Expression and Function of Atrial Myosin Light Chain1 in the Porcine Right Ventricle of Normal and Pulmonary Hypertensive animals

Journal of Applied Physiology

Nagle

2003

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. A number of studies have shown that the characteristics of cardiac myocytes vary across the width of the ventricular wall. We have previously shown that endurance exercise training alters the Ca2+ sensitivity of tension as well as contractile protein isoform expression in rat cardiac myocytes. We tested the hypothesis that these effects of training are not uniform across the ventricular wall but are more pronounced in the subendocardial (Endo) region of the myocardium. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from the Endo region of the myocardium and from the subepicardial (Epi) region of both T and C hearts. We found an increase in the Ca2+ sensitivity of tension in T cells compared with C cells, but this difference was larger in the Endo cells than in the Epi cells. In addition, we found a training-induced increase in atrial myosin light chain 1 (aMLC1) expression that was larger in the Endo compared with Epi samples. We conclude that effects of exercise training on myocyte contractile and biochemical properties are greater in myocytes from the Endo region of the myocardium than those from the Epi region. In addition, these results provide evidence that the increase in aMLC1 expression may be responsible for some of the training-induced increase in myocyte Ca2+ sensitivity of tension.

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Regional differences in effects of exercise training on contractile and biochemical properties of rat cardiac myocytes

Journal of Applied Physiology

Nagle

2003

“…PDQuest software (version 6.0, Bio-Rad) was used for gel image analysis. The locations of the aMLC-1 and ventricular MLC-1 (vMLC-1) spots were determined based on the predicted isoelectric point and molecular mass of these proteins as well as by comparison to previously published 2-D gel analysis of these proteins (20,25).…”

Section: Exercise Training Protocolmentioning

confidence: 99%

Microarray expression analysis of effects of exercise training: increase in atrial MLC-1 in rat ventricles

American Journal of Physiology-Heart and Circulatory Physiology

Seversen

Stein

et al. 2003

Previous studies have shown that endurance exercise training increases myocardial contractility. We have previously described training-induced alterations in myocardial contractile function at the cellular level, including an increase in the Ca(2+) sensitivity of tension. To determine the molecular mechanism(s) of these changes, oligonucleotide microarrays were used to analyze the gene expression profile in ventricles from endurance-trained rats. We used an 11-wk treadmill training protocol that we have previously shown results in increased contractility in cardiac myocytes. After the training, the hearts were removed and RNA was isolated from the ventricles of nine trained and nine control rats. With the use of an Affymetrix Rat Genome U34A Array, we detected altered expression of 27 genes. Several genes previously found to have increased expression in hypertrophied myocardium, such as atrial natriuretic factor and skeletal alpha-actin, were decreased with training in this study. From the standpoint of altered contractile performance, the most significant finding was an increase in the expression of atrial myosin light chain 1 (aMLC-1) in the trained ventricular tissue. We confirmed microarray results for aMLC-1 using RT-PCR and also confirmed a training-induced increase in aMLC-1 protein using two-dimensional gel electrophoresis. aMLC-1 content has been previously shown to be increased in human cardiac hypertrophy and has been associated with increased Ca(2+) sensitivity of tension and increased power output. These results suggest that increased expression of aMLC-1 in response to training may be responsible, at least in part, for previously observed training-induced enhancement of contractile function.

Moderate Intensity, but Not High Intensity, Treadmill Exercise Training Alters Power Output Properties in Myocardium From Aged Rats

Chung

The Journals of Gerontology Series A: Biological Sciences and M

2012

Aging is characterized by a progressive decline in cardiac function, but endurance exercise training has been shown to retard a number of deleterious effects of aging. However, underlying mechanisms by which exercise training improves age-related decrements in myocardial contractile function are not well understood. The purpose of this study was to determine the effects of exercise training on power output properties in permeablized (skinned) myocytes of old rats. Thirty-month-old rats were divided into sedentary control (C) and groups undergoing 11 weeks of treadmill exercise training at moderate intensity (MI) and at high intensity (HI). Peak power output normalized to maximal force was significantly increased in MI but not in HI compared to C with significant increases in atrial myosin light chain 1 in ventricle. These results suggest that MI exercise training is beneficial as a significant increase was seen in the ability of the myocardium to do work, but this effect was not seen with HI training.