Exercise Training Post-MI Favorably Modifies Heart Extracellular Matrix in the Rat

Yengo, Christopher M.; Zimmerman, Scott; McCormick, Richard J.; Thomas, D. P.

doi:10.1249/mss.0b013e318244bc8a

Cited by 15 publications

(12 citation statements)

References 37 publications

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“…As a potential underlying mechanism of decreased scar thinning, LV collagen synthesis in the infarct area was significantly attenuated in exercised mice. This is in accordance with other reports (70,86). Matrix turnover is regulated by several factors, among which MMPs play a major role (51,61,67,78).…”

Section: H354 Exercise Limits Post-mi Scar Thinningsupporting

confidence: 93%

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Puhl

Müller

Wagner

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Although exercise mediates beneficial effects in patients after myocardial infarction (MI), the underlying mechanisms as well as the question of whether an early start of exercise after MI is safe or even beneficial are incompletely resolved. The present study analyzed the effects of exercise before and reinitiated early after MI on cardiac remodeling and function. Male C57BL/6N mice were housed sedentary or with the opportunity to voluntarily exercise for 6 wk before MI induction (ligation of the left anterior descending coronary artery) or sham operation. After a 5-day exercise-free phase after MI, mice were allowed to reexercise for another 4 wk. Exercise before MI induced adaptive hypertrophy with moderate increases in heart weight, cardiomyocyte diameter, and left ventricular (LV) end-diastolic volume, but without fibrosis. In sedentary mice, MI induced eccentric LV hypertrophy with massive fibrosis but maintained systolic LV function. While in exercised mice gross LV end-diastolic volumes and systolic function did not differ from sedentary mice after MI, LV collagen content and thinning of the infarcted area were reduced. This was associated with ameliorated activation of inflammation, mediated by TNF-␣, IL-1␤, and IL-6, as well as reduced activation of matrix metalloproteinase 9. In contrast, no differences in the activation patterns of various MAPKs or adenosine receptor expressions were observed 5 wk after MI in sedentary or exercised mice. In conclusion, continuous exercise training before and with an early reonset after MI ameliorates adverse LV remodeling by attenuating inflammation, fibrosis, and scar thinning. Therefore, an early reonset of exercise after MI can be encouraged. exercise; remodeling; scar thinning; magnetic resonance imaging; fibrosis; myocardial infarction NEW & NOTEWORTHY Our data provide new insights into the exercise-mediated cardioprotection by implying that an early reinitiation of exercise after myocardial infarction attenuates left ventricular fibrosis and scar thinning, presumably by attenuating the coordinated proinflammatory response involving TNF-␣, IL-6, and IL-1␤. These findings could translate into clinical benefits in patients.CORONARY ARTERY DISEASE is the single most frequent cause of death worldwide. In Europe, every sixth man and every seventh woman will die of myocardial infarction (MI) (71). Those patients who survive MI frequently develop systolic heart failure due to the infarct-induced loss of functional myocardium per se and remodeling of the remainder of the left ventricular (LV) myocardium, which is frequently associated with thinning of the LV wall in the area of MI and its border zone, LV dilation, and systolic dysfunction. These parameters of myocardial remodeling are important prognostic markers for the long-term outcome of these patients. For instance, regional wall thinning is associated with postinfarction ventricular arrhythmia (36) and adverse outcome in patients undergoing coronary artery bypass surgery (87).Scar formation occurs secondary to isc...

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Section: H354 Exercise Limits Post-mi Scar Thinningsupporting

confidence: 93%

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Puhl

Müller

Wagner

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…Exercise reduces adverse ventricular remodeling and cardiac dysfunction when initiated after infarction in animal models (Bansal et al, 2010; Wan et al, 2007; Xu et al, 2008; Xu et al, 2010; Yengo et al, 2012) and humans (Haykowsky et al, 2011), attenuating fibrosis, dilatation, and cardiac dysfunction. To assess the possible protective role of miR-222 expression in this context, Tg-miR-222 mice were withdrawn from doxycycline and then subjected to ischemia-reperfusion injury (IRI) induced by 30 minutes coronary ligation and reperfusion.…”

Section: Resultsmentioning

confidence: 99%

miR-222 Is Necessary for Exercise-Induced Cardiac Growth and Protects against Pathological Cardiac Remodeling

et al. 2015

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SUMMARY Exercise induces physiological cardiac growth and protects the heart against pathological remodeling. Recent work suggests exercise also enhances the heart’s capacity for repair, which could be important for regenerative therapies. While microRNAs are important in certain cardiac pathologies, less is known about their functional roles in exercise-induced cardiac phenotypes. We profiled cardiac microRNA expression in two distinct models of exercise and found microRNA-222 (miR-222) was upregulated in both. Downstream miR-222 targets modulating cardiomyocyte phenotype were identified, including HIPK1 and Homeobox-1. Inhibition of miR-222 in vivo completely blocked cardiac and cardiomyocyte growth in response to exercise, while reducing markers of cardiomyocyte proliferation. Importantly, mice with inducible cardiomyocyte miR-222 expression were resistant to adverse cardiac remodeling and dysfunction after ischemic injury. These studies implicate miR-222 as necessary for exercise-induced cardiomyocyte growth and proliferation in the adult mammalian heart and show that it is sufficient to protect the heart against adverse remodeling.

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“…We hypothesized that the LV dilation associated with pericardiectomy alone would contribute to the dilation seen in the infarcted mouse that had also undergone a prerequisite pericardiectomy. As we had previously seen no additional effect of exercise on LV/BW in infarcted rats, we hypothesized that there would be no additional training-induced hypertrophy employing infarcted mice in the current study [36].…”

Section: Introductionmentioning

confidence: 83%

Effects of pericardiectomy on training- and myocardial infarction-induced left ventricular hypertrophy, chamber dimensions and gene expression

Wolff

Rasmussen²,

Wichern³

et al. 2016

Int J Sports Med

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The primary purpose of the study was to evaluate whether a pericardiectomy (PERI) alters training- or myocardial infarction (MI)-induced left ventricular hypertrophy (LVH), chamber geometry, gene expression and/or running performance. Mice were randomized into 6 groups: naïve control (CONT)-sedentary (Sed), CONT-trained (Tr), PERI-Sed, PERI-Tr, MI-Sed and MI-Tr. MI mice also received a pericardiectomy as part of the MI surgical procedure. 10 weeks of treadmill running resulted in enhanced running performance-to-exhaustion in all 3 trained groups (CONT-Tr, PERI-Tr, MI-Tr) compared to sedentary cohorts (<0.001). Training also resulted in similar increases in normalized LVH (LV/BW) in CONT-Tr and PERI-Tr mice. 2D-echocardiographic evaluation of LV internal chamber dimensions revealed that stroke diameter (SD) was larger in PERI compared to MI (<0.01) but not CONT mice. Ventricular B-type natriuretic peptide mRNA (BNP) was elevated only in the 2 MI groups. Left ventricle β-adrenergic receptor (β-AR) and melusin transcripts both demonstrated an overall increase in trained compared to sedentary mice (both <0.05). Additionally long-term pericardiectomy did not further enhance running performance or increase LV/BW in either sedentary or trained mice.

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Exercise Training Post-MI Favorably Modifies Heart Extracellular Matrix in the Rat

Abstract: Because increased HP cross-linking in the heart is associated with decreased chamber compliance, these findings may help to explain the improved heart function seen after daily exercise in cardiac rehabilitation patients.

Cited by 15 publications

References 37 publications

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

miR-222 Is Necessary for Exercise-Induced Cardiac Growth and Protects against Pathological Cardiac Remodeling

Effects of pericardiectomy on training- and myocardial infarction-induced left ventricular hypertrophy, chamber dimensions and gene expression

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