Mutsuko Yoshizawa

Effect of 12 weeks of moderate–intensity resistance training on arterial stiffness: a randomised controlled trial in women aged 32–59 years

Background: Resistance training has been increasingly incorporated into the overall exercise programme because of its effect on muscle strength, functional capacity and osteoporosis. High-intensity resistance training increases arterial stiffness. However, the effect of moderate-intensity resistance training on arterial stiffness is unknown. Objective: To determine whether 12 weeks of moderate-intensity resistance training increases arterial stiffness in middle-aged women. Methods: 35 middle-aged women (age range 32 to 59 years) volunteered to participate. The subjects were randomly assigned to one of three groups: resistance training (RT) group, aerobic exercise training (AET) group or control group. The RT and AET groups performed 12 weeks of moderate-intensity resistance training or aerobic exercise training (two days/week). Results: In the RT group, one-repetition maximum strength significantly increased after the intervention. Interestingly, aortic (carotid–femoral) pulse wave velocity (PWV; an index of arterial stiffness), and peripheral (femoral–ankle) PWV did not change with moderate-intensity resistance training. In contrast, in the AET group, carotid–femoral PWV significantly decreased after the intervention. Resistance training and aerobic exercise training did not affect blood pressure. Conclusions: This study found that moderate-intensity resistance training did not increase arterial stiffness in middle-aged women, which may have great importance for health promotion with resistance training.

Effect of weight reduction with dietary intervention on arterial distensibility and endothelial function in obese men

Obesity and reduction in central arterial distensibility, respectively, have been identified as powerful and independent risk factors for cardiovascular disease. However, the effect of weight reduction on central arterial function in obese subjects has not yet been clarified. We investigated whether low-calorie diet-induced weight reduction affects central arterial distensibility and endothelial function in middle-aged obese men. Twelve obese men (age: 45+2 yrs, BMI: 30+1 kg/m 2) completed a 12-week dietary intervention. Caloric restriction induced significantly weight loss and decrease in BMI. After the program, carotid arterial compliance significantly increased and b-stiffness index and aortic pulse-wave velocity remarkably decreased. Concentrations of plasma endothelin-1 (ET-1) significantly decreased and plasma nitric oxide (NO) markedly increased after the program. Weight reduction by low-calorie diet in obese men increases central arterial distensibility, which may contribute to the improvement in endothelial function, as noted by a decrease in ET-1 and an increase in NO.

Additive beneficial effects of lactotripeptides and aerobic exercise on arterial compliance in postmenopausal women

Central arterial compliance plays an important role in the functional abilities of the vasculature. Two active tripeptides, valine-proline-proline and isoleucine-proline-proline, were isolated from sour milk and were referred to as lactotripeptides (LTP). Because LTP appears to act as an angiotensin-converting enzyme inhibitor, it is plausible to hypothesize that LTP improves arterial compliance. We determined the effects of LTP ingestion alone or in combination with regular aerobic exercise on arterial compliance. A total of 55 postmenopausal women (50-65 yr old) were randomly divided into four groups: placebo, LTP, exercise and placebo (Ex + placebo), or exercise and LTP (Ex + LTP). LTP or placebo was administered orally for 8 wk. The exercise groups completed an 8-wk moderate aerobic exercise intervention. There were no differences in baseline arterial compliance and most other key dependent variables among the groups. Carotid arterial compliance increased significantly in the LTP (0.93 + or - 0.07 vs. 0.99 + or - 0.08 mm(2)/mmHg x 10(-1)), Ex + placebo (0.92 + or - 0.04 vs. 1.00 + or - 0.05 mm(2)/mmHg x 10(-1)), and Ex + LTP groups (0.86 + or - 0.06 vs. 1.00 + or - 0.06 mm(2)/mmHg x 10(-1)), whereas no such changes were observed in the placebo control group (0.86 + or - 0.06 vs. 0.85 + or - 0.07 mm(2)/mmHg x 10(-1)). The magnitude of increases in carotid arterial compliance was significantly greater in the Ex + LTP group (19 + or - 4%) than in other groups. The improvements in arterial compliance with LTP were associated with the corresponding reductions in arterial blood pressure and plasma angiotensin II concentrations. We concluded that LTP ingestion improves carotid arterial compliance and that the combination of LTP ingestion and regular exercise is additive and synergistic in improving arterial compliance in postmenopausal women.

Effect of Habitual Aerobic Exercise on Body Weight and Arterial Function in Overweight and Obese Men

The effect of habitual exercise on vascular function, including central arterial distensibility and endothelial function, in obese subjects has not yet been clarified. We investigated whether aerobic exercise training affects central arterial distensibility and endothelial function in middle-age overweight and obese men. A total of 21 overweight and obese men (age 50 +/- 2 years, body mass index 30 +/- 1 kg/m(2)) completed a 12-week aerobic exercise intervention. Aerobic exercise training significantly reduced their body weight and resulted in a significant decrease in body mass index. After the weight-reduction exercise program, carotid arterial compliance (determined by simultaneous B-mode ultrasonography and arterial applanation tonometry on the common carotid artery) significantly increased; and the beta-stiffness index, an index of arterial compliance adjusted for distending pressure, significantly decreased. The concentrations of plasma endothelin-1, a potent vasoconstrictor peptide produced by vascular endothelial cells, significantly decreased and plasma nitric oxide (measured as the stable end product [nitrite/nitrate]), a potent vasodilator produced by vascular endothelial cells, significantly increased after the weight-reduction exercise program. In conclusion, weight reduction by aerobic exercise training in overweight and obese men increased the central arterial distensibility. This increase might contribute to the improvement in endothelial function, as assessed by a decrease in endothelin-1 and an increase in nitric oxide, after exercise training-induced weight loss.

Involvement of endothelin-1 in habitual exercise-induced increase in arterial compliance.

Aim:  Habitual aerobic exercise results in a significant increase in central arterial compliance. Endothelin‐1 (ET‐1) is a potent endothelium‐derived vasoconstrictor peptide and could play a role in mediating the habitual aerobic exercise‐induced increase in central arterial compliance. The aim of the present study was to examine whether ET‐1 is involved in the mechanisms underlying the increase in central arterial compliance with aerobic exercise training.

Additive beneficial effects of lactotripeptides intake with regular exercise on endothelium-dependent dilatation in postmenopausal women.

BACKGROUND Peripheral conduit artery endothelium-dependent dilatation decreases with aging in humans. Lactotripeptides (LTPs) and regular exercise can improve endothelium-dependent dilatation, but combining these lifestyle modifications may be more effective than either treatment alone. We conducted a randomized, place-controlled trial with four different intervention arms. METHODS A total of 43 postmenopausal women (50-65 years old) were randomly divided into placebo, LTP, exercise and placebo (Ex+placebo), or exercise and LTP (Ex+LTP) groups. LTP or placebo was administered orally for 8 weeks. The exercise groups completed an 8-week moderate aerobic exercise (walking or cycling) intervention. RESULTS There were no statistically significant differences in baseline flow-mediated dilatation (FMD) and most other key dependent variables among the groups. FMD significantly increased in the LTP, Ex+placebo, and Ex+LTP groups whereas no such changes were observed in the placebo control group. The magnitude of increases in FMD was significantly greater in the Ex+LTP group than other intervention groups. CONCLUSION We concluded that LTP ingestion combined with regular aerobic exercise improves endothelium-dependent dilatation to a greater extent than monotherapy with either intervention alone in postmenopausal women.

Regular endurance exercise in young men increases arterial baroreflex sensitivity through neural alteration of baroreflex arc

Endurance exercise training increases arterial baroreflex sensitivity that corresponds to alteration in vessel wall compliance of the carotid artery in elderly men. Here, we examined whether regular endurance exercise increases arterial baroreflex sensitivity through neural alteration of the baroreflex arc in young men. We assessed arterial baroreflex sensitivity in eight sedentary men (age 24 +/- 1 yr) and nine men trained in endurance exercise (age 23 +/- 1 yr) during phase IV of the Valsalva maneuver [systolic arterial blood pressure (SAP)-R-R interval relationship]. Arterial baroreflex sensitivity was further analyzed by dividing the mechanical component [SAP-end-systolic carotid lumen diameter relationship (ultrasonography)] and the neural component (end-systolic carotid lumen diameter-R-R interval relationship). Carotid arterial compliance was determined using B-mode ultrasound and arterial applanation tonometry on the common carotid artery. Arterial baroreflex sensitivity and its neural component were greater in the exercise-trained group (P < 0.05). In contrast, carotid arterial compliance and the mechanical component of arterial baroreflex sensitivity did not differ between groups. These results suggest that regular endurance exercise in young men increases arterial baroreflex sensitivity through changes in the neural component of the baroreflex arc and not through alterations in vessel wall compliance of the carotid artery.

Combination of polymorphisms in the β2-adrenergic receptor and nitric oxide synthase 3 genes increases the risk for hypertension

Objective Hypertension is a major risk factor for cardiovascular disease. Polymorphism in the β2-adrenergic receptor (ADRB2) and nitric oxide synthase 3 (NOS3) genes is associated with clinical cardiovascular phenotypes. The Arg16Gly and Glu298Asp polymorphisms of ADRB2 and NOS3 genes, respectively, have been reported to be associated with hypertension. We hypothesized that a combination of these two polymorphisms increases the risk for hypertension. Hence, we examined the effect of this combination of single-nucleotide polymorphisms on the risk for hypertension. Methods Our cross-sectional study comprised 402 middle-aged and elderly human participants. We determined the genotypes of Arg16Gly and Glu298Asp single-nucleotide polymorphisms in ADRB2 and NOS3, respectively, by TaqMan PCR method; we also measured the resting blood pressure. Results The odds ratio for the presence of hypertension in individuals having the Gly/Gly genotype of ADRB2 compared with those having the other genotypes (Arg/Arg and Arg/Gly) was 2.87. With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79. Interestingly, the odds ratio was 7.64 for individuals having a combination of the Gly/Gly genotype of ADRB2 and Glu/Glu genotype of NOS3 when compared with those having a combination of Arg/Arg and Arg/Gly genotypes of ADRB2 and Asp/Asp and Asp/Glu genotypes of NOS3. Conclusion We revealed that a combination of the Arg16Gly and Glu298Asp polymorphisms in ADRB2 and NOS3, respectively, remarkably increased the risk for hypertension in middle-aged and elderly humans.

High circulating levels of oxidized LDL in strength-trained athletes

Oxidized low-density lipoprotein (oxLDL) has been shown to play a major role in the progression of atherosclerosis and cardiovascular disease. Aerobic exercise training has been reported to decrease plasma oxLDL levels. However, until now, there have been no studies regarding the effect of strength exercise training on plasma oxLDL levels. The purpose of this study was to investigate the plasma oxLDL. concentration and antioxidant capacity of plasma in strength-trained athletes. We specifically assessed the total scavenging activity against plasma hydroxyl radical (HO,) and alkoxyl radical (RO,) by using the electron spin resonance (ESR) technique, as both radicals are involved in oxLDL production. The subjects included young strength-trained athletes (SA group; shot put, hammer, javelin throwers, or power lifters; n=9) and sedentary individuals (control group; n=9). We measured plasma oxLDL concentrations and total scavenging activity against HO, and RO. Maximal muscle strength, as assessed by isokinetic tests of the knee and elbow joints and maximal handgrip strength, was significantly greater in the SA group than in the control group. Plasma oxl.DL concentrations were found to be significantly higher in the SA group than in the control group. The total scavenging activity of plasma against HO, and RO. did not differ between the two groups. These results suggest that high-intensity strength training increases plasma oxLDL concentration without upregulating the total scavenging activity against plasma HO, and RO.