ABSTRACT
Decreased anabolic androgen levels are followed by impaired brain energy support and sensing with loss of neural connectivity during physiological aging, providing a neurobiological basis for hormone supplementation. Here, we investigated whether nandrolone decanoate (ND) administration mediates hypothalamic AMPK activation and glucose metabolism, thus affecting metabolic connectivity in brain areas of adult and aged mice. Metabolic interconnected brain areas of rodents can be detected by positron emission tomography using 18FDG-mPET. Albino CF1 mice at 3 and 18 months of age were separated into 4 groups that received daily subcutaneous injections of either ND (15 mg/kg) or vehicle for 15 days. At the in vivo baseline and on the 14th day, brain 18FDG-microPET scans were performed. Hypothalamic pAMPKT172/AMPK protein levels were assessed, and basal mitochondrial respiratory states were evaluated in synaptosomes. A metabolic connectivity network between brain areas was estimated based on 18FDG uptake. We found that ND increased the pAMPKT172/AMPK ratio in both adult and aged mice but increased 18FDG uptake and mitochondrial basal respiration only in adult mice. Furthermore, ND triggered rearrangement in the metabolic connectivity of adult mice and aged mice compared to age-matched controls. Altogether, our findings suggest that ND promotes hypothalamic AMPK activation, and distinct glucose metabolism and metabolic connectivity rearrangements in the brains of adult and aged mice.
Subject(s)
Anabolic Agents , Nandrolone , AMP-Activated Protein Kinases/metabolism , Anabolic Agents/metabolism , Animals , Brain/diagnostic imaging , Brain/metabolism , Dietary Supplements , Fluorodeoxyglucose F18 , Glucose/metabolism , Mice , Nandrolone/metabolism , Nandrolone/pharmacology , Nandrolone Decanoate , Positron-Emission TomographyABSTRACT
AIM: Since studies on resistance exercise and oxidative stress markers show contradictory results, it is not clear whether different intensities of exercise are the determinant of changes in such markers. The objective of this study was to investigate the acute effects of different intensities of resistance exercise on lipid peroxidation and total glutathione in previously resistance trained men. METHODS: Eight male subjects with at least 2 years of resistance training experience performed two different resistance exercise protocols: low-intensity (LI), 60% of one repetition maximum (1RM) and high-intensity (HI), 85% of 1RM. Both protocols involved seven exercises and subjects performed one set of each exercise. Blood samples were obtained before and immediately after exercise for lipid peroxidation and total glutathione analysis. RESULTS: The results indicated a significant difference in total workload (load multiplied by repetitions performed) between the LI and HI protocols (P<0.05) and no differences on lipid peroxidation and total glutathione after both LI and HI protocols. CONCLUSION: This study suggests that resistance exercise protocols composed of a single set of seven exercises, regardless of the intensity or total workload do not induce to oxidative stress, suggesting that volume is the main variable to induce oxidative stress in previously resistance trained individuals.
