Abstract
Aerobic exercise confers many health benefits. However, numerous reports have shown that acute aerobic exercise can injure the heart. We tested the general hypothesis that acute moderate‐intensity exercise in rodents induces cardiomyocyte damage and stimulates mesenchymal stem cells (MSCs) to increase paracrine‐mediated protective effects on cardiomyocytes. A single session of treadmill running (13 m/min, 0% grade, for 45 min) in untrained C57BL/6 male mice (n = 18) increased cleaved poly ADP‐ribose polymerase (PARP), a marker of apoptosis, in the myocardium 24 h postexercise. Microarray analysis of mouse myocardium identified 11 relevant apoptotic genes and several shifts in matrix remodeling transcripts over the postexercise window. Postexercise cardiomyocyte death was recapitulated in neonatal rat cardiomyocytes (NRCMs) by culturing cells in 2% plasma harvested from exercised rats. The increased cell death observed in exercise‐treated NRCMs was attenuated by β‐adrenergic blockade, but not antioxidant treatment. MSC survival, proliferation, and chemotaxis showed no significant differences between sedentary and exercise plasma conditions, despite increased IL‐6, TNF‐α, IL‐1β, and IFN‐γ secretions from MSCs treated with exercise plasma. NRCM survival was increased nearly 500% when cocultured with MSCs, but this effect was not altered under exercise plasma culture conditions. Our results suggest acute moderate‐intensity aerobic treadmill running in exercise‐naïve rodents induces temporal cardiomyocyte death due to plasma‐borne factors, namely, catecholaminergic stress. Even though exercise conditions prompt an inflammatory response in MSCs, the exercise milieu does not alter the MSC‐protective phenotype on cardiomyocytes.
Highlights
Several studies have shown that the heart exhibits cardiomyocyte renewal mechanisms that persist throughout the life span (Bergmann et al 2009; van Berlo et al 2014)
We hypothesized that a single bout of treadmill exercise would induce apoptosis and prompt repair mechanisms by mesenchymal stem cells (MSCs) on the heart
Our results in rodents showed that myocardial apoptosis was induced in the heart 24 h postexercise, and was in part due to catecholaminergic stress, but not oxidative stress
Summary
Several studies have shown that the heart exhibits cardiomyocyte renewal mechanisms that persist throughout the life span (Bergmann et al 2009; van Berlo et al 2014). While cardiomyocyte renewal is a multifactorial process, stem cells are thought to play a regulatory role (van Berlo et al 2014). As MSC therapeutic potency is known to be stimulated after deleterious stimuli such as hypoxia and inflammation, their response to physiological stresses such as acute exercise has received limited attention. This is a significant issue because acute aerobic exercise has been shown by unknown mechanisms to induce transient a 2017 The Authors.
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