The objective of this study was to investigate the effect of the NaHCO 3 ingestion on the judo performance. Six male athletes in-gested 0.3 g • kg-1 body weight of NaHCO 3 or CaCO 3 (placebo) 2 h before 3 fights of 5 min, with 15 min recovery. Immediately after-wards, and 15 min after each fight, the athletes related their perceived exertion. The blood lactate concentration was verified in rest, after warming up, 0, 3, 5, 7, 10 and 15 min after each fight. The same experimental protocol was repeated twice by each athlete, except for the ingested substance. The study adopted the counterbalanced double-blind model. There was no significant difference for the performance variables. The perceived exertion did not differ among the treatments, and the blood lactate concentration was significantly greater (p < 0.05) after NaHCO 3 ingestion in the first moments of the protocol. In conclusion, the ergogenic effects of NaH-CO 3 are not enough to contribute to the improvement of the performance in judo fights. However, the model limitations must be considered when generalizing these results. Future studies should use other tools to evaluate the performance in judo.

The high forces undergone during repetitive eccentric, or lengthening, contractions place skeletal muscle under considerable stress, in particular if unaccustomed. Although muscle is highly adaptive, the responses to stress may not be optimally regulated by the body. Reactive oxygen species (ROS) are one component of the stress response that may contribute to muscle damage after eccentric exercise. Antioxidants may in turn scavenge ROS, thereby preventing or attenuating muscle damage. The antioxidant vitamins C (ascorbic acid) and E (tocopherol) are among the most commonly used sport supplements, and are often taken in large doses by athletes and other sportspersons because of their potential protective effect against muscle damage. This review assesses studies that have investigated the effects of these two antioxidants, alone or in combination, on muscle damage and oxidative stress. Studies have used a variety of supplementation strategies, with variations in dosage, timing and duration of supplementation. Although there is some evidence to show that both antioxidants can reduce indices of oxidative stress, there is little evidence to support a role for vitamin C and/or vitamin E in protecting against muscle damage. Indeed, antioxidant supplementation may actually interfere with the cellular signalling functions of ROS, thereby adversely affecting muscle performance. Furthermore, recent studies have cast doubt on the benign effects of long-term, high-dosage antioxidant supplementation. High doses of vitamin E, in particular, may increase all-cause mortality. Although some equivocation remains in the extant literature regarding the beneficial effects of antioxidant vitamin supplementation on muscle damage, there is little evidence to support such a role. Since the potential for long-term harm does exist, the casual use of high doses of antioxidants by athletes and others should perhaps be curtailed.

McGinley C, Bishop DJ. Influence of training intensity on adaptations in acid/base transport proteins, muscle buffer capacity, and repeated-sprint ability in active men. J Appl Physiol 121: 1290-1305, 2016. First published October 14, 2016; doi:10.1152/japplphysiol.00630.2016-This study measured the adaptive response to exercise training for each of the acid-base transport protein families, including providing isoform-specific evidence for the monocarboxylate transporter (MCT)1/4 chaperone protein basigin and for the electrogenic sodium-bicarbonate cotransporter (NBCe)1. We investigated whether 4 wk of work-matched, high-intensity interval training (HIIT), performed either just above the lactate threshold (HIITΔ20; n = 8), or close to peak aerobic power (HIITΔ90; n = 8), influenced adaptations in acid-base transport protein abundance, nonbicarbonate muscle buffer capacity (βm), and exercise capacity in active men. Training intensity did not discriminate between adaptations for most proteins measured, with abundance of MCT1, sodium/hydrogen exchanger (NHE) 1, NBCe1, carbonic anhydrase (CA) II, and CAXIV increasing after 4 wk, whereas there was little change in CAIII and CAIV abundance. βm also did not change. However, MCT4 protein content only increased for HIITΔ20 [effect size (ES): 1.06, 90% confidence limits × / ÷ 0.77], whereas basigin protein content only increased for HIITΔ90 (ES: 1.49, × / ÷ 1.42). Repeated-sprint ability (5 × 6-s sprints; 24 s passive rest) improved similarly for both groups. Power at the lactate threshold only improved for HIITΔ20 (ES: 0.49; 90% confidence limits ± 0.38), whereas peak O uptake did not change for either group. Detraining was characterized by the loss of adaptations for all of the proteins measured and for repeated-sprint ability 6 wk after removing the stimulus of HIIT. In conclusion, 4 wk of HIIT induced improvements in each of the acid-base transport protein families, but, remarkably, a 40% difference in training intensity did not discriminate between most adaptations.

What is the central question of this study? Following a training intervention, how is the interpretation of adaptations in skeletal muscle H transporters influenced by biopsy timing in the context of individual protein and mRNA kinetics after the final exercise bout? What is the main finding and its importance? We show that distinct postexercise protein and mRNA kinetics for monocarboxylate transporter 1/4 and sodium-hydrogen exchanger 1 indicate that timing of a single end-point biopsy after a training intervention can influence the inferences made. Furthermore, we found the intrasubject, intersample variability of the muscle buffer capacity titration assay to be greater than the typical training effect. In order to gain a better understanding of training-induced adaptations in skeletal muscle pH regulation, in this study we measured protein and mRNA kinetics of proton (H ) transporters for 72 h following a bout of high-intensity interval exercise (HIIE), conducted after 4 weeks of similar training. We also assayed muscle buffer capacity (βm) by a titration technique (βm ) over the same period. Sixteen active men cycled for seven bouts of 2 min at ∼80% of peak aerobic power, interspersed with 1 min rest. Compared with the first 9 h postexercise, monocarboxylate transporter (MCT) 1 protein content was ∼1.3-fold greater 24-72 h post-HIIE, whereas there was no such change in MCT4 protein content. Conversely, MCT1 and MCT4 mRNA expression progressively decreased 9-72 h post-HIIE. Sodium-hydrogen exchanger 1 (NHE1) protein content was lower 9 h post-HIIE (∼0.8-fold) compared with every other postexercise time point, but NHE1 mRNA expression was 2.2 to 2.9-fold greater 24-72 h post-HIIE, compared with the first 24 h post-HIIE. Furthermore, we determined the intrasubject, intersample variability (11.5%) of βm for resting samples taken on consecutive days to be greater than the typical training effect (mean 6%; 95% confidence limits ±4%). In conclusion, the delay in steady-state protein turnover should inform biopsy timing in studies investigating the response to training of the H transport proteins, whereas the temporal resolution provided by single time points has been shown to be of limited epistemological value for their corresponding mRNA expression. Finally, our data cast doubt on the ecological validity of the βm assay for measuring true changes in βm.