Aerobic exercise training (AER) induces the browning of white adipose tissue, turning adipocytes multilocular, highly vascularized and expressing uncoupling protein 1 (UCP-1). The current study compared the efficiency of resistance to aerobic exercise training to promote a brown-like phenotype. Our results suggest that both types of training similarly induce subcutaneous and visceral adipose tissue browning.

Purpose: To compare the efficiency of an aerobic physical training program prescribed according to either velocity associated with maximum oxygen uptake (vVO2max) or peak running speed obtained during an incremental treadmill test (Vpeak_K) in mice.Methods: Twenty male Swiss mice, 60 days old, were randomly divided into two groups with 10 animals each: 1. group trained by vVO2max (GVO2), 2. group trained by Vpeak_K (GVP). After the adaptation training period, an incremental test was performed at the beginning of each week to adjust training load and to determine the amount of VO2 and VCO2 fluxes consumed, energy expenditure (EE) and run distance during the incremental test. Mice were submitted to 4 weeks of aerobic exercise training of moderate intensity (velocity referring to 70% of vVO2max and Vpeak_K) in a programmable treadmill. The sessions lasted from 30 to 40 min in the first week, to reach 60 min in the fourth week, in order to provide the mice with a moderate intensity exercise, totaling 20 training sessions.Results: Mice demonstrated increases in VO2max (ml·kg−1·min−1) (GVO2 = 49.1% and GVP = 56.2%), Vpeak_K (cm·s−1) (GVO2 = 50.9% and GVP = 22.3%), EE (ml·kg−0,75·min−1) (GVO2 = 39.9% and GVP = 51.5%), and run distance (cm) (GVO2 = 43.5% and GVP = 33.4%), after 4 weeks of aerobic training (time effect, P < 0.05); there were no differences between the groups.Conclusions: Vpeak_K, as well as vVO2max, can be adopted as an alternative test to determine the performance and correct prescription of systemized aerobic protocol training to mice.

Deletion of mTORC2 essential component Rictor by a Cre recombinase under control of the broad, non-adipocyte specific aP2/FABP4 promoter impairs thermoregulation and brown adipose tissue (BAT) glucose uptake upon acute cold exposure. We investigated herein whether adipocyte-specific mTORC2 deficiency affects BAT and inguinal white adipose tissue (iWAT) signaling, metabolism and thermogenesis in cold-acclimated mice. For this, 8-weeks old male mice bearing Rictor deletion and therefore mTORC2 deficiency in adipocytes (adiponectin-Cre) and littermates controls were either kept at thermoneutrality (30 ± 1ºC) or cold-acclimated (10 ± 1ºC) for 14 days and evaluated for BAT and iWAT signaling, metabolism and thermogenesis. Cold acclimation inhibited mTORC2 in BAT and iWAT, but its residual activity is still required for the cold-induced increases in BAT adipocyte number, total UCP-1 content and mRNA levels of proliferation markers Ki67 and cyclin 1D and de novo lipogenesis enzymes ATP-citrate lyase and acetyl-CoA carboxylase. In iWAT, mTORC2 residual activity is partially required for the cold-induced increases in multilocular adipocytes, mitochondrial mass and UCP-1 content. Conversely, BAT mTORC1 activity and BAT and iWAT glucose uptake were upregulated by cold independently of mTORC2. Noteworthy, the impairment in BAT and iWAT total UCP-1 content and thermogenic capacity induced by adipocyte mTORC2 deficiency had no major impact on whole-body energy expenditure in cold-acclimated mice due to a compensatory activation of muscle shivering. In conclusion, adipocyte mTORC2 deficiency impairs, through different mechanisms, BAT and iWAT total UCP-1 content and thermogenic capacity in cold-acclimated mice, without affecting glucose uptake and whole-body energy expenditure.

No abstract