Superior bioavailability of the calcium salt form of ß-hydroxy-ß-methylbutyrate compared with the free acid form.

We investigated the bioavailability of the calcium salt (HMB-Ca) and the free acid (HMB-FA) forms of ß-hydroxy-ß-methylbutyrate (HMB). Sixteen young individuals received the following treatments on three different occasions in a counterbalanced crossover fashion: (1) HMB-FA in clear capsules; (2) HMB-Ca in gelatine capsules; (3) HMB-Ca dissolved in water. All treatments provided 1 g of HMB. Blood samples were taken before and on multiple time points following ingestion. The following parameters were calculated: peak plasma (Cmax), time to peak (Tmax), slope of HMB appearance in blood, area under the curve (AUC), half-life time (t1/2) and relative bioavailability (HMB-Ca in water set as reference). All treatments led to rapid and large increases in plasma HMB. HMB-Ca in capsules and in water showed similar plasma HMB values across time (p = 0.438). HMB-FA resulted in lower concentrations vs. the other treatments (both p < 0.001). AUC (HMB-Ca in capsules: 50,078 ± 10,507; HMB-Ca in water: 47,871 ± 10,783; HMB-FA: 29,130 ± 12,946 µmol L-1 × 720 min), Cmax (HMB-Ca in capsules: 229.2 ± 65.9; HMB-Ca in water: 249.7 ± 49.7; HMB-FA: 139.1 ± 67.2 µmol L-1) and relative bioavailability (HMB-Ca in capsules: 104.8 ± 14.9%; HMB-FA: 61.5 ± 17.0%) were lower in HMB-FA vs. HMB-Ca (all p < 0.001). HMB-Ca in water resulted in the fastest Tmax (43 ± 22 min) compared to HMB-Ca in capsules (79 ± 40 min) and HMB-FA (78 ± 21 min) (all p < 0.05), while t1/2 was similar between treatments. To conclude, HMB-Ca exhibited superior bioavailability compared to HMB-FA, with HMB-Ca in water showing faster absorption. Elimination kinetics were similar across all forms, suggesting that the pharmaceutical form of HMB affects the absorption rates, but not its distribution or elimination.

Trehalose Improved 20-min Cycling Time-Trial Performance After 100-min Cycling in Amateur Cyclists.

Carbohydrate (CHO) supplementation during endurance exercise can improve performance. However, it is unclear whether low glycemic index (GI) CHO leads to differential ergogenic and metabolic effects compared with a standard high GI CHO. This study investigated the ergogenic and metabolic effects of CHO supplementation with distinct GIs, namely, (a) trehalose (30 g/hr), (b) isomaltulose (30 g/hr), (c) maltodextrin (60 g/hr), and (d) placebo (water). In this double-blind, crossover, counterbalanced, placebo-controlled study, 13 male cyclists cycled a total of 100 min at varied exercise intensity (i.e., 10-min stages at 1.5, 2.0, and 2.5 W/kg; repeated three times plus two 5-min stages at 1.0 W/kg before and after the protocol), followed by a 20-min time trial on four separated occasions. Blood glucose and lactate (every 20 min), heart rate, and ratings of perceived exertion were collected throughout, and muscle biopsies were taken before and immediately after exercise. The results showed that trehalose improved time-trial performance compared with placebo (total work done 302 ± 39 vs. 287 ± 48 kJ; p = .01), with no other differences between sessions (all p ≥ .07). Throughout the 100-min protocol, blood glucose was higher with maltodextrin compared with the other supplements at all time points (all p < .05). Heart rate, ratings of perceived exertion, muscle glycogen content, blood glucose, and lactate were not different between conditions when considering the 20-min time trial (all p > .05). Trehalose supplementation throughout endurance exercise improved cycling performance and appears to be an appropriate CHO source for exercise tasks up to 2 hr. No ergogenic superiority between the different types of CHO was established.

Commentary: Aldehyde dehydrogenase, redox balance and exercise physiology: What is missing?

Aldehyde dehydrogenase 2 (ALDH2) is a mitochondrial enzyme involved in reactive aldehyde detoxification. Approximately 560 million people (about 8% of the world's population) carry a point mutation in the aldehyde dehydrogenase 2 gene (ALDH2), identified as ALDH2*2, which leads to decreased ALDH2 catalytic activity. ALDH2*2 variant is associated with an accumulation of toxic reactive aldehydes and consequent disruption of cellular metabolism, which contributes to the establishment and progression of several degenerative diseases. Consequences of aldehyde accumulation include impaired mitochondrial functional, hindered anabolic signaling in the skeletal muscle, impaired cardiovascular and pulmonary function, and reduced osteoblastogenesis. Considering that aldehydes are endogenously produced through redox processes, it is expected that conditions that have a high energy demand, such as exercise, might be affected by impaired aldehyde clearance in ALDH2*2 individuals. Despite the large body of evidence supporting the importance of ALDH2 to ethanol metabolism, redox homeostasis and overall health, specific research investigating the impact of ALDH2*2 on phenotypes relevant to exercise performance are notoriously scarce. In this commentary, we highlight the consolidated knowledge on the impact of ALDH2*2 on physiological processes that are relevant to exercise.

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.

Insulin stimulates ß-alanine uptake in skeletal muscle cells in vitro.

We evaluated whether insulin could stimulate ß-alanine uptake by skeletal muscle cells in vitro. Mouse myoblasts (C2C12) (n = 3 wells per condition) were cultured with ß-alanine (350 or 700 µmol·L-1), with insulin (100 µU·mL-1) either added to the media or not. Insulin stimulated the ß-alanine uptake at the lower (350 µmol·L-1) but not higher (700 µmol·L-1) ß-alanine concentration in culture medium, indicating that transporter saturation might blunt the stimulatory effects of insulin.

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.

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.

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.

Efficacy and safety of creatine supplementation in juvenile dermatomyositis: A randomized, double-blind, placebo-controlled crossover trial.

INTRODUCTION: It has been suggested that creatine supplementation is safe and effective for treating idiopathic inflammatory myopathies, but no pediatric study has been conducted to date. The objective of this study was to examine the efficacy and safety of creatine supplementation in juvenile dermatomyositis (JDM) patients. METHODS: In this study, JDM patients received placebo or creatine supplementation (0.1 g/kg/day) in a randomized, crossover, double-blind design. Subjects were assessed at baseline and after 12 weeks. The primary outcome was muscle function. Secondary outcomes included body composition, aerobic conditioning, health-related quality of life, and muscle phosphocreatine (PCr) content. Safety was assessed by laboratory parameters and kidney function measurements. RESULTS: Creatine supplementation did not affect muscle function, intramuscular PCr content, or any other secondary outcome. Kidney function was not affected, and no side effects were reported. CONCLUSIONS: Twelve weeks of creatine supplementation in JDM patients were well-tolerated and free of adverse effects, but treatment did not affect muscle function, intramuscular PCr, or any other parameter.

Dose-Response of Sodium Bicarbonate Ingestion Highlights Individuality in Time Course of Blood Analyte Responses.

To defend against hydrogen cation accumulation and muscle fatigue during exercise, sodium bicarbonate (NaHCO3) ingestion is commonplace. The individualized dose-response relationship between NaHCO3 ingestion and blood biochemistry is unclear. The present study investigated the bicarbonate, pH, base excess and sodium responses to NaHCO3 ingestion. Sixteen healthy males (23 ± 2 years; 78.6 ± 15.1 kg) attended three randomized order-balanced, nonblinded sessions, ingesting a single dose of either 0.1, 0.2 or 0.3 g·kg-1BM of NaHCO3 (Intralabs, UK). Fingertip capillary blood was obtained at baseline and every 10 min for 1 hr, then every 15 min for a further 2 hr. There was a significant main effect of both time and condition for all assessed blood analytes (p ≤ .001). Blood analyte responses were significantly lower following 0.1 g·kg-1BM compared with 0.2 g·kg-1BM; bicarbonate concentrations and base excess were highest following ingestion of 0.3 g·kg-1BM (p ≤ .01). Bicarbonate concentrations and pH significantly increased from baseline following all doses; the higher the dose the greater the increase. Large interindividual variability was shown in the magnitude of the increase in bicarbonate concentrations following each dose (+2.0-5; +5.1-8.1; and +6.0-12.3 mmol·L-1 for 0.1, 0.2 and 0.3 g·kg-1BM) and in the range of time to peak concentrations (30-150; 40-165; and 75-180 min for 0.1, 0.2 and 0.3 g·kg-1BM). The variability in bicarbonate responses was not affected by normalization to body mass. These results challenge current practices relating to NaHCO3 supplementation and clearly show the need for athletes to individualize their ingestion protocol and trial varying dosages before competition.

Can creatine supplementation form carcinogenic heterocyclic amines in humans?

There is a long-standing concern that creatine supplementation could be associated with cancer, possibly by facilitating the formation of carcinogenic heterocyclic amines (HCAs). This study provides compelling evidence that both low and high doses of creatine supplementation, given either acutely or chronically, does not cause a significant increase in HCA formation. HCAs detection was unrelated to creatine supplementation. Diet was likely to be the main factor responsible for HCAs formation after either placebo (n = 6) or creatine supplementation (n = 3). These results directly challenge the recently suggested biological plausibility for the association between creatine use and risk of testicular germ cell cancer. Creatine supplementation has been associated with increased cancer risk. In fact, there is evidence indicating that creatine and/or creatinine are important precursors of carcinogenic heterocyclic amines (HCAs). The present study aimed to investigate the acute and chronic effects of low- and high-dose creatine supplementation on the production of HCAs in healthy humans (i.e. 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (8-MeIQx), 2-amino-(1,6-dimethylfuro[3,2-e]imidazo[4,5-b])pyridine (IFP) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (4,8-DiMeIQx)). This was a non-counterbalanced single-blind crossover study divided into two phases, in which low- and high-dose creatine protocols were tested. After acute (1 day) and chronic supplementation (30 days), the HCAs PhIP, 8-MeIQx, IFP and 4,8-DiMeIQx were assessed through a newly developed HPLC-MS/MS method. Dietary HCA intake and blood and urinary creatinine were also evaluated. Out of 576 assessments performed (from 149 urine samples), only nine (3 from creatine and 6 from placebo) showed quantifiable levels of HCAs (8-MeIQx: n = 3; 4,8-DiMeIQx: n = 2; PhIP: n = 4). Individual analyses revealed that diet rather than creatine supplementation was the main responsible factor for HCA formation in these cases. This study provides compelling evidence that both low and high doses of creatine supplementation, given either acutely or chronically, did not cause increases in the carcinogenic HCAs PhIP, 8-MeIQx, IFP and 4,8-DiMeIQx in healthy subjects. These findings challenge the long-existing notion that creatine supplementation could potentially increase the risk of cancer by stimulating the formation of these mutagens.

Embryonic stem cells improve skeletal muscle recovery after extreme atrophy in mice.

INTRODUCTION: We injected embryonic stem cells into mouse tibialis anterior muscles subjected to botulinum toxin injections as a model for reversible neurogenic atrophy. METHODS: Muscles were exposed to botulinum toxin for 4 weeks and allowed to recover for up to 6 weeks. At the onset of recovery, a single muscle injection of embryonic stem cells was administered. The myofiber cross-sectional area, single twitch force, peak tetanic force, time-to-peak force, and half-relaxation time were determined. RESULTS: Although the stem cell injection did not affect the myofiber cross-sectional area gain in recovering muscles, most functional parameters improved significantly compared with those of recovering muscles that did not receive the stem cell injection. CONCLUSIONS: Muscle function recovery was accelerated by embryonic stem cell delivery in this durable neurogenic atrophy model. We conclude that stem cells should be considered a potential therapeutic tool for recovery after extreme skeletal muscle atrophy.

Influence of training status on high-intensity intermittent performance in response to ß-alanine supplementation.

Recent investigations have suggested that highly trained athletes may be less responsive to the ergogenic effects of ß-alanine (BA) supplementation than recreationally active individuals due to their elevated muscle buffering capacity. We investigated whether training status influences the effect of BA on repeated Wingate performance. Forty young males were divided into two groups according to their training status (trained: T, and non-trained: NT cyclists) and were randomly allocated to BA and a dextrose-based placebo (PL) groups, providing four experimental conditions: NTPL, NTBA, TPL, TBA. BA (6.4 g day(-1)) or PL was ingested for 4 weeks, with participants completing four 30-s lower-body Wingate bouts, separated by 3 min, before and after supplementation. Total work done was significantly increased following supplementation in both NTBA (p = 0.03) and TBA (p = 0.002), and it was significantly reduced in NTPL (p = 0.03) with no difference for TPL (p = 0.73). BA supplementation increased mean power output (MPO) in bout 4 for the NTBA group (p = 0.0004) and in bouts 1, 2 and 4 for the TBA group (p ≤ 0.05). No differences were observed in MPO for NTPL and TPL. BA supplementation was effective at improving repeated high-intensity cycling performance in both trained and non-trained individuals, highlighting the efficacy of BA as an ergogenic aid for high-intensity exercise regardless of the training status of the individual.

Creatine supplementation prevents acute strength loss induced by concurrent exercise.

PURPOSE: To investigate the effect of creatine (CR) supplementation on the acute interference induced by aerobic exercise on subsequent maximum dynamic strength (1RM) and strength endurance (SE, total number of repetitions) performance. METHODS: Thirty-two recreationally strength-trained men were submitted to a graded exercise test to determine maximal oxygen consumption (VO2max: 41.56 ± 5.24 ml kg(-1) min(-1)), anaerobic threshold velocity (ATv: 8.3 ± 1.18 km h(-1)), and baseline performance (control) on the 1RM and SE (4 × 80 % 1RM to failure) tests. After the control tests, participants were randomly assigned to either a CR (20 g day(-1) for 7 days followed by 5 g day(-1) throughout the study) or a placebo (PL-dextrose) group, and then completed 4 experimental sessions, consisting of a 5-km run on a treadmill either continuously (90 % ATv) or intermittently (1:1 min at vVO2max) followed by either a leg- or bench-press SE/1RM test. RESULTS: CR was able to maintain the leg-press SE performance after the intermittent aerobic exercise when compared with C (p > 0.05). On the other hand, the PL group showed a significant decrease in leg-press SE (p ≤ 0.05). CR supplementation significantly increased bench-press SE after both aerobic exercise modes, while the bench-press SE was not affected by either mode of aerobic exercise in the PL group. Although small increases in 1RM were observed after either continuous (bench press and leg press) or intermittent (bench press) aerobic exercise in the CR group, they were within the range of variability of the measurement. The PL group only maintained their 1RM. CONCLUSIONS: In conclusion, the acute interference effect on strength performance observed in concurrent exercise may be counteracted by CR supplementation.

The effects of two different doses of calcium lactate on blood pH, bicarbonate, and repeated high-intensity exercise performance.

We investigated the effects of low- and high-dose calcium lactate supplementation on blood pH and bicarbonate (Study A) and on repeated high-intensity performance (Study B). In Study A, 10 young, physically active men (age: 24 ± 2.5 years; weight: 79.2 ± 9.45 kg; height: 1.79 ± 0.06 m) were assigned to acutely receive three different treatments, in a crossover fashion: high-dose calcium lactate (HD: 300 mg · kg(-1) body mass), low-dose calcium lactate (LD: 150 mg · kg(-1) body mass) and placebo (PL). During each visit, participants received one of these treatments and were assessed for blood pH and bicarbonate 0, 60, 90, 120, 150, 180, and 240 min following ingestion. In Study B, 12 young male participants (age: 26 ± 4.5 years; weight: 82.0 ± 11.0 kg; height: 1.81 ± 0.07 m) received the same treatments of Study A. Ninety minutes after ingestion, participants underwent 3 bouts of the upper-body Wingate test and were assessed for blood pH and bicarbonate 0 and 90 min following ingestion and immediately after exercise. In Study A, both HD and LD promoted slight but significant increases in blood bicarbonate (31.47 ± 1.57 and 31.69 ± 1.04 mmol · L(-1, respectively) and pH levels (7.36 ± 0.02 and 7.36 ± 0.01, respectively), with no effect of PL. In Study B, total work done, peak power, mean power output were not affected by treatments. In conclusion, low- and high-dose calcium lactate supplementation induced similar, yet very discrete, increases in blood pH and bicarbonate, which were not sufficiently large to improve repeated high-intensity performance.

Predicting punching acceleration from selected strength and power variables in elite karate athletes: a multiple regression analysis.

This study investigated the relationship between punching acceleration and selected strength and power variables in 19 professional karate athletes from the Brazilian National Team (9 men and 10 women; age, 23 ± 3 years; height, 1.71 ± 0.09 m; and body mass [BM], 67.34 ± 13.44 kg). Punching acceleration was assessed under 4 different conditions in a randomized order: (a) fixed distance aiming to attain maximum speed (FS), (b) fixed distance aiming to attain maximum impact (FI), (c) self-selected distance aiming to attain maximum speed, and (d) self-selected distance aiming to attain maximum impact. The selected strength and power variables were as follows: maximal dynamic strength in bench press and squat-machine, squat and countermovement jump height, mean propulsive power in bench throw and jump squat, and mean propulsive velocity in jump squat with 40% of BM. Upper- and lower-body power and maximal dynamic strength variables were positively correlated to punch acceleration in all conditions. Multiple regression analysis also revealed predictive variables: relative mean propulsive power in squat jump (W·kg-1), and maximal dynamic strength 1 repetition maximum in both bench press and squat-machine exercises. An impact-oriented instruction and a self-selected distance to start the movement seem to be crucial to reach the highest acceleration during punching execution. This investigation, while demonstrating strong correlations between punching acceleration and strength-power variables, also provides important information for coaches, especially for designing better training strategies to improve punching speed.