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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 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.

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.

We determined the effect of suppressing lipolysis via administration of nicotinic acid (NA) on fuel substrate selection and half-marathon running capacity. In a single-blinded, Latin square design, 12 competitive runners completed four trials involving treadmill running until volitional fatigue at a pace based on 95% of personal best half-marathon time. Trials were completed in a fed or overnight fasted state: 1) carbohydrate (CHO) ingestion before (2 g CHO·kg−1·body mass−1) and during (44 g/h) [CFED]; 2) CFED plus NA ingestion [CFED-NA]; 3) fasted with placebo ingestion during [FAST]; and 4) FAST plus NA ingestion [FAST-NA]. There was no difference in running distance (CFED, 21.53 ± 1.07; CFED-NA, 21.29 ± 1.69; FAST, 20.60 ± 2.09; FAST-NA, 20.11 ± 1.71 km) or time to fatigue between the four trials. Concentrations of plasma free fatty acids (FFA) and glycerol were suppressed following NA ingestion irrespective of preexercise nutritional intake but were higher throughout exercise in FAST compared with all other trials ( P < 0.05). Rates of whole-body CHO oxidation were unaffected by NA ingestion in the CFED and FAST trials, but were lower in the FAST trial compared with the CFED-NA trial ( P < 0.05). CHO was the primary substrate for exercise in all conditions, contributing 83-91% to total energy expenditure with only a small contribution from fat-based fuels. Blunting the exercise-induced increase in FFA via NA ingestion did not impair intense running capacity lasting ∼85 min, nor did it alter patterns of substrate oxidation in competitive athletes. Although there was a small but obligatory use of fat-based fuels, the oxidation of CHO-based fuels predominates during half-marathon running.

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

A major goal of training to improve the performance of prolonged, continuous, endurance events lasting up to 3 h is to promote a range of physiological and metabolic adaptations that permit an athlete to work at both higher absolute and relative power outputs/speeds and delay the onset of fatigue (i.e., a decline in exercise intensity). To meet these goals, competitive endurance athletes undertake a prodigious volume of training, with a large proportion performed at intensities that are close to or faster than race pace and highly dependent on carbohydrate (CHO)-based fuels to sustain rates of muscle energy production [i.e., match rates of adenosine triphosphate (ATP) hydrolysis with rates of resynthesis]. Consequently, to sustain muscle energy reserves and meet the daily demands of training sessions, competitive athletes freely select CHO-rich diets. Despite renewed interest in high-fat, low-CHO diets for endurance sport, fat-rich diets do not improve training capacity or performance, but directly impair rates of muscle glycogenolysis and energy flux, limiting high-intensity ATP production. When highly trained athletes compete in endurance events lasting up to 3 h, CHO-, not fat-based fuels are the predominant fuel for the working muscles and CHO, not fat, availability becomes rate limiting for performance.