Background:Adipose depots have different responses when subjected to certain situations. Sertie et al. shown in periepididymal white adipose tissue that physical detraining reversed
adaptations acquired through continuous training sessions increasing rate of weight gain.
Methods:Used Wistar rats of 6 weeks under standard conditions of temperature, 12/12h cycle, food and water ad libitum. The treadmill training was an intensity of 50-60% of the maximum
capacity. A group trained daily 60min, 5X per week for 12 weeks (T); another trained for 8wk (D) and then detraining for 4wk and a sedentary group (S). The metabolic assay of oxidation and lipogenesis
was realized from glucose marked with 14C and the radiation was measured by beta counter. The activity of citrate synthase (CS) was determined by the method described by Alp et al. Statistical
analysis was performed by T student test and ANOVA.
Results:The body weight of rats S (392g +/-26) and T (348g +/-26) in the 8th wk and at end of the protocol showed significant differences. The water consumption exhibit no
differences. The food intake in the first 8 weeks was significantly different between S (26g +/-2) and T (24g +/-2). The depot of mesenteric fat presented no difference between the groups S (2,4g
+/-0,9), T (2,2g +/-0,7) and D (2,1g +/-0,5). Isolated adipocytes showed an increase in cell diameter of D (64µm +/-16) compared to T (52µm +/-5). Glucose oxidation showed increase at basal condition
in D when compared with S, and on maximum stimulation T and D exhibited increased in regarding S. The basal lipogenesis not presented difference between none of the groups. However, when maximally
stimulated with insulin T reveal increment in regarding S. The trails of CS showed no statistical differences.
Conclusions: Physical training developed in the first 8 weeks of the protocol showed the ability to reduce the increase at the body weight by T compared to S. The group D was able to
reverse the consequences of physical training. The diameter of adipocytes showed a cellular hypertrophy by group D, despite the depot weight not shown differences, possibly due to cell turnover
(balance apoptosis and adipogenesis). There was an increase of oxidative process in T that could be explained by the increase in energy expenditure inherent of the exercise and the energy necessary to
achievement of the lipogenesis. On D the detraining time was unable to reverse the oxidative increase caused by the training, when the cell maximally stimulated by insulin. However, the response to
detraining is visible in lipogenesis, leading to suggest that the weight increase found must occur days after the start of detraining.