The study evaluates whether the intrinsic capacity for physical exercise influences dopamine neuroplasticity induced by physical training. Male rats were submitted to three progressive tests until fatigue. Based on the maximal time of exercise (TE), rats were considered as low performance (LP), standard performance (SP) or high performance (HP) to exercise. Eight animals from each group (LP, SP, and HP) were randomly subdivided in sedentary (SED) or trained (TR). Physical training was performed for 6 wk. After that, concentrations of dopamine (DA), serotonin (5-HT), and their metabolites and mRNA levels of D1 receptor ( Drd1), D2 receptor ( Drd2), dopamine transporter ( Dat), tyrosine hydroxylase ( Th), glia cell line neurotrophic factor ( Gdnf), and brain-derived neurotrophic factor ( Bdnf) were determined in the caudate-putamen (CPu). TE was increased with training in all performance groups. However, the relative increase was markedly higher in LP rats, and this was associated with a training-induced increase in dopaminergic activity in the CPu, which was determined by the 3,4-dihydroxyphenylacetic acid (DOPAC)/DA ratio. An opposite monoamine response was found in HP-TR rats, in which physical training decreased the DOPAC/DA ratio in the CPu. Moreover, LP-SED rats displayed higher levels of Drd2 in the CPu compared with the other SED groups, and this higher expression was decreased by physical training. Physical training also decreased Dat and increased Gdnf in the CPu of LP rats. Physical training decreased Bdnf in the CPu only in HP rats. Thus, we provide evidence that the intrinsic capacity to exercise affects the neuroplasticity of the dopaminergic system in response to physical training. NEW & NOTEWORTHY The findings reported reveal that dopaminergic neuroplasticity in caudate-putamen induced by physical training is influenced by the intrinsic capacity to exercise in rats. To evaluate the dopaminergic neuroplasticity, we analyzed mRNA levels of D1 receptor, D2 receptor, dopamine transporter, tyrosine hydroxylase, glia cell line neurotrophic factor, and brain-derived neurotrophic factor as well as concentrations of dopamine, serotonin, and their metabolites. These results expand our knowledge about the interrelationship between genetic background, physical training, and dopaminergic neuroplasticity.

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This study aimed to investigate the effects of physical training on thermoregulatory adjustments during running exercise and its effects on brain neuronal nitric oxide synthase (n‐NOS) expression. Male spontaneously hypertensive (SHR) and normotensive Wistar rats (NWR) at 8‐weeks age old were divided into four groups: untrained NWR (NWR‐U), trained NWR (NWR‐T), untrained SHR (SHR‐U) and trained SHR (SHR‐T). Experimental procedures were approved by the CEUA‐UFMG (#21/2015). Aerobic exercise training was performed on a treadmill running for 8 weeks. On the day of the experiments, the rats were subjected to a constant‐speed (60% of Vmáx) protocol until fatigue at 25°C. Tail skin temperature (Ts) and abdominal temperature (Ta) were measured every minute throughout the exercise trials. The preoptic area (POA) and paraventricular nuclei (PVN) of hypothalamus was collected to quantification of n‐NOS(ser852) by western blot. During exercise, the SHR‐U group showed greater increase in Ta compared to with NWR‐U group from the 16th min until the 23th min (min 23: 1.62 ± 0.15 °C vs. 1.21 ± 0.12 °C, p<0.05) and lower Ts from the 1th until the 16th min of exercise (min 16: 0.09 ± 0.95 °C vs. 1.39 ± 0.41 °C, p<0.05). Physical training in SHRs group did not change Ta response during exercise (fatigue: SHR‐T: 1.54 ± 0.29 °C vs. SHR‐U: 1.70 ± 0.18 °C, p<0.05) but caused a greater increase in Ts in SHR‐T group (min 12: −0.54 ± 0.93 °C vs. −2.64 ± 0.80 °C, p<0.05). Physical training in NWR group did not change Ta response during exercise (fatigue: NWR‐T: 1.62 ± 0.26 °C vs. NWR‐U: 1.71 ± 0.26 °C, p<0.05) but caused a greater increase in Ts in NWR‐T group (fatigue: 3.65 ± 0.38 °C vs. 1.60 ± 0.47 °C, p<0.05). The p‐nNOS expression in APO was lower in SHR‐U group when compared to the NWR‐U (0.06 ± 0.01 u.a. vs. 0.09 ± 0.01 u.a., p<0.05). Physical training increased the p‐nNOS expression in the APO in the SHR group (0.10 ± 0.01 u.a. vs. 0.06 ± 0.01 u.a., p<0.05). The p‐nNOS expression in PVN was similar between SHR‐U and NWR‐U groups (SHR‐U: 1.10 ± 0.19 u.a vs. NWR NT: 0.94 ± 0.13 u.a., p>0.05). Physical training increased p‐NOS expression in the APO in both SHR group (1.58 ± 0.17 u.a. vs. 1.10 ± 0.19 u.a., p<0.05) and NWR group (1.56 ± 0.25 u.a vs. 0.94 ± 0.13 u.a., p<0.05). We conclude that physical training increases the efficiency of thermoregulatory control during exercise in hypertensive animals, which can be explained, at least in part, to an increase in the activity of neuronal nitric oxide synthase in trained animals. Support or Funding Information Fapemig, Capes, and CNPq. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The aim of study was to investigate the aerobic running performance of hypertensive rats in exercise capacity test at different ages and stages of hypertension. Male spontaneously hypertensive rat (SHR, n = 10) and normotensive wistar rats (NWR, n = 10) of 5, 8, 12 and 16 weeks were used. Experimental procedures were approved by the CEUA‐UFMG (#49/2015). Systolic blood pressure (SBP) and body mass was measured in 4 different ages. All animals were submitted to the exercise capacity test: initial speed was set to 10 m.min−1, with increments of 1 m.min−1 every 3 min until fatigue and the inclination of treadmill was maintained at 5°. The exercise time was measured and the workload was calculated as follows: body weight (kg) x exercise time (min) x treadmill speed (m.min−1) x sinα (treadmill inclination) x acceleration of gravity. The hypertensive rats had lower body mass in comparison to normotensive animals at all four ages (NWR‐5: 175 ± 5 g vs. SHR‐5:119 ± 3 g; NWR‐8: 321 ± 9 g vs. SHR‐8: 233 ± 4 g; NWR‐12: 368 ± 13 g vs. SHR‐12: 264 ± 7 g; NWR‐16: 391 ± 13 g vs. SHR‐16: 324 ± 5 g; p < 0.05, two‐way ANOVA). As expected, the SHR group presented higher SBP when compared to the NWR group at all four ages (NWR‐5: 98.7 ± 3.5 mmHg vs. SHR‐5:128.8 ± 2.6 mmHg; NWR‐8: 108.1 ± 5.4 mmHg vs. SHR‐8: 169.2 ± 3.3 mmHg; NWR‐12: 112.2 ± 2.0 mmHg vs. SHR‐12: 176.5 ± 2.0 mmHg; NWR‐16: 119.8 ± 3.3 mmHg vs. SHR‐16: 195.1 ± 7.3 mmHg; p < 0.05, two‐way ANOVA). When analyzing the physical performance measured only in the exercise time, it can be observed that all the groups showed similar physical performance in all the four moments (NWR‐5: 50.6 ± 4.1 min vs. SHR‐5: 49.6 ± 2.0 min; NWR‐8: 50.0 ± 2.5 min vs. SHR‐8: 46.8 ± 2.2 min; NWR‐12: 49.8 ± 4.2 min vs. SHR‐12: 44.8 ± 1.6 min; NWR‐16: 34.5 ± 2.1 min vs. SHR‐16: 35.2 ± 1.4 min; p > 0.05, two‐way ANOVA). However, when analyzing physical running capacity was measured by workload, it can be observed that the hypertensive animals showed a lower physical performance in comparison to normotensive animals at all four ages (NWR‐5: 140 ± 17 J vs. SHR‐5: 84 ± 6 J; NWR‐8: 206 ± 18 J vs. SHR‐8: 153 ± 8 J; NWR‐12: 264 ± 29 J vs. SHR‐12: 170 ± 9 J; NWR‐16: 195 ± 13 J vs. SHR‐16: 154 ± 9 J; p < 0.05, two‐way ANOVA). In conclusion, the present results indicate that hypertensive rats exhibit reduced physical performance compared to normotensive controls, since, the most reliable index to assess physical performance when there is difference in body mass between strains is workload.Support or Funding InformationFAPEMIG, CAPES and CNPqThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.