Can Exercise Teach Us How to Treat Heart Disease?
Cardiovascular Division, Beth Israel Deaconess Medical Center, 3 Blackfan Circle, CLS-9, Boston, MA 02215. . Circulation
(Impact Factor: 14.43).
11/2012; 126(22):2625-35. DOI: 10.1161/CIRCULATIONAHA.111.060376
Available from: Joao A Paulo
- "The health benefits of physical activity and exercise are well recognized (Hawley et al., 2014; Mann and Rosenzweig, 2012; Voss et al., 2013). Exercise is the first line of therapy for various metabolic diseases like diabetes and obesity, but exercise also improves outcomes in diseases involving other tissues, such as the heart and brain. "
[Show abstract] [Hide abstract]
ABSTRACT: Exercise provides many health benefits, including improved metabolism, cardiovascular health, and cognition. We have shown previously that FNDC5, a type I transmembrane protein, and its circulating form, irisin, convey some of these benefits in mice. However, recent reports questioned the existence of circulating human irisin both because human FNDC5 has a non-canonical ATA translation start and because of claims that many human irisin antibodies used in commercial ELISA kits lack required specificity. In this paper we have identified and quantitated human irisin in plasma using mass spectrometry with control peptides enriched with heavy stable isotopes as internal standards. This precise state-of-the-art method shows that human irisin is mainly translated from its non-canonical start codon and circulates at ∼3.6 ng/ml in sedentary individuals; this level is increased to ∼4.3 ng/ml in individuals undergoing aerobic interval training. These data unequivocally demonstrate that human irisin exists, circulates, and is regulated by exercise.
Copyright © 2015 Elsevier Inc. All rights reserved.
Cell metabolism 08/2015; 22(4). DOI:10.1016/j.cmet.2015.08.001 · 17.57 Impact Factor
Available from: Camila Ferreira Leite
- "In cardiac hypertrophy associated with pathological processes, it has been shown that CSCs participate in the reparative processes (Ellison et al., 2013; Leri et al., 2005); however, extensive damage cannot be completely reversed, indicating that the regenerative potential of these stem cells during a damage challenge is limited (Chan et al., 2009; Hatzistergos et al., 2010B; Bailey et al., 2009). For the physiological cardiac hypertrophy observed in exercise training (Waring et al., 2014; Xiao et al., 2014b), pregnancy (Xiao et al., 2014a) or postnatal growth (Mann and Rosenzweig, 2012), little is known about the role of resident CSCs. Waring et al. (2014) have demonstrated that c-Kit + CSCs play an active role during physiological cardiac hypertrophy in mice specifically for exercise training. "
[Show abstract] [Hide abstract]
ABSTRACT: Physical activity evokes well-known adaptations in the cardiovascular system. Although exercise training induces cardiac remodeling, whether multipotent stem cells play a functional role in the hypertrophic process remains unknown. To evaluate this possibility, C57BL/6 mice were subjected to swimming training aimed at achieving cardiac hypertrophy, which was morphologically and electrocardiographically characterized. Subsequently, c-Kit(+)Lin(-) and Sca-1(+)Lin(-) cardiac stem cells (CSCs) were quantified using flow cytometry while cardiac muscle-derived stromal cells (CMSCs, also known as cardiac-derived mesenchymal stem cells) were assessed using in vitro colony-forming unit fibroblast assay (CFU-F). Only the number of c-Kit(+)Lin(-) cells increased in the hypertrophied heart. To investigate a possible extracardiac origin of these cells, a parabiotic eGFP transgenic/wild-type mouse model was used. The parabiotic pairs were subjected to swimming, and the wild-type heart in particular was tested for eGFP(+) stem cells. The results revealed a negligible number of extracardiac stem cells in the heart, allowing us to infer a cardiac origin for the increased amount of detected c-Kit(+) cells. In conclusion, the number of resident Sca-1(+)Lin(-) cells and CMSCs was not changed, whereas the number of c-Kit(+)Lin(-) cells was increased during physiological cardiac hypertrophy. These c-Kit(+)Lin(-) CSCs may contribute to the physiological cardiac remodeling that result from exercise training.
Copyright © 2015. Published by Elsevier B.V.
Stem Cell Research 05/2015; 170. DOI:10.1016/j.scr.2015.05.011 · 3.69 Impact Factor
Available from: Fabio Santos Lira
- "The metabolic, cardiovascular, autonomic, and anti-inflammatory benefits of a physically active life style have led many researchers to suggest exercise training (ET) as an important nonpharmacological tool in the prevention and treatment of CVD [7–11]. The effectiveness of ET as a great tool in the treatment of patients with established CAD (either with or without MI) has been widely reported in the literature [7, 12–16]. "
[Show abstract] [Hide abstract]
ABSTRACT: The cardiovascular autonomic imbalance in patients after myocardial infarction (MI) provides a significant increase in mortality rate, and seems to precede metabolic, hormonal, and immunological changes. Moreover, the reduction in the parasympathetic function has been associated with inflammatory response in different pathological conditions. Over the years, most of the studies have indicated the exercise training (ET) as an important nonpharmacological tool in the management of autonomic dysfunction and reduction in inflammatory profile after a myocardial infarction. In this work, we reviewed the effects of ET on autonomic imbalance after MI, and its consequences, particularly, in the post-MI inflammatory profile. Clinical and experimental evidence regarding relationship between alterations in autonomic regulation and local or systemic inflammation response after MI were also discussed.
Mediators of Inflammation 06/2014; 2014:702473. DOI:10.1155/2014/702473 · 3.24 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.