Effect of Various Types of Exercise Training on 5′-Nucleotidase and Adenosine Deaminase Activities in Rat Heart: Influence of a Single Bout of Endurance Exercise

Langfort, Józef; Czarnowski, D.; Pilis, Wiesław; Wójcik, Beata; Górski, Jan

doi:10.1006/bmme.1996.0060

Cited by 20 publications

(19 citation statements)

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“…Since these are all typical features of exercise-induced adaptive remodeling, it is plausible that A 2a R stimulation may have contributed to these effects. Increased activity of CD73 (5=-ectonucleotidase), the main regulator of adenosine metabolism, has been documented in exercising rats (38). We and others have shown that adenosine receptor expression can rapidly be increased in the presence of adenosine itself or stress induced by the addition of lipopolysaccharide (16,17,53,76,80).…”

Section: Adenosine Receptors Are Upregulated By Exercise: a Potentialmentioning

confidence: 88%

“…One possible mediator of the beneficial effects on LV remodeling induced by exercise could be adenosine. In the rat heart, it has been shown that endurance training leads to increased activity of 5=-ectonucleotidase, a key regulator of adenosine metabolism (38). Adenosine is known to reduce infarct size, increase coronary flow, and attenuate myocardial fibrosis (23,42,45) in the context of ischemic preconditioning and cardiac remodeling and to prevent TNF-␣-induced cardiomyocyte hypertrophy (40).…”

Section: H355 Exercise Limits Post-mi Scar Thinningmentioning

confidence: 99%

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Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Puhl

Müller

Wagner

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Although exercise mediates beneficial effects in patients after myocardial infarction (MI), the underlying mechanisms as well as the question of whether an early start of exercise after MI is safe or even beneficial are incompletely resolved. The present study analyzed the effects of exercise before and reinitiated early after MI on cardiac remodeling and function. Male C57BL/6N mice were housed sedentary or with the opportunity to voluntarily exercise for 6 wk before MI induction (ligation of the left anterior descending coronary artery) or sham operation. After a 5-day exercise-free phase after MI, mice were allowed to reexercise for another 4 wk. Exercise before MI induced adaptive hypertrophy with moderate increases in heart weight, cardiomyocyte diameter, and left ventricular (LV) end-diastolic volume, but without fibrosis. In sedentary mice, MI induced eccentric LV hypertrophy with massive fibrosis but maintained systolic LV function. While in exercised mice gross LV end-diastolic volumes and systolic function did not differ from sedentary mice after MI, LV collagen content and thinning of the infarcted area were reduced. This was associated with ameliorated activation of inflammation, mediated by TNF-␣, IL-1␤, and IL-6, as well as reduced activation of matrix metalloproteinase 9. In contrast, no differences in the activation patterns of various MAPKs or adenosine receptor expressions were observed 5 wk after MI in sedentary or exercised mice. In conclusion, continuous exercise training before and with an early reonset after MI ameliorates adverse LV remodeling by attenuating inflammation, fibrosis, and scar thinning. Therefore, an early reonset of exercise after MI can be encouraged. exercise; remodeling; scar thinning; magnetic resonance imaging; fibrosis; myocardial infarction NEW & NOTEWORTHY Our data provide new insights into the exercise-mediated cardioprotection by implying that an early reinitiation of exercise after myocardial infarction attenuates left ventricular fibrosis and scar thinning, presumably by attenuating the coordinated proinflammatory response involving TNF-␣, IL-6, and IL-1␤. These findings could translate into clinical benefits in patients.CORONARY ARTERY DISEASE is the single most frequent cause of death worldwide. In Europe, every sixth man and every seventh woman will die of myocardial infarction (MI) (71). Those patients who survive MI frequently develop systolic heart failure due to the infarct-induced loss of functional myocardium per se and remodeling of the remainder of the left ventricular (LV) myocardium, which is frequently associated with thinning of the LV wall in the area of MI and its border zone, LV dilation, and systolic dysfunction. These parameters of myocardial remodeling are important prognostic markers for the long-term outcome of these patients. For instance, regional wall thinning is associated with postinfarction ventricular arrhythmia (36) and adverse outcome in patients undergoing coronary artery bypass surgery (87).Scar formation occurs secondary to isc...

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Section: Adenosine Receptors Are Upregulated By Exercise: a Potentialmentioning

confidence: 88%

Section: H355 Exercise Limits Post-mi Scar Thinningmentioning

confidence: 99%

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Puhl

Müller

Wagner

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…Animals were housed in standard conditions (21 ± 2 °C, 12 h light/12 h dark cycle) with free access to tap water and food pellets. The animals were randomly divided into two groups ( N = 8 in each group): (1) sedentary (control) (2) trained for 5 weeks on an electrically driven treadmill according to the following protocol [28]: 1st week 1 h daily at a speed of 960 m/h. The same running time was applied during successive weeks but the running speed was increased as follows: 2nd week 1,200 m/h, 3rd week 1,440 m/h, 4th–6th week 1,680 m/h.…”

Section: Methodsmentioning

confidence: 99%

Aerobic Training in Rats Increases Skeletal Muscle Sphingomyelinase and Serine Palmitoyltransferase Activity, While Decreasing Ceramidase Activity

Błachnio-Zabielska

Baranowski

Górski

2010

Lipids

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Sphingolipids are important components of cell membranes that may also serve as cell signaling molecules; ceramide plays a central role in sphingolipid metabolism. The aim of this study was to examine the effect of 5 weeks of aerobic training on key enzymes and intermediates of ceramide metabolism in skeletal muscles. The experiments were carried out on rats divided into two groups: (1) sedentary and (2) trained for 5 weeks (on a treadmill). The activity of serine palmitoyltransferase (SPT), neutral and acid sphingomyelinase (nSMase and aSMase), neutral and alkaline ceramidases (nCDase and alCDase) and the content of sphingolipids was determined in three types of skeletal muscle. We also measured the fasting plasma insulin and glucose concentration for calculating HOMA-IR (homeostasis model assessment) for estimating insulin resistance. We found that the activities of aSMase and SPT increase in muscle in the trained group. These changes were followed by elevation in the content of sphinganine. The activities of both isoforms of ceramidase were reduced in muscle in the trained group. Although the activities of SPT and SMases increased and the activity of CDases decreased, the ceramide content did not change in any of the studied muscle. Although ceramide level did not change, we noticed increased insulin sensitivity in trained animals. It is concluded that training affects the activity of key enzymes of ceramide metabolism but also activates other metabolic pathways which affect ceramide metabolism in skeletal muscles.

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“…Stimuli including physical exercise (Pierce et al 1989;Langfort et al 1996;Delgado et al 1999), pressure loading (Panagia et al 1986;Czarnowski et al 1996), estradiol (Dubey et al 2000, thyroxine (Daly et al 1986;Smolenski et al 1995), dietary lipid composition (Baracca et al 1994), alpha-adrenergic stimulation Sato et al 1997) as well as hypoxia and ischemia (Bak and Ingwall 1994;Minamino et al 1995;Kitakaze et al 1996;Gustafson and Kroll 1998) were studied. Also, age-related changes were investigated (Awad and Chattopadhyay 1983;Wang et al 1987;De Jong et al 1990;Torii and Ito 1990;Grosso et al 1992;Lorbar et al 1999).…”

Section: Regulation Of Adenosine Metabolismmentioning

confidence: 99%

Metabolic flux rates of adenosine in the heart

Deußen

2000

Naunyn-Schmied Arch Pharmacol

101

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The quantitatively most important source of adenosine under well-oxygenated conditions is 5'-AMP hydrolyzed by cytosolic 5'-nucleotidase N-I. Hydrolysis of S-adenosylhomocysteine and extracellular dephosphorylation of 5'-AMP further contribute to total production. More than 90% of the total production occur intracellularly under well-oxygenated conditions. Besides cardiomyocytes, endothelial cells and smooth muscle contribute significantly to total cardiac adenosine production. Rapid enzymatic conversion of adenosine is provided by adenosine kinase and adenosine deaminase, keeping the cytosolic adenosine concentration in the nanomolar range. Due to the high intracellular rates of adenosine rephosphorylation and deamination the cytosolic is normally below the extracellular adenosine concentration, making the cytosol to a sink rather than a source of adenosine. It is for this reason that blockers of membrane transport enhance the plasma adenosine concentration. With increasing catabolism of adenine nucleotides the rate of intracellular adenosine production exceeds the rate of adenosine deamination and rephosphorylation. Thus, this condition will result in a concentration gradient from intra- to extracellular. Thence, membrane transport blockers would be expected to increase the intracellular adenosine concentration. A considerable insecurity on the importance of experimental data results from species differences of purine metabolism. Cardiac adenosine metabolism has recently been described in quantitative terms using mathematical model analysis. This analysis tool may prove useful in future when (1) clarifying the importance of various regulatory actions described for the different pathways of adenosine metabolism, (2) making quantitative comparisons of different experimental models possible and (3) deepening the insight from experimental data.

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Effect of Various Types of Exercise Training on 5′-Nucleotidase and Adenosine Deaminase Activities in Rat Heart: Influence of a Single Bout of Endurance Exercise

Cited by 20 publications

References 0 publications

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Exercise attenuates inflammation and limits scar thinning after myocardial infarction in mice

Aerobic Training in Rats Increases Skeletal Muscle Sphingomyelinase and Serine Palmitoyltransferase Activity, While Decreasing Ceramidase Activity

Metabolic flux rates of adenosine in the heart

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