Vitamin D and the Athlete: Current Perspectives and New Challenges

The last decade has seen a dramatic increase in general interest in and research into vitamin D, with many athletes now taking vitamin D supplements as part of their everyday dietary regimen. The most recognized role of vitamin D is its regulation of calcium homeostasis; there is a strong relationship between vitamin D and bone health in non-athletic individuals. In contrast, data have consistently failed to demonstrate any relationship between serum 25[OH]D and bone health, which may in part be due to the osteogenic stimulus of exercise. Vitamin D may interact with extra-skeletal tissues such as muscle and the immune system to modulate recovery from damaging exercise and infection risk. Given that many athletes now engage in supplementation, often consuming extreme doses of vitamin D, it is important to assess whether excessive vitamin D can be detrimental to health. It has been argued that toxic effects only occur when serum 25[OH] D concentrations are greater than 180 nmol·l −1 , but data from our laboratory have suggested high-dose supplementation could be problematic. Finally, there is a paradoxical relationship between serum 25[OH]D concentration, ethnicity, and markers of bone health: Black athletes often present with low serum 25[OH] D without physiological consequences. One explanation for this could be genetic differences in vitamin D binding protein due to ethnicity, resulting in greater concentrations of bioavailable (or free) vitamin D in some ethnic groups. In the absence of any pathology, screening may be unnecessary and could result in incorrect supplementation. Data must now be re-examined, taking into consideration bioavailable or “free” vitamin D in ethnically diverse groups to enable new thresholds and target concentrations to be established; perhaps, for now, it is time to “set vitamin D free”. © 2018 The Author(s

Murine myoblast migration: influence of replicative ageing and nutrition

Cell migration is central to skeletal muscle repair following damage. Leucine and β-Hydroxy β-methylbutyric acid (HMB) are supplements consumed for recovery from muscle damaging exercise in humans, however, their impact on muscle cell migration with age is not yet understood. We hypothesised that replicatively aged (“aged”; P46–P48) myoblasts would be less efficient at basal and supplemented repair versus parental controls (“control”; P12–P16). Aged and control myoblasts were scratch-damaged and migration velocity, directionality and distance assessed over 48 h in the absence and presence of leucine (10 mM) or HMB (10 mM) ± PI3K/Akt (LY294002 10 μM), ERK (PD98059 5 μM) or mTOR (rapamycin 0.5 μM) inhibition. Opposing our hypothesis, aged cells displayed increased velocities, directionality and distance migrated (P < 0.001) versus control. Leucine and HMB significantly increased (P < 0.001) the same parameters in control cells. The supplements were with smaller, albeit significant impact on aged cell velocity (P < 0.001) and in the presence of HMB only, distance (P = 0.041). Inhibitor studies revealed that, PI3K and ERK activation were essential for velocity, directionality and migration distance of aged cells in basal conditions, whereas mTOR was important for directionality only. While PI3K activation was critical for all parameters in control cells (P < 0.001), inhibition of ERK or mTOR improved, rather than reduced, control cell migration distance. Enhanced basal velocity, directionality and distance in aged cells required ERK and PI3K activation. By contrast, in control cells, basal migration was underpinned by PI3K activation, and facilitated by leucine or HMB supplementation, to migration levels seen in aged cells. These data suggest that replicatively aged myoblasts are not anabolically resistant per se, but are capable of efficient repair, underpinned by altered signaling pathways, compared with unaged control myoblasts

Carbohydrate and caffeine improves high intensity running of elite rugby league interchange players during simulated match play.

The study examined the effects of carbohydrate and caffeine ingestion on simulated rugby league interchange performance. Eight male elite rugby league forwards completed two trials of a rugby league simulation protocol for interchange players seven days apart in a randomized crossover design, ingesting either carbohydrate (CHO; 40 g·h-1) or carbohydrate and caffeine (CHO-C) (40 g·h-1 + 3 mg·kg-1) drink. Movement characteristics, heart rate, ratings of perceived exertion (RPE), and countermovement jump height (CMJ) were measured during the protocol. CHO-C resulted in likely to very likely higher mean running speeds (ES 0.43 to 0.75), distance in high intensity running (ES 0.41 to 0.64) and mean sprint speeds (ES 0.39 to 1.04) compared to CHO. Heart rate was possibly to very likely higher (ES 0.32 to 0.74) and RPE was likely to very likely lower (ES -0.53 to 0.86) with CHO-C. There was a likely trivial to possibly higher CMJ in CHO-C compared to CHO (ES 0.07 to 0.25). The co-ingestion of carbohydrate with caffeine has an ergogenic effect to reduce the sense of effort and increase high intensity running capability that might be employed to enhance interchange running performance in elite rugby league players

Male Flat Jockeys Do Not Display Deteriorations in Bone Density or Resting Metabolic Rate in Accordance With Race Riding Experience: Implications for RED-S.

Despite consistent reports of poor bone health in male jockeys, it is not yet known if this is a consequence of low energy availability or lack of an osteogenic stimulus. Given the rationale that low energy availability is a contributing factor in low bone health, we tested the hypothesis that both hip and lumbar bone mineral density (BMD) should progressively worsen in accordance with the years of riding. In a cross-sectional design, male apprentice (n=17) and senior (n=14) jockeys (matched for body mass and fat free mass) were assessed for hip and lumbar spine BMD as well as both measured and predicted resting metabolic rate (RMR). Despite differences (P0.05) in hip (-0.9 ± 1.1 v -0.8 ± 0.7) and lumbar Z-scores (-1.3 ± 1.4 v -1.5 ± 1) or measured RMR (1459 ± 160 v 1500 ± 165 kcal.d-1) between apprentices and senior jockeys, respectively. Additionally, years of race riding did not demonstrate any significant correlations (P>0.05) with either hip or lumbar spine BMD. Measured RMR was also not different (P>0.05) from predicted RMR in either apprentice (1520 ± 44 kcal.d-1) or senior jockeys (1505 ± 70 kcal.d-1). When considered with previously published data examining under-reporting of energy intake and direct assessments of energy expenditure, we suggest that low BMD in jockeys is not due to low energy availability per se, but rather, the lack of an osteogenic stimulus associated with riding

Prevalence, Severity and Potential Nutritional Causes of Gastrointestinal Symptoms during a Marathon in Recreational Runners.

The purpose of the present study was to investigate the prevalence of gastrointestinal symptoms (GIS) amongst recreational runners during a marathon race, and potential nutritional factors that may contribute. Recreational runners of the 2017 Liverpool (n = 66) and Dublin (n = 30) marathons were recruited. GIS were reported post-marathon and we considered GIS in the 7 days prior to the marathon and during the marathon using the Gastrointestinal Symptom Rating Scale (GSRS). Nutritional intake was recorded using food diaries for the day before the race, morning of the race, and during the race; 43% of participants reported moderate (&ge;4) GIS in the 7 days prior to the marathon and 27% reported moderate symptoms during the marathon with most common symptoms being flatulence (16%) during training, and nausea (8%) during the marathon race. Correlations between all nutritional intake and GIS were not statistically significant (p > 0.05). There were significant correlations between total GIS score (r = 0.510, p < 0.001), upper GIS score (r = 0.346, p = 0.001) and lower GIS score (r = 0.483, p < 0.001) in training and during the marathon. There appears to be a modest prevalence of GIS in recreational runners, in the week prior to a marathon and during marathon running, although there was no association with nutritional intake before or during the race

GB Apprentice Jockeys Do Not Have the Body Composition to Make Current Minimum Race Weights: Is It Time to Change the Weights or Change the Jockeys?

Flat jockeys in Great Britain (GB) are classified as apprentices if they are aged less than 26 years and/or have ridden less than 95 winners. To gain experience, apprentices are allocated a weight allowance of up to 7 lb (3.2 kg). Given that there is no off-season in GB flat horseracing, jockeys are required to maintain their racing weight all year round. In light of recent work determining that current apprentices are considerably heavier than previous generations and that smaller increases have been made in the minimum weight, the aim of this study was to assess if the minimum weight in GB was achievable. To make the minimum weight (50.8 kg) with the maximal weight allowance requires a body mass of ∼46.6 kg while maintaining a fat mass >2.5 kg (the lowest fat mass previously reported in weight-restricted males). Thirty-two male apprentice jockeys were assessed for body composition using dual-energy X-ray absorptiometry. The mean (SD) total mass and fat mass were 56 (2.9) kg and 7.2 (1.8) kg, respectively. Given that the lowest theoretical body mass for this group was 51.2 (2.3) kg, only one of 32 jockeys was deemed feasible to achieve the minimum weight with their current weight allowance and maintaining fat mass >2.5 kg. Furthermore, urine osmolality of 780 (260) mOsmol/L was seen, with 22 (out of 32) jockeys classed as dehydrated (>700 mOsmols/L), indicating that body mass would be higher when euhydrated. Additionally, we observed that within new apprentice jockeys licensed during this study (N = 41), only one jockey was able to achieve the minimum weight. To facilitate the goal of achieving race weight with minimal disruptions to well-being, the authors’ data suggest that the minimum weight for GB apprentices should be raised

Why don't serum vitamin D concentrations associate with BMD by DXA? A case of being 'bound' to the wrong assay? Implications for vitamin D screening.

BACKGROUND: The association between bone mineral density (BMD) and serum25-hydroxyvitamin D (25(OH)D) concentration is weak, particularly in certain races (eg, BlackAfrican vs Caucasian) and in athletic populations. We aimed to examine if bioavailable vitamin D rather than serum 25(OH)D was related to markers of bone health within a racially diverse athletic population. METHODS: In 604 male athletes (Arab (n=327), Asian (n=48), Black(n=108), Caucasian (n=53)and Hispanic (n=68)), we measured total 25(OH)D, vitamin D-binding protein and BMD by DXA. Bioavailable vitamin D was calculated using the free hormone hypothesis. RESULTS: From 604 athletes, 21.5% (n=130) demonstrated severe 25(OH)D deficiency, 37.1% (n=224) deficiency, 26% (n=157) insufficiency and 15.4% (n=93) sufficiency. Serum 25(OH)D concentrations were not associated with BMD at any site. After adjusting for age and race, bioavailable vitamin D was associated with BMD (spine, neck and hip). Mean serum vitamin D binding protein concentrations were not associated with 25(OH)D concentrations (p=0.392). CONCLUSION: Regardless of age or race, bioavailable vitamin D and not serum 25(OH)D was associated with BMD in a racially diverse athletic population. If vitamin D screening is warranted, clinicians should use appropriate assays to calculate vitamin D binding protein and bioavailable vitamin D levels concentrations than serum 25(OH)D. In turn, prophylactic vitamin D supplementation to 'correct' insufficient athletes should not be based on serum 25(OH)D measures

Acute high-intensity interval running increases markers of damage and permeability but not gastrointestinal symptoms.

Purpose: To investigate the effects of high-intensity interval (HIIT) running on markers of gastrointestinal (GI) damage and permeability alongside subjective symptoms of GI discomfort. Methods: Eleven male runners completed an acute bout of HIIT (eighteen 400 m runs at 120%O2max ) where markers of GI permeability, intestinal damage and GI discomfort symptoms were assessed and compared with resting conditions. Results: Compared to rest, HIIT significantly increased serum lactulose:rhamnose ratio (0.051 ± 0.016 vs. 0.031 ± 0.021, p = 0.0047; 95% CI = 0.006 - 0.036) and sucrose concentrations (0.388 ± 0.217 vs 0.137 ± 0.148 mg.l-1; p < 0.001; 95% CI = 0.152 - 0.350). In contrast, urinary lactulose:rhamnose (0.032 ± 0.005 vs 0.030 ± 0.005; p = 0.3; 95% CI = -0.012 - 0.009) or sucrose concentrations (0.169 ± 0.168% vs 0.123 ± 0.120%; p = 0.54; 95% CI = -0.199 - 0.108) did not differ between HIIT and resting conditions. Plasma I-FABP was significantly increased (p < 0.001) during and in the recovery period from HIIT whereas no changes were observed during rest. Mild-symptoms of GI discomfort, were reported immediately- and 24 h post-HIIT, although these symptoms did not correlate to GI permeability or I-FABP. Conclusion Acute HIIT increased GI permeability and intestinal I-FABP release, although these do not correlate with symptoms of GI discomfort. Furthermore, by using serum sampling, we provide data showing that it is possible to detect changes in intestinal permeability that is not observed using urinary sampling over a shorter time-period

Fuel for the Work Required: A Theoretical Framework for Carbohydrate Periodization and the Glycogen Threshold Hypothesis.

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

Efficacy of High Dose Vitamin D Supplements for Elite Athletes.

PURPOSE: Supplementation with dietary forms of vitamin D is commonplace in clinical medicine, elite athletic cohorts and the general population, yet the response of all major vitamin D metabolites to high doses of vitamin D is poorly characterized. We aimed to identify the responses of all major vitamin D metabolites to moderate and high dose supplemental vitamin D3. METHODS: A repeated measures design was implemented in which 46 elite professional European athletes were block randomized based on their basal 25[OH]D concentration into two treatment groups. Athletes received either 35,000 or 70,000 IU.week vitamin D3 for 12 weeks and 42 athletes completed the trial. Blood samples were collected over 18 weeks to monitor the response to supplementation and withdrawal from supplementation. RESULTS: Both doses led to significant increases in serum 25[OH]D and 1,25[OH]2D3. 70,000 IU.week also resulted in a significant increase of the metabolite 24,25[OH]2D at weeks 6 and 12 that persisted following supplementation withdrawal at week 18, despite a marked decrease in 1,25[OH]2D3. Intact PTH was decreased in both groups by week 6 and remained suppressed throughout the trial. CONCLUSIONS: High dose vitamin D3 supplementation (70,000 IU.week) may be detrimental for its intended purposes due to increased 24,25[OH]2D production. Rapid withdrawal from high dose supplementation may inhibit the bioactivity of 1,25[OH]2D3 as a consequence of sustained increases in 24,25[OH]2D that persist as 25[OH]D and 1,25[OH]2D concentrations decrease. These data imply that lower doses of vitamin D3 ingested frequently may be most appropriate and gradual withdrawal from supplementation as opposed to rapid withdrawal may be favorable