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Mitsuo Matsuda

Publications and source records attributed to Mitsuo Matsuda.

28 records · Page 2Linked to original sources

Influence of regular exercise on age-related changes in arterial elasticity: mechanistic insights from wall compositions in rat aorta.

Arterial stiffness increases with age in healthy sedentary adults. We previously reported that the age-related increases in arterial stiffness are absent or attenuated in regularly exercising adults. However, the mechanism underlying this training effect is unknown. One possibility is that regular exercise minimizes age-related changes in the arterial wall composition of elastin and collagen. To gain insight into this issue, we studied four groups of rats (N = 23): young (42-46 wks) and old (80-84 wks), sedentary and exercise-trained. The exercise group swam 1 hr.d-1, 6 d.wk-1 for 17-21 weeks. There was no significant difference in the incremental elastic modulus between young sedentary and exercise-trained rats. The elastic moduli of the old exercise-trained rats were 31% lower than in the old sedentary controls. As such, the magnitude of age-related increase in the elastic modulus was smaller in the exercise-trained (110%) vs. the sedentary group (151%) (p < 0.05). In both activity groups, elastin content was lower and collagen content was higher in old vs. young rats (p < 0.05). However, there were no significant differences between the two activity groups. These results are not consistent with the hypothesis that regular physical exercise minimizes age-related compositional changes in the arterial wall and attenuates the age-related increase in arterial stiffness.

Animals↗

Cardiac hypertrophy by hypertension and exercise training exhibits different gene expression of enzymes in energy metabolism.

Hypertension-induced pathological cardiac hypertrophy (hypertensive heart) and exercise training-induced physiological cardiac hypertrophy (athletic heart) have differences in cardiac properties. We hypothesized that gene expression of energy metabolic enzymes differs between these two types of cardiac hypertrophy. To investigate whether mRNA expression of key enzymes in the long-chain fatty acid (FA), glucose, and lactic acid metabolic pathways differs between these two types of cardiac hypertrophy, we used the hearts of spontaneously hypertensive rats (SHR; 19 weeks old) as a model of the hypertensive heart, swim-trained rats (Trained; 19 weeks old, swimming training for 15 weeks) as a model of the athletic heart, and sedentary Wistar-Kyoto rats (Control; 19 weeks old). SHR developed hypertensive cardiac hypertrophy, of which cardiac function was deteriorated, whereas Trained rats developed an athletic heart, of which cardiac function was enhanced. The mRNA expression of CD36, which involved in uptake of long-chain FA, in the heart was almost never detected in the SHR group. Furthermore, the mRNA expression of key enzymes in the long-chain FA metabolic pathway (acyl CoA synthase [ACoAS], carnitine palmitoyl transferase [CPT]-I, CPT-II, and isocitrate dehydrogenase [ISCD]) in the heart was significantly higher in the SHR group compared with the Control group. The mRNA expression of ACoAS, CPT-I, ISCD, and CD36 in the heart did not differ between Trained group and Control group, whereas that of CPT-II in the Trained group was significantly higher compared with the Control group. The mRNA expression of key enzymes (phosphofructokinase and lactate dehydrogenase) in glycolytic metabolic pathway in the heart was markedly higher in the SHR group compared with the Control group, whereas these mRNA expressions did not differ between Trained group and Control group. These findings suggest that the molecular phenotypes in the energy metabolic system differ in hypertension-induced pathological and exercise training-induced physiological cardiac hypertrophy, and these differences may participate in the differences in cardiac function.

Animals↗

The effects of low-intensity single-leg exercise on regional arterial stiffness.

We examined the effect of low-intensity single-leg exercise (20 or 30 watt, 5 min) on pulse wave velocity from the femoral to the ankle arteries in 18 young men. After the exercise, the velocity significantly decreased in the exercised leg, but not in the counterpart, suggesting that the decrease in arterial stiffness in the exercised leg was induced mainly by exercise-related regional factors.

Adult↗

Involvement of endogenous endothelin-1 in exercise-induced redistribution of tissue blood flow: an endothelin receptor antagonist reduces the redistribution.

BACKGROUND: Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor peptide. Exercise results in a significant redistribution of tissue blood flow, which greatly increases blood flow in active muscles but decreases it in the splanchnic circulation. We reported that exercise causes an increase of ET-1 production in the internal organ and then hypothesized that ET-1 participates in the exercise-induced redistribution of tissue blood flow. We investigated the effects of acute endothelin-A (ETA)-receptor blockade on regional tissue blood flow during exercise in rats. METHODS AND RESULTS: Regional blood flow in the kidney, spleen, stomach, intestine, and muscles was measured using the microsphere technique before and during treadmill running of 30 minutes duration at 30 m/min after pretreatment with either an ETA-receptor antagonist (TA-0201; 0.5 mg/kg) or vehicle in rats. Blood flow in the kidney, spleen, stomach, and intestine was decreased by exercise, but the magnitude of the decrease after pretreatment with TA-0201 was significantly smaller than that after pretreatment with vehicle. Furthermore, the increase in blood flow to active muscles induced by exercise was significantly smaller in rats pretreated with TA-0201 than those pretreated with vehicle. CONCLUSIONS: The present study revealed that ET-1-mediated vasoconstriction participates in the decrease of blood flow in the internal organs of rats during exercise, and therefore, that these actions of endogenous ET-1 partly contribute to the increase of blood flow in active muscles during exercise. The data suggest that endogenous ET-1 participates in the exercise-induced redistribution of tissue blood flow.

Animals↗

Exercise causes a tissue-specific change of NO production in the kidney and lung.

Nitric oxide (NO) is produced in the vascular endothelium and is a potent vasodilator substance that participates in the regulation of local vascular tone. Exercise causes peculiar changes in systemic and regional blood flow, i.e., an increase of systemic blood flow and a redistribution of local tissue blood flow, by which the blood flow is greatly increased in the working muscles, whereas it is decreased in some organs such as the kidney and intestine. Thus we hypothesized that exercise causes a tissue-specific change of NO production in some internal organs. We studied whether exercise affects expression of NO synthase (NOS) mRNA and protein, NOS activity, and tissue level of nitrite/nitrate (stable end products of NO) in the kidneys (in which blood flow during exercise is decreased) and lungs (in which blood flow during exercise is increased with the increase of cardiac output) of rat. Rats ran on a treadmill for 45 min at a speed of 25 m/min. Immediately after this exercise, kidneys and lungs were quickly removed. Control rats remained at rest during this 45-min period. Expression of endothelial NOS (eNOS) mRNA in the kidneys was markedly lower in exercise rats than in control rats, whereas that in the lungs was significantly higher in exercise rats than in control rats. Western blot analysis confirmed down- and upregulation of eNOS protein in the kidney and lung, respectively, after exercise. On the other hand, neither expression of neuronal NOS (nNOS) mRNA and nNOS protein nor inducible NOS (iNOS) mRNA and iNOS protein in the kidneys and lungs differed between exercise and control rats. NOS activity in the kidney was significantly lower in exercise rats than in control rats, whereas that in the lung was significantly higher in exercise rats than in control rats. On the other hand, the iNOS activity in the kidneys and lungs did not differ between exercise rats and control rats. Tissue nitrite/nitrate level in the kidneys was markedly lower in exercise rats, whereas that in the lungs was significantly higher in exercise rats. The present results show that production of NO is markedly and tissue-specifically changed in the kidney and lung by exercise.

Animals↗

Moderate physical exercise induces the oxidation of human blood protein thiols.

Exercise is known to induce the oxidation of blood low-molecular-weight (LMW) thiols such as reduced glutathione (GSH). We previously reported that full-marathon running induced a decrease in human plasma levels of protein-bound sulfhydryl groups (p-SHs). Moderate exercise, a 30-min running at the intensity of the individual ventilatory threshold, performed by untrained healthy females caused a significant decrease in erythrocyte levels of p-SHs (mostly hemoglobin cysteine residues) and LMW thiols, but their levels returned to each baseline by 2 h. No significant change in plasma LMW thiols was observed. However, plasma levels of p-SHs significantly decreased after running and remained unchanged after 24 h. These results suggest that moderate exercise causes the oxidation of blood thiols, especially protein-bound thiols.

Adult↗

Effects of exercise training on expression of endothelin-1 mRNA in the aorta of aged rats.

Aging impairs endothelial function and the vascular tone regulation, although the precise mechanism remains unclear. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. Because ET-1 has a potent vasoconstrictor effect on vessels, it may be involved in the regulation of vascular tonus. We hypothesized that aging causes a decrease in ET-1 expression in aorta, and that exercise training improves the aging-induced decrease in ET-1 expression in aorta. This study was performed to examine whether gene expression of ET-1 in the aorta of rats is altered by aging and subsequent exercise training. We studied expression of ET-1 mRNA in the aortas of sedentary young rats (Sedentary young group, 4 months old), sedentary aged rats (Sedentary aged group, 23 months old), and swim trained aged rats (Training aged group, 23 months old; swimming training for 8 weeks, 5 days/week, 90 min/day). The expression of ET-1 mRNA in the aorta was analysed by real-time quantitative PCR. Body weight and resting heart rate were significantly lower in the Training aged group compared with the Sedentary aged group. These results suggest that the Training aged rats exhibited physiological effects from exercise training. The expression of ET-1 mRNA in the aorta was markedly lower in Sedentary aged group compared with the Sedentary young group, whereas it was significantly higher in Training aged group compared with the Sedentary aged group. These results show that the expression of ET-1 mRNA in the aorta is decreased by aging, and that the expression is increased by exercise training. Therefore, the present study provides a possibility that exercise training improves endothelial function through up-regulation of the aging-induced decrease in ET-1 expression in the aorta.

Aging↗

Effects of aging and subsequent exercise training on gene expression of endothelin-1 in rat heart.

Endothelin-1 (ET-1) is produced by endothelial cells and cardiac myocytes. ET-1 has potent positive inotropic and chronotropic effects on heart and induces myocardial cell hypertrophy. We investigated whether gene expression of ET-1 in rat hearts is altered by aging and subsequent exercise training. We also investigated whether gene expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which participate in some pathological cardiac conditions, in the rat hearts is altered by aging and subsequent exercise training. We studied mRNA expression of ET-1, ANP and BNP in hearts of sedentary young rats (Sedentary young; 4 months old), sedentary aged rats (Sedentary aged; 23 months old), and swim-trained aged rats (Trained aged; 23 months old, swimming training for 8 weeks). The left ventricle weight mass index for body weight and left ventricular end-diastolic dimension were significantly higher in the Trained aged group compared with the Sedentary aged group. These results showed that Trained aged rats developed cardiac hypertrophy with improvement of cardiac function. The mRNA expression of ET-1 in the heart was significantly higher in Sedentary aged group compared with Sedentary young group, and was significantly higher in the Trained aged group compared with the Sedentary aged group. The mRNA expression of ANP and BNP in the heart was significantly higher in Sedentary aged group compared with Sedentary young group, and was significantly higher in the Trained aged group compared with the Sedentary aged group. The present results show that mRNA expression of ET-1 in the heart is increased by aging, and that the mRNA expression is further increased by exercise-induced cardiac hypertrophy, suggesting that ET-1 in the heart may participate in these physiological cardiac adaptations.

Aging↗

Aging-induced decrease in the PPAR-alpha level in hearts is improved by exercise training.

Peroxisome proliferator-activated receptor (PPAR)-alpha, a transcriptional activator, regulates genes of fatty acid (FA) metabolic enzymes. To study the contribution of PPAR-alpha to exercise training-induced improvement of FA metabolic capacity in the aged heart, we investigated whether PPAR-alpha signaling and expression of its target genes in the aged heart are affected by exercise training. We used hearts of sedentary young rat (4 mo old), sedentary aged rat (23 mo old), and swim-trained aged rat (23 mo old, training for 8 wk). The mRNA and protein expression of PPAR-alpha in the heart was significantly lower in the sedentary aged rats compared with the sedentary young rats and was significantly higher in the swim-trained aged rats compared with the sedentary aged rats. The activity of PPAR-alpha DNA binding to the transcriptional regulating region on the FA metabolic enzyme genes, the mRNA expression of 3-hydroxyacyl CoA dehydrogenase (HAD) and carnitine palmitoyl transferase-I, which are PPAR-alpha target genes, and the enzyme activity of HAD in the heart altered in association with changes of the myocardial PPAR-alpha mRNA and protein levels. These findings suggest that exercise training improves aging-induced downregulation in myocardial PPAR-alpha-mediated molecular system, thereby contributing to the improvement of the FA metabolic enzyme activity in the trained-aged hearts.

3-Hydroxyacyl CoA Dehydrogenases↗

[Changes in blood volume in the muscles of the thigh and calf during exercise and recovery and their relationships to exercise tolerance in patients with cardiac disease].

OBJECTIVES: This study compared the blood-volume changes and recovery in the thigh and calf during leg exercise and evaluated the relationships to exercise tolerance. METHODS: The peak oxygen uptake and total hemoglobin level(blood-volume index), oxyhemoglobin level, and deoxyhemoglobin level in the thigh and calf were measured by near-infrared spectroscopy during leg ergometer exercise and recovery in 13 patients with cardiac disease(mean age: 66 +/- 6 years, left ventricular ejection fraction: 31-82%). RESULTS: There was no significant difference between the increase in blood-volume index during exercise in the thigh and that in the calf. The increase in the blood-volume index during recovery in the calf was significantly greater than that in the thigh, mainly due to the difference in deoxyhemoglobin levels. There were no positive relationships between the peak oxygen uptake and increases in blood-volume index except for the increase in blood-volume index in the thigh during exercise(r = 0.73). CONCLUSIONS: There was no significant difference between the increase in blood-volume index in the thigh and that in the calf during exercise, whereas the increase in blood-volume index during recovery in the calf was significantly greater than that in the thigh in patients with cardiac disease. Only the increase in the blood-volume index in the thigh during exercise is related to the leg-exercise tolerance in patients with cardiac disease.

Aged↗