In vitro effects of exercise on the heart

Abstract

Pathologic and physiologic factors acting on the heart can produce consistent pressure changes, volume overload, or increased cardiac output. These changes may then lead to cardiac remodeling, ultimately resulting in cardiac hypertrophy. Exercise can also induce hypertrophy, primarily physiologic in nature. To determine the mechanisms responsible for each type of remodeling, it is important to examine the heart at the functional unit, the cardiomyocyte. Tests of individual cardiomyocyte function in vitro provide deeper understanding of the changes occurring within the heart during hypertrophy. Examination of cardiomyocyte function during exercise primarily follows one of two pathways: the addition of hypertrophic inducing agents in vitro to normal cardiomyocytes, or the use of trained animal models and isolating cells following the development of hypertrophy in vivo. Due to the short lifespan of adult cardiomyocytes, a proportionately scant amount of research exists involving the direct stimulation of cells in vitro to induce hypertrophy. These attempts provide the only current evidence, as it is difficult to gather extensive data demonstrating cell growth as a result of in vitro physical stimulation. Researchers have created ways to combine skeletal myocytes with cardiomyocytes to produce functional muscle cells used to repair pathologic heart tissue, but continue to struggle with the short lifespan of these cells. While there have been promising findings regarding the mechanisms that surround cardiac hypertrophy in vitro, the translation of in vitro findings to in vivo function is not consistent. Therefore, the focus of this review is to highlight recent studies that have investigated the effect of exercise on the heart, both in vitro and in vivo.

Can fish oil supplementation and physical training improve oxidative metabolism in aged rat hearts?

“…When moderate exercise is practiced regularly, it can decrease the chances of dying from cardiovascular disease by the reduction of risk factors such as hypertension, obesity and hyperlipidemia, and physical activity; it also enhances longevity by mechanisms independent of these risk factors [15,16]. In addition, there are results demonstrating that moderate physical exercise plays a key role on reducing the risk of cardiovascular diseases in elderly subjects [17,18].…”

(Myocardium Remodelling: From Adaptation Mechanisms to Heart Failure Development)

“…Při tlakovém přetížení se vyvine koncentrická hypertrofi e, kardiomyocyty se individuálně rozšiřují zapojením nových sarkomer paralelně a tloušťka srdeční stěny se zvětší. 2,7 Pro zachování funkce komor při tlakovém přetížení není ovšem hypertrofi e vždy potřeba. Za určitých podmínek může představovat adaptivní i maladaptivní typ remodelace.…”

“…Většina sportovních aktivit kombinuje izotonický a izometrický druh svalové práce. 7,18,19 Pojem atletické srdce zahrnuje soubor remodelačních změn vzniklých v reakci na dlouhodobou opakovanou intenzivní fyzickou zátěž. Významný rozvoj atletického srdce byl popsán u osob věnujících se vytrvalostním sportům.…”

Energy Metabolism in Exercise-Induced Physiologic Cardiac Hypertrophy

“…Initially, the increasing expression of myocardial peroxisome proliferator-activated receptor (PPARα) was detected during treadmill training in mice ( Dobrzyn et al., 2013 ). Later, it was found that the level of PPARα also increased in exercise-induced physiologic hypertrophic cardiomyocytes ( Youtz et al., 2014 ). In addition, some experiments found that gene expression of PPARα was reduced in pathological cardiac hypertrophy, suggesting that upregulation of PPAR-α expression may limit pathological cardiac hypertrophy ( Barger et al., 2000 ).…”