes in preparation for endurance events undertaken in hot and humid conditions

OBJECTIVE: Blood doping in endurance sport is a growing problem. The purpose of this study was to determine the reliability of total hemoglobin mass (Hb(mass)) measurement in the field and to establish the variability of Hb(mass) during a cycling race, to assess its viability as an additional antidoping detection parameter. DESIGN: Control-matched longitudinal study. SETTING: International Cycling Union's (UCI) ProTour stage race. PARTICIPANTS: Six professional cyclists and 5 recreationally active controls. INTERVENTIONS: Seventy-two Hb(mass) tests using the optimized carbon monoxide rebreathing method were performed over 7 consecutive days, before and throughout the tour. Fasted venous blood was obtained for measurement of hematocrit (Hct) and hemoglobin concentration [Hb] in the morning before stages 1, 3, and 6 (D1, D3, and D6). MAIN OUTCOME MEASURES: Reliability of Hb(mass) measurement was established using typical error calculated from 2 baseline measures. Individual change scores and coefficients of variation were used to assess stability during racing. RESULTS: Typical error for Hb(mass) was 1.3% [95% confidence limits (CL): 0.9%, 2.5%]. Calculated 95% and 99.99% CL for percent change in Hb(mass) were +/-3.6% and +/-7.2%, respectively. Mean Hb(mass) remained within +/-1.9% of baseline in cyclists and +/-0.5% in controls. In all cases, individual change scores for both cyclists and controls fell within the 95% CL. There was a decrease in Hct (8.1% +/- 2.8%) and [Hb] (9.7% +/- 3.2%) throughout the tour in cyclists but not in controls. CONCLUSIONS: We demonstrate that Hb(mass) can be measured reliably via CO-rebreathing during a cycling tour. Unlike [Hb] and Hct, Hb(mass) remains stable over 6 days of racing in professional cyclists and may have potential in an antidoping context.

We investigated the effect of carbohydrate ingestion after maximal lengthening contractions of the knee extensors on circulating concentrations of myocellular proteins and cytokines, and cytokine mRNA expression in muscle. Using a cross-over design, 10 healthy males completed 5 sets of 10 lengthening (eccentric) contractions (unilateral leg press) at 120% 1 repetition-maximum. Subjects were randomized to consume a carbohydrate drink (15% weight per volume; 3 g/kg BM) for 3 h after exercise using one leg, or a placebo drink after exercise using the contralateral leg on another day. Blood samples (10 mL) were collected before exercise and after 0, 30, 60, 90, 120, 150, and 180 min of recovery. Muscle biopsies (vastus lateralis) were collected before exercise and after 3 h of recovery. Following carbohydrate ingestion, serum concentrations of glucose (30-90 min and at 150 min) and insulin (30-180 min) increased (P < 0.05) above pre-exercise values. Serum myoglobin concentration increased (similar to 250%; P < 0.05) after both trials. In contrast, serum cytokine concentrations were unchanged throughout recovery in both trials. Muscle mRNA expression for IL-8 (6.4-fold), MCP-1 (4.7-fold), and IL-6 (7.3-fold) increased substantially after carbohydrate ingestion. TNF-alpha mRNA expression did not change after either trial. Carbohydrate ingestion during early recovery from exercise-induced muscle injury may promote proinflammatory reactions within skeletal muscle.

The purpose of this study was to investigate the effects of sodium bicarbonate (NaHCO3), caffeine, and their combination on repeated 200-m freestyle performance. Six elite male freestyle swimmers ingested NaHCO3 (0.3 g/kg; B), caffeine (6.2 ± 0.3 mg/kg; C), a combination of both (B+C), and placebo (P) on 4 separate occasions before completing 2 maximal 200-m freestyle time trials (TT1 and TT2) separated by 30 min. No significant differences (p = .06) were observed for performance in TT1 (B 2:03.01 ± 0:03.68 min, C 2:02.42 ± 0:03.17 min, B+C 2:01.69 ± 0:03.19 min, P 2:03.77 ± 0:03.21 min) or TT2 (B 2:02.62 ± 0:04.16 min, C 2:03.90 ± 0:03.58 min, B+C 2:01.70 ± 0:02.84 min, P 2:04.22 ± 0:03.75 min). The drop-off in performance time from TT1 to TT2, however, was significantly greater when C was ingested than with B (−1.5%, p = .002) or B+C (–1.2%, p = .024). This is likely because of the lower blood pH and slower recovery of blood HCO3 post-TT1 after C ingestion. These findings suggest that the ergogenic benefit of taking C alone for repeated 200-m swimming performance appears limited. When combined with NaHCO3, however, its negative impact on repeated maximal exercise performance is reversed.