Exercise training alters length dependence of contractile properties in rat myocardium

Diffee, Gary M.; Nagle, Daniel F.

doi:10.1152/japplphysiol.00565.2002

Cited by 32 publications

(39 citation statements)

References 46 publications

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“…Experiments utilizing transgenic mice (25) and rats (1) (discussed in detail in ELC Transgenic Animal Models) supported these earlier findings obtained from human fibers and demonstrated an overall increase in the kinetic properties of the ventricular tissue expressing ELC a . Interestingly, increased levels of ELC a expression in rat ventricles due to chronic exercise were also shown to be associated with improvement of cardiac contractility (17)(18)(19). The ELC a -mediated enhancement in cardiac function was verified by Khalina et al (38) at the myosin level, utilizing synthetic filaments of ventricular myosin reconstituted with recombinant human ELC a (38).…”

Section: Effect Of Elc On Myosin Cross-bridge Kineticsmentioning

confidence: 91%

Myosin essential light chain in health and disease

Hernandez¹,

Jones²,

Guzman³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

117

113

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The essential light chain of myosin (ELC) is known to be important for structural stability of the ␣-helical lever arm domain of the myosin head, but its function in striated muscle contraction is poorly understood. Two ELC isoforms are expressed in fast skeletal muscle, a long isoform and its NH 2-terminal ϳ40 amino acid shorter counterpart, whereas only the long ELC is observed in the heart. Biochemical and structural studies revealed that the NH 2-terminus of the long ELC can make direct contacts with actin, but the effects of the ELC on the affinity of myosin for actin, ATPase, force, and the kinetics of force generating myosin cross-bridges are inconclusive. Myosin containing the long ELC has been shown to have slower cross-bridge kinetics than myosin with the short isoform. A difference was also reported among myosins with long isoforms. Increased shortening velocity was observed in atrial compared with ventricular muscle fibers. The common findings suggest that ELC provides the fine tuning of the myosin motor function, which is regulated in an isoform and tissue-dependent manner. The functional importance of the ELC is further implicated by the discovery of ELC mutations associated with Familial Hypertrophic Cardiomyopathy. The pathological phenotypes vary in severity, but more notably, almost all ELC mutations result in sudden cardiac death at a young age. This review summarizes the functional roles of striated muscle ELC in normal healthy muscle and in disease. Transgenic animal models and phenotypic characterization of ELC-mediated remodeling of the heart are also discussed.cross-bridge kinetics; striated muscle contraction; familial hypertrophic cardiomyopathy; sarcomeric mutations; failing heart; sudden cardiac death STRIATED MUSCLE MYOSIN

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Section: Effect Of Elc On Myosin Cross-bridge Kineticsmentioning

confidence: 91%

Myosin essential light chain in health and disease

Hernandez¹,

Jones²,

Guzman³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

117

113

View full text Add to dashboard Cite

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“…Notwithstanding, studies showing changes in the resting force-length relationship exist (DiVee and Nagle 2003;DiVee 2004). In contrast, Nutter ; and detrained 4 weeks (closed diamond).…”

Section: Variablesmentioning

confidence: 99%

Exercise training-induced enhancement in myocardial mechanics is lost after 2 weeks of detraining in rats

et al. 2010

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Exercise training is assumed to improve myocardial function; however, the role of detraining and its effect on myocardial parameters are still unclear. The aim of the present study was to evaluate the effect of detraining on ventricular remodeling and myocardial mechanical parameters after an 8 week (5 days/week, 60 min/day) swimming training period. Forty-three female Wistar rats were distributed into six groups: trained (T, n = 9), detrained 2 weeks (D2, n = 8), detrained 4 weeks (D4, n = 8) and their respective controls: untrained (U, n = 5), untrained 2 weeks (U2, n = 5) and untrained 4 weeks (U4, n = 5). Detrained rats underwent training and then remained sedentary (i.e., "detraining") for 2 or 4 weeks. After training, the T group demonstrated increased physical capacity, left ventricular (LV) posterior wall thickness, and LV end-diastolic diameter, along with decreased heart rate, as evaluated by echocardiogram. In addition, the inotropism and lusitropism parameters studied on papillary muscles showed improvement in the T group (P < 0.05). However, after just 2 weeks of detraining, all parameters regressed back to values which were similar to those of the untrained groups. In conclusion, our results confirmed that exercise training is capable of inducing myocardial remodeling and improving contractile performance; however, these changes are completely lost after a short period of detraining.

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“…Cell isolation was performed as described previously 36,37 (please see the online Data Supplement for details), and the technique for image analysis is outlined in the online Data Supplement.…”

Section: Myocyte Isolation and Assessment Of Cell Morphometrymentioning

confidence: 99%

Dietary-Induced Obesity Hastens the Progression From Concentric Cardiac Hypertrophy to Pump Dysfunction in Spontaneously Hypertensive Rats

et al. 2009

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Abstract-We explored whether dietary-induced obesity hastens the transition from concentric left ventricular (LV) hypertrophy to pump dysfunction in spontaneously hypertensive rats (SHRs) and the mechanisms thereof. After feeding rats a diet for 4 to 5 months, obesity was induced in SHRs and Wistar-Kyoto (WKY) control rats. Obesity was not associated with abnormal blood glucose control (glycosylated hemoglobin) or with increases in systolic blood pressure. However, in SHRs, but not in WKY rats, obesity was associated with a reduced LV chamber systolic function, as determined by echocardiography, and in isolated perfused heart studies. A marked increase in LV end diastolic diameter and a right shift in the LV diastolic pressure-volume relation were noted in obese SHRs but not in obese WKY rats. Moreover, LV intrinsic myocardial systolic function, as determined from the slope of the linearized LV systolic stress-strain relationship (LV myocardial end systolic elastance), was markedly reduced in obese as compared with lean SHRs, whereas LV myocardial end systolic elastance was maintained in obese WKY rats. Obesity increased LV weight, cardiomyocyte width, cardiomyocyte apoptosis (TUNEL), the activity of myocardial matrix metalloproteinases (zymography), and serum leptin concentrations in SHRs but not in WKY rats. In conclusion, SHRs are susceptible to the adverse effects of dietary-induced obesity on the heart, an effect that hastens the progression from concentric LV hypertrophy to pump dysfunction independent of blood pressure changes or alterations in glycosylated hemoglobin. This effect may be mediated through a proclivity of SHRs to developing both obesity-induced effects on cardiomyocyte apoptosis and activation of myocardial collagenases through leptin resistance and obesity-induced hypertrophy. Key Words: obesity Ⅲ ventricular function Ⅲ rats inbred spontaneously hypertensive rats Ⅲ dilatation Ⅲ ventricular remodeling O besity is an independent risk factor for heart failure. [1][2][3] As adjustments for cardiac systolic chamber function abolish the relationship between obesity and heart failure, 2 it is possible that heart failure in obesity is caused by pump dysfunction rather than diastolic abnormalities. There is increasing evidence from both human 4,5 and animal studies 6,7 that obesity is associated with myocardial contractile disturbances. However, a cause-effect relationship between obesity and cardiac systolic dysfunction is controversial. Indeed, weight loss produced by lifestyle modification or gastric bypass does not influence left ventricular (LV) myocardial systolic dysfunction. 8,9 Moreover, although some studies have reported a decreased LV pump function associated with obesity, 10 -13 the majority indicate a normal or even increased LV pump function. 4,5,14 -22 Because pump dysfunction is an established predictor of the development of heart failure, 23 clarity on the role of obesity in the development of pump dysfunction is required.Obesity may augment the impact of hypertension on LV hyp...

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Exercise training alters length dependence of contractile properties in rat myocardium

Cited by 32 publications

References 46 publications

Myosin essential light chain in health and disease

Myosin essential light chain in health and disease

Exercise training-induced enhancement in myocardial mechanics is lost after 2 weeks of detraining in rats

Dietary-Induced Obesity Hastens the Progression From Concentric Cardiac Hypertrophy to Pump Dysfunction in Spontaneously Hypertensive Rats

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