Ten healthy, non-cycling trained males (age: 21.2 ± 2.2 years, body mass: 75.9 ± 13.4 kg, height: 178 ± 6 cm, [Vdot]O2PEAK: 46 ± 10 ml · kg(-1) · min(-1)) performed a graded incremental exercise test, two familiarisation trials and six experimental trials. Experimental trials consisted of cycling to volitional exhaustion at 100%, 110% and 120% WPEAK, 60 min after ingesting either 0.3 g · kg(-1) body mass sodium bicarbonate (NaHCO3) or 0.1 g · kg(-1) body mass sodium chloride (placebo). NaHCO3 ingestion increased cycling capacity by 17% at 100% WPEAK (327 vs. 383 s; P = 0.02) although not at 110% WPEAK (249 vs. 254 s; P = 0.66) or 120% WPEAK (170 vs. 175 s; P = 0.60; placebo and NaHCO3 respectively). Heart rate (P = 0.02), blood lactate (P = 0.001), pH (P < 0.001), [HCO3 (-)], (P < 0.001), and base excess (P < 0.001) were greater in all NaHCO3 trials. NaHCO3 attenuated localised ratings of perceived exertion (RPEL) to a greater extent than placebo only at 100% WPEAK (P < 0.02). Ratings of abdominal discomfort and gut fullness were mild but higher for NaHCO3. NaHCO3 ingestion significantly improves continuous constant load cycling at 100% WPEAK due to, in part, attenuation of RPEL.

Caffeine (CAF) is widely consumed across sport and exercise for its reputed ergogenic properties, including central nervous stimulation and enhanced muscular force development. However, expectancy and the related psychological permutations that are associated with oral CAF ingestion are generally not considered in most experimental designs and these could be important in understanding if/how CAF elicits an ergogenic effect. The present paper reviews 17 intervention studies across sport, exercise, and cognitive performance. All explore CAF expectancies, in conjunction with/without CAF pharmacology. Thirteen out of 17 studies indicated expectancy effects of varying magnitudes across a range of exercise tasks and cognitive skills inclusive off but not limited to; endurance capacity, weightlifting performance, simple reaction time and memory. Factors, such as motivation, belief, and habitual CAF consumption habits influenced the response. In many instances, these effects were comparable to CAF pharmacology. Given these findings and the lack of consistency in the experimental design, future research acknowledging factors, such as habitual CAF consumption habits, habituated expectations, and the importance of subjective post-hoc analysis will help to advance knowledge within this area.

The aim of this study was to assess the effects of post-exercise sodium bicarbonate (NaHCO3) ingestion (0.3 g.kg−1 body mass) on the recovery of acid-base balance (pH, HCO3-, and the SID) and subsequent exercise performance in elite boxers. Seven elite male professional boxers performed an initial bout of exhaustive exercise comprising of a boxing specific high-intensity interval running (HIIR) protocol, followed by a high-intensity run to volitional exhaustion (TLIM1). A 75 min passive recovery then ensued, whereby after 10 min recovery, participants ingested either 0.3 g.kg−1 body mass NaHCO3, or 0.1 g.kg−1 body mass sodium chloride (PLA). Solutions were taste matched and administered double-blind. Participants then completed a boxing specific punch combination protocol, followed by a second high-intensity run to volitional exhaustion (TLIM2). Both initial bouts of TLIM1 were well matched between PLA and NaHCO3 (ICC; r = 0.94, p = 0.002). The change in performance from TLIM1 to TLIM2 was greater following NaHCO3 compared to PLA (+164 ± 90 vs. +73 ± 78 sec; p = 0.02, CI = 45.1, 428.8, g = 1.0). Following ingestion of NaHCO3, pH was greater prior to TLIM2 by 0.11 ± 0.02 units (1.4%) (p < 0.001, CI = 0.09, 0.13, g = 3.4), whilst HCO3- was greater by 8.8 ± 1.5 mmol.l−1 (26.3%) compared to PLA (p < 0.001, CI = 7.3, 10.2, g = 5.1). The current study suggests that these significant increases in acid base balance during post-exercise recovery facilitated the improvement in the subsequent bout of exercise. Future research should continue to explore the role of NaHCO3 supplementation as a recovery aid in boxing and other combat sports.

Polyphenols are secondary metabolites involved in a myriad of critical processes in plants. Over recent decades, special attention has been paid to the anti-oxidative role of fruit-derived polyphenols in the human diet, with evidence supporting the contribution of polyphenols in the prevention of numerous non-communicable disease outcomes. However, due to the low concentration in biological fluids in vivo, the antioxidant properties of polyphenols seem to be related to an enhanced endogenous antioxidant capacity induced via signaling through the nuclear respiratory factor 2 pathway. Polyphenols also seem to possess anti-inflammatory and antioxidant properties and have been shown to enhance vascular function via nitric oxide mediated mechanisms. Consequently, there is rationale to support fruit-derived polyphenol supplementation to enhance exercise performance, possibly via improved muscle perfusion. Fruit-derived polyphenol supplementation in exercise studies have included a variety of fruits, e.g., New Zealand blackcurrant, pomegranate, and cherry, in the form of extracts (multicomponent or purified), juices and infusions to varying degrees of benefit. For example, research has yet to link the health-related benefits of black elderberry (Sambucus nigra L.) ingestion to exercise performance in spite of the purported health benefits associated with black elderberry provision in vitro and in vivo models, which has been attributed to their high antioxidant capacity and polyphenol content. This review summarizes the existing evidence supporting a beneficial effect of fruit-derived polyphenols on various biological processes and outlines the potential for black elderberry ingestion to improve nitric oxide production, exercise performance, and the associated physiological responses before-, during- and post-exercise.

The present work aimed to evaluate the effect of 3 mg·kg−1 caffeine consumption on the standing and dynamic balance performance of older adults and sought to establish if caffeine ingestion can modulate the influence of a cognitive dual task on balance performance. Twelve apparently healthy participants (8 females) aged >65 years (72 ± 3.7 years) completed the study. Bipedal postural sway, four square step test, timed up and go, Y-balance (anterior reach only) and force-time characteristics of sit-to-stand performance were used to assess standing and dynamic balance. Attention and working memory were assessed using a serial 3s and 7s subtraction task during seated rest and completion of the bipedal standing assessment and Y-balance test. This battery of assessments was completed on two separate occasions, once following the consumption of a non-ergogenic placebo and again following the consumption of 3 mg·kg−1 caffeine. The administration of treatments was randomised, counterbalanced and double-blind. Caffeine reduced performance in the bipedal standing balance assessments, evidenced by an increase in COPML, COPPath, COPVelocity. Performance during the dynamic balance tests was unaffected, other than rate of force development during the sit-to-stand, which was improved following caffeine ingestion. The introduction of a cognitive dual task had either limited effects, or improved facets of bipedal standing balance, whilst performance during the dynamic balance task was significantly reduced. In both balance assessments, there was evidence for a reduction in the performance of the cognitive task when both the balance and cognitive tests were performed simultaneously, with this effect not modulated by caffeine consumption. These findings refute the idea that caffeine ingestion may have positive effects on balance performance. However, despite a caffeine-induced reduction in bipedal standing balance, it is unlikely that caffeine ingestion would exacerbate fall risk given the limited effects in the dynamic balance tests. Future work should establish if these effects are generalisable to older frail participants and if caffeine can modulate the detrimental effects of an acute exercise bout on balance performance.

This study evaluated the ingestion of sodium bicarbonate (NaHCO3) on postexercise acid-base balance recovery kinetics and subsequent high-intensity cycling time to exhaustion. In a counterbalanced, crossover design, nine healthy and active males (age: 23 ± 2 years, height: 179 ± 5 cm, body mass: 74 ± 9 kg, peak mean minute power (Wpeak) 256 ± 45 W, peak oxygen uptake (V̇O2peak) 46 ± 8 ml.kg-1.min-1) performed a graded incremental exercise test, two familiarization and two experimental trials. Experimental trials consisted of cycling to volitional exhaustion (TLIM1) at 100% WPEAK on two occasions (TLIM1 and TLIM2) interspersed by a 90 min passive recovery period. Using a double-blind approach, 30 min into a 90 min recovery period participants ingested either 0.3 g.kg-1 body mass sodium bicarbonate (NaHCO3) or a placebo (PLA) containing 0.1 g.kg-1 body mass sodium chloride (NaCl) mixed with 4 ml.kg-1 tap water and 1 ml.kg-1 orange squash. The mean differences between TLIM2 and TLIM1 was larger for PLA compared with NaHCO3 (-53 ± 53 vs. -20 ± 48 s; p = .008, d = 0.7, CI =-0.3, 1.6), indicating superior subsequent exercise time to exhaustion following NaHCO3. Blood lactate [Bla-] was similar between treatments post TLIM1, but greater for NaHCO3 post TLIM2 and 5 min post TLIM2. Ingestion of NaHCO3 induced marked increases (p < .01) in both blood pH (+0.07 ± 0.02, d = 2.6, CI = 1.2, 3.7) and bicarbonate ion concentration [HCO3-] (+6.8 ± 1.6 mmo.l-1, d = 3.4, CI = 1.8, 4.7) compared with the PLA treatment, before TLIM2. It is likely both the acceleration of recovery, and the marked increases of acid-base after TLIM1 contributed to greater TLIM2 performance compared with the PLA condition.

This study examined the effects of elevated buffer capacity [~32 mM HCO₃(-)] through administration of sodium bicarbonate (NaHCO₃) on maximally stimulated isolated mouse soleus (SOL) and extensor digitorum longus (EDL) muscles undergoing cyclical length changes at 37 °C. The elevated buffering capacity was of an equivalent level to that achieved in humans with acute oral supplementation. We evaluated the acute effects of elevated [HCO₃(-)] on (1) maximal acute power output (PO) and (2) time to fatigue to 60 % of maximum control PO (TLIM60), the level of decline in muscle PO observed in humans undertaking similar exercise, using the work loop technique. Acute PO was on average 7.0 ± 4.8 % greater for NaHCO₃-treated EDL muscles (P < 0.001; ES = 2.0) and 3.6 ± 1.8 % greater for NaHCO₃-treated SOL muscles (P < 0.001; ES = 2.3) compared to CON. Increases in PO were likely due to greater force production throughout shortening. The acute effects of NaHCO₃ on EDL were significantly greater (P < 0.001; ES = 0.9) than on SOL. Treatment of EDL (P = 0.22; ES = 0.6) and SOL (P = 0.19; ES = 0.9) with NaHCO₃ did not alter the pattern of fatigue. Although significant differences were not observed in whole group data, the fatigability of muscle performance was variable, suggesting that there might be inter-individual differences in response to NaHCO₃ supplementation. These results present the best indication to date that NaHCO₃ has direct peripheral effects on mammalian skeletal muscle resulting in increased acute power output.

This study evaluated the effects of ingesting sodium bicarbonate (NaHCO3) or caffeine individually or in combination on high-intensity cycling capacity. In a counterbalanced, crossover design, 13 healthy, noncycling trained males (age: 21 ± 3 years, height: 178 ± 6 cm, body mass: 76 ± 12 kg, peak power output (Wpeak): 230 ± 34 W, peak oxygen uptake: 46 ± 8 mL·kg(-1)·min(-1)) performed a graded incremental exercise test, 2 familiarisation trials, and 4 experimental trials. Trials consisted of cycling to volitional exhaustion at 100% Wpeak (TLIM) 60 min after ingesting a solution containing either (i) 0.3 g·kg(-1) body mass sodium bicarbonate (BIC), (ii) 5 mg·kg(-1) body mass caffeine plus 0.1 g·kg(-1) body mass sodium chloride (CAF), (iii) 0.3 g·kg(-1) body mass sodium bicarbonate plus 5 mg·kg(-1) body mass caffeine (BIC-CAF), or (iv) 0.1 g·kg(-1) body mass sodium chloride (PLA). Experimental solutions were administered double-blind. Pre-exercise, at the end of exercise, and 5-min postexercise blood pH, base excess, and bicarbonate ion concentration ([HCO3(-)]) were significantly elevated for BIC and BIC-CAF compared with CAF and PLA. TLIM (median; interquartile range) was significantly greater for CAF (399; 350-415 s; P = 0.039; r = 0.6) and BIC-CAF (367; 333-402 s; P = 0.028; r = 0.6) compared with BIC (313: 284-448 s) although not compared with PLA (358; 290-433 s; P = 0.249, r = 0.3 and P = 0.099 and r = 0.5, respectively). There were no differences between PLA and BIC (P = 0.196; r = 0.4) or between CAF and BIC-CAF (P = 0.753; r = 0.1). Relatively large inter- and intra-individual variation was observed when comparing treatments and therefore an individual approach to supplementation appears warranted