Association between the increase in brain temperature and physical performance at different exercise intensities and protocols in a temperate environment

There is evidence that brain temperature (Tbrain) provides a more sensitive index than other core body temperatures in determining physical performance. However, no study has addressed whether the association between performance and increases in Tbrain in a temperate environment is dependent upon exercise intensity, and this was the primary aim of the present study. Adult male Wistar rats were subjected to constant exercise at three different speeds (18, 21, and 24 m/min) until the onset of volitional fatigue. Tbrain was continuously measured by a thermistor inserted through a brain guide cannula. Exercise induced a speed-dependent increase in Tbrain, with the fastest speed associated with a higher rate of Tbrain increase. Rats subjected to constant exercise had similar Tbrain values at the time of fatigue, although a pronounced individual variability was observed (38.7-41.7°C). There were negative correlations between the rate of Tbrain increase and performance for all speeds that were studied. These results indicate that performance during constant exercise is negatively associated with the increase in Tbrain, particularly with its rate of increase. We then investigated how an incremental-speed protocol affected the association between the increase in Tbrain and performance. At volitional fatigue, Tbrain was lower during incremental exercise compared with the Tbrain resulting from constant exercise (39.3±0.3 vs 40.3±0.1°C; P<0.05), and no association between the rate of Tbrain increase and performance was observed. These findings suggest that the influence of Tbrain on performance under temperate conditions is dependent on exercise protocol

Passiflora edulis peel intake improves insulin sensitivity, increasing incretins and hypothalamic satietogenic neuropeptide in rats on a high-fat diet

This study aimed to investigate the effect of Passiflora edulis peel flour (PEPF) intake on hypothalamic neuropeptides messenger RNA expression, insulin sensitivity, and other metabolic parameters in Sprague-Dawley rats fed a high-fat (HF) diet. Methods: Sprague-Dawley rats were divided in 3 groups: a control group, fed on a normal fat diet; a HF group, fed on a high-fat diet (35% fat [w/w]); and a high-fat Passiflora flour (HFPF) group, fed on a HF diet containing PEPF. The rats from the HFPF group as well as the HF group were kept on an HF diet for the first 4 wk to induce metabolic conditions related to obesity. Then the HFPF group was switched to a HF diet containing PEPF for additional 6 wk. Other groups were kept on normal-fat and HF diet without addition of PEPF during the whole period of experiment. The glucose tolerance and insulin sensitivity were evaluated through the glucose tolerance test (GTT) and the insulin tolerance test (ITT). Gut hormones and adipokines were measured through an immunoassay. The hypothalamic neuropeptides expression was assessed by real-time polymerase chain reaction. Results: The PEPF intake increased the hypothalamic cocaine- and amphetamine-regulated transcript expression (CART) (P < 0.05), counteracted cumulative body weight gain (P < 0.001), decreased adiposity (P < 0.05) and leptin level (P < 0.01), whereas increased adiponectin (P < 0.01), glucose-dependent insulinotropic polypeptide (P < 0.01), and glucagon-like peptide-1 (GLP-1) (P < 0.001) improved the insulin sensitivity in diet-induced obesity rats by increasing the kITT (glucose disappearance rate) (P < 0.01), which was calculated during the ITT. Other gut hormones (peptide tyrosine tyrosine, pancreatic polypeptide, and amylin) and interleukins (IL) (IL-6, tumor necrosis factor-α, IL-1β, and monocyte chemoattractant protein-1) were not changed by the PEPF intake. Conclusion: Our findings provide a further understanding of how the PEPF works as a dietary component to improve glucose homeostasis and demonstrate a molecular mechanism that may increase satiety by PEPF in diet-induced obesity.327-8863870CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPSem informação2012/12322-