Habitual isomaltulose intake reduces arterial stiffness associated with postprandial hyperglycemia in middle-aged and elderly people: a randomized controlled trial.

Endothelin-1 (ET-1), produced by vascular endothelial cells, plays a pivotal role in the regulation of vascular tone. Isomaltulose, a naturally occurring sweetener and structural isomer of sucrose, reduces postprandial hyperglycemia, but its effect on arteriosclerosis due to hyperglycemia is unknown. The effects of 12 weeks of isomaltulose administration on ET-1 levels, a peptide that regulates arterial stiffness, blood pressure, and vascular tone, were tested before and after an oral glucose tolerance test. Fifty-four healthy middle-aged and older adults (30 men and 24 women) were divided into two groups: (1) a 25 g isomaltulose jelly drink intake group (Group I, 27 participants, mean age 55 ± 1 years) and (2) a sucrose jelly drink intake group (Group S, 27 participants, mean age 55 ± 1 years), each consuming isomaltulose or sucrose daily for 12 weeks, and a randomized, controlled study was conducted. Participants visited the laboratory before the intervention and 4, 8, and 12 weeks after the intervention to measure carotid-femoral (cf) and brachial-ankle (ba) pulse wave velocity (PWV), systolic blood pressure (BP), plasma glucose (PG), insulin, and ET-1 levels before and 60 and 120 min after a 75-g OGTT. baPWV, and ET-1 levels before intervention were significantly increased after 75-g OGTT compared to before 75-g OGTT in both groups (p < 0.05). The post-intervention baPWV, and ET-1 levels were significantly increased after 75-g OGTT in Group S compared to before 75-g OGTT (p < 0.05), whereas no significant changes were observed in Group I. These results suggest that consumption of isomaltulose, which has a lower GI than sucrose, is more effective in preventing the increases in systemic arterial stiffness associated with postprandial hyperglycemia in healthy middle-aged and older adults.

Effect of aerobic exercise training frequency on arterial stiffness in middle-aged and elderly females.

[Purpose] This study aimed to determine the effects of aerobic exercise training frequency on arterial stiffness in postmenopausal females. [Participants and Methods] This study included 45 postmenopausal females randomly assigned to one of the following three groups: 1) low-frequency training group (aerobic exercise training twice per week); 2) high-frequency training group (aerobic exercise training four times per week); and 3) control group (no training). Each group was subjected to an 8-week intervention period. Both traditional and newer indexes were measured immediately before and after the 8-week intervention period. [Results] In the low-frequency training group, carotid-femoral pulse wave velocity and arterial velocity pulse index decreased post 8 weeks compared with those at baseline. In the high-frequency training group, carotid-femoral, brachial-ankle, and heart-brachial pulse wave velocities and arterial velocity pulse and arterial pressure-volume indexes decreased post 8 weeks compared to those at baseline. In the control group, no change in any indices post 8 weeks compared to those at baseline was observed. [Conclusion] Carotid-femoral pulse wave velocity was lower after aerobic training than before training in both the exercise groups. Thus, aerobic exercise training might have a beneficial effect on aortic stiffness, regardless of the training frequency in this population.

Effects of Different Types of Carbohydrates on Arterial Stiffness: A Comparison of Isomaltulose and Sucrose.

Increased arterial stiffness during acute hyperglycemia is a risk factor for cardiovascular disease, but the type of carbohydrate that inhibits it is unknown. The purpose of this study was to determine the efficacy of low-glycemic-index isomaltulose on arterial stiffness during hyperglycemia in middle-aged and older adults. Ten healthy middle-aged and older adult subjects orally ingested a solution containing 25 g of isomaltulose (ISI trial) and sucrose (SSI trial) in a crossover study. In the SSI trial, the brachial-ankle (ba) pulse wave velocity (PWV) increased 30, 60, and 90 min after ingestion compared with that before ingestion (p < 0.01); however, in the ISI trial, the baPWV did not change after ingestion compared with that before ingestion. Blood glucose levels 30 min after intake were lower in the ISI trial than in the SSI trial (p < 0.01). The baPWV and systolic blood pressure were positively correlated 90 min after isomaltulose and sucrose ingestion (r = 0.640, p < 0.05). These results indicate that isomaltulose intake inhibits an acute increase in arterial stiffness. The results of the present study may have significant clinical implications on the implementation of dietary programs for middle-aged and elderly patients.

The Effect of Aerobic Exercise Training Frequency on Arterial Stiffness in a Hyperglycemic State in Middle-Aged and Elderly Females.

The frequency of aerobic exercise training in reducing the increase in arterial stiffness during acute hyperglycemia, a risk factor for cardiovascular disease, is unknown. The aim of the study was to determine the aerobic exercise training frequency on arterial stiffness in a hyperglycemic state in middle-aged and elderly females. Twenty healthy elderly people were randomly assigned to a two-times-a-week (T2, n = 10) and four-times-a-week (T4, n = 10) exercise group. All participants exercised for 35 min per session, which consisted of jogging exercises with a heart rate intensity of 65%. Brachial-ankle (ba), and heart-brachial (hb) pulse wave velocity (PWV) were measured before, 4 and 8 weeks after intervention; before the oral ingestion of 75-g of glucose; and 30, 60, and 90 min after ingestion. The baPWV before and 4 weeks after the intervention increased in both groups (p < 0.05), but only increased 8 weeks after intervention in the T2 group. hbPWV was unchanged before, 4 and 8 weeks after intervention in both groups. These findings show that frequent aerobic exercise suppresses the increase in arterial stiffness following glucose intake. The results of this study can be used to support the implementation of exercise programs for middle-aged and elderly patients.

Identification of the Core Activate Position for a Seated Subject: Proposal of a new Exercise Method for Maintenance Rehabilitation.

OBJECTIVES: This study aimed to identify a position for core muscle activation (core activate position) for a seated subject and to design an exercise method using this position for rehabilitation during the daily maintenance or maintenance stages. METHODS: Thirteen young men participated as subjects in this study. We manufactured a chair in which the seat had an adjustable forward tilt angle. The subjects underwent ultrasonographic measurements of the thickness of the transversus abdominis, internal oblique, and external oblique muscles while sitting in the chair with the seat angle adjusted to 0°, 6°, or 12°. Further, we conducted image analysis to determine the positional relationships of these muscles using the following four points as landmarks: the anterior superior iliac spine, the posterior superior iliac spine, the fourth lumbar vertebra, and the seventh thoracic vertebra. RESULTS: Significant increases in the thickness of the transversus abdominis and external oblique muscles were observed when the seat forward tilt angle was adjusted to 12° (P <0.05). In the core activate position (which demonstrated effective activation of the transversus abdominis), the posterior superior iliac spine, the fourth lumbar vertebra, and the seventh thoracic vertebra were aligned in a straight line that was nearly perpendicular to the line connecting the anterior superior iliac spine and the posterior superior iliac spine. CONCLUSIONS: This postural guidance can be applied to core exercise methods during maintenance rehabilitation.

Acute effects of difference in glucose intake on arterial stiffness in healthy subjects.

BACKGROUND: Post-prandial hyperglycemia is associated with higher cardiovascular risk, which causes arterial stiffening and impaired function. Although post-prandial increases in blood glucose are proportional to the level of intake, the acute effects of different glucose intakes on arterial stiffness have not been fully characterized. The present study aimed to determine the acute effects of differences in glucose intake on arterial stiffness. METHODS: Six healthy middle-aged and elderly individuals (mean age, 60.0 ± 12.1 years) were orally administered 15, 20, and 25 g of glucose on separate days in a randomized, controlled, cross-over fashion. Brachial-ankle pulse wave velocity, heart-brachial pulse wave velocity, cardio-ankle vascular index, brachial and ankle blood pressure, heart rate, and blood glucose and serum insulin concentrations before and 30, 60, and 90 min after glucose ingestion were measured. RESULTS: Compared to baseline, brachial-ankle pulse wave velocity was higher at 30, 60 and 90 min after ingestion of 25 g glucose, and higher at 90 min after ingestion of 20 g glucose, but at no time points after ingestion of 15 g. Cardio-ankle vascular index was higher at 60 min than at baseline after ingestion of 25 g glucose, but not after ingestion of 15 or 20 g. CONCLUSIONS: These results suggest that brachial-ankle pulse wave velocity and cardio-ankle vascular index is affected by the quantity of glucose ingested. Proposed presently is that glucose intake should be reduced at each meal to avoid increases in brachial-ankle pulse wave velocity and cardio-ankle vascular index during acute hyperglycemia.

Effects of a short-term increase in physical activity on arterial stiffness during hyperglycemia.

We examined the effects of increasing physical activity on arterial stiffness during hyperglycemia. Nineteen glucose-intolerant elderly participated in the study. We randomly assigned 10 participants to increase their daily activity in everyday life, regardless of the time or intensity, for 1 month (PAI group) (age, 74.6 ± 1.3 years; mean ± SE) and nine participants to maintain their level of activity (CON group) (age, 79.2 ± 2.1 years; mean ± SE). The 75-g oral glucose tolerance test was conducted in each participant in both groups before and after the start of the intervention to confirm glucose intolerance. Brachial-ankle pulse wave velocity and cardio-ankle vascular index significantly increased from baseline at 30, 60, and 90 min after the 75-g glucose ingestion after the intervention in the CON group (p<0.05), but not in the PAI group. Heart-brachial pulse wave velocity did not change compared to baseline after the 75-g glucose ingestion in either group and did not change from baseline at 30, 60, and 90 min after the 75-g glucose ingestion before and after the intervention in both groups. The present findings indicate that a short-term increase in physical activity suppresses the increase in arterial stiffness after glucose intake.

Effects of different intensities and durations of aerobic exercise training on arterial stiffness.

[Purpose] In the present study, we investigated the effects of regular aerobic training with different intensities and durations on new indices of arterial stiffness measured via an upper-arm oscillometric device. [Participants and Methods] We gathered data from 41 middle-aged and older people (age 65.0 ± 11.7 years). Participants were randomly divided into five groups: (1) 15 minutes of low intensity aerobic training (n=10); (2) 30 minutes of low intensity training (n=7); (3) 15 minutes of moderate-intensity training (n=9); (4) 30 minutes of moderate-intensity training (n=8); and (5) a non-training group (n=7). Training was conducted for 8 weeks, three times per week. Arterial pulse wave index, arterial pressure-volume index, brachial-ankle and heart-brachial pulse wave velocity, cardio-ankle vascular index, brachial and ankle blood pressure, heart rate, and peak oxygen uptake were measured before and after the intervention. [Results] All indicators of arterial stiffness and brachial and ankle blood pressure in the exercise groups were significantly lower after versus before the intervention. Peak oxygen uptake did not differ before versus after the intervention. [Conclusion] The present findings indicate that regular aerobic exercise may be important in reducing arterial stiffness regardless of the intensity or duration of aerobic exercise.

Arterial stiffness during hyperglycemia in older adults with high physical activity vs low physical activity.

We compared arterial stiffness after glucose intake in active and inactive elderly people with impaired glucose tolerance and clarified whether physical activity was associated with arterial stiffness after ingestion of glucose. Twenty older adults with impaired glucose tolerance were analyzed in a cross-sectional design. Based on the international physical activity questionnaire, participants were divided into the active group (daily step count: 10,175.9 ± 837.8 steps/day, n = 10) or the inactive group (daily step count: 4,125.6 ± 485.9 steps/day, n = 10). Brachial-ankle (systemic) and heart-brachial (aortic) pulse wave velocity and cardio-ankle vascular index (systemic) were increased at 30, 60, and 90 min compared to baseline after a 75-g oral glucose tolerance test in the inactive but not the active group. Heart-brachial pulse wave velocity did not change compared to baseline after a 75-g oral glucose tolerance test in either group. The area under the curve for brachial-ankle pulse wave velocity was associated with daily living activity (r = -0.577, p = 0.008), daily step activity (r = -0.546, p = 0.013), and the daily step count (r = -0.797, p = 0.0001). The present findings indicate that physical activity or inactivity is associated with arterial stiffness following glucose ingestion.

New indices of arterial stiffness measured with an upper-arm oscillometric device in active versus inactive women.

Arterial velocity pulse index (AVI) and arterial pressure-volume index (API), new indicators of arterial stiffness, are risk factors for the development of cardiovascular disease. Regular aerobic exercise decreases arterial stiffness. In fact, pulse wave velocity (PWV), index of arterial stiffness, is lower in endurance-trained than in untrained young adults. However, the effect of regular aerobic exercise on AVI and API remains unknown. This study investigates the effect of regular aerobic exercise on AVI and API, new indicators of arterial stiffness. We gathered data from 18 recreationally active females (active group, age: 18 ± 1 years, 2 ± 2 h/week, 3 ± 2 times/week, ≥2 years of aerobic endurance training) and 18 recreationally inactive females (inactive group, age: 18 ± 1 years, ≥2 years without such training) in a cross-sectional study. Height, body weight, body mass index, AVI, API, brachial blood pressure, heart rate, and 20-m multistage shuttle run test were measured in a quiet room at a temperature between 24°C and 25°C. AVI and API were lower in the active group than in the inactive group (P < 0.01). Number of 20-m shuttles was negatively correlated with AVI (P < 0.01, r = -0.8) and API (P < 0.01, r = -0.8). These results suggest that regular aerobic exercise training decreases AVI and API in young females.

Masked function of amino acid sensors on pancreatic hormone secretion in ventromedial hypothalamic (VMH) lesioned rats with marked hyperinsulinemia.

SUMMARY: In neural regulation of the endocrine pancreas, there is much evidence to suggest that vagal efferents alter insulin and glucagon secretion, but less information on the effects of vagal afferents. In this study, we investigated the role and function of afferent fibers of the vagus nerve in normal and ventromedial hypothalamic (VMH) lesioned rats with marked hyperinsulinemia. In normal rats, hepatic vagotomy was associated with intraperitoneal (ip) arginine-induced enhancement of insulin and glucagon secretion without an accompanying change in blood glucose levels, ip leucine induced enhancement of insulin secretion accompanied by a decrease in blood glucose levels, and ip alanine-induced enhancement of glucagon secretion accompanied by an increase in blood glucose levels. In VMH lesioned rats with marked hyperinsulinemia, none of these amino acids caused significant changes in insulin and glucagon secretion. We conclude that amino acid sensors in normal rats inhibit excess release of pancreatic hormones induced directly by intake of amino acids, such as that in excess protein ingestion, and maintain blood glucose levels within the normal range. In contrast, in VMH lesioned rats with marked hyperinsulinemia, the function of the amino acid sensors is masked due to the marked hyperinsulinemia in these rats.:

Enhanced exercise-induced muscle damage and muscle protein degradation in streptozotocin-induced type 2 diabetic rats.

UNLABELLED: Aims/Introduction: The effects of 5-day voluntary exercise on muscle damage and muscle protein degradation were investigated in a streptozotocin-induced rat model of moderately glycemic, uncontrolled, type 2 diabetes. MATERIALS AND METHODS: In the preliminary experiment, an oral glucose tolerance (1.0 g/kg) test was carried out to confirm the development of diabetes 3 days after streptozotocin treatment (30 mg/kg). In the genuine experiment, rats were divided into four groups: (i) non-diabetic rats without exercise (controls); (ii) non-diabetic rats with exercise; (iii) diabetic rats without exercise; and (iv) diabetic rats with exercise. After 5 days of voluntary wheel running exercise, blood and 24-h urine were collected, and levels of serum creatine kinase, a marker of muscle damage, and 24-h urinary excretion of muscle degradation products were determined. RESULTS: Type 2 diabetic rats with insulin deficiency that exercised had higher serum creatine kinase and greater urinary excretions of creatinine, urea nitrogen and 3-methylhistidine compared with both type 2 diabetic rats with insulin deficiency and non-diabetic rats that did not exercise. However, there were no differences in serum creatine kinase and urinary excretions of creatinine, urea nitrogen and 3-methylhistidine between non-diabetic rats that did and did not exercise. CONCLUSIONS: These findings suggest that muscle damage is induced and muscle protein degradation are enhanced by chronic moderate exercise in moderately glycemic uncontrolled type 2 diabetic rats with insulin deficiency at an intensity level of exercise that does not affect muscle damage and muscle protein degradation in non-diabetic rats. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00130.x, 2011).

Effects of gastric vagotomy on visceral cell proliferation induced by ventromedial hypothalamic lesions: role of vagal hyperactivity.

In rats, ventromedial hypothalamic (VMH) lesions induce cell proliferation in the visceral organs (stomach, small intestine, liver, and pancreas) due to hyperactivity of the vagus nerve. To investigate the effects of selective gastric vagotomy on VMH lesion-induced cell proliferation and secretion of gastric acid, we assessed the mitotic index (the number of proliferating cell nuclear antigen (PCNA)-immunopositive cells per 1,000 cells in the gastric mucosal cell layer) and measured the volume of secreted basal gastric acid. Furthermore, to explore whether or not ethanol-induced acute gastric mucosal lesions (AGML) lead to ulcer formation in VMH-lesioned rats, we assessed the ulcer index of both sham-operated and VMH-lesioned rats after administration of ethanol. VMH lesions resulted in an increased mitotic index and thickness of the gastric mucosal cell layer and gave rise to the hypersecretion of gastric acid. Selective gastric vagotomy restored these parameters to normal without affecting cell proliferation in other visceral organs. Ethanol-induced AGML caused ulcers in sham VMH-lesioned rats, whereas VMH-lesioned rats were less likely to exhibit such ulcers. These results suggest that VMH lesion-induced vagally mediated cell proliferation in the visceral organs is associated with hyperfunction in these organs, and VMH lesion-induced resistance to ethanol may be due to thickening of the gastric mucosal cell layer resulting from cell proliferation in the gastric mucosa-this in turn is due to hyperactivity of the vagus nerve.