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Moderate physical training is often associated with improved cardiorespiratory fitness in athletes and the general population. In animals, studies are designed to investigate basic physiology that could be invasive and uncomfortable for humans. The standardization of an exercise training protocol for rats based on maximal consumption of oxygen (VO(2)max) is needed. This study validated a program of moderate physical training for Wistar rats based on VO(2)max determined once a week. A 10-stage treadmill running test was developed to measure VO(2)max through an indirect, open circuit calorimeter. Thirty male Wistar rats (210-226 g) were randomly assigned to either a nontrained group or a trained group. The animals were evaluated weekly to follow their VO(2)max during 8 weeks of moderate training and to adjust the intensity of the protocol of training. The soleus muscle was removed for determination of citrate synthase activity. Trained animals maintained their values of VO(2)max during a moderate running training and showed a significant less body weight gain. An increase of 42% in citrate synthase activity of the soleus muscle from trained rats was found after the training program. Our study presents a protocol of moderate physical training for Wistar rats based on VO(2)max. Peripheral adaptations such as the values of citrate synthase activity also responded to the moderate training program imposed as observed for VO(2)max. Other studies can use our protocol of moderate training to study the physiologic adaptations underlying this specific intensity of training. It will provide support for study with humans.

The aim of this study was to investigate the effects of malnutrition, induced by a regional basic diet (RBD), on motor development. RBD is a 7.87%-protein diet based on aliments typical of Northeastern Brazil, elaborated after nutritional investigation by Teodosio et al. (1979). Female rats were treated with RBD during lactation. The reflex ontogenesis and the development of locomotor activity in their offspring were assessed. Malnourished (MN) rats showed a delay in reflex maturation and in locomotor activity evolution. The decreased locomotor activity may be related to the reduced movement experiences induced by the delay in the reflex maturation. Occurring during the critical period of brain development, this fact could jeopardize all the steps in future locomotion evolution. The present results confirm deleterious effects of RDB-induced malnutrition on the somatic development and maturation of the nervous system (NS).

We evaluated the effects of moderate-to low-intensity physical training during gestation on reflex ontogeny in neonate rats whose mothers were undernourished. Virgin female Wistar rats were divided into four groups as follows: untrained (NT, n 7); trained (T, n 7); untrained with a low-protein diet (NT þ LP, n 7); trained with a low-protein diet (T þ LP, n 4). Trained rats were subjected to a protocol of moderate physical training on a treadmill over a period of 4 weeks (5 d/week and 60 min/d, at 65 % of VO 2max ). After confirming the pregnancy, the intensity and duration of the exercise were reduced. Low-protein groups were provided with an 8 % casein diet, and controls were provided with a 17 % casein diet. Their respective offspring were evaluated (during the 10th -17th days of postnatal life) in terms of physical feature maturation, somatic growth and reflex ontogeny. Pups born to mothers provided with the low-protein diet during gestation and lactation showed delayed physical feature and reflex maturation and a deficit in somatic growth when compared with controls. However, most of these deficiencies were attenuated in pups of undernourished mothers undergoing training. In conclusion, physical training during gestation attenuates the effects of perinatal undernutrition on some patterns of maturation in the central nervous system during development.

FFMFat-free mass KTK K€ orper Koordination Test f€ ur Kinder VO 2max Maximal oxygen consumption AIM The aim of this study was to analyse the influence of birthweight on motor performance and body composition in children. Further, we investigated whether associations between birthweight and motor performance changed after adjustment for current height, body mass index (BMI), fat-free mass (FFM), and % body fat.METHOD A total of 483 children (251 males and 232 females) aged 7 to 10 years (mean 8.78, SD 1.0y) born in Vit oria Santo Antão (northeast Brazil) were sampled. Motor performance was operationalized using different physical fitness components and gross motor coordination. Physical fitness was measured by handgrip strength, muscle endurance, explosive power, flexibility, agility, running speed, and maximal oxygen consumption (VO 2max ). Gross motor coordination was evaluated by means of the K€ orper Koordination Test f€ ur Kinder (KTK).RESULTS Positive correlations between birthweight and height, BMI, and FFM were found.Birthweight was positively correlated with handgrip strength and negatively correlated with 20-meter sprint time, even after controlling for age, height, BMI, FFM, and % body fat. Birthweight was negatively associated with relative VO 2max (mL/kg/min); however, the association was no longer significant after inclusion of BMI or FFM in the model. INTERPRETATIONBirthweight significantly predicted height, BMI, FFM, and performance in strength and velocity tests, but did not influence gross motor coordination.Physical activity and fitness have a protective effect on metabolic risk factors during childhood, 1 as well as on premature morbidity and mortality in adulthood. 2,3 Poor motor performance could lead to reduced participation in physical activity and sports, which could potentially increase the health risks associated with physical inactivity. Thus, a better understanding of the determinants of poor motor performance may lead to the development of better intervention strategies with the long-term potential of improving physical activity and health.Previous studies have indicated that low birthweight is associated with faster infant growth, abdominal fat accumulation, high blood pressure during adolescence, and the risk of metabolic diseases in adulthood. 4 A recent metaanalysis conducted by Yu et al. 5 showed that low birthweight was associated with decreased odds of obesity (OR 0.61; 95% CI 0.46-0.80), while high birthweight (>4000g) was associated with increased odds of obesity (OR 2.07; 95% CI 1.91-2.24). Similarly, low birthweight was also associated with a decreased odds of overweight (OR 0.67; 95% CI 0.59-0.76), while high birthweight (>4000g) was associated with increased odds of overweight (OR 1.66; 95% CI 1.55-1.77).6 Using a twin sample (aged 8.9y old), a previous study reported that birthweight accounted for up to 11% of the total variance of neuromotor performance. 7 Our previous study showed that low birthweight alone cannot be considered as a biological determinant of physi...

This combined analysis suggests that LBW alone can be not considered as a biological determinant of growth, body composition, or physical fitness in children, but is a predictor of muscle strength and running speed.

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The goal of the present study was to investigate morphological changes in the serotonergic neurons/terminals in the dorsal (DR) and median (MnR) raphe nuclei and on the hippocampal dentate gyrus (DG) in neonatal rats treated from the 1st to the 21st postnatal day with fluoxetine (10 mg/kg sc, daily) or drug vehicle (0.9% saline 1 ml/kg). The results show that postnatal chronic treatment with fluoxetine promoted: (1) a smaller body weight increase during the pre-weaning period; (2) smaller number of 5-HT neurons in the DR; (3) smaller 5-HT neuronal cell bodies (area, perimeter and diameter) in the DR and the MnR and (4) diminished serotonergic terminals in the DG. These data suggest that the development of the serotonergic system was impaired and that early exposure to fluoxetine damaged the morphology of 5-HT neurons in young adult rats. While these findings are consistent with other work, more studies are needed to better clarify the effects of postnatal chronic treatment with fluoxetine on the serotonergic system and, consequently, on the functions modulated by serotonin.