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Review
. 2014 Oct 29;116(2):67-73.
doi: 10.1016/j.lfs.2014.08.015. Epub 2014 Sep 8.

In vitro effects of exercise on the heart

Affiliations
Review

In vitro effects of exercise on the heart

Dane J Youtz et al. Life Sci. .

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.

Keywords: Exercise; Heart; Hypertrophy; Myocyte; Signaling mechanisms.

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References

    1. Barry SP, Townsend Pa, Latchman DS, Stephanou A. Role of the JAK-STAT pathway in myocardial injury. Trends in molecular medicine. 2007;13:82–9. - PubMed
    1. Bernardo BC, Weeks KL, Pretorius L, McMullen JR. Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. Pharmacology & therapeutics. 2010;128:191–227. - PubMed
    1. Berry JM, Naseem RH, Rothermel Ba, Hill Ja. Models of cardiac hypertrophy and transition to heart failure. Drug Discovery Today: Disease Models. 2007;4:197–206.
    1. Birla RK, Dow DE, Huang Y-C, Migneco F, Khait L, Borschel GH, et al. Methodology for the formation of functional, cell-based cardiac pressure generation constructs in vitro. In vitro cellular & developmental biology Animal. 2008;44:340–50. - PubMed
    1. Blaauw E, van Nieuwenhoven Fa, Willemsen P, Delhaas T, Prinzen FW, Snoeckx LH, et al. Stretch-induced hypertrophy of isolated adult rabbit cardiomyocytes. American journal of physiology Heart and circulatory physiology. 2010;299:H780–7. - PubMed

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