| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Kinesiology, Biodynamics Laboratory, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: gmdiffee{at}facstaff.wisc.edu.
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 sub-endocardial region of the myocardium. Female Sprague-Dawley rats were divided into sedentary control(C) and exercise trained (T) groups. The T rats underwent 11 weeks of progressive treadmill exercise. Myocytes were isolated from the sub-endocardial (ENDO) region of the myocardium and from the sub-epicardial region (EPI) of both T and C hearts. We found an increase in the Ca2+ sensitivity of tension in trained cells compared to control 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 to 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.
This article has been cited by other articles:
|
|
 |
|
  J. E. Stelzer, H. S. Norman, P. P. Chen, J. R. Patel, and R. L. Moss Transmural variation in myosin heavy chain isoform expression modulates the timing of myocardial force generation in porcine left ventricle J. Physiol., November 1, 2008; 586(21): 5203 - 5214. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Nottin, G. Doucende, I. Schuster-Beck, M. Dauzat, and P. Obert Alteration in left ventricular normal and shear strains evaluated by 2D-strain echocardiography in the athlete's heart J. Physiol., October 1, 2008; 586(19): 4721 - 4733. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Tshori, A. Sonnenblick, N. Yannay-Cohen, G. Kay, H. Nechushtan, and E. Razin Microphthalmia Transcription Factor Isoforms in Mast Cells and the Heart Mol. Cell. Biol., June 1, 2007; 27(11): 3911 - 3919. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Cazorla, Y. Ait Mou, L. Goret, G. Vassort, M. Dauzat, A. Lacampagne, S. Tanguy, and P. Obert Effects of high-altitude exercise training on contractile function of rat skinned cardiomyocyte Cardiovasc Res, September 1, 2006; 71(4): 652 - 660. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.-C. Battista, E. Calvo, A. Chorvatova, B. Comte, J. Corbeil, and M. Brochu Intra-uterine growth restriction and the programming of left ventricular remodelling in female rats J. Physiol., May 15, 2005; 565(1): 197 - 205. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. A. McCrossan, R. Billeter, and E. White Transmural changes in size, contractile and electrical properties of SHR left ventricular myocytes during compensated hypertrophy Cardiovasc Res, August 1, 2004; 63(2): 283 - 292. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
