Abstract
Bone morphogenetic protein 4 (BMP4) plays an important role in bone remodeling and in heart failure pathogenesis. The aim of this study was to evaluate the effect of spontaneous physical activity on the expression of BMP4 in the heart and tibia of the transgenic (Tgαq*44) mice, representing a model of chronic heart failure. Tgαq*44 and wild‐type FVB mice (WT) were randomly assigned either to sedentary or to trained groups undergoing 8 weeks of spontaneous wheel running. The BMP4 protein expression in heart and tibiae was evaluated using Western immunoblotting and the phosphorus and calcium in the tibiae was assessed using the X‐ray microanalysis. BMP4 content in the hearts of the Tgαq*44‐sedentary mice was by ~490% higher than in the WT‐sedentary mice, whereas in tibiae the BMP4 content of the Tgαq*44‐sedentary mice was similar to that in the WT‐sedentary animals. Tgαq*44 mice revealed by ~28% poorer spontaneous physical activity than the WT mice. No effect of performed physical activity on the BMP4 content in the hearts of either in the Tgαq*44 or WT mice was observed. However, 8‐week spontaneous wheel running resulted in a decrease in the BMP4 expression in tibiae (by ~43%) in the group of Tgαq*44 mice only, with no changes in their bone phosphorus and calcium contents. We have concluded that prolonged period of spontaneous physical exercise does not increase the risk of the progression of the BMP4‐mediated pathological cardiac hypertrophy and does not affect bone mineral status in the chronic heart failure mice.
Highlights
Heart failure (HF) is a clinical syndrome characterized by a progressive deterioration of the cardiac function, leading to a decrease in capacity of the heart to meet the body requirements for blood flow (Grassi et al, 2017; Poole, Richardson, Haykowsky, Hirai, & Musch, 2018)
In this study we have found that: (a) the Bone morphogenetic protein 4 (BMP4) expression in the heart of the transgenic mouse model of chronic heart failure (Tgαq*4 mice) was about 490% higher than in the heart of the healthy (WT) mice, (b) the spontaneous physical activity of 8 weeks did not affect the BMP4 expression in the heart muscle of the Tgαq*4 mice nor in the wild-type FVB mice (WT) mice, (c) the performed physical activity decreased the BMP4 content in bone (~43%), but only in the group of Tgαq*44 mice, with no significant effect on the mineral part of bones
We have presented the impact of relatively long-lasting spontaneous physical activity on the BMP4 content in the heart and bone of the healthy mice and the mice with chronic heart failure
Summary
Heart failure (HF) is a clinical syndrome characterized by a progressive deterioration of the cardiac function, leading to a decrease in capacity of the heart to meet the body requirements for blood flow (Grassi et al, 2017; Poole, Richardson, Haykowsky, Hirai, & Musch, 2018). One of the most prominent effects of the endurance training on skeletal muscles is an increase in the mitochondrial enzyme activity (Holloszy, 1967), mitochondrial content (Hoppeler et al, 1985), and muscle mitochondria efficiency (Zoladz, Koziel, Woyda-Ploszczyca, Celichowski, & Jarmuszkiewicz, 2016), leading to an increase in the metabolic stability during exercise and enhancement of exercise tolerance (Dudley, Tullson, & Terjung, 1987; Korzeniewski & Zoladz, 2004; Zoladz, Grassi, & Szkutnik, 2019; Zoladz, Korzeniewski, & Grassi, 2006). At the heart muscle level, the endurance training has been shown to increase the activity/content of mitochondrial proteins (Momken, Lechêne, Ventura-Clapier, & Veksler, 2004) and mitochondrial volume and density (Vettor et al, 2014)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
