Chronic exercise alters contractility and morphology of isolated rat cardiac myocytes

Moore, Russell L.; Musch, Timothy I.; Yelamarty, R. V.; Scaduto, Russell C.; Semanchick, A. M.; Elensky, M.; Cheung, Joseph Y.

doi:10.1152/ajpcell.1993.264.5.c1180

Cited by 91 publications

(103 citation statements)

References 18 publications

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“…We found that training alone elicited a small (ϳ6%) but significant increase in cell length. This type of adaptation is similar to that previously described in younger healthy rat models of training (31,36). The fact that LWR did not increase with training indicates that the longitudinal cardiocyte growth was also accompanied by cross-sectional myocyte growth.…”

Section: Discussionsupporting

confidence: 88%

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Emter

McCune²,

Sparagna³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats. Am J Physiol Heart Circ Physiol 289: H2030 -H2038, 2005. First published July 1, 2005; doi:10.1152/ajpheart.00526.2005.-Data regarding the effectiveness of chronic exercise training in improving survival in patients with congestive heart failure (CHF) are inconclusive. Therefore, we conducted a study to determine the effect of exercise training on survival in a well-defined animal model of heart failure (HF), using the lean male spontaneously hypertensive HF (SHHF) rat. In this model, animals typically present with decompensated, dilated HF between ϳ18 and 23 mo of age. SHHF rats were assigned to sedentary or exercise-trained groups at 9 and 16 mo of age. Exercise training consisted of 6 mo of low-intensity treadmill running. Exercise training delayed the onset of overt HF and improved survival (P Ͻ 0.01), independent of any effects on the hypertensive status of the rats. Training delayed the myosin heavy chain (MyHC) isoform shift from ␣-to ␤-MyHC that was seen in sedentary animals that developed HF. Exercise was associated with a concurrent increase in cardiomyocyte length (Ϸ6%), width, and area and prevented the increase in the length-to-width ratio seen in sedentary animals in HF. The increases in proteinuria, plasma atrial natriuretic peptide, and serum leptin levels observed in rats with HF were suppressed by low-intensity exercise training. No significant alterations in sarco (endo)plasmic reticulum Ca 2ϩ ATPase, phospholamban, or Na ϩ / Ca 2ϩ exchanger protein expression were found in response to training. Our results indicate that 6 mo of low-intensity exercise training delays the onset of decompensated HF and improves survival in the male SHHF rat. Similarly, exercise intervention prevented or suppressed alterations in several key variables that normally occur with the development of overt CHF. These data support the idea that exercise may be a useful and inexpensive intervention in the treatment of HF. myosin heavy chain; proteinuria; cardiomyocyte morphology; atrial natriuretic peptide; leptin HEART DISEASE is a leading cause of death among men and women in Western industrialized societies. Cardiovascular disease (CVD) currently affects over 70 million Americans, 65 million of which are estimated to have high blood pressure and nearly 5 million are diagnosed with congestive heart failure (CHF) (2). With the diagnosis of CHF, life expectancy decreases dramatically and chances of survival decrease with 70 -80% of patients dying within 8 yr (2). Although chronic exercise training has clearly been shown to be beneficial in attenuating risk factors for CVD, including high blood pressure and cholesterol levels, insulin resistance, and obesity (9,14,53,58), the utility of exercise as a clinical intervention for patients with developing CHF is less clear. Currently, there is a lack of clarity regarding the efficacy of chronic exercise training as a treatment and in reducing mortali...

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Section: Discussionsupporting

confidence: 88%

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Emter

McCune²,

Sparagna³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Both cell length and width increased, whereas only lengthening was observed in rats (29,42). No differences in cardiomyocyte dimension between the sexes were found, even though males had greater ventricle mass, which may suggest a higher number of cardiomyocytes in males.…”

Section: Discussionmentioning

confidence: 79%

“…Until recently, findings appeared somewhat contradictory. Treadmill running with fixed exercise intensity induced only minor increments in ventricular mass and cardiomyocyte dimensions (2,3,28,29) or did not induce any effects (16,18). However, 10-20% improvements in V O 2 max and work economy had been demonstrated (16,30).…”

mentioning

confidence: 94%

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Kemi

Loennechen

Wisløff

et al. 2002

Journal of Applied Physiology

243

265

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. Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy. J Appl Physiol 93: 1301-1309. First published May 24, 2002 10.1152/japplphysiol.00231.2002-Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored and call for an effective and wellcharacterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (V O2 max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent V O2 max with 0.98 test-retest correlation was found at 25°treadmill grade. Running for 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of V O2 max and 2 min at 50% (adjusted to weekly V O2 max testing) increased V O2 max to a plateau 49% above sedentary females and 29% in males. Running economy improved in both sexes, and echocardiography indicated significantly increased left ventricle posterior wall thickness. Ventricular weights increased by 19-29 and 12-17% in females and males, respectively, whereas cardiomyocyte dimensions increased by 20-32, and 17-23% in females and males, respectively; skeletal muscle mass increased by 12-18%. Thus the model mimics human responses to exercise and can be used in future studies of molecular mechanisms underlying these adaptations. maximal oxygen uptake; work economy; respiratory exchange ratio; cardiomyocyte; allometric scaling SEVERAL NOVEL SIGNALING PATHWAYS of pathological cardiac hypertrophy have been unveiled in the powerful model of mechanical overloading by thoracic aorta constriction in genetically modified mice (8,22). Thus far, the molecular mechanisms of adaptive cardiac hypertrophy in response to physiological stimuli remain virtually unexplored because of a paucity of effective and well-controlled experimental models in this species. Ideally, the outcome should mimic typical results of exercise training in humans, e.g., increased maximal oxygen uptake (V O 2 max ) and work economy (21). In healthy individuals, increased exercise capacity is dependent on functional and structural adaptations in skeletal muscle, blood vessels, and heart. Cardiac adaptation includes increased ventricular chamber volumes and weights, cardiomyocyte hypertrophy, increased cardiac output, and improved contractile function measured in isolated cardiomyocytes and in the intact heart (2, 3).At present, there are few well-controlled endurance training studies in mice. Training is usually carried out as voluntary exercise regimens, with little control of exercise intensity and the individual's fitness level. Voluntary wheel running is most frequently used. V O 2 max has been shown to increase by 12-30% after a 7-to 12-wk period of free wheel running (11,40). The latter study also demonstrated a 6% decreased respiratory exchange ratio (RER) at V O 2 max in trained mice. Exercise capacity and adaptations have al...

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“…The better response of the stressed rats may be due to increase in myofilament calcium-sensitivity 31,32 and increased sarcoplasmic reticulum calcium uptake 33,34 induced by chronic stress. These postulations are extrapolated from a previous study 35 that observed better inotropic response to calcium in rats subjected to exercise training.…”

Section: Discussionmentioning

confidence: 99%

Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Bruder‐Nascimento

Campos

Leopoldo

et al. 2012

Arq. Bras. Cardiol.

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Chronic exercise alters contractility and morphology of isolated rat cardiac myocytes

Cited by 91 publications

References 18 publications

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

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