Craig Sale

The absorption of orally supplied β-alanine and its effect on muscle carnosine synthesis in human vastus lateralis

Summary.β-Alanine in blood-plasma when administered as A) histidine dipeptides (equivalent to 40 mg · kg−1 bwt of β-alanine) in chicken broth, or B) 10, C) 20 and D) 40 mg · kg−1 bwt β-alanine (CarnoSyn™, NAI, USA), peaked at 428 ± SE 66, 47 ± 13, 374 ± 68 and 833 ± 43 µM. Concentrations regained baseline at 2 h. Carnosine was not detected in plasma with A) although traces of this and anserine were found in urine. Loss of β-alanine in urine with B) to D) was <5%. Plasma taurine was increased by β-alanine ingestion but this did not result in any increased loss via urine. Pharmacodynamics were further investigated with 3 × B) per day given for 15 d. Dietary supplementation with I) 3.2 and II) 6.4 g · d−1 β-alanine (as multiple doses of 400 or 800 mg) or III) L-carnosine (isomolar to II) for 4 w resulted in significant increases in muscle carnosine estimated at 42.1, 64.2 and 65.8%.

Influence of β-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity

Summary.Muscle carnosine synthesis is limited by the availability of β-alanine. Thirteen male subjects were supplemented with β-alanine (CarnoSyn™) for 4 wks, 8 of these for 10 wks. A biopsy of the vastus lateralis was obtained from 6 of the 8 at 0, 4 and 10 wks. Subjects undertook a cycle capacity test to determine total work done (TWD) at 110% (CCT110%) of their maximum power (Wmax). Twelve matched subjects received a placebo. Eleven of these completed the CCT110% at 0 and 4 wks, and 8, 10 wks. Muscle biopsies were obtained from 5 of the 8 and one additional subject. Muscle carnosine was significantly increased by +58.8% and +80.1% after 4 and 10 wks β-alanine supplementation. Carnosine, initially 1.71 times higher in type IIa fibres, increased equally in both type I and IIa fibres. No increase was seen in control subjects. Taurine was unchanged by 10 wks of supplementation. 4 wks β-alanine supplementation resulted in a significant increase in TWD (+13.0%); with a further +3.2% increase at 10 wks. TWD was unchanged at 4 and 10 wks in the control subjects. The increase in TWD with supplementation followed the increase in muscle carnosine.

Effect of beta-alanine supplementation on muscle carnosine concentrations and exercise performance

High-intensity exercise results in reduced substrate levels and accumulation of metabolites in the skeletal muscle. The accumulation of these metabolites (e.g. ADP, Pi and H+) can have deleterious effects on skeletal muscle function and force generation, thus contributing to fatigue. Clearly this is a challenge to sport and exercise performance and, as such, any intervention capable of reducing the negative impact of these metabolites would be of use. Carnosine (β-alanyl-l-histidine) is a cytoplasmic dipeptide found in high concentrations in the skeletal muscle of both vertebrates and non-vertebrates and is formed by bonding histidine and β-alanine in a reaction catalysed by carnosine synthase. Due to the pKa of its imidazole ring (6.83) and its location within skeletal muscle, carnosine has a key role to play in intracellular pH buffering over the physiological pH range, although other physiological roles for carnosine have also been suggested. The concentration of histidine in muscle and plasma is high relative to its Km with muscle carnosine synthase, whereas β-alanine exists in low concentration in muscle and has a higher Km with muscle carnosine synthase, which indicates that it is the availability of β-alanine that is limiting to the synthesis of carnosine in skeletal muscle. Thus, the elevation of muscle carnosine concentrations through the dietary intake of carnosine, or chemically related dipeptides that release β-alanine on absorption, or supplementation with β-alanine directly could provide a method of increasing intracellular buffering capacity during exercise, which could provide a means of increasing high-intensity exercise capacity and performance. This paper reviews the available evidence relating to the effects of β-alanine supplementation on muscle carnosine synthesis and the subsequent effects on exercise performance. In addition, the effects of training, with or without β-alanine supplementation, on muscle carnosine concentrations are also reviewed.

Blood hemostasis in exercise and training

Formation of the blood clot is a slow but normal physiological process occurring as a result of the activation of blood coagulation pathways. Natures guard against unwanted blood clots is the fibrinolytic enzyme system. In healthy people, there is a delicate dynamic balance between blood clot formation and blood clot dissolution. Available evidence suggests that exercise and physical training evoke multiple effects on blood hemostasis in normal healthy subjects and in patients. A single bout of exercise is usually associated with a transient increase in blood coagulation as evidenced by a shortening of activated partial thromboplastin time (APTT) and increased Factor VIII (FVIII). The rise in FVIII is intensity dependent and continues into recovery. The effects of acute exercise on plasma fibrinogen have yielded conflicting results. Thus, the issue of whether exercise-induced blood hypercoagulability in vitro mirrors an in vivo thrombin generation and fibrin formation remains disputable. Exercise-induced enhancement of fibrinolysis has been repeatedly demonstrated using a wide range of exercise protocols incorporating various exercise intensities and durations. Moderate exercise appears to enhance blood fibrinolytic activity without a concomitant activation of blood coagulation mechanisms, whereas, very heavy exercise induces simultaneous activation of blood fibrinolysis and coagulation. The increase in fibrinolysis is due to a rise in tissue-type plasminogen activator (tPA) and decrease in plasminogen activator inhibitor (PAI). The mechanism of exercise-induced hyperfibrinolysis is poorly understood, and the physiological utility of such activation remains unresolved. Strenuous exercise elicits a transient increase in platelet count, but there are conflicting results concerning the effect of exercise on platelet aggregation and activation. Few comprehensive studies exist concerning the influence of exercise training on blood hemostasis, making future investigation necessary to identify whether there are favorable effects of exercise training on blood coagulation, fibrinolysis, and platelet functions.

Effects of resistance training and detraining on muscle strength and blood lipid profiles in postmenopausal women

Objectives: To study the effects of eight weeks of supervised, low intensity resistance training (80% of 10 repetition maximum (10RM)) and eight weeks of detraining on muscle strength and blood lipid profiles in healthy, sedentary postmenopausal women. Subjects: Fifteen postmenopausal women, aged 49–62 years, took part in the study. Subjects were assigned to either a control (n = 7) or training (n = 8) group. The training regimen consisted of three sets of eight repetitions of leg press, bench press, knee extension, knee flexion, and lat pull-down, three days a week at 80% of 10RM. Dynamic leg strength, 10RM, and blood lipid profiles (total cholesterol (TC), low and high density lipoprotein cholesterol (LDL-C, HDL-C), triglycerides, and very low density lipoprotein cholesterol (VLDL-C)) were measured at baseline, after eight weeks of training, and after a further eight weeks of detraining. Results: Eight weeks of resistance training produced significant increases in knee extension (F1,13 = 12.60; p<0.01), bench press (F1,13 = 13.79; p<0.01), leg press (F1,13 = 15.65; p<0.01), and lat pull-down (F1,13 = 16.60; p<0.005) 10RM strength tests. Although 10RM strength decreased after eight weeks of detraining, the results remained significantly elevated from baseline measures. Eight weeks of training did not result in any significant alterations in blood lipid profiles, body composition, or dynamic isokinetic leg strength. There were no significant differences in any of the variables investigated over the 16 week period in the control group. Conclusions: These data suggest that a short, low intensity resistance training programme produces substantial improvements in muscle strength. Training of this intensity and duration was not sufficient to produce significant alterations in blood lipid concentrations.

Effect of β-alanine plus sodium bicarbonate on high-intensity cycling capacity.

PURPOSE We examined the effect of β-alanine supplementation plus sodium bicarbonate on high-intensity cycling capacity. METHODS Twenty males (age = 25 ± 5 yr, height = 1.79 ± 0.06 m, body mass = 80.0 ± 10.3 kg) were assigned to either a placebo (P) or a β-alanine (BA; 6.4 g·d(-1) for 4 wk) group based on power max, completing four cycling capacity tests at 110% of power max (CCT110%) to determine time to exhaustion (TTE) and total work done. A CCT(110%) was performed twice (habituation and baseline) before supplementation (with maltodextrin [MD]) and twice after supplementation (with MD and with sodium bicarbonate [SB]), using a crossover design with 2 d of rest between trials, creating four study conditions (PMD, PSB, BAMD, and BASB). Blood pH, Lactate, bicarbonate and base excess were determined at baseline, before exercise, immediately after exercise, and 5 min after exercise. Data were analyzed using repeated-measures ANOVA. RESULTS TTE was increased in all conditions after supplementation (+1.6% PMD, +6.5% PSB, +12.1% BAMD, and +16.2% BASB). Both BAMD and BASB resulted in significantly improved TTE compared with that before supplementation (P ≤ 0.01). Although further increases in TTE (4.1%) were shown in BASB compared with BAMD, these differences were not significant (P = 0.74). Differences in total work done were similar to those of TTE. Blood bicarbonate concentrations were significantly (P ≤ 0.001) elevated before exercise in PSB and BASB but not in PMD or BAMD. Blood lactate concentrations were significantly elevated after exercise, remaining elevated after 5 min of recovery (P ≤ 0.001) and were highest in PSB and BASB. CONCLUSIONS Results show that BA improved high-intensity cycling capacity. However, despite a 6-s (∼4%) increase in TTE with the addition of SB, this did not reach statistical significance, but magnitude-based inferences suggested a ∼70% probability of a meaningful positive difference.

The Effect of Training Status on the Metabolic Response of Bone to an Acute Bout of Exhaustive Treadmill Running

CONTEXT Strenuous exercise increases bone resorption but not formation. The effect of improved training status is unknown. OBJECTIVE Our objective was to examine the metabolic response of bone to strenuous running in recreationally active (RA) and endurance-trained (ET) men. DESIGN Eleven RA, 10 ET, and 10 control (CON) subjects completed one 8-d trial. On d 4, RA and ET completed an exhaustive treadmill run. Blood was obtained at baseline (BASE), during exercise, during 2 h of recovery, and on four follow-up (FU) days (FU1-FU4). CON rested throughout, providing blood samples at BASE and on FU1-FU4. Markers of bone resorption [C-terminal telopeptide region of collagen type 1 (beta-CTX)] and bone formation [N-terminal propeptides of procollagen type 1 (P1NP) and bone alkaline phosphatase (ALP)], osteoprotegerin (OPG), PTH, albumin-adjusted calcium (ACa), and phosphate (PO4) were measured. RESULTS There were no significant differences between ET and RA and no changes in CON for any variable. Exercise increased beta-CTX at FU1-FU4 (P<0.001) but had no effect on P1NP or bone ALP. OPG was increased after 20 min of exercise (P<0.001) and remained elevated at FU1 (P<0.001). PTH, ACa, and PO4 were increased throughout exercise (P<0.01). ACa and PO4 remained elevated in the 2 h after exercise (P<0.001), whereas PTH was lower than BASE from 1-2 h after exercise (P<0.001). CONCLUSION After acute, exhaustive running, bone resorption but not formation was increased for 4 d in RA and ET men. The increased bone resorption might be related to the increase in PTH, whereas increased OPG might be a compensatory response to increased bone resorption. Training status did not significantly affect the metabolic response of bone to exhaustive running.

Carnosine: from exercise performance to health

Carnosine was first discovered in skeletal muscle, where its concentration is higher than in any other tissue. This, along with an understanding of its role as an intracellular pH buffer has made it a dipeptide of interest for the athletic population with its potential to increase high-intensity exercise performance and capacity. The ability to increase muscle carnosine levels via β-alanine supplementation has spawned a new area of research into its use as an ergogenic aid. The current evidence base relating to the use of β-alanine as an ergogenic aid is reviewed here, alongside our current thoughts on the potential mechanism(s) to support any effect. There is also some emerging evidence for a potential therapeutic role for carnosine, with this potential being, at least theoretically, shown in ageing, neurological diseases, diabetes and cancer. The currently available evidence to support this potential therapeutic role is also reviewed here, as are the potential limitations of its use for these purposes, which mainly focusses on issues surrounding carnosine bioavailability.

The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise.

We compared the effects of exercise intensity (EI) on bone metabolism during and for 4 days after acute, weight-bearing endurance exercise. Ten males [mean ± SD maximum oxygen uptake (Vo(2max)): 56.2 ± 8.1 ml·min(-1)·kg(-1)] completed three counterbalanced 8-day trials. Following three control days, on day 4, subjects completed 60 min of running at 55%, 65%, and 75% Vo(2max). Markers of bone resorption [COOH-terminal telopeptide region of collagen type 1 (β-CTX)] and formation [NH(2)-terminal propeptides of procollagen type 1 (P1NP), osteocalcin (OC), bone-alkaline phosphatase (ALP)], osteoprotegerin (OPG), parathyroid hormone (PTH), albumin-adjusted calcium (ACa), phosphate (PO(4)), and cortisol were measured during and for 3 h after exercise and on four follow-up days (FU1-FU4). At 75% Vo(2max), β-CTX was not significantly increased from baseline by exercise but was higher compared with 55% (17-19%, P < 0.01) and 65% (11-13%, P < 0.05) Vo(2max) in the first hour postexercise. Concentrations were decreased from baseline in all three groups by 39-42% (P < 0.001) at 3 h postexercise but not thereafter. P1NP increased (P < 0.001) during exercise only, while bone-ALP was increased (P < 0.01) at FU3 and FU4, but neither were affected by EI. PTH and cortisol increased (P < 0.001) with exercise at 75% Vo(2max) only and were higher (P < 0.05) than at 55% and 65% Vo(2max) during and immediately after exercise. The increases (P < 0.001) in OPG, ACa, and PO(4) with exercise were not affected by EI. Increasing EI from 55% to 75% Vo(2max) during 60 min of running resulted in higher β-CTX concentrations in the first hour postexercise but had no effect on bone formation markers. Increased bone-ALP concentrations at 3 and 4 days postexercise suggest a beneficial effect of this type of exercise on bone mineralization. The increase in OPG was not influenced by exercise intensity, whereas PTH was increased at 75% Vo(2max) only, which cannot be fully explained by changes in serum calcium or PO(4) concentrations.

The psychometric properties of the short version of the Cybernetic Coping scale: A multigroup confirmatory factor analysis across four samples

Throughout the literature, there appears to be little support for the psychometric characteristics of scales measuring coping behaviour. This article explores the psychometric properties of the 20-item version of the Cybernetic Coping Scale (CCS; Edwards & Baglioni, 1993). Initially, confirmatory factor analysis and internal reliability analysis were conducted on large samples of data from four different studies in order to conduct an exhaustive examination of the scale. Results provided moderate support for the 20-item version of the CCS. However, improved model modification produced moderate to strong support for a 15-item version. Multigroup confirmatory factor analysis was then conducted on the 15-item version of the CCS in order to cross-validate the measurement model across groups. Findings revealed a well-fitting model with a stable factor structure and partial measurement invariance. Both versions produced acceptable to high internal reliability. Findings indicate support for the use of the 15-item version of the CCS and suggest that this short version of the CCS is the best fitting model of all the other previously developed CCS scales.