The present study investigated the effects of acute melatonin administration on the biomarkers of energy substrates, GLUT4, and FAT/CD36 of skeletal muscle and its performance in rats subjected to exhaustive swimming exercise at an intensity corresponding to the maximal aerobic capacity (tlim). The incremental test was performed to individually determine the exercise intensity prescription and 48 h after, the animals received melatonin (10 mg·kg⁻¹) or vehicles 30 min prior totlim. Afterwards, the animals were euthanized 1 or 3 h after the exhaustion for blood and muscles storage. The experiment 1 found that melatonin increased the content of glycogen and GLUT4 in skeletal muscles of the animals that were euthanized 1 (p < 0.05; 22.33% and 41.87%) and 3 h (p < 0.05; 37.62% and 57.87%) after the last procedures. In experiment 2, melatonin enhanced thetlim (p = 0.01; 49.42%), the glycogen content (p < 0.05; 40.03%), GLUT4 and FAT/CD36 in exercised skeletal muscles (F = 26.83 and F = 25.28, p < 0.01). In summary, melatonin increased energy substrate availability prior to exercise, improved the exercise tolerance, and accelerated the recovery of muscle energy substrates after thetlim, possibly through GLUT4 and FAT/CD36.

A deficit of estrogen is associated with energy substrate imbalance, raising the risk of metabolic diseases. Physical training (PT) is a potent metabolic regulator through oxidation and storage of substrates transported by GLUT4 and FAT CD36 in skeletal muscle. However, little is known about the effects of PT on these carriers in an estrogen-deficit scenario. Thus, the aim of this study was to determine the influence of 12 weeks of PT on metabolic variables and GLUT4 and FAT CD36 expression in the skeletal muscle of animals energetically impaired by ovariectomy (OVX). The trained animals swam 30 min/day, 5 days/week, at 80% of the critical load intensity. Spontaneous physical activity was measured biweekly. After training, FAT CD36 and GLUT4 expressions were quantified by immunofluorescence in the soleus, as well as muscular glycogen and triglyceride of the soleus, gluteus maximus and gastrocnemius. OVX significantly reduced FAT CD36, GLUT4 and spontaneous physical activity (p < 0.01), while PT significantly increased FAT CD36, GLUT4 and spontaneous physical activity (p < 0.01). PT increased soleus glycogen, and OVX decreased muscular triglyceride of gluteus maximus. Therefore, OVX can cause energy disarray through reduction in GLUT4 and FAT CD36 and their muscle substrates and PT prevented these metabolic consequences, masking ovarian estrogen’s absence.

Metabolic diseases are associated with hypoestrogenism owing to their lower energy expenditure and consequent imbalance. Physical training promotes energy expenditure through PGC-1α and NRF-1, which are muscle proteins of the oxidative metabolism. However, the influence of physical training on protein expression in individuals with hypoestrogenism remains uncertain. Thus, the aim of this study is to determine the effect of 12 weeks of moderate-intensity swimming training on the muscle expression of PGC-1α, NRF-1, glycogen and triglyceride in ovariectomised rats. OVX and OVX+TR rats were subjected to ovariectomy. The trained animals swam for 30 minutes, 5 days/week, at 80% of the critical load intensity. Soleus was collected to quantify PGC-1α and NRF-1 expressions, while gastrocnemius and gluteus maximus were collected to measure glycogen and triglyceride. Blood glucose was also evaluated. Whereas ovariectomy decreased PGC-1α expression (p<0.05) without altering NRF-1 (p=0.48), physical training increased PGC-1α (p<0.01) and NRF-1 (p<0.05). Ovariectomy reduced glycogen (p<0.05) and triglyceride (p<0.05), whereas physical training increased glycogen (p<0.05) but did not change triglyceride (p=0.06). Ovariectomy increased blood glucose (p<0.01), while physical training reduced it (p<0.01). In summary, 12 weeks of individualized and moderate-intensity training were capable of preventing muscle metabolic consequences caused by ovariectomy.

Background and Objectives: The hormonal state of hypoestrogenism is associated with the accumulation of white adipose tissue, which can induce an increase in pro-inflammatory markers, leading to progressive health complications. Melatonin can act on adipose tissue mass, promoting its reduction and influencing inflammation, reducing IL-6 and releasing IL-10, pro- and anti-inflammatory markers, respectively. However, the role of melatonin regarding such parameters under the context of hypoestrogenism remains unknown. The aim of this study was to determine the effect of 12 weeks of hypoestrogenism and melatonin on white adipose tissue mass and circulating levels of IL-6, IL-10, TGF-β-1, and leukotriene C4 (LTC4). Materials and Methods: The animals (Wistar rats with sixteen weeks of age at the beginning of the experiment) under hypoestrogenism were submitted to the surgical technique of bilateral ovariectomy. The animals received melatonin (10 mg·kg⁻¹) or vehicles by orogastric gavage every day for 12 weeks and administration occurred systematically 1 h after the beginning of the dark period. White adipose tissue (perigonadal, peritoneal, and subcutaneous) was collected for mass recording, while blood was collected for the serum determination of IL-6, IL-10, TGF-β-1, and LTC4. Results: Hypoestrogenism increased the perigonadal and subcutaneous mass and IL-6 levels. Melatonin kept hypoestrogenic animals in physiological conditions similar to the control group and increased thymus tissue mass. Conclusions: Hypoestrogenism appears to have a negative impact on white adipose tissue mass and IL-6 and although melatonin commonly exerts a significant effect in preventing these changes, this study did not have a sufficiently negative impact caused by hypoestrogenism for melatonin to promote certain benefits.

This study investigated whether, 24 hours after the exercise-induced muscle damage protocol (EIMDP), melatonin administration performed 30 minutes prior to the protocol exhibited responses about inflammatory and redox status. Control (CG), exercised (EG), and exercised+melatonin (EMG) groups were submitted to the incremental test through swimming exercise to determine the intensity of the maximal aerobic capacity (iMAC). Melatonin (10 mg kg⁻¹) was administered, and after 30 min, the EIMDP was induced through swimming exercise (10 sets of 1 min with 30-s interval at 120% of iMAC, followed by 20 minutes continuous exercise at 100% of iMAC). The animals were euthanized 24 hours after the EIMDP. No effect on superoxide dismutase but lower activities (p<0.05) of glutathione S-transferase for EMG in relation to EG and of catalase for EMG in relation to CG were observed. EMG showed lower (p<0.05) carbonylated protein and lipid peroxidation in relation to EG and CG, respectively. Hematoxylin–eosin (HE) demonstrated higher connective tissue for EG in relation to EMG. Integrated Biomarker Responses version 2 attested the melatonin capacity in reducing antioxidant enzyme activity and muscle oxidative damage. This study demonstrated the protective role of melatonin in reducing muscle oxidative stress caused after 24 hours of the EIMDP. Received: 29 October 2024 Accepted after revision: 21 August 2025 Article published online: 10 September 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany