Sodium bicarbonate supplementation and the female athlete: A brief commentary with small scale systematic review and meta-analysis.

ABSTRACTSodium bicarbonate (SB) is considered an effective ergogenic supplement for improving high-intensity exercise capacity and performance, although recent data suggests that women may be less amenable to its ergogenic effects than men. Currently, an apparent paucity of data on women means no consensus exists on whether women benefit from SB supplementation. The aim of the current study was to quantify the proportion of the published literature on SB supplementation that includes women, and to synthesise the evidence regarding its effects on blood bicarbonate and exercise performance in women by performing a systematic review and meta-analysis. Electronic searches of the literature were undertaken using three databases (MEDLINE, Embase, SPORTDiscus) to identify relevant articles. All meta-analyses were performed within a Bayesian framework. A total of 149 SB articles were identified, 11 of which contained individual group data for women. Results indicated a pooled blood bicarbonate increase of 7.4 [95%CrI: 4.2-10.4 mmol·L-1] following supplementation and a pooled standardised exercise effect size of 0.37 [95%CrI: -0.06-0.92]. The SB literature is skewed, with only 20% (30 studies) of studies employing female participants, of which only 11 studies (7.4%) provided group analyses exclusively in women. Despite the small amount of available data, results are consistent in showing that SB supplementation in women leads to large changes in blood bicarbonate and that there is strong evidence for a positive ergogenic effect on exercise performance that is likely to be small to medium in magnitude.HighlightsThis study aimed to quantify the proportion of the published literature on sodium bicarbonate supplementation that includes women and to synthesise the evidence regarding its ergogenic effect on women, using a systematic review and meta-analytic approach.The sodium bicarbonate literature is skewed, with only 30 studies (20%) employing female participants, of which only 11 studies (7.4%) provided group analyses exclusively in women.Despite the small amount of available data, results are consistent in showing that sodium bicarbonate supplementation in women leads to large changes in blood bicarbonate and that there is strong evidence for a positive ergogenic effect on exercise performance that is likely small to medium in magnitude.Based on these findings, we do not believe there is any evidence to support sex-specific sodium bicarbonate dosing recommendations and that current recommendations of 0.2-0.3 g·kg-1BM of SB taken 60-180 min prior to high-intensity exercise appear appropriate for the female athlete.

Warm-Up Intensity Does Not Affect the Ergogenic Effect of Sodium Bicarbonate in Adult Men.

This study determined the influence of a high- (HI) versus low-intensity (LI) cycling warm-up on blood acid-base responses and exercise capacity following ingestion of sodium bicarbonate (SB; 0.3 g/kg body mass) or a placebo (PLA; maltodextrin) 3 hr prior to warm-up. Twelve men (21 ± 2 years, 79.2 ± 3.6 kg body mass, and maximum power output [Wmax] 318 ± 36 W) completed a familiarization and four double-blind trials in a counterbalanced order: HI warm-up with SB, HI warm-up with PLA, LI warm-up with SB, and LI warm-up with PLA. LI warm-up was 15 min at 60% Wmax, while the HI warm-up (typical of elites) featured LI followed by 2 × 30 s (3-min break) at Wmax, finishing 30 min prior to a cycling capacity test at 110% Wmax. Blood bicarbonate and lactate were measured throughout. SB supplementation increased blood bicarbonate (+6.4 mmol/L; 95% confidence interval, CI [5.7, 7.1]) prior to greater reductions with HI warm-up (-3.8 mmol/L; 95% CI [-5.8, -1.8]). However, during the 30-min recovery, blood bicarbonate rebounded and increased in all conditions, with concentrations ∼5.3 mmol/L greater with SB supplementation (p < .001). Blood bicarbonate significantly declined during the cycling capacity test at 110%Wmax with greater reductions following SB supplementation (-2.4 mmol/L; 95% CI [-3.8, -0.90]). Aligned with these results, SB supplementation increased total work done during the cycling capacity test at 110% Wmax (+8.5 kJ; 95% CI [3.6, 13.4], ∼19% increase) with no significant main effect of warm-up intensity (+0.0 kJ; 95% CI [-5.0, 5.0]). Collectively, the results demonstrate that SB supplementation can improve HI cycling capacity irrespective of prior warm-up intensity, likely due to blood alkalosis.

Individual Participant Data Meta-Analysis Provides No Evidence of Intervention Response Variation in Individuals Supplementing With Beta-Alanine.

Currently, little is known about the extent of interindividual variability in response to beta-alanine (BA) supplementation, nor what proportion of said variability can be attributed to external factors or to the intervention itself (intervention response). To investigate this, individual participant data on the effect of BA supplementation on a high-intensity cycling capacity test (CCT110%) were meta-analyzed. Changes in time to exhaustion (TTE) and muscle carnosine were the primary and secondary outcomes. Multilevel distributional Bayesian models were used to estimate the mean and SD of BA and placebo group change scores. The relative sizes of group SDs were used to infer whether observed variation in change scores were due to intervention or non-intervention-related effects. Six eligible studies were identified, and individual data were obtained from four of these. Analyses showed a group effect of BA supplementation on TTE (7.7, 95% credible interval [CrI] [1.3, 14.3] s) and muscle carnosine (18.1, 95% CrI [14.5, 21.9] mmol/kg DM). A large intervention response variation was identified for muscle carnosine (σIR = 5.8, 95% CrI [4.2, 7.4] mmol/kg DM) while equivalent change score SDs were shown for TTE in both the placebo (16.1, 95% CrI [13.0, 21.3] s) and BA (15.9, 95% CrI [13.0, 20.0] s) conditions, with the probability that SD was greater in placebo being 0.64. In conclusion, the similarity in observed change score SDs between groups for TTE indicates the source of variation is common to both groups, and therefore unrelated to the supplement itself, likely originating instead from external factors such as nutritional intake, sleep patterns, or training status.

Histidine dipeptides are key regulators of excitation-contraction coupling in cardiac muscle: Evidence from a novel CARNS1 knockout rat model.

Histidine-containing dipeptides (HCDs) are abundantly expressed in striated muscles. Although important properties have been ascribed to HCDs, including H+ buffering, regulation of Ca2+ transients and protection against oxidative stress, it remains unknown whether they play relevant functions in vivo. To investigate the in vivo roles of HCDs, we developed the first carnosine synthase knockout (CARNS1-/-) rat strain to investigate the impact of an absence of HCDs on skeletal and cardiac muscle function. Male wild-type (WT) and knockout rats (4 months-old) were used. Skeletal muscle function was assessed by an exercise tolerance test, contractile function in situ and muscle buffering capacity in vitro. Cardiac function was assessed in vivo by echocardiography and cardiac electrical activity by electrocardiography. Cardiomyocyte contractile function was assessed in isolated cardiomyocytes by measuring sarcomere contractility, along with the determination of Ca2+ transient. Markers of oxidative stress, mitochondrial function and expression of proteins were also evaluated in cardiac muscle. Animals were supplemented with carnosine (1.8% in drinking water for 12 weeks) in an attempt to rescue tissue HCDs levels and function. CARNS1-/- resulted in the complete absence of carnosine and anserine, but it did not affect exercise capacity, skeletal muscle force production, fatigability or buffering capacity in vitro, indicating that these are not essential for pH regulation and function in skeletal muscle. In cardiac muscle, however, CARNS1-/- resulted in a significant impairment of contractile function, which was confirmed both in vivo and ex vivo in isolated sarcomeres. Impaired systolic and diastolic dysfunction were accompanied by reduced intracellular Ca2+ peaks and slowed Ca2+ removal, but not by increased markers of oxidative stress or impaired mitochondrial respiration. No relevant increases in muscle carnosine content were observed after carnosine supplementation. Results show that a primary function of HCDs in cardiac muscle is the regulation of Ca2+ handling and excitation-contraction coupling.

The role of chronic muscle (in)activity on carnosine homeostasis: a study with spinal cord-injured athletes.

To examine the role of chronic (in)activity on muscle carnosine (MCarn) and how chronic (in)activity affects MCarn responses to ß-alanine supplementation in spinal cord-injured athletes, 16 male athletes with paraplegia were randomized (2:1 ratio) to receive ß-alanine (n = 11) or placebo (PL, n = 5). They consumed 6.4 g/day of ß-alanine or PL for 28 days. Muscle biopsies of the active deltoid and the inactive vastus lateralis (VL) were taken before and after supplementation. MCarn in the VL was also compared with the VL of a group of individuals without paraplegia (n = 15). MCarn was quantified in whole muscle and in pools of individual fibers by high-performance liquid chromatography. MCarn was higher in chronically inactive VL vs. well-trained deltoid (32.0 ± 12.0 vs. 20.5 ± 6.1 mmol/kg DM; P = 0.018). MCarn was higher in inactive vs. active VL (32.0 ± 12.0 vs. 21.2 ± 7.5 mmol/kg DM; P = 0.011). In type-I fibers, MCarn was significantly higher in the inactive VL than in the active deltoid (38.3 ± 4.7 vs. 27.3 ± 11.8 mmol/kg DM, P = 0.014). MCarn increased similarly between inactive VL and active deltoid in the ß-alanine group (VL: 68.9 ± 55.1%, P = 0.0002; deltoid: 90.5 ± 51.4%, P < 0.0001), with no changes in the PL group. MCarn content was higher in the inactive VL than in the active deltoid and the active VL, but this is probably a consequence of fiber type shift (type I to type II) that occurs with chronic inactivity. Chronically inactive muscle showed an increase in MCarn after BA supplementation equally to the active muscle, suggesting that carnosine accretion following ß-alanine supplementation is not influenced by muscle inactivity.

Potential of Creatine in Glucose Management and Diabetes.

Creatine is one of the most popular supplements worldwide, and it is frequently used by both athletic and non-athletic populations to improve power, strength, muscle mass and performance. A growing body of evidence has been identified potential therapeutic effects of creatine in a wide variety of clinical conditions, such as cancer, muscle dystrophy and neurodegenerative disorders. Evidence has suggested that creatine supplementation alone, and mainly in combination with exercise training, may improve glucose metabolism in health individuals and insulin-resistant individuals, such as in those with type 2 diabetes mellitus. Creatine itself may stimulate insulin secretion in vitro, improve muscle glycogen stores and ameliorate hyperglycemia in animals. In addition, exercise induces numerous metabolic benefits, including increases in insulin-independent muscle glucose uptake and insulin sensitivity. It has been speculated that creatine supplementation combined with exercise training could result in additional improvements in glucose metabolism when compared with each intervention separately. The possible mechanism underlying the effects of combined exercise and creatine supplementation is an enhanced glucose transport into muscle cell by type 4 glucose transporter (GLUT-4) translocation to sarcolemma. Although preliminary findings from small-scale trials involving patients with type 2 diabetes mellitus are promising, the efficacy of creatine for improving glycemic control is yet to be confirmed. In this review, we aim to explore the possible therapeutic role of creatine supplementation on glucose management and as a potential anti-diabetic intervention, summarizing the current knowledge and highlighting the research gaps.

Kinetics of Muscle Carnosine Decay after ß-Alanine Supplementation: A 16-wk Washout Study.

PURPOSE: This study aimed to describe the kinetics of carnosine washout in human skeletal muscle over 16 wk. METHODS: Carnosine washout kinetics were studied in 15 young, physically active omnivorous men randomly assigned to take 6.4 g·d-1 of ß-alanine (n = 11) or placebo (n = 4) for 8 wk. Muscle carnosine content (M-Carn) was determined before (PRE), immediately after (POST), and 4, 8, 12, and 16 wk after supplementation. High-intensity exercise tests were performed at these same time points. Linear and exponential models were fitted to the washout data, and the leave-one-out method was used to select the model with the best fit for M-Carn decay data. Repeated-measures correlation analysis was used to assess the association between changes in M-Carn and changes in performance. RESULTS: M-Carn increased from PRE to POST in the ß-alanine group only (+91.1% ± 29.1%; placebo, +0.04% ± 10.1%; P < 0.0001). M-Carn started to decrease after cessation of ß-alanine supplementation and continued to decrease until week 16 (POST4, +59% ± 40%; POST8, +35% ± 39%; POST12, +18% ± 32%; POST16, -3% ± 24% of PRE M-Carn). From week 12 onward, M-Carn was no longer statistically different from PRE. Both linear and exponential models displayed very similar fit and could be used to describe carnosine washout, although the linear model presented a slightly better fit. The decay in M-Carn was mirrored by a similar decay in high-intensity exercise tolerance; M-Carn was moderately and significantly correlated with total mechanical work done (r = 0.505; P = 0.032) and time to exhaustion (r = 0.72; P < 0.001). CONCLUSIONS: Carnosine washout takes 12-16 wk to complete, and it can be described either by linear or exponential curves. Changes in M-Carn seem to be mirrored by changes in high-intensity exercise tolerance. This information can be used to optimize ß-alanine supplementation strategies.

Insulin does not stimulate ß-alanine transport into human skeletal muscle.

To test whether high circulating insulin concentrations influence the transport of ß-alanine into skeletal muscle at either saturating or subsaturating ß-alanine concentrations, we conducted two experiments whereby ß-alanine and insulin concentrations were controlled. In experiment 1, 12 men received supraphysiological amounts of ß-alanine intravenously (0.11 g·kg-1·min-1 for 150 min), with or without insulin infusion. ß-Alanine and carnosine were measured in muscle before and 30 min after infusion. Blood samples were taken throughout the infusion protocol for plasma insulin and ß-alanine analyses. ß-Alanine content in 24-h urine was assessed. In experiment 2, six men ingested typical doses of ß-alanine (10 mg/kg) before insulin infusion or no infusion. ß-Alanine was assessed in muscle before and 120 min following ingestion. In experiment 1, no differences between conditions were shown for plasma ß-alanine, muscle ß-alanine, muscle carnosine and urinary ß-alanine concentrations (all P > 0.05). In experiment 2, no differences between conditions were shown for plasma ß-alanine or muscle ß-alanine concentrations (all P > 0.05). Hyperinsulinemia did not increase ß-alanine uptake by skeletal muscle cells, neither when substrate concentrations exceed the Vmax of ß-alanine transporter TauT nor when it was below saturation. These results suggest that increasing insulin concentration is not necessary to maximize ß-alanine transport into muscle following ß-alanine intake.

Leucine Supplementation Has No Further Effect on Training-induced Muscle Adaptations.

INTRODUCTION: Several acute studies have suggested that leucine is a key amino acid to drive muscle protein synthesis. However, there are very few studies on the long-term effects of leucine supplementation on resistance training (RT)-induced gains in muscle mass and strength. We sought to determine the impact of 10 g of leucine on muscle mass and strength in response to RT in healthy young men. METHODS: Twenty-five, resistance-trained men (27 ± 5 yr; 78.4 ± 11.6 kg; 24.8 ± 3.0 kg·m) consuming 1.8 ± 0.4 g protein·kg·d, were randomly assigned to receive 2 × 5 g·d supplementation of either free leucine (LEU n = 12) or alanine (PLA n = 13) while undergoing a supervised 12-wk, twice-weekly lower-limb RT program. One-repetition maximum (leg-press 1RM) and muscle cross-sectional area (mCSA) of the vastus lateralis were determined before (PRE) and after (POST) the intervention. Additionally, three 24-h dietary recalls were also performed at PRE and POST. RESULTS: Protein intake was roughly double that of the RDA in both groups and remained unchanged across time with no differences detected between groups. Similar increases were observed between groups in leg-press 1RM (LEU, 19.0% ± 9.4% and PLA, 21.0% ± 10.4%, P = 0.31) and mCSA (LEU, 8.0% ± 5.6% and PLA, 8.4% ± 5.1%, P = 0.77). CONCLUSIONS: High-dose leucine supplementation did not enhance gains in muscle strength and mass after a 12-wk RT program in young resistance-trained males consuming adequate amounts of dietary protein.

24-Week ß-alanine ingestion does not affect muscle taurine or clinical blood parameters in healthy males.

PURPOSE: To investigate the effects of chronic beta-alanine (BA) supplementation on muscle taurine content, blood clinical markers and sensory side-effects. METHODS: Twenty-five healthy male participants (age 27 ± 4 years, height 1.75 ± 0.09 m, body mass 78.9 ± 11.7 kg) were supplemented with 6.4 g day-1 of sustained-release BA (N = 16; CarnoSyn™, NAI, USA) or placebo (PL; N = 9; maltodextrin) for 24 weeks. Resting muscle biopsies of the m. vastus lateralis were taken at 0, 12 and 24 weeks and analysed for taurine content (BA, N = 12; PL, N = 6) using high-performance liquid chromatography. Resting venous blood samples were taken every 4 weeks and analysed for markers of renal, hepatic and muscle function (BA, N = 15; PL, N = 8; aspartate transaminase; alanine aminotransferase; alkaline phosphatase; lactate dehydrogenase; albumin; globulin; creatinine; estimated glomerular filtration rate and creatine kinase). RESULTS: There was a significant main effect of group (p = 0.04) on muscle taurine, with overall lower values in PL, although there was no main effect of time or interaction effect (both p > 0.05) and no differences between specific timepoints (week 0, BA: 33.67 ± 8.18 mmol kg-1 dm, PL: 27.75 ± 4.86 mmol kg-1 dm; week 12, BA: 35.93 ± 8.79 mmol kg-1 dm, PL: 27.67 ± 4.75 mmol kg-1 dm; week 24, BA: 35.42 ± 6.16 mmol kg-1 dm, PL: 31.99 ± 5.60 mmol kg-1 dm). There was no effect of treatment, time or any interaction effects on any blood marker (all p > 0.05) and no self-reported side-effects in these participants throughout the study. CONCLUSIONS: The current study showed that 24 weeks of BA supplementation at 6.4 g day-1 did not significantly affect muscle taurine content, clinical markers of renal, hepatic and muscle function, nor did it result in chronic sensory side-effects, in healthy individuals. Since athletes are likely to engage in chronic supplementation, these data provide important evidence to suggest that supplementation with BA at these doses for up to 24 weeks is safe for healthy individuals.

Effects of ß-alanine and sodium bicarbonate supplementation on the estimated energy system contribution during high-intensity intermittent exercise.

The effects of ß-alanine (BA) and sodium bicarbonate (SB) on energy metabolism during work-matched high-intensity exercise and cycling time-trial performance were examined in 71 male cyclists. They were randomised to receive BA + placebo (BA, n = 18), placebo + SB (SB, n = 17), BA + SB (BASB, n = 19), or placebo + placebo (PLA, n = 18). BA was supplemented for 28 days (6.4 g day-1) and SB (0.3 g kg-1) ingested 60 min before exercise on the post-supplementation trial. Dextrose and calcium carbonate were placebos for BA and SB, respectively. Before (PRE) and after (POST) supplementation, participants performed a high-intensity intermittent cycling test (HICT-110%) consisting of four 60-s bouts at 110% of their maximal power output (60-s rest between bouts). The estimated contribution of the energy systems was calculated for each bout in 39 of the participants (BA: n = 9; SB: n = 10; BASB: n = 10, PLA: n = 10). Ten minutes after HICT-110%, cycling performance was determined in a 30-kJ time-trial test in all participants. Both groups receiving SB increased estimated glycolytic contribution in the overall HICT-110%, which approached significance (SB: + 23%, p = 0.068 vs. PRE; BASB: + 18%, p = 0.059 vs. PRE). No effects of supplementation were observed for the estimated oxidative and ATP-PCr systems. Time to complete 30 kJ was not significantly changed by any of the treatments, although a trend toward significance was shown in the BASB group (p = 0.06). We conclude that SB, but not BA, increases the estimated glycolytic contribution to high-intensity intermittent exercise when total work done is controlled and that BA and SB, either alone or in combination, do not improve short-duration cycling time-trial performance.

Is Bypassing the Stomach a Means to Optimize Sodium Bicarbonate Supplementation? A Case Study With a Postbariatric Surgery Individual.

Sodium bicarbonate (SB) is an ergogenic supplement shown to improve high-intensity exercise via increased blood bicarbonate buffering. Substantial amounts of the ingested bicarbonate are neutralized in the stomach. Bariatric surgery results in a small gastric pouch which dramatically reduces exposure time of any ingested food in the stomach. The aim of this study was to examine the pharmacokinetics of orally ingested SB in a postgastric bypass individual to determine the magnitude of changes in blood bicarbonate and associated side effects. We hypothesized that SB supplementation in a gastric bypass model would result in greater blood bicarbonate increases and fewer side effects than in healthy individuals due to minimal bicarbonate losses in the stomach. One postbariatric male ingested 0.3 g/kg·body mass of SB on three occasions (SB1, SB2, and SB3) and 0.3 g/kg·body mass of placebo on a further occasion. Blood bicarbonate was determined before and every 10 min following supplement ingestion for 3 hr and then every 20 min for a further 1 hr. Side effects were reported using an adapted questionnaire at identical time points. Maximal increases in blood bicarbonate with SB were +20.0, +15.2, and +12.6 mM, resulting in maximal bicarbonate concentrations of 42.8, 39.3, and 36.2 mM. Area under the curve was SB1: 8,328 mM/min; SB2: 7,747 mM/min; SB3: 7,627 mM/min, and 6,436 mM/min for placebo. Side effects with SB were scarce. Maximal bicarbonate increases were well above those shown previously, with minimal side effects, indicative of minimal neutralization of bicarbonate in the stomach. The large increases in circulating bicarbonate and minimal side effects experienced by our postgastric surgery bypass patient are indicative that minimizing neutralization of bicarbonate in the stomach, as would occur with enteric coated capsules, may optimize SB supplementation and thus warrants investigation.

Sodium bicarbonate ingestion increases glycolytic contribution and improves performance during simulated taekwondo combat.

PURPOSE: To investigate the effect of sodium bicarbonate (NaHCO3) on performance and estimated energy system contribution during simulated taekwondo combat. METHODS: Nine taekwondo athletes completed two experimental sessions separated by at least 48 h. Athletes consumed 300 mg/kg body mass of NaHCO3 or placebo (CaCO3) 90 min before the combat simulation (three rounds of 2 min separated by 1 min passive recovery), in a double-blind, randomized, repeated-measures crossover design. All simulated combat was filmed to quantify the time spent fighting in each round. Lactate concentration [La-] and rating of perceived exertion (RPE) were measured before and after each round, whereas heart rate (HR) and the estimated contribution of the oxidative (WOXI), ATP (adenosine triphosphate)-phosphocreatine (PCr) (WPCR), and glycolytic (W[La-]) systems were calculated during the combat simulation. RESULTS: [La-] increased significantly after NaHCO3 ingestion, when compared with the placebo condition (+14%, P = 0.04, d = 3.70). NaHCO3 ingestion resulted in greater estimated glycolytic energy contribution in the first round when compared with the placebo condition (+31%, P = 0.01, d = 3.48). Total attack time was significantly greater after NaHCO3 when compared with placebo (+13%, P = 0.05, d = 1.15). WOXI, WPCR, VO2, HR and RPE were not different between conditions (P > 0.05). CONCLUSION: NaHCO3 ingestion was able to increase the contribution of glycolytic metabolism and, therefore, improve performance during simulated taekwondo combat.

Effect of age, diet, and tissue type on PCr response to creatine supplementation.

Creatine/phosphorylcreatine (PCr) responses to creatine supplementation may be modulated by age, diet, and tissue, but studies assessing this possibility are lacking. Therefore we aimed to determine whether PCr responses vary as a function of age, diet, and tissue. Fifteen children, 17 omnivorous and 14 vegetarian adults, and 18 elderly individuals ("elderly") participated in this study. Participants were given placebo and subsequently creatine (0.3 g·kg-1·day-1) for 7 days in a single-blind fashion. PCr was measured through phosphorus magnetic resonance spectroscopy (31P-MRS) in muscle and brain. Creatine supplementation increased muscle PCr in children (P < 0.0003) and elderly (P < 0.001), whereas the increase in omnivores did not reach statistically significant difference (P = 0.3348). Elderly had greater PCr increases than children and omnivores (P < 0.0001 for both), whereas children experienced greater PCr increases than omnivores (P = 0.0022). In relation to diet, vegetarians (P < 0.0001), but not omnivores, had significant increases in muscle PCr content. Brain PCr content was not affected by creatine supplementation in any group, and delta changes in brain PCr (-0.7 to +3.9%) were inferior to those in muscle PCr content (+10.3 to +27.6%; P < 0.0001 for all comparisons). PCr responses to a standardized creatine protocol (0.3 g·kg-1·day-1 for 7 days) may be affected by age, diet, and tissue. Whereas creatine supplementation was able to increase muscle PCr in all groups, although to different extents, brain PCr was shown to be unresponsive overall. These findings demonstrate the need to tailor creatine protocols to optimize creatine/PCr accumulation both in muscle and in brain, enabling a better appreciation of the pleiotropic properties of creatine.NEW & NOTEWORTHY A standardized creatine supplementation protocol (0.3 g·kg-1·day-1 for 7 days) effectively increased muscle, but not brain, phosphorylcreatine. Older participants responded better than younger participants whereas vegetarians responded better than omnivores. Responses to supplementation are thus dependent on age, tissue, and diet. This suggests that a single "universal" protocol, originally designed for increasing muscle creatine in young individuals, may lead to heterogeneous muscle responses in different populations or even no responses in tissues other than skeletal muscle.

Dispelling the myth that habitual caffeine consumption influences the performance response to acute caffeine supplementation.

This study investigates the influence of habitual caffeine intake on aerobic exercise-performance responses to acute caffeine supplementation. A double-blind, crossover, counterbalanced study was performed. Forty male endurance-trained cyclists were allocated into tertiles, according to their daily caffeine intake: low (58 ± 29 mg/d), moderate (143 ± 25 mg/d), and high (351 ± 139 mg/d) consumers. Participants completed three trials in which they performed simulated cycling time trials (TTs) in the fastest time possible following ingestion of the following: caffeine (CAF: 6 mg/kg body mass), placebo (PLA), and no supplement (CON). A mixed-model analysis revealed that TT performance was significantly improved in CAF compared with PLA and CON (29.92 ± 2.18 vs. 30.81 ± 2.67 and 31.14 ± 2.71 min, respectively; P = 0.0002). Analysis of covariance revealed no influence of habitual caffeine intake as a covariate on exercise performance (P = 0.47). TT performance was not significantly different among tertiles (P = 0.75). No correlation was observed between habitual caffeine intake and absolute changes (CAF - CON) in TT performance with caffeine (P = 0.524). Individual analysis showed that eight, seven, and five individuals improved above the variation of the test in CAF in the low, moderate, and high tertiles, respectively. A Fisher's exact test did not show any significant differences in the number of individuals who improved in CAF among the tertiles (P > 0.05). Blood lactate and ratings of perceived exertion were not different between trials and tertiles (P > 0.05). Performance effects of acute caffeine supplementation during an ~30-min cycling TT performance were not influenced by the level of habitual caffeine consumption.NEW & NOTEWORTHY There has been a long-standing paradigm that habitual caffeine intake may influence the ergogenicity of caffeine supplementation. Low, moderate, and high caffeine consumers showed similar absolute and relative improvements in cycling time-trial performance following acute supplementation of 6 mg/kg body mass caffeine. Performance effects of acute caffeine were not influenced by the level of habitual caffeine consumption, suggesting that high habitual caffeine intake does not negate the benefits of acute caffeine supplementation.

Twenty-four Weeks of ß-Alanine Supplementation on Carnosine Content, Related Genes, and Exercise.

INTRODUCTION: Skeletal muscle carnosine content can be increased through ß-alanine (BA) supplementation, but the maximum increase achievable with supplementation is unknown. No study has investigated the effects of prolonged supplementation on carnosine-related genes or exercise capacity. PURPOSE: This study aimed to investigate the effects of 24 wk of BA supplementation on muscle carnosine content, gene expression, and high-intensity cycling capacity (CCT110%). METHODS: Twenty-five active males were supplemented with 6.4 g·d of sustained release BA or placebo for a 24 wk period. Every 4 wk participants provided a muscle biopsy and performed the CCT110%. Biopsies were analyzed for muscle carnosine content and gene expression (CARNS, TauT, ABAT, CNDP2, PHT1, PEPT2, and PAT1). RESULTS: Carnosine content was increased from baseline at every time point in BA (all P < 0.0001; week 4 = +11.37 ± 7.03 mmol·kg dm, week 8 = +13.88 ± 7.84 mmol·kg dm, week 12 = +16.95 ± 8.54 mmol·kg dm, week 16 = +17.63 ± 8.42 mmol·kg dm, week 20 = +21.20 ± 7.86 mmol·kg dm, and week 24 = +20.15 ± 7.63 mmol·kg dm) but not placebo (all P > 0.05). Maximal increases were +25.66 ± 7.63 mmol·kg dm (range = +17.13 to +41.32 mmol·kg dm), and absolute maximal content was 48.03 ± 8.97 mmol·kg dm (range = 31.79 to 63.92 mmol·kg dm). There was an effect of supplement (P = 0.002) on TauT; no further differences in gene expression were shown. Exercise capacity was improved in BA (P = 0.05) with possible to almost certain improvements across all weeks. CONCLUSIONS: Twenty-four weeks of BA supplementation increased muscle carnosine content and improved high-intensity cycling capacity. The downregulation of TauT suggests it plays an important role in muscle carnosine accumulation with BA supplementation, whereas the variability in changes in muscle carnosine content between individuals suggests that other determinants other than the availability of BA may also bear a major influence on muscle carnosine content.

Beta-alanine supplementation enhances judo-related performance in highly-trained athletes.

OBJECTIVES: In official judo competitions, athletes usually engage in 5-7 matches in the same day, performing numerous high-intensity efforts interspersed by short recovery intervals. Thus, glycolytic demand in judo is high and acidosis may limit performance. Carnosine is a relevant intracellular acid buffer whose content is increased with beta-alanine supplementation. Thus, we hypothesized that beta-alanine supplementation could attenuate acidosis and improve judo performance. DESIGN: Twenty-three highly-trained judo athletes were randomly assigned to receive either beta-alanine (6.4gday-1) or placebo (dextrose, same dosage) for 4 weeks. METHODS: Performance was assessed before (PRE) and after (POST) supplementation through a 5-min simulated fight (randori) followed by 3 bouts of the Special Judo Fitness Test (SJFT). Blood samples were collected for blood pH, bicarbonate (HCO3-) and lactate determination. RESULTS: Beta-alanine supplementation improved the number of throws per set and the total number of throws (both p<0.05). Placebo did not change these variables (both p>0.05). Blood pH and HCO3- reduced after exercise (all p<0.001), with no between-group differences (all p>0.05). However, the lactate response to exercise increased in the beta-alanine group as compared to placebo (p<0.05). CONCLUSIONS: In conclusion, 4 weeks of beta-alanine supplementation effectively enhance judo-related performance in highly-trained athletes.

Effects of Four Weeks of ß-Alanine Supplementation on Repeated Sprint Ability in Water Polo Players.

The purpose of this study was to investigate the effect of four weeks of ß-alanine supplementation on repeated sprint ability in water polo players. Twenty-two male water polo players participated in the study, divided randomly into two homogeneous groups (placebo and ß-alanine groups). The study design was double-blind, parallel and placebo controlled. Before and after the supplementation period (28 days), the athletes performed two specific repeated sprint ability tests interspaced by a 30-minute swimming test. Participants received 4.8g∙day-1 of the supplement (dextrose or ß-alanine) on the first 10 days and 6.4g∙day-1 on the final 18 days. There was no significant group-time interaction for any variable. The qualitative inference for substantial changes demonstrated a likely beneficial effect in the ß-alanine group (ß-alanine vs placebo) for mean time (6.6±0.4s vs 6.7±0.4s; 81% likely beneficial), worst time (6.9±0.5s vs 7.1±0.5s; 78% likely beneficial) and total time (39.3±2.5s vs 40.4±2.5s; 81% likely beneficial) in the first repeated sprint ability set and for worst time (7.2±0.6s vs 7.5±0.6s; 57% possible beneficial) in the second repeated sprint ability set. Further, was found substantial change for total time for both repeated sprint ability tests (80.8±5.7s vs 83.4±5.6s; 52% possible beneficial). To conclude, four weeks of ß-alanine supplementation had a likely beneficial effect in the first set of repeated sprint ability tests and a possible beneficial effect for worst time in the second set performed in a specific protocol in water polo players.