Effect of chronic exercise on glucose uptake and activities of glycolytic enzymes measured regionally in rat heart

Kainulainen, Heikki; Komulainen, Jyrki; Takala, Timo; Vihko, V.

doi:10.1007/bf01907927

Cited by 21 publications

(10 citation statements)

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“…Moreover, we reported that the CS activities in cardiac ventricle muscle were unchanged after 8-wk endurance treadmill training in both groups of 1 and 48 h after the final session of exercise training, a finding that agrees with the majority of the previous findings. There is little evidence in the literature reporting that exercise training promotes an increase in CS activity in rat cardiac muscle (10). Our findings are consistent with previously published data indicating that CS activity is not altered after endurance training in rat cardiac muscle (1,2,17,18,30).…”

Section: Discussionsupporting

confidence: 92%

“…Several studies have been conducted to determine the influence of exercise training in the mitochondrial enzyme adaptation in cardiac muscles (2,10,11,18,19). Although the majority of previous studies suggest that the traininginduced alteration of mitochondrial enzymes is not noticeable in cardiac muscle (1,2,17,18,30), a few discrepant results regarding the changes were reported (10). Moreover, among the studies that have been conducted to examine the exercise-induced response of CS in cardiac muscle, very few have provided data regarding the transcriptional, translational, and/or posttranslational processes.…”

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confidence: 99%

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Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Siu

Donley

Bryner

2003

Journal of Applied Physiology

117

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. Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles. J Appl Physiol 94: 555-560, 2003; 10.1152/ japplphysiol.00821.2002.-The present study was designed to examine the acute and chronic effects of endurance treadmill training on citrate synthase (CS) gene expression and enzymatic activity in rat skeletal and cardiac muscles. Adult rats were endurance trained for 8 wk on a treadmill. They were killed 1 h (T1, n ϭ 8) or 48 h (T48, n ϭ 8) after their last bout of exercise training. Eight rats were sedentary controls (C) during the training period. CS mRNA levels and enzymatic activities of the soleus and ventricle muscles were determined. Training resulted in higher CS mRNA levels in both the soleus muscles (21% increase in T1; 18% increase in T48, P Ͻ 0.05) and ventricle muscles (23% increase in T1; 17% increase in T48, P Ͻ 0.05) when compared with the C group. The CS enzyme activities were 42 (P Ͻ 0.01) and 25% (P Ͻ 0.01) greater in the soleus muscles of T1 and T48 groups, respectively, when compared with that of the C group. Soleus CS enzyme activity was significantly greater in the T1 vs. T48 groups (P Ͻ 0.05). However, no appreciable alterations in CS enzyme activities were observed in the ventricle muscles in both training groups. These findings suggest differential responses of skeletal and cardiac muscles in CS enzymatic activity but similar responses in CS gene expression at 1 and 48 h after the last session of endurance training. Moreover, our data support the existence of an acute effect of exercise on the training-induced elevation in CS activity in rat soleus but not ventricle muscles. physical activity; oxidative enzyme; gene transcriptional expression; soleus muscle; heart muscle CITRATE SYNTHASE (CS) is one of the key regulatory enzymes in the energy-generating metabolic pathway that catalyzes the condensation of oxaloacetate and acetyl coenzyme A to form citrate in the tricarboxylic acid cycle. It has been extensively used as a metabolic marker in assessing oxidative and respiratory capacity (22). More than 30 years ago, Holloszy and his colleagues (8) reported that endurance exercise training increases the oxidative enzyme activities in skeletal muscle. After that, numerous studies were conducted to examine the effect of exercise training on muscle oxidative capacity and metabolic characteristics (7,15,20,22,29). It is generally recognized that the skeletal muscle oxidative capacity and the activities of mitochondrial enzymes are elevated by endurance exercise training.

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Section: Discussionsupporting

confidence: 92%

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confidence: 99%

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Siu

Donley

Bryner

2003

Journal of Applied Physiology

117

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“…Free fatty acid level is higher and carnitine content lower in Endo than in Epi (41). Glucose uptake is higher in Endo (42) and activity of several glycolytic enzymes, e.g., that of phosphofructokinase (22), are higher in Endo. There is also evidence that longitudinal and latitudinal systolic stress is greater in Endo than in Epi (19) and that Endo undergoes greater shortening than Epi during the systole (36,38), suggesting greater work load in Endo.…”

Section: Discussionmentioning

confidence: 96%

Regional differences of substrate oxidation capacity in rat hearts: Effects of extra load and endurance training

Kainulainen¹,

Komulainen

Leinonen

et al. 1990

Basic Res Cardiol

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Male rats, aged 17 weeks at the end of experiments, were divided into four groups. Two groups lived in normal cage conditions with or without extra load (20% of the body weight) and two groups were trained by running with or without extra load for 8 weeks. Oxidation rates of succinate, glutamate + malate, palmitoylcarnitine, and pyruvate, and the activities of lactate dehydrogenase, citrate synthase, isocitrate dehydrogenase and cytochrome oxidase were measured in homogenates of the right ventricle and in those of the subendocardial and subepicardial layers of the left ventricle. Oxidation rates of succinate and palmitoylcarnitine tended to be higher in the subendocardium than in the subepicardium of sedentary control animals (p less than 0.1 and p less than 0.05, respectively). Transmural differences of succinate and palmitoylcarnitine oxidation rates were even more clear after running training (p less than 0.01 and p less than 0.05, respectively), after carrying extra load (p less than 0.001 and p less than 0.001, respectively) and after training carrying extra load (p less than 0.001 and p less than 0.05, respectively). Training also enhanced pyruvate oxidation rate in the subendocardium. Oxidation rates of all substrates were lower in the right ventricle than in the left ventricle. In control animals there were no regional differences in the myocardial enzyme activities and the training- or extra-load-induced changes were modest compared with the changes in the oxidation rates. The most significant change was the training-induced enhancement in the lactate dehydrogenase activity of the subendocardium (p less than 0.001 vs subepicardium). These results show greater subendocardial than subepicardial oxidation rates of certain substrates in the normal heart. These results also suggest that the myocardium adapts to increased work by increasing the subendocardial oxidation rate of some but not all substrates, indicating further that there may be qualitative mitochondrial differences in the different regions of the heart.

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“…a differential (i.e., Sed vs. Tr) inhibition of K ATP channels via the effects of subsarcolemmal glycolysis seems highly unlikely in view of the fact that our anoxia condition included the use of 2-deoxy-D-glucose to inhibit glycolysis and to accelerate cellular ATP depletion. We hasten to point out that, in a more physiological context, this hypothetical mechanism might be important because there are reports that training can increase myocardial glucose transport rate and/or an upregulation in the activities of several glycolytic enzymes, including pyruvate kinase (12,17,18,40,43). It is possible that a training-induced increase in glycolytic ATP production in close proximity to sarcolemmal K ATP channels would serve to suppress anoxia-induced IK ATP expression via an enhanced glycolysis-mediated maintenance of [ATP] ss .…”

Section: Discussionmentioning

confidence: 99%

Exercise training alters an anoxia-induced, glibenclamide-sensitive current in rat ventricular cardiocytes

Jew

Moore

2002

Journal of Applied Physiology

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The effect of training on properties of a sarcolemmal ATP-sensitive K+ current (I(K(ATP))) was examined in left ventricular cardiocytes isolated from sedentary (Sed) and trained (Tr) female Sprague-Dawley rats. Whole cell patch-clamp techniques were used to characterize I(K(ATP)), an anoxia-inducible, glibencamide-sensitive current. An anoxic condition was induced by superfusing cells with a buffer that was equilibrated with 100% N(2), maintained under a layer of argon, and that contained 2-deoxy-D-glucose. Over a 1-h period of anoxia, 59% of Tr cells and 85% Sed cells expressed I(K(ATP)). In those cells that did express I(K(ATP)), the time to expression of the current during the anoxic period occurred significantly later in cells from the Tr group compared with the Sed. Peak I(K(ATP)) density was significantly lower in the Tr cells compared with the Sed cells. These results indicate that the onset and magnitude of I(K(ATP)) were altered by training. These alterations in I(K(ATP)) may be reflective of processes that contribute to training-induced cardioprotection against ischemia-reperfusion damage.

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Effect of chronic exercise on glucose uptake and activities of glycolytic enzymes measured regionally in rat heart

Cited by 21 publications

References 60 publications

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Regional differences of substrate oxidation capacity in rat hearts: Effects of extra load and endurance training

Exercise training alters an anoxia-induced, glibenclamide-sensitive current in rat ventricular cardiocytes

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