supplementation. Participants identified which supplement they believed they had 29 ingested ("caffeine", "placebo", "don't know") pre-and post-exercise. Subsequently, 30 participants were allocated to subgroups for analysis according to their identifications. 31Overall and subgroup analyses were performed using mixed-model and magnitude 32 based inference analyses. Caffeine improved performance vs. PLA and CON 33 (P≤0.001). Correct pre-and post-exercise identification of caffeine in CAF improved 34 exercise performance (+4.8 and +6.5%) vs. CON, with slightly greater relative 35 increases than the overall effect of caffeine (+4.1%). Performance was not different 36 between PLA and CON within subgroups (all P>0.05), although there was a tendency 37 towards improved performance when participants believed they had ingested caffeine 38 post-exercise (P=0.06; 87% likely beneficial). Participants who correctly identified 39 placebo in PLA showed possible harmful effects on performance compared to CON. 40 Supplement identification appeared to influence exercise outcome and may be a 41 source of bias in sports nutrition. 42

26Objective: To investigate the influence of habitual caffeine intake on aerobic exercise performance responses 27 to acute caffeine supplementation. Methods: A double-blind, crossover, counterbalanced study was performed. 28Forty male endurance-trained cyclists were allocated into tertiles according to their daily caffeine intake: low suggesting that high habitual caffeine intake does not negate the benefits of acute caffeine supplementation.

Purpose: To describe the reliability of blood bicarbonate pharmacokinetics in response to sodium bicarbonate (SB) supplementation across multiple occasions and assess, using putative thresholds, whether individual variation indicated a need for individualised ingestion timings. Methods: Thirteen m en (age 27±5 y; body mass (BM) 77.4±10.5 kg; height 1.75 ±0.06 m) ingested 0.3 g•kg -1 BM SB in gelatine capsules on 3 occasions. One hour after a standardised meal, venous blood was obtained before and every 10 min following ingestion for 3 h, then every 20 min for a further hour. Time-to-peak (Tmax), absolute-peak (Cmax), absolute-peak-change (∆Cmax) and area under the curve (AUC) were analysed using mixed models, intraclass correlation coefficient (ICC), coefficient of variation (CV) and typical error. Individual variation in pharmacokinetic responses was assessed using Bayesian simulation with multilevel models with random intercepts. Results: No significant differences between sessions were shown for blood bicarbonate regarding Cmax, ∆Cmax or AUC (p>0.05), although Tmax occurred earlier in SB2 (127±36 min) than in SB1 (169±54 min, p=0.0088) and SB3 (159±42 min, p=0.05). ICC, CV and typical error showed moderate to poor reliability. Bayesian modelling estimated that >80% of individuals from the population experience elevated blood bicarbonate levels above + 5 mmol•L -1 between 75-240 min after ingestion, and between 90-225 min above +6 mmol•L -1 . Conclusion: Assessing SB supplementation using discrete values showed only moderate reliability at the group level, and poor reliability at the individual level, while Tmax was not reproducible. However, when analysed as modelled curves, a 0.3 g•kg -1 BM dose was shown to create a long-lasting window of ergogenic potential, challenging the notion that SB ingestion individualised to time-topeak is a necessary strategy, at least when SB is ingested in capsules.

Study Design 132A double-blind, placebo-controlled, crossover, counterbalanced study was conducted. 133Participants visited the laboratory on six separate occasions, separated by 2-7 days, to undertake 134 4 bouts of the upper-body Wingate anaerobic test. The first and second visits were performed to 135 familiarise the participants with the protocol, while the third session was undertaken following 136 no treatment (control). The remaining three sessions were undertaken following the acute 137 ingestion of calcium lactate, sodium bicarbonate or placebo. The order of the treatments was 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 P R O O F 6 chosen at random in a fully counterbalanced manner. To further confirm that the order of the 139 tests did not influence performance, we compared overall total mechanical work (TMW) 140 obtained in the experimental sessions between the three visits (see more details below). As 141 expected, no significant differences were found (visit 1: 33462 ± 5122 J; visit 2: 33813 ± 5371 142 J; visit 3: 33436 ± 4928 J; F = 0.70, p = 0.50). All tests were performed during the same period 143 of the day to account for circadian variation (Atkinson & Reilly 1996). 144The volunteers were instructed to arrive at the laboratory in a well fed and hydrated 145 state, without having ingested any food in the 2 h preceding the tests. In order to minimise the 146 influence of diet on performance, athletes were requested to maintain the same diet prior to all 147 trials and this was confirmed by the analysis of all individual's 72 h food recall prior to each 148 test. The participants were also informed to refrain from strenuous exercise and caffeine in the 149 24 hours preceding the experimental sessions. Compliance with these requests was verbally 150 confirmed before each trial. Body fat was estimated by hydrostatic weighing measuring body 151 volume density and calculating perceptual body fat using the equation proposed by Siri (1961). 152Participants performed four bouts of the Wingate upper-body anaerobic test during 153 every session. Blood samples were collected at rest (baseline), immediately after and 5 min after 154 the fourth bout of the Wingate test. The efficacy of the blind procedure was verified during all 155 trials; immediately after exercise, participants were asked to report which treatment they 156 believed they had received, and to describe all perceived side effects. 157 158 High-Intensity Intermittent Performance 159High-intensity intermittent exercise performance was assessed using 4 bouts of the 160 upper-body Wingate Anaerobic Test, a protocol that has been previously used to assess the 161 effects of metabolic induced alkalosis on performance in athletes (Artioli, Gualano 2007; 162 Tobias, Benatti 2013). Athletes warmed up by performing arm-cranking with no resistance for 3 163 ...

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34Beta-alanine (BA) supplementation increases muscle carnosine content (MCarn), and is ergogenic in many situations. Currently, many questions on the 35 nature of the Mcarn response to supplementation are open, and the response to these has considerable potential to enhance the efficacy and applications 36 of this supplementation strategy. Objective: To conduct a Bayesian analysis of available data on the Mcarn response to BA supplementation. Methods: A 37 systematic review with meta-analysis of individual and published aggregate data using a dose response (Emax) model was conducted. The protocol was 38 designed according to PRISMA guidelines. A three-step screening strategy was undertaken to identify studies that measured the Mcarn response to BA 39 supplementation. In addition, individual data from 5 separate studies conducted in the authors' laboratory were analysed. Data were extracted from all 40 controlled and uncontrolled supplementation studies conducted on healthy humans. Meta-regression was used to consider the influence of potential 41 moderators (including dose, sex, age, baseline Mcarn and analysis method used) on the primary outcome. Results and Conclusion: The Emax model 42 indicated that human skeletal muscle has large capacity for non-linear Mcarn accumulation, and that commonly used BA supplementation protocols may 43 not come close to saturating muscle carnosine content. Neither baseline values, nor sex, appear to influence subsequent response to supplementation. 44 Analysis of individual data indicated that Mcarn is relatively stable in the absence of intervention, and effectually all participants respond to BA 45 supplementation (99.3% response [95%CrI: 96.2 -100]).46 47

To examine the role of chronic (in)activity on muscle carnosine (MCarn) and how chronic (in)activity affects MCarn responses to β-alanine supplementation in spinal-cord injured athletes, sixteen male athletes with paraplegia were randomized (2:1 ratio) to receive β-alanine (n=11) or placebo (PL, n=5). They consumed 6.4 g‧d-1 of β-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-1 DM; p=0.018). MCarn was higher in inactive vs. active VL (32.0±12.0 vs. 21.2±7.5 mmol‧kg-1 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-1 DM, p=0.014). MCarn increased similarly between inactive VL and active deltoid in the β-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 β-alanine supplementation is not influenced by muscle inactivity.

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