title: 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 a 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.
authors.affiliation: College of Nursing, The Ohio State University, Columbus, OH, USA.
authors.forename: Dane J
authors.initials: DJ
authors.lastname: Youtz
authors.affiliation: College of Medicine, The Ohio State University, Columbus, OH, USA.
authors.forename: Michael C
authors.initials: MC
authors.lastname: Isfort
authors.affiliation: College of Nursing, The Ohio State University, Columbus, OH, USA.
authors.forename: Clayton M
authors.initials: CM
authors.lastname: Eichenseer
authors.affiliation: College of Medicine, The Ohio State University, Columbus, OH, USA.
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Nelin
authors.affiliation: College of Nursing, The Ohio State University, Columbus, OH, USA; College of Medicine, The Ohio State University, Columbus, OH, USA; Department of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, OH, USA; Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH, USA. Electronic address: Loren.Wold@osumc.edu.
authors.forename: Loren E
authors.initials: LE
authors.lastname: Wold
mesh_terms: D000328:Adult; D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D015444:Exercise / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D018485:Muscle Fibers, Skeletal / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D020257:Ventricular Remodeling
keywords: Exercise; Heart; Hypertrophy; Myocyte; Signaling mechanisms