ABC | Volume 114, Nº1, January 2019

Short Editorial Mendes & Martins Effects of physical training in remodelling, inflammation and oxidative stress Arq Bras Cardiol. 2020; 114(1):106-108 of ovariectomized mice muscle, has demonstrated the lower capability of activating adenosine monophosphate kinase (AMPK) phosphorylation. 10 This protein is important for glucose uptake and lipid oxidation inmuscle, being implicated in energy production, needed to produce muscle contractions. 1,11,12 Associated to physical activity is the generation of reactive species of oxygen (ROS) that may damage cell membranes lipids, proteins as well as both mitochondrial and nuclear DNA in case of oxidative stress, that can result in serious or mortal cellular injury. 13,14 Novais et al. 15 reported that with eight weeks of exercise training in the trained hypertensive menopausal group, aerobic training was effective in promoting an increase in superoxide dismútase (SOD) and catalase, antioxidant agents, which have a crucial role in oxidative stress modulation. Also in animal studies, Claudio et al . 16 demonstrated that eight weeks of interval training programs significantly increased SOD and catalase expression, contributing to the reduction of cardiac superoxide production in rats with ovariectomized, in this case with hypertension, which may prevent coronary heart disease in hypertensive postmenopausal women. 1,7,14 Brianezi et al. 4 conclude that moderate-intensity aerobic training acts on the volume of collagen fibres and on the collagen remodelling, with reduced oxidative stress in left ventricles of mice ovariectomized LDLr Knockout. It is known that after menopause, different factors contribute to the decline in muscle mass, the combination of physical inactivity, protein intake and oxidative stress 16 clearly contribute the increase to this process. 16 Associated with the oxidative stress increase, characterized by the imbalance between the production and the removal of free radicals, usually due to an inadequate antioxidant system. 16,17 Oxidative stress is related to a higher ROS production from the mitochondria, which can induce cell apoptosis. 18 Meaning that the mitochondrial DNA may be damaged due to oxidative stress, affecting mitochondria capacity to produce energy, contributing to a higher susceptibility to apoptosis which finally intensifies muscle fibre atrophy or death and muscle mass decrease. 1 Taking together, the results of Brianeziet et al . 4 conclude that physical exercise contributes positively influencing the control and dyslipidemic groups in the parameter of density and volume of collagen fibres of type I and the control group in relation to oxidative stress. The mechanisms underlying the pathophysiology of menopausal alterations are complex and implicate estrogen-MMP-metabolic deregulation with age-driven vascular changes. Acknowledgements Foundation for Science and Technology (FCT), Portugal (Strategic Projects UID/NEU/04539/2013 and UID/ NEU/04539/2019), and COMPETE-FEDER (POCI-01-0145- FEDER-007440). 1. MaltaisML, Desroches J,Donne IJ. Changes inmusclemass and strength after enopause. J Musculoskelet Neuronal Interact. 2009;9(4):, 186–97. 2. Carter CS, Justice JN,Thompson L. Lipotoxicity, aging, and muscle contractility: does fiber type matter? GeroScience.2019;41(3);297-308. 3. Calmels P, Vico L, Alexandre C, Minaire P. Cross-sectional study of muscle strength and bone mineral density in a population of 106 women between the ages of 44 and 87 years: relationship with age and menopause. Eur J Appl Physiol Occup Physiol.1995;70(2):180-6. 4. Brianezi L, Ornelas E, Gehrke FS, Fonseca LA, Alves BC, Sousa VA, et al. Efeitos do treinamento físico sobre o miocárdio de camundongos LDLr Knockut ovariectomizadas: MMP -2c-9, Colageno I/II, inflamação e estresse oxidativo. Arq Bras Cardiol. 2020; 114(1):100-105. 5. Lurbe E, Cifkova R, Cruickshank JK, Dillon MJ, Ferreira I, Invitti C, et al. Management of high blood pressure in children and adolescents: recommendations of the European Society of Hypertension. J. Hypertens.2009;27(2):1719-42. 6. Lekontseva O, Jiang Y, Davidg ST. Estrogen replacement increases matrix metalloproteinase contribution to vasoconstriction in a rat model of menopause. J Hypertens.2009;27(8):1602-8. 7. Lin YY, Lee SD. Cardiovascular Benefits of Exercise Training in Postmenopausal Hypertension. Int J Mol Sci.2018;9.pii e2523 8. Myers J. Cardiology patient pages. Exercise and cardiovascular health. Circulation.2003;107(1):e2-5. 9. Fagard FH. Exercise Therapy in Hypertensive Cardiovascular Disease. Prog Cardiovasc Dis.2011;53(6):404-11. 10. Wohlers L M,Sweeney SM., Ward CW, Lovering R M, Spangenburg E E. Changes in contraction-induced phosphorylation of AMP-activated protein kinase and mitogen-activated protein kinases in skeletal muscle after ovariectomy. J Cell Biochem. 2009; 107(1):171-8. 11. Jørgensen S B, Richter E A, Wojtaszewski J] F P. Role of AMPK in skeletal muscle metabolic regulation and adaptation in relation to exercise. J Physiol.2006;574(Pt1):17-31. 12. OslerME, Zierath JR. Minireview: Adenosine 5’-Monophosphate-Activated Protein Kinase Regulation of Fatty Acid Oxidation in Skeletal Muscle. Endocrinology.2008;149(3):935-41. 13. Cheng TL,Lin YY, Su CT, Hu CC, Yang AL. Improvement of Acetylcholine- Induced Vasodilation by Acute Exercise in Ovariectomized Hypertensive Rats. Chin J Physiol. 2016;59(3):165-72. 14. Claudio ER, Almeida SA, Mengal V, Brasil GA, Santuzzi CH, Tiradentes RV. Swimming training prevents coronary endothelial dysfunction in ovariectomized spontaneously hypertensive rats. Braz J Med Biol Res. 2017;50(1):e5495 15. Novais IP, Jarrete AP, Puga G, Araujo HN, Delbin MA, Zanesco A. Effect of aerobic exercise training on GMP levels and blood pressure in treated hypertensive postmenopausal women. Motriz. 2017;23(1):1-6. References 107