scholarly journals Lack of Effect of Running Training at Two Intensities on Cardiac Myosin Isozyme Composition in Rats.

2000 ◽  
Vol 50 (6) ◽  
pp. 577-583 ◽  
Author(s):  
Shuichi Machida ◽  
Fumihiko Kariya ◽  
Keizo Kobayashi ◽  
Mitsuo Narusawa
Keyword(s):  
Cardiac Myosin ◽  
Running Training ◽  
Myosin Isozyme

scholarly journals Age-Related Differences in the Effect of Running Training on Cardiac Myosin Isozyme Composition in Rats

2002 ◽  
Vol 57 (9) ◽  
pp. B339-B343 ◽  
Author(s):  
S. Machida ◽  
H. Tsujimoto ◽  
H. Suzuki ◽  
N. Kasuga ◽  
K. Kobayashi ◽  
...  
Keyword(s):  
Cardiac Myosin ◽  
Running Training ◽  
Age Related ◽  
Myosin Isozyme

Exercise alters cardiac myosin isozyme distribution in obese Zucker and Wistar rats

1990 ◽  
Vol 69 (1) ◽  
pp. 380-383 ◽  
Author(s):  
G. S. Morris ◽  
K. M. Baldwin ◽  
J. M. Lash ◽  
R. L. Hamlin ◽  
W. M. Sherman
Keyword(s):  
Exercise Training ◽  
Atpase Activity ◽  
Functional Capacity ◽  
Wistar Rats ◽  
Cardiac Contractility ◽  
Cardiac Myosin ◽  
Endurance Exercise Training ◽  
Obese Rats ◽  
Myosin Isozyme ◽  
Glucose Availability

Recent evidence suggests that exercise training may significantly increase the expression of the cardiac myosin isozyme V1 in the diabetic heart, a change associated with improved cardiac functional capacity. To test this hypothesis, cardiac myofibrillar adenosinetriphosphatase (ATPase) activity and myosin isozyme profiles were determined in trained and sedentary male hyperinsulinemic obese Zucker (OZT, OZS) and obese Wistar (OWT, OWS) rats. Lean sedentary (LZS, LWS) animals served as age-matched controls. Myofibrillar ATPase activity and the relative quantity of the high-ATPase isozyme V1 was significantly lower in both strains of sedentary obese rats than in the respective lean sedentary controls (P less than 0.05). Both 5 (OZT) and 10 wk (OWT) of moderate treadmill training increased these markers of cardiac myosin biochemistry in the obese animals (P less than 0.05). Thus, endurance exercise training remodels the cardiac isomyosin profile of hyperinsulinemic rats and, in doing so, may enhance cardiac contractility and functional capacity. Such changes may reflect an improvement in glucose availability and utilization in these hearts.

Altered Expression of Cardiac Myosin Isozymes Associated with the Malignant Hyperthermia Genotype in Swine

2000 ◽  
Vol 93 (5) ◽  
pp. 1312-1319 ◽  
Author(s):  
Ying-Ming Liou ◽  
Meei Jyh Jiang ◽  
Ming-Che Wu
Keyword(s):  
Atpase Activity ◽  
Malignant Hyperthermia ◽  
Myofibrillar Atpase ◽  
Cardiac Myosin ◽  
Long Term Effects ◽  
Altered Expression ◽  
Cardiac Symptoms ◽  
Myofibrillar Atpase Activity ◽  
Malignant Hyperthermia Susceptible ◽  
Myosin Isozyme

Background Anesthetic-induced malignant hyperthermia (MH) in humans and pigs is associated with dramatic alterations in cardiac function. However, it remains controversial as to whether MH-associated cardiac symptoms represent a primary difference of myocardium or a secondary alteration consequent to increases in the hyperthermic stress. Here the authors describe changes in myosin isoform expression in the hearts of MH-susceptible pigs with and without prior exposure to halothane. Methods One group of pigs was diagnosed as MH susceptible by halothane challenge and Hal-1843 nucleotide examination. To determine if there is an effect of halothane exposure, another group of pigs was diagnosed by simple MH genotyping without exposure to halothane. After diagnosis and genotyping, animals with and without exposure to halothane were killed to study cardiac myosin isozyme distributions, cardiac myofibrillar adenosine triphosphatase (ATPase) activity, and the steepness of the Ca2+-ATPase activity relation in the hearts of normal and susceptible pigs. The altered myosin isozyme expression was analyzed by pyrophosphate gel electrophoresis. Results Malignant hyperthermia-susceptible animals with the prior halothane challenge showed an increased V1 myosin (-44%) expression, increased myofibrillar ATPase activity (-25%) and increased steepness of the Ca2+-ATPase activity relation. Without exposure to halothane, no change of myofibrillar ATPase activity was found in the hearts of different genotyped pigs, but there was a small increase in expression of V1 myosin (-5%) in the mutant (TT). Conclusions The potential modulation of V1 myosin expression occurs in the hearts of MH-susceptible pigs. The added stress by halothane challenge would further cause a V3 --> V1 shift, which may be attributed to the long-term effects of hyperthermic stress.

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