ABC | Volume 114, Nº1, January 2019

Short Editorial The Impact Of Exercise On Inflammation, Oxidative Stress And Remodelling In Cardiac Muscle Fernando Mendes 1,2,3, 4 a nd Diana Martins 1,5 Politécnico de Coimbra - Departamento de Ciências Biomédicas Laboratoriais ESTeSC, 1 Coimbra – Portugal Consórcio CNC.IBILI/ Centro de Biomedicina Inovadora e Biotecnologia (CIBB), Universidade de Coimbra, 2 Coimbra – Portugal Instituto de Biofísica e Instituto de Investigação Clínica e Biomédica de Coimbra (iCBR) área de Meio Ambiente Genética e Oncobiologia (CIMAGO), Faculdade de Medicina, Universidade de Coimbra, 3 Coimbra – Portugal European Association for Professions in Biomedical Sciences, 4 Bruxelles – Belgium I3S, Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 5 Porto – Portugal Short Editorial related to the article: Effects of Physical Training on the Myocardium of Oxariectomized LDLr Knockout Mice: MMP 2/9, Collagen I/III, Inflammation and Oxidative Stress Mailing Address: Fernando Mendes • Escola Superior de Tecnologia da Saúde de Coimbra - Departamento de Ciências Biomédicas Laboratoriais, Gabinete 1.9 - Rua 5 de Outubro - SM Bispo - Apartado 7006. Postal Code 3046-854 Coimbra – Portugal E-mail: fjmendes@estescoimbra.pt Keywords Coronary Artery Disease; Exercise; Menopause; Dyslipidemias; Physical activity; Collagen; Oxidative Stress; Inflammation; Mice. DOI: https://doi.org/10.36660/abc.20190735 Aging is naturally connected with a decline, in some if not all physiological functions, namely loss of bone mass density (BMD) and strength associated with the loss of muscle mass. 1-3 This muscle loss happens mainly due to an imbalance between muscle protein synthesis and muscle protein breakdown. The increase of catabolic factors such as oxidative stress and inflammation contribute significantly to the above process. Nevertheless, the weakening of strength and muscle loss is not linear, occurring differently in all sexes. Other factors such as a decline in hormonal levels due to menopause phenomenon are thought to be also implicated in this process. 1 In fact, some authors proposed that, in females, an accelerated loss of muscle mass and strength arises at an earlier age than in males, around the time of menopause. 1 A good body of evidence supports that the decline in muscle mass may be in line with the estrogen decrease that typifies menopausal years. 3 The present study published at Arquivos Brasileiros de Cardiologia by Brianezi et al. 4 proposed to investigate the aerobic exercise training on the left ventricle in low-density lipoprotein (LDL) knockout ovariectomized mice, mimicking the effects of menopause, exercise and its effects on muscles of the mouse. It is well known that estrogen decrease contributes to the loss of BMD, as well as to the redistribution of subcutaneous fat to the visceral area, associated to an increased risk of cardiovascular disease, affecting the quality of life of females. To worsen the undesirable impact of menopause on female’s health, the decrease in estrogen levels may also have a direct effect on muscle tissue. 1,3 In order to better understand the above-mentioned effects, Ledimar et al. , 4 design the following experiment; a group of thirty animals were divided into 6 groups, each with 5 mice: non-ovariectomized sedentary control, ovariectomized sedentary control, ovariectomized trained control, non‑ovariectomized sedentary LDL knockout, ovariectomized sedentary LDL knockout, ovariectomized LDL knockout trained. The animals were ovariectomized at 9 months according to the protocol described, after that the animals were exposed to two different tests, one regarding the max training test and a second one training exercises. Then animals were euthanized and parameters such as the average volume density type I and III collagen fibres, matrix metalloproteinases (MMP) 2 and 9, oxidative stress (OS) were analysed. Their results revealed that the exercise protocol altered the volume of collagen fibres in type I and collagen remodelling parameters namely MMP-2, and further reduced the OS parameter of 8-hydroxy-2’-deoxyguanosine (8-OhdG). In females, aging of the vascular system only occurs due to a decline of ovarian function along with the decline in associated circulating hormones, in particular estrogen. 5 Although the risk factors, age and estrogen deficiency are well characterized, the mechanism of estrogen action in the vasculature compromised by aging are not well determined. Inflammation is associated with the aging of the vascular system, mainly due to the elevated levels of proinflammatory cytokines, such as tumour necrosis factor (TNF), which is also known to induce MMP. For example, MMP2 can specifically cleavage big endothelin-1, suggesting the role of this proteolytic enzyme in the vascular wall. Also, an interesting study found increased MMP2 activity in the mesenteric arteries from aged/estrogen-deficient animals, which was restored when the animals were treated with an anti‑inflammatory agent targeting TNF. 6 Also, the major source of MMP-9 are leucocytes, major key players in inflammatory process, suggesting that MMPs are critical modulators of vascular disease in an aging/estrogen-deficient model. Although estrogen replacement had been proposed for the management of cardiovascular risk associated with aging in female, its efficacy is controversial. Physical activity seems to be an effective alternative to estrogen supplementation in post-menopausal females, improving aerobic fitness and physiological adaptations of the cardiovascular system. 7-9 There is some intriguing evidence related to the loss of estrogen in mice showing a role in muscle contractile properties. Wohlers et al. 10 studied the contractile properties 106