Voluntary Wheel Running and Pacing-Induced Dysfunction in Hypertension

Abstract

These data suggest that voluntary wheel running in SHR does not protect from pacing-induced myocardial dysfunction, and adenylyl cyclase agonism during pacing stress can functionally protect the heart. These data reiterate the importance of a competent myocardial beta-adrenergic signaling cascade.

Cardiac Effects of Exercise Training in Hypertension

“…us one of the major bene�ts of exercise training in hypertension is the preservation of cardiomyocyte cell number. Despite the potential for exercise training to increase myocardial mass in pressure overload, most studies have reported an improved phenotype aer training [25,30,46,61,[80][81][82][83][84][85][86][87]. One of the most proli�c bene�ts of exercise training is its improvement on adrenergic signaling.…”

Is exercise really deleterious for the hypertensive heart?

“…The authors emphatically concluded that 'high physical activity in hypertensives must be considered as an important risk factor rather than a therapeutic intervention' . Given that the results of this paper conflict with multiple exercise training studies in various models of pressure overload (Scheuer et al 1982;MacDonnell et al 2005;Konhilas et al 2006;Libonati & Gaughan, 2006;Reger et al 2006;Renna et al 2006;Kolwicz et al 2007Kolwicz et al , 2008Kolwicz et al , 2009Chicco et al 2008;Garciarena et al 2009;Libonati et al 2011;Rossoni et al 2011;Huang et al 2012;Marshall et al 2012), I feel it is imperative to further address its implications. Their paper is particularly interesting in light of reports in both humans (Oxbourough et al 2010;O'Keefe et al 2012) and animals (Schultz et al 2007;Huang et al 2009;Benito et al 2011) showing that extreme levels of exercise can, in fact, be damaging to the heart.…”

Modulation of Anthracycline-Induced Cardiotoxicity by Aerobic Exercise in Breast Cancer

“…This notion has not been examined in cancer models, however Kolwicz et al 74 found that exercise attenuated cardiomyocyte apoptosis, increased CPC proliferation by ~200% and augmented the presence of KIT positive cells (a stem cell factor crucial for the mobilization of progenitor cells to sites of injury) in the heart. 75 Together, this led to a higher abundance of cardiomyocytes in exercised relative to sedentary animals.…”