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

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.

Download Full-text

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

Anesthesiology ◽

10.1097/00000542-200011000-00026 ◽

2000 ◽

Vol 93 (5) ◽

pp. 1312-1319 ◽

Cited By ~ 3

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.

Download Full-text

High-volume endurance exercise training stimulates hematopoiesis by increasing ACE NH2-terminal activity

Clinical Science ◽

10.1042/cs20210739 ◽

2021 ◽

Author(s):

Flávio de Castro Magalhães ◽

Tiago Fernandes ◽

Vinícius Bassaneze ◽

Katt Coelho Mattos ◽

Isolmar Schettert ◽

...

Keyword(s):

Exercise Training ◽

Endurance Exercise ◽

Wistar Rats ◽

High Volume ◽

Erythroid Progenitor ◽

Hematopoietic Stem ◽

Endurance Exercise Training ◽

First Time ◽

Captopril Treatment

One of the health benefits of endurance exercise training (ET) is the stimulation of hematopoiesis. However, the mechanisms underlying ET-induced hematopoietic adaptations are understudied. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits proliferation of early hematopoietic progenitor cells. The angiotensin-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP. Here we demonstrate for the first time the role of ACE NH2-terminal in ET-induced hematopoietic adaptations. Wistar rats were subjected to 10 weeks of moderate-(T1) and high-(T2) volume swimming-training. Although both protocols induced classical ET-associated adaptations, only T2 increased plasma ACE NH2-domain activity (by 40%, p=0.0003) and reduced Ac-SDKP levels (by 50%, p<0.0001). T2 increased the number of hematopoietic stem cells (~200%, p=0.0008), early erythroid progenitor colonies (~300%, p<0.0001) and reticulocytes (~500%, p=0.0007), and reduced erythrocyte lifespan (~50%, p=0.022). Following, Wistar rats were subjected to T2 or T2 combined with ACE NH2-terminal inhibition (captopril treatment: 10 mg.kg-1.d-1). T2 combined with ACE NH2-terminal inhibition prevented Ac-SDKP decrease and attenuated ET-induced hematopoietic adaptations. Altogether, our findings show that ET-induced hematopoiesis was at least partially associated to increased ACE NH2-terminal activity and reduction of the hematopoietic inhibitor Ac-SDKP.

Download Full-text

Effects of exercise on cardiac myosin isozyme composition during the aging process

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.2.880 ◽

1988 ◽

Vol 64 (2) ◽

pp. 880-883 ◽

Cited By ~ 9

Author(s):

R. P. Farrar ◽

J. W. Starnes ◽

G. D. Cartee ◽

P. Y. Oh ◽

H. L. Sweeney

Keyword(s):

Atpase Activity ◽

Exercise Program ◽

Cardiac Performance ◽

Fischer 344 Rats ◽

Cardiac Myosin ◽

Equal Distribution ◽

Fischer 344 ◽

Age Related ◽

Myosin Isozyme ◽

Effects Of Aging

The effects of aging and exercise on isoforms of cardiac myosin and Ca2+-activated actomyosin adenosinetriphosphatase (ATPase) activity were examined in Fischer 344 rats. Rats were divided into running (R) and age-matched sedentary (S) groups. The groups initiated their exercise program at either 3, 4, or 18 mo of age. Rats were killed at 10, 12, 24, or 27 mo of age. ATPase activity decreased 25% in the S group and 28% in the R group from 12 to 27 mo of age. The myosin isozyme patterns shifted in both S and R groups from a predominantly V1 isozyme form (63.8%) at 10 mo of age to a more equal distribution of isozyme forms at 24 mo (V1, V2, and V3 comprising 40.0, 27.8, and 31.9%, respectively). Age-related shifts in myosin composition occurred despite chronic endurance training at an intensity of approximately 75% maximum O2 consumption. Improvement of cardiac performance through training during aging is not accompanied by attenuating shifts in myosin isozyme composition.

Download Full-text