Key result
Physical detraining in rats significantly increased adipocyte cross-sectional area compared to continuous training and sedentary groups (3,474 vs 1,945.7 and 2,492.4 μm2, respectively; P<0.05).
Why the study?
Does physical detraining change metabolism and adipocyte cellularity in male Wistar rats?
Does physical detraining change metabolism and adipocyte cellularity in male Wistar rats?
Absolute Event Rate: 3474% vs 1945.7%
p-value: p=<0.05
Physical detraining in rats leads to significant adipocyte hypertrophy and increased lipogenic capacity, suggesting that adipose tissue changes after detraining are obesogenic.
Detraining may promote obesogenic adipose changes in rats; hypothesis-generating with no implications for human practice.
All of the adaptations acquired through physical training are reversible with inactivity. Although significant reductions in maximal oxygen uptake (Vo2max) can be observed within 2 to 4 wk of detraining, the consequences of detraining on the physiology of adipose tissue are poorly known. Our aim was therefore to investigate the effects of discontinuing training (physical detraining) on the metabolism and adipocyte cellularity of rat periepididymal (PE) adipose tissue. Male Wistar rats, aged 6 wk, were divided into three groups and studied for 12 wk under the following conditions: 1) trained (T) throughout the period; 2) detrained (D), trained during the first 8 wk and detrained during the remaining 4 wk; and 3) age-matched sedentary (S). Training consisted of treadmill running sessions (1 h/day, 5 days/wk, 50-60% Vo2max). The PE adipocyte size analysis revealed significant differences between the groups. The adipocyte cross-sectional area (in μm(2)) was significantly larger in D than in the T and S groups (3,474 ± 68.8; 1,945.7 ± 45.6; 2,492.4 ± 49.08, respectively, P < 0.05). Compared with T, the isolated adipose cells (of the D rats) showed a 48% increase in the ability to perform lipogenesis (both basal and maximally insulin-stimulated) and isoproterenol-stimulated lipolysis. No changes were observed with respect to unstimulated lipolysis. A 15% reduction in the proportion of apoptotic adipocytes was observed in groups T and D compared with group S. The gene expression levels of adiponectin and PPAR-gamma were upregulated by factors of 3 and 2 in D vs. S, respectively. PREF-1 gene expression was 3-fold higher in T vs. S. From these results, we hypothesize that adipogenesis was stimulated in group D and accompanied by significant adipocyte hypertrophy and an increase in the lipogenic capacity of the adipocytes. The occurrence of apoptotic nuclei in PE fat cells was reduced in the D and T rats; these results raise the possibility that the adipose tissue changes after detraining are obesogenic.
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Sertié et al. (2013) studied Physical detraining. Physical detraining vs. Continuous training or sedentary was evaluated on Adipocyte cross-sectional area (in μm2) (p=<0.05). Physical detraining in rats significantly increased adipocyte cross-sectional area compared to continuous training and sedentary groups (3,474 vs 1,945.7 and 2,492.4 μm2, respectively; P<0.05).
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