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Few data are available that describe how probiotics influence systemic metabolism during endurance exercise. Metabolomic profiling of endurance athletes will elucidate mechanisms by which probiotics may confer benefits to the athlete. In this study, twenty-four runners (20 male, 4 female) were block randomised into two groups using a double-blind matched-pairs design according to their most recent Marathon performance. Runners were assigned to 28-days of supplementation with a multi-strain probiotic (PRO) or a placebo (PLB). Following 28-days of supplementation, runners performed a competitive track Marathon race. Venous blood samples and muscle biopsies (vastus lateralis) were collected on the morning of the race and immediately post-race. Samples were subsequently analysed by untargeted 1H-NMR metabolomics. Principal component analysis (PCA) identified a greater difference in the post-Marathon serum metabolome in the PLB group vs. PRO. Univariate tests identified 17 non-overlapped metabolites in PLB, whereas only seven were identified in PRO. By building a PLS-DA model of two components, we revealed combinations of metabolites able to discriminate between PLB and PRO post-Marathon. PCA of muscle biopsies demonstrated no discernible difference post-Marathon between treatment groups. In conclusion, 28-days of probiotic supplementation alters the metabolic perturbations induced by a Marathon. Such findings may be related to maintaining the integrity of the gut during endurance exercise.

INTRODUCTION: Sodium bicarbonate (NaHCO3) is a well-established nutritional ergogenic aid that is typically ingested as a beverage or consumed in gelatin capsules. Whilst capsules may delay NaHCO3 release and reduce gastrointestinal (GI) side-effects compared with a beverage, it is currently unclear whether capsule size may influence acid-base responses and GI symptoms following supplementation. AIM: To determine the effects of NaHCO3 supplementation administered in different sized capsules on acid-base responses, GI symptoms and palatability. METHODS: Ten healthy males (mean ± SD: age 20 ± 2 y; height 1.80 ± 0.09 m; weight 78.0 ± 11.9 kg) underwent three testing sessions whereby 0.3 g∙kg–1 body mass NaHCO3 was consumed in either small (size 3), medium (size 0) or large (size 000) capsules. Capillary blood samples were procured pre-ingestion and every 10 min post-ingestion for 180 min. Blood samples were analysed using a Radiometer (Radiometer ABL800, Denmark) to determine blood bicarbonate concentration ([HCO3–]) and potential hydrogen (pH). Gastrointestinal (GI) symptoms were measured using a questionnaire at the same timepoints, whereas palatability was recorded pre-consumption. RESULTS: Capsule size had a significant effect on lag time (the time [HCO3-] changed Tlag) and the timing of peak blood [HCO3–](Tmax). Bicarbonate Tlag was significantly higher in the large (28 ± 4 min) compared with the small (13 ± 2 min) sized capsules (P = 0.009). Similarly, Tmax was significantly lower in the small capsule (13 ± 2 min) compared with both the medium (22 ± 6 min; P = 0.005) and large (28 ± 4 min; P = 0.001) sized capsules. The GI symptom scores were similar for small (3 ± 3 AU,), medium (5 ± 3 AU) and large (3 ± 3 AU) sized capsules, with no significant difference between symptom scores (F = 1.3, P = 0.310). Similarly, capsule size had no effect on palatability (F = 0.8, P = 0.409), with similar scores between different capsule sizes. CONCLUSION: Small capsu

The timing of sodium bicarbonate (NaHCO3) supplementation has been suggested to be most optimal when coincided with a personal time that bicarbonate (HCO3–) or pH peaks in the blood following ingestion. However, the ergogenic mechanisms supporting this ingestion strategy are strongly contested. It is therefore plausible that NaHCO3 may be ergogenic by causing beneficial shifts in the strong ion difference (SID), though the time course of this blood acid base balance variable is yet to be investigated. Twelve highly trained, adolescent swimmers (age: 15.9 ± 1.0 years, body mass: 65.3 ± 9.6 kg) consumed their typical pre-competition nutrition 1–3 hours before ingesting 0.3 g∙kg BM-1 NaHCO3 in gelatine capsules. Capillary blood samples were then taken during seated rest on nine occasions (0, 60, 75, 90, 105, 120, 135, 150, 165 min post-ingestion) to identify the time course changes in HCO3–, pH, and the SID. No significant differences were found in the time to peak of each blood measure (HCO3–: 130 ± 35 min, pH: 120 ± 38 min, SID: 98 ± 37 min; p = 0.08); however, a large effect size was calculated between time to peak HCO3– and the SID (g = 0.88). Considering that a difference between time to peak blood HCO3– and the SID was identified in adolescents, future research should compare the ergogenic effects of these two individualized NaHCO3 ingestion strategies compared to a traditional, standardized approach.

As a nitric oxide (NO) enhancer, citrulline malate (CM) has recently been touted as a potential ergogenic aid to both resistance and high-intensity exercise performance, as well as the recovery of muscular performance. The mechanism has been associated with enhanced blood flow to active musculature, however, it might be more far-reaching as either ammonia homeostasis could be improved, or ATP production could be increased via greater availability of malate. Moreover, CM might improve muscle recovery via increased nutrient delivery and/or removal of waste products. To date, a single acute 8 g dose of CM on either resistance exercise performance or cycling has been supplemented, which has produced equivocal results. This makes the effectiveness of CM to improve exercise performance difficult to determine. Reasons for the disparity in conclusions seem to be due to methodological discrepancies such as the testing protocols and the associated test-retest reliability, dosing strategy (i.e. amount and timing), and the recent discovery of quality control issues with some manufacturers stated (i.e. citrulline:malate ratios). Further exploration of the optimal dose is therefore required including quantification of the bioavailability of NO, citrulline, and malate following ingestion of a range of CM doses. Similarly, further well-controlled studies using highly repeatable exercise protocols with a large aerobic component are required to assess the mechanisms associated with this supplement appropriately. Until such studies are completed, the efficacy of CM supplementation to improve exercise performance remains ambiguous.

This study investigated the effects of two sodium bicarbonate (NaHCO3) doses on estimated energy system contribution and performance during an intermittent high-intensity cycling test (HICT), and time-to-exhaustion (TTE) exercise. Twelve healthy males (stature: 1.75 ± 0.08 m; body mass: 67.5 ± 6.3 kg; age: 21.0 ± 1.4 years; maximal oxygen consumption: 45.1 ± 7.0 ml.kg.min−1) attended four separate laboratory visits. Maximal aerobic power (MAP) was identified from an incremental exercise test. During the three experimental visits, participants ingested either 0.2 g.kg−1 BM NaHCO3 (SBC2), 0.3 g.kg−1 BM NaHCO3 (SBC3), or 0.07 g.kg−1 BM sodium chloride (placebo; PLA) at 60 min pre-exercise. The HICT involved 3 × 60 s cycling bouts (90, 95, 100% MAP) interspersed with 90 s recovery, followed by TTE cycling at 105% MAP. Blood lactate was measured after each cycling bout to calculate estimates for glycolytic contribution to exercise. Gastrointestinal (GI) upset was quantified at baseline, 30 and 60 min post-ingestion, and 5 min post-exercise. Cycling TTE increased for SBC2 (+20.2 s; p = 0.045) and SBC3 (+31.9 s; p = 0.004) compared to PLA. Glycolytic contribution increased, albeit non-significantly, during the TTE protocol for SBC2 (+7.77 kJ; p = 0.10) and SBC3 (+7.95 kJ; p = 0.07) compared to PLA. GI upset was exacerbated post-exercise after SBC3 for nausea compared to SBC2 and PLA (p < 0.05), whilst SBC2 was not significantly different to PLA for any symptom (p > 0.05). Both NaHCO3 doses enhanced cycling performance and glycolytic contribution, however, higher doses may maximize ergogenic benefits.

Background In this Position Statement, the International Society of Sports Nutrition (ISSN) provides an objective and critical review of the literature pertinent to nutritional considerations for training and racing in single-stage ultra-marathon. Recommendations for Training. i) Ultra-marathon runners should aim to meet the caloric demands of training by following an individualized and periodized strategy, comprising a varied, food-first approach; ii) Athletes should plan and implement their nutrition strategy with sufficient time to permit adaptations that enhance fat oxidative capacity; iii) The evidence overwhelmingly supports the inclusion of a moderate-to-high carbohydrate diet (i.e., ~ 60% of energy intake, 5-8 g·kg- 1·d- 1) to mitigate the negative effects of chronic, training-induced glycogen depletion; iv) Limiting carbohydrate intake before selected low-intensity sessions, and/or moderating daily carbohydrate intake, may enhance mitochondrial function and fat oxidative capacity. Nevertheless, this approach may compromise performance during high-intensity efforts; v) Protein intakes of ~ 1.6 g·kg- 1·d- 1 are necessary to maintain lean mass and support recovery from training, but amounts up to 2.5 g.kg- 1·d- 1 may be warranted during demanding training when calorie requirements are greater; Recommendations for Racing. vi) To attenuate caloric deficits, runners should aim to consume 150-400 Kcal·h- 1 (carbohydrate, 30-50 g·h- 1; protein, 5-10 g·h- 1) from a variety of calorie-dense foods. Consideration must be given to food palatability, individual tolerance, and the increased preference for savory foods in longer races; vii) Fluid volumes of 450-750 mL·h- 1 (~ 150-250 mL every 20 min) are recommended during racing. To minimize the likelihood of hyponatraemia, electrolytes (mainly sodium) may be needed in concentrations greater than that provided by most commercial products (i.e., > 575 mg·L- 1 sodium). Fluid and electrolyte requirements will be elevat