Brain serotonin and dopamine are neurotransmitters related to fatigue, a feeling that leads to reduced intensity or interruption of physical exercises, thereby regulating performance. The present review aims to present advances on the understanding of fatigue, which has recently been proposed as a defense mechanism instead of a “physiological failure” in the context of prolonged (aerobic) exercises. We also present recent advances on the association between serotonin, dopamine and fatigue. Experiments with rodents, which allow direct manipulation of brain serotonin and dopamine during exercise, clearly indicate that increased serotoninergic activity reduces performance, while increased dopaminergic activity is associated with increased performance. Nevertheless, experiments with humans, particularly those involving nutritional supplementation or pharmacological manipulations, have yielded conflicting results on the relationship between serotonin, dopamine and fatigue. The only clear and reproducible effect observed in humans is increased performance in hot environments after treatment with inhibitors of dopamine reuptake. Because the serotonergic and dopaminergic systems interact with each other, the serotonin-to-dopamine ratio seems to be more relevant for determining fatigue than analyzing or manipulating only one of the two transmitters. Finally, physical training protocols induce neuroplasticity, thus modulating the action of these neurotransmitters in order to improve physical performance.

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This study examined the effects of precooling on performance and pacing during 30-km cycling exercise in hot and temperate environments. 8 trained male cyclists performed 4 trials involving either cooling (PREC and PREC) or no-cooling interventions (TEMP and HOT) prior to a 30-km self-paced cycling exercise in either a hot (35°C, 68% relative humidity) or temperate environment (24°C, 68% relative humidity). Exercise time was longer in HOT (60.62±3.47 min) than in TEMP (58.28±3.30 min; <0.001), and precooling attenuated this thermal strain performance impairment (PREC 58.28±3.30 min; =0.048), but it was still impaired compared with TEMP (=0.02). Exercise performance in PREC (54.58±4.35 min) was no different from TEMP. Initial power output was sustained until the end of the exercise in both TEMP and PREC, but was reduced from the 12 km until the end of the trial in HOT (P<0.05). This reduction was delayed by precooling because power output was reduced only after the 20 km during PREC (P<0.05). Heart rate was similar in all conditions throughout almost the entire exercise, suggesting the maintenance of similar relative intensities. In conclusion, precooling was effective in attenuating, but not completely reversing thermal strain performance impairment and offered no ergogenic effect in the temperate environment.

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New Findings r What is the central question of this study?Clinical studies suggest that obesity 'protects' against osteoporosis. However, these studies used only bone densitometry and assessed only one bone site, which is insufficient to enable conclusions to be drawn about the response of the whole skeleton. Furthermore, the effects of exercise on bone responses in obesity have not been explored previously. r What is the main finding and what is its importance?We show that obesity causes osteopetrosis. Therefore, the classical perspective of 'protective effects of obesity' needs to be reviewed, and exercise is an important tool to avoid these alterations and to maintain the homeostasis of bone.A sedentary lifestyle and obesity induce systemic inflammatory responses. Although the effects of physical inactivity on osseous tissue have been well established, the effects of obesity on bone tissue remain controversial. Furthermore, the effects of physical training on bone tissue responses in the presence of diet-induced obesity are unknown. Our aim was to investigate the effects of obesity and physical training at multiple bone sites in rats. Female Wistar rats were divided into the following four groups: (i) control diet, non-trained (C-NT); (ii) high-refined carbohydrate-containing diet, non-trained (HC-NT); (iii) control diet, trained (C-T); and (iv) high-refined carbohydrate-containing diet, trained (HC-T). At 5 months of age, the rats were submitted to daily exercise for 30 min day −1 . After 13 weeks, blood samples, adipose and skeletal tissues were harvested. Two-way ANOVA was applied to detect differences (significance accepted when P ࣘ 0.05). The HC-NT group exhibited increased body mass, adiposity, serum leptin, serum insulin, insulin resistance index and concentrations of tumour necrosis factor-α and interleukin-6. Obese rats (HC-NT) exhibited thickening of nasal bones, trabecular bones in the lumbar vertebrae and long bones in a site-dependent manner. The HC-T group exhibited similar adiposity and inflammatory results. Morphological analysis of the lumbar vertebrae in rats fed the HC diet revealed characteristics of osteopetrosis that were inhibited by exercise. In conclusion, the HC diet induced obesity and inflammatory/hormonal alterations and increased the trabecular bone in a site-dependent manner. However, obesity caused osteopetrosis in the lumbar vertebrae, which could be inhibited by physical training. Although exercise inhibited the

Antarctic climate is challenging, since the cold, wind and sensory monotony are stressful stimuli to individuals. Moreover, camp activities and heavy clothes may contribute to increase physiological strain. Thus, we aimed to characterise the physiological demand of a 24-day period in the Antarctic field and then to evaluate the effect of this expedition on the aerobic fitness in individuals with heterogeneous initial aerobic fitness (as determined by estimating maximum oxygen consumption – V̊O2MAX). Before and after the 24-day period in Antarctica, 7 researchers and 2 mountaineers were subjected to incremental tests to estimate their V̊O2MAX. Field effort was characterised by measuring heart rate (HR). During the field trips, their HR remained 33.4% of the recording time between 50–60% HRMAX, 22.3% between 60–70% HRMAX, and only 1.4% between 80 and 90% HRMAX. The changes in estimated V̊O2MAX during the expedition depended on the pre-expedition aerobic fitness. The post-expedition V̊O2MAX increased by 5.9% and decreased by 14.3%in individuals with lower (researchers) and higher (mountaineers) initial V̊O2MAX, respectively. We concluded that physical effort in the Antarctic field is characterised as predominantly of low- to moderate-intensity. This effort represented an effective training load for individuals with lower initial V̊O2MAX, but not for those with higher V̊O2MAX.

There is a growing consensus that the balance between the persistence of infection and the host immune response is crucial for chronification of Chagas heart disease. Extrapolation for chagasic megacolon is hampered because research in humans and animal models that reproduce intestinal pathology is lacking. The parasite-host relationship and its consequence to the disease are not well-known. Our model describes the temporal changes in the mice intestine wall throughout the infection, parasitism, and the development of megacolon. It also presents the consequence of the infection of primary myenteric neurons in culture with Trypanosoma cruzi (T. cruzi). Oxidative neuronal damage, involving reactive nitrogen species induced by parasite infection and cytokine production, results in the denervation of the myenteric ganglia in the acute phase. The long-term inflammation induced by the parasite's DNA causes intramuscular axonal damage, smooth muscle hypertrophy, and inconsistent innervation, affecting contractility. Acute phase neuronal loss may be irreversible. However, the dynamics of the damages revealed herein indicate that neuroprotection interventions in acute and chronic phases may help to eradicate the parasite and control the inflammatory-induced increase of the intestinal wall thickness and axonal loss. Our model is a powerful approach to integrate the acute and chronic events triggered by T. cruzi, leading to megacolon.