We examined the isolated and combined effects of beta-alanine (BA) and sodium bicarbonate (SB) on high-intensity intermittent upper-body performance in judo and jiu-jitsu competitors. 37 athletes were assigned to one of four groups: (1) placebo (PL)+PL; (2) BA+PL; (3) PL+SB or (4) BA+SB. BA or dextrose (placebo) (6.4 g day−1) was ingested for 4 weeks and 500 mg kg−1 BM of SB or calcium carbonate (placebo) was ingested for 7 days during the 4th week. Before and after 4 weeks of supplementation, the athletes completed four 30-s upper-body Wingate tests, separated by 3 min. Blood lactate was determined at rest, immediately after and 5 min after the 4th exercise bout, with perceived exertion reported immediately after the 4th bout. BA and SB alone increased the total work done in +7 and 8 %, respectively. The co-ingestion resulted in an additive effect (+14 %, p < 0.05 vs. BA and SB alone). BA alone significantly improved mean power in the 2nd and 3rd bouts and tended to improve the 4th bout. SB alone significantly improved mean power in the 4th bout and tended to improve in the 2nd and 3rd bouts. BA+SB enhanced mean power in all four bouts. PL+PL did not elicit any alteration on mean and peak power. Post-exercise blood lactate increased with all treatments except with PL+PL. Only BA+SB resulted in lower ratings of perceived exertion (p = 0.05). Chronic BA and SB supplementation alone equally enhanced high-intensity intermittent upper-body performance in well-trained athletes. Combined BA and SB promoted a clear additive ergogenic effect.

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The purpose of this study was to determine the physiological, anthropometric, performance, and nutritional characteristics of the Brazil Canoe Polo National Team. Ten male canoe polo athletes (age 26.7 ± 4.1 years) performed a battery of tests including assessments of anthropometric parameters, upper-body anaerobic power (Wingate), muscular strength, aerobic power, and nutritional profile. In addition, we characterized heart rate and plasma lactate responses and the temporal pattern of the effort/recovery during a simulated canoe polo match. The main results are as follows: body fat, 12.3 ± 4.0%; upper-body peak and mean power, 6.8 ± 0.5 and 4.7 ± 0.4 W · kg(-1), respectively; 1-RM bench press, 99.1 ± 11.7 kg; peak oxygen uptake, 44.3 ± 5.8 mL · kg(-1) · min(-1); total energy intake, 42.8 ± 8.6 kcal · kg(-1); protein, carbohydrate, and fat intakes, 1.9 ± 0.1, 5.0 ± 1.5, and 1.7 ± 0.4 g · kg(-1), respectively; mean heart rate, 146 ± 11 beats · min(-1); plasma lactate, 5.7 ± 3.8 mmol · L(-1) at half-time and 4.6 ± 2.2 mmol · L(-1) at the end of the match; effort time (relative to total match time), 93.1 ± 3.0%; number of sprints, 9.6 ± 4.4. The results of this study will assist coaches, trainers, and nutritionists in developing more adequate training programmes and dietary interventions for canoe polo athletes.

Cancer alters the function of multiple organs beyond those targeted by metastasis 1,2 . Here we show that inflammation, fatty liver and dysregulated metabolism are hallmarks of systemically affected livers in mouse models and in patients with extrahepatic metastasis. We identified tumour-derived extracellular vesicles and particles (EVPs) as crucial mediators of cancer-induced hepatic reprogramming, which could be reversed by reducing tumour EVP secretion via depletion of Rab27a. All EVP subpopulations, exosomes and principally exomeres, could dysregulate hepatic function. The fatty acid cargo of tumour EVPs-particularly palmitic acid-induced secretion of tumour necrosis factor (TNF) by Kupffer cells, generating a proinflammatory microenvironment, suppressing fatty acid metabolism and oxidative phosphorylation, and promoting fatty liver formation. Notably, Kupffer cell ablation or TNF blockade markedly decreased tumour-induced fatty liver generation. Tumour implantation or pre-treatment with tumour EVPs diminished cytochrome P450 gene expression and attenuated drug metabolism in a TNF-dependent manner. We also observed fatty liver and decreased cytochrome P450 expression at diagnosis in tumour-free livers of patients with pancreatic cancer who later developed extrahepatic metastasis, highlighting the clinical relevance of our findings. Notably, tumour EVP education enhanced side effects of chemotherapy, including bone marrow suppression and cardiotoxicity, suggesting that metabolic reprogramming of the liver by tumour-derived EVPs may limit chemotherapy tolerance in patients with cancer. Our results reveal how tumour-derived EVPs dysregulate hepatic function and their targetable potential, alongside TNF inhibition, for preventing fatty liver formation and enhancing the efficacy of chemotherapy.Cancer is a systemic disease that is mediated by the release of soluble factors, including EVPs 1,3 . Tumour-derived EVPs establish pre-metastatic niches (PMNs) and reprogramme cell function in multiple metastasis-free organs 3,4 . Liver functional reprogramming in the absence of metastasis during cancer progression has not been widely studied. However, the liver has been identified as one of the primary organs targeted by tumour-derived EVPs 5-9 , prompting us to investigate the roles of EVPs in altering liver function. Here, by applying multi-omic analyses to multiple mouse tumour models and liver tissues from patients with cancer, we demonstrate that saturated fatty acids packaged in tumour EVPs induce metabolic dysregulation, which, in turn, promotes fatty liver formation and diminishes the drug-metabolizing capacity of the liver. Remote tumours alter liver metabolismTo investigate how cancer affects the liver, we orthotopically implanted mouse B16F10 melanoma or K7M2 osteosarcoma cells, which preferentially metastasize to the lung 10,11 . Three to four weeks after implantation, we observed no liver metastasis in either model, but detected lung metastases in the K7M2 model by histology (Extended Data Fig. 1a-c). Further...