Biomedical subjects

M Iemitsu

Publications and source records attributed to M Iemitsu.

12 recordsLinked to original sources

PubMed2006

Effects of leg resistance training on arterial function in older men.

BACKGROUND: Little information is available on the effect of strength training on vascular function, particularly in older people. OBJECTIVE: To determine the effect of resistance training on arterial stiffness and endothelial function in older adults. METHOD: Eleven healthy men (mean (SEM) age 64 (1) years) performed 12 weeks of resistance training involving knee flexion and extension (three sets a day, two days a week). RESULTS: Resistance training increased maximal muscle power by 16% (p<0.0001). Arterial stiffness as assessed by aortic pulse wave velocity did not change with resistance training. Plasma concentration of nitric oxide (NO), measured as its stable end product (nitrite/nitrate), had increased (p<0.05) after resistance training (61.2 (10.4) v 39.6 (3.2) micromol/l). There was no change in plasma concentration of endothelin-1. CONCLUSION: The results suggest that short term resistance training may increase NO production without stiffening central arteries in healthy older men.

Aged↗

PubMed2006

Contribution of systemic arterial compliance and systemic vascular resistance to effective arterial elastance changes during exercise in humans.

BACKGROUND: Effective arterial elastance (Ea), an index of arterial load, increases with elevations in left ventricular elastance to maximize the efficiency of left ventricular stroke work during exercise. Systemic arterial compliance (C) and vascular resistance (R) are the primary components contributing to Ea, and R plays a greater role in determining Ea at rest. We hypothesized that the contribution of C to Ea increases during exercise to maintain an optimal balance between arterial load and ventricular elastance, and that the increase in Ea is due primarily to a reduction in C. AIM: The aim of this study was to investigate the contributions of C and R to Ea during exercise. METHODS: Ea (0.9 x systolic blood pressure/stroke volume), C (stroke volume/pulse pressure), R (mean blood pressure/cardiac output), and cardiac cycle length (T) were measured at rest and during exercise of 40%, 60% and 80% maximal oxygen uptake (O(2max)) using Doppler echocardiography in 45 healthy men. RESULTS: Ea did not differ between rest and 40%O(2max), but it was greater at 60% and 80%O(2max). C markedly decreased during exercise in an exercise intensity-dependent manner. The changes in R/T during exercise were small, whereas it decreased at 40%O(2max) and gradually increased at 60% and 80%O(2max). CONCLUSIONS: The present results suggest that the contribution of systemic arterial compliance to effective arterial elastance increases during exercise. Therefore, we propose that the increase in arterial load during exercise is mainly driven by a reduction in systemic arterial compliance.

Adult↗

PubMed2005

Acute exercise causes an enhancement of tissue renin-angiotensin system in the kidney in rats.

AIMS: Initially, the renin-angiotensin system (RAS) produced through the classical endocrine pathway was well known for its regulation of blood pressure. However, it was revealed that a local autocrine and/or paracrine RAS may exist in a number of tissues (such as kidney). Exercise causes a redistribution of tissue blood flow, by which the blood flow is greatly increased in active muscles, whereas it is decreased in the splanchnic circulation (such as in the kidney). We hypothesized that exercise causes an enhancement of tissue RAS in the kidney. METHODS: We studied whether exercise affects expression of angiotensinogen and angiotensin-converting enzyme (ACE) and tissue angiotensin II level in the kidney. The rats performed treadmill running for 30-min. Immediately after this exercise, kidney was quickly removed. Control rats remained at rest during this 30-min period. RESULTS: The expression of angiotensinogen mRNA in the kidney was markedly higher in the exercise rats than in the control rats. ACE mRNA in the kidney was significantly higher in the exercise rats than in the control rats. Western blot analysis confirmed significant upregulation of ACE protein in the kidney after exercise. Tissue angiotensin II level was also increased by exercise. CONCLUSION: The present study suggests that the exercise-induced enhancement of tissue RAS in the kidney causes vasoconstriction and hence decreases blood flow in the kidney, which are helpful in increasing blood flow in active muscles, thereby contributing to the redistribution of blood flow during exercise.

Angiotensin II↗

PubMed2005

Gene expression profiling of exercise-induced cardiac hypertrophy in rats.

AIMS: Exercise training causes physiological cardiac hypertrophy, which acts to enhance cardiac function during exercise. However, the underlying molecular mechanisms are unclear. We investigated gene expression profile of exercise training-induced cardiac hypertrophy using left ventricle (LV) excised from exercise-trained and sedentary control rats (12-week old). METHOD: Rats in the training group exercised on a treadmill for 8-week. RESULTS: Left ventricular mass index and wall thickness in the exercise-trained group were significantly greater than that in the control group, indicating that the trained rats developed cardiac hypertrophy. Of the 3800 genes analysed in the microarray analyses, a total of 75 relevant genes (upregulation of 33 genes and downregulation of 42 genes) displayed alterations with exercise training. Among these genes, we focused on glycogen synthase kinase (GSK)-3beta, calcineurin-inhibitor (Cain), and endothelin (ET)-1 for their implicated roles in pathological cardiac hypertrophy, and confirmed the results of microarray analysis at mRNA and protein/peptide levels using quantitative PCR, Western blot, and EIA analyses. The gene expression of GSK-3beta decreased significantly and those of Cain and ET-1 increased significantly with exercise training. Furthermore, LV mass index was significantly correlated with GSK-3beta protein activity (r = -0.70, P < 0.01) and tissue ET-1 concentration (r = 0.52, P < 0.05). There were no changes in gene expressions in brain natriuretic peptide (BNP), angiotensin-correcting enzyme (ACE), interleukin-6, and vascular cell adhesion molecule (VCAM)-1. CONCLUSION: These findings suggest that physiological and pathological LV hypertrophy may share some of the same molecular mechanisms in inducing LV hypertrophy (e.g. GSK-3beta, Cain, and ET-1) and that other genes (e.g. BNP, ACE) may differentiate physiological from pathological LV hypertrophy.

Adaptation, Physiological↗

PubMed2003

Non-invasive assessment of cardiac output during exercise in healthy young humans: comparison between Modelflow method and Doppler echocardiography method.

AIMS: The Modelflow method can estimate cardiac output from arterial blood pressure waveforms using a three-element model of aortic input impedance (aortic characteristic impedance, arterial compliance, and systemic vascular resistance). We tested the reliability of a non-invasive cardiac output estimation during submaximal exercise using the Modelflow method from finger arterial pressure waveforms collected by Portapres in healthy young humans. METHODS: The Doppler echocardiography method was used as a reference method. Sixteen healthy young subjects (nine males and seven females) performed a multi-stage cycle ergometer exercise at an intensity corresponding to 70, 90, 110 and 130% of their individual ventilatory threshold for 2 min each. The simultaneous estimation of cardiac output (15 s averaged data) using the Modelflow and Doppler echocardiography methods was performed at rest and during exercise. RESULTS AND CONCLUSION: The Modelflow-estimated cardiac output correlated significantly with the simultaneous estimates by the Doppler method in all subjects (r = 0.87, P < 0.0001) and the SE of estimation was 1.93 L min-1. Correlation coefficients in each subject ranged from 0.91 to 0.98. Although the Modelflow method overestimated cardiac output, the errors between two estimates were not significantly different among the exercise levels. These results suggest that the Modelflow method using Portapres could provide a reliable estimation of the relative change in cardiac output non-invasively and continuously during submaximal exercise in healthy young humans, at least in terms of the relative changes in cardiac output.

Adult↗

PubMed2003

Exercise training improves ageing-induced decrease in eNOS expression of the aorta.

AIMS: Ageing impairs endothelial function such as the regulation of vascular tone. The release of nitric oxide (NO), which has a potent vasodilator effect and antiatherosclerotic property, is decreased in the aorta of aged rats. Exercise training, however, has been reported to increase the expression of endothelial NO synthase (eNOS) in the aorta of young rats. In aged rats, it is not known whether the expression of eNOS is altered by exercise training. We hypothesized that exercise training would improve the ageing-induced decrease in eNOS expression in vessels, and examined the messenger RNA (mRNA) and protein expression of eNOS in the aorta 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(-1), 90 min day(-1)). RESULTS: Body weight was significantly lower, and citrate synthase activity in the epitrochlearis muscle was significantly higher in the training-aged group compared with the sedentary-aged group. The mRNA expression of eNOS in the aorta was significantly higher in the training-aged group than in the sedentary-aged group, while it was significantly lower in both the sedentary-aged and training-aged groups than in the sedentary-young group. The expression of eNOS protein in the aorta was also significantly higher in the training-aged group than in the sedentary-aged group, while it was also significantly lower in the sedentary-aged group, but not in the training-aged group, than in the sedentary-young group. CONCLUSION: The present results revealed that the production of eNOS in the aorta decreases with ageing, and that the decreased production is increased by exercise training in aged rats, which may produce beneficial effects on the impaired cardiovascular system caused by ageing.

Aging↗

PubMed2001

Effects of exercise training of 8 weeks and detraining on plasma levels of endothelium-derived factors, endothelin-1 and nitric oxide, in healthy young humans.

Vascular endothelial cells produce nitric oxide (NO), which is a potent vasodilator substance and has been proposed as having antiatherosclerotic property. Vascular endothelial cells also produce endothelin-1 (ET-1), which is a potent vasoconstrictor peptide and has potent proliferating activity on vascular smooth muscle cells. Therefore, ET-1 has been implicated in the progression of atheromatous vascular disease. Because exercise training has been reported to produce an alteration in the function of vascular endothelial cells in animals, we hypothesized that exercise training influences the production of NO and ET-1 in humans. The purpose of the present study was to examine whether chronic exercise could influence the plasma levels of NO (measured as the stable end product of NO, i.e., nitrite/nitrate [NOx]) and ET-1 in humans. Eight healthy young subjects (20.3 +/- 0.5 yr old) participated in the study and exercised by cycling on a leg ergometer (70% VO2max for 1 hour, 3-4 days/week) for 8 weeks. Venous plasma concentrations of NOx and ET-1 were measured before and after (immediately before the end of 8-week exercise training) the exercise training, and also after the 4th and 8th week after the cessation of training. The VO2max significantly increased after exercise training. After the exercise training, the plasma concentration of NOx significantly increased (30.69 +/- 3.20 vs. 48.64 +/- 8.16 micromol/L, p < 0.05), and the plasma concentration of ET-1 significantly decreased (1.65 +/- 0.14 vs. 1.23 +/- 0.12 pg/mL, p < 0.05). The increase in NOx level and the decrease in ET-1 level lasted to the 4th week after the cessation of exercise training and these levels (levels of NOx and ET-1) returned to the basal levels (the levels before the exercise training) in the 8th week after the cessation of exercise training. There was a significant negative correlation between plasma NOx concentration and plasma ET-1 concentration. The present study suggests that chronic exercise causes an increase in production of NO and a decrease in production of ET-1 in humans, which may produce beneficial effects (i.e., vasodilative and antiatherosclerotic) on the cardiovascular system.

Adult↗

PubMed2001

Physiological and pathological cardiac hypertrophy induce different molecular phenotypes in the rat.

Pressure overload, such as hypertension, to the heart causes pathological cardiac hypertrophy, whereas chronic exercise causes physiological cardiac hypertrophy, which is defined as athletic heart. There are differences in cardiac properties between these two types of hypertrophy. We investigated whether mRNA expression of various cardiovascular regulating factors differs in rat hearts that are physiologically and pathologically hypertrophied, because we hypothesized that these two types of cardiac hypertrophy induce different molecular phenotypes. We used the spontaneously hypertensive rat (SHR group; 19 wk old) as a model of pathological hypertrophy and swim-trained rats (trained group; 19 wk old, swim training for 15 wk) as a model of physiological hypertrophy. We also used sedentary Wistar-Kyoto rats as the control group (19 wk old). Left ventricular mass index for body weight was significantly higher in SHR and trained groups than in the control group. Expression of brain natriuretic peptide, angiotensin-converting enzyme, and endothelin-1 mRNA in the heart was significantly higher in the SHR group than in control and trained groups. Expression of adrenomedullin mRNA in the heart was significantly lower in the trained group than in control and SHR groups. Expression of beta(1)-adrenergic receptor mRNA in the heart was significantly higher in SHR and trained groups than in the control group. Expression of beta(1)-adrenergic receptor kinase mRNA, which inhibits beta(1)-adrenergic receptor activity, in the heart was markedly higher in the SHR group than in control and trained groups. We demonstrated for the first time that the manner of mRNA expression of various cardiovascular regulating factors in the heart differs between physiological and pathological cardiac hypertrophy.

Actins↗

PubMed2000

Whole-body energy mapping under physical exercise using positron emission tomography.

We attempted to visualize dynamic adjustment of glucose utilization in humans in the whole-body organs during physical exercise by using three-dimensional positron emission tomography (3D-PET) and [18F]-2-fluoro-deoxy-glucose (FDG). Twelve healthy male volunteers collaborated on the study; six subjects were assigned to the resting control group (C) and the other six to the running group (E). Group E subjects performed running on a flat road for 35 min. After 15 min of running, subjects injected FDG and kept on running thereafter for another 20 min. Group C subjects sat on a comfortable chair in a quiet room for 35 min after the injection of FDG. After scanning by PET, the regions of interest (ROIs) were manually set on brain, heart, thorax, abdomen, lower extremities, and the rest of the body on the corresponding transaxial images. The uptake of FDG in each region was evaluated as the % fraction of FDG accumulation relative to the total amount of whole-body accumulation. The results revealed increase of FDG uptake after running in the lower leg muscles from 24.6 +/- 9.5% to 43.1 +/- 4.7% and in the heart from 2.3 +/- 0.4% to 2.8 +/- 0.6%. The differences were significant (P < 0.05). These increases reflect the rise in energy consumption in leg and heart muscles and were balanced by the reduction of energy consumption in the other part of the body. FDG uptake in the abdominal region reduced from 37.3 +/- 7.2% to 19.7 +/- 4.9%. However, FDG uptake in the brain remained stable, i.e., 11.9 +/- 2.8% at rest and 10.3 +/- 2.5% after exercise. Thus, 3D-PET is a tool to visualize the dynamic adjustment of energy consumption during physical exercise in humans.

Adult↗

PubMed2000

Intense exercise causes decrease in expression of both endothelial NO synthase and tissue NOx level in hearts.

Cardiac myocytes produce nitric oxide (NO). We studied the effects of intense exercise on the expression of NO synthase (NOS) and the tissue level of nitrite (NO(2)(-))/nitrate (NO(3)(-)) (i.e., NOx), which are stable end products of NO in the heart. Rats ran on a treadmill for 45 min. Immediately after this exercise, the heart was quickly removed. Control rats remained at rest during the same 45-min period. The mRNA level of endothelial NOS (eNOS) in the heart was markedly lower in the exercised rats than in the control rats. Western blot analysis confirmed downregulation of eNOS protein in the heart after exercise. Tissue NOx level in the heart was significantly lower in the exercised rats than in the control rats. The present study revealed for the first time that production of NO in the heart is decreased by intense exercise. Because NO attenuates positive inotropic and chronotropic responses to beta(1)-adrenergic stimulation in the heart, the decrease in cardiac production of NO by intense exercise may contribute to the acceleration of increase in myocardial contractility and heart rate during intense exercise.

Animals↗

PubMed1998

Effects of endurance training on the size and blood flow of the arterial conductance vessels in humans.

The aim of the present study was to determine non-invasively the effects of endurance training on both the size and blood flow of the arterial conductance vessels during exercise by men. Twelve healthy male subjects were assigned to either an exercise-trained group (ET, n = 7) or a sedentary control group (S, n = 5). The ET group underwent cycle-endurance training for 8 weeks (80% VO2max, 40 min day-1, 5 days week-1). The S group led normal lives during the 8-week period. Before and after the training period, cross-sectional areas (CSA) of the ascending and abdominal aorta were measured by echography. Measurements were taken in the semisupine position on a cycle ergometer fitted with a backrest, at rest and during 40, 60 and 80% VO2max of exercise. In addition, Doppler ultrasonographic velocity and flow in the ascending aorta were simultaneously measured. The CSA of the ascending and abdominal aorta after training were significantly larger than those before training in the ET group. Although there were no significant differences in the peak and mean velocities in the ascending aorta before and after the training in the ET group, the blood flow in the ascending aorta during exercise after training was significantly larger than that found before training at each relative intensity. There were no significant differences in any of the Doppler echographic parameters in the S group. These findings suggest that the arterial conductance vessels can be morphologically altered in an adaptive response to the endurance training. Furthermore, the dilation of the conductance vessels with endurance training contributes to an increase in blood flow to the exercising muscles without a rise in blood velocity. In other words, the arterial conductance vessels adapt to maintain adequate blood velocity and shear stress.

Adaptation, Physiological↗

PubMed1998

Prolonged exercise causes an increase in endothelin-1 production in the heart in rats.

Cardiac myocytes produce endothelin-1 (ET-1). ET-1 has potent positive inotropic and chronotropic effects. We investigated whether production of ET-1 in the heart is altered by prolonged exercise in rats. Rats ran on a treadmill for 45 min. Immediately after this exercise the heart and lungs were quickly removed. Control rats remained at rest during this 45-min period. Expression of preproET-1 mRNA in the heart was markedly higher in the exercised than in the control rats. The peptide level of ET-1 in the heart was also markedly higher in the exercised rats. Expression of endothelin type A- and type B-receptor mRNA and endothelin-converting enzyme mRNA in the heart did not differ between the groups. The peptide level of ET-1 and the preproET-1 mRNA level in the lungs of the exercised rats did not differ from those in the control rats. The present results show that production of ET-1 is markedly increased tissue specifically in the heart by exercise without appreciable changes in endothelin-converting enzyme and endothelin receptor expression. The present study suggests that myocardial ET-1 may participate in modulation of cardiac function during exercise.

Animals↗