Independent metabolic costs of supporting body weight and accelerating body mass during walking.

The metabolic cost of walking is determined by many mechanical tasks, but the individual contribution of each task remains unclear. We hypothesized that the force generated to support body weight and the work performed to redirect and accelerate body mass each individually incur a significant metabolic cost during normal walking. To test our hypothesis, we measured changes in metabolic rate in response to combinations of simulated reduced gravity and added loading. We found that reducing body weight by simulating reduced gravity modestly decreased net metabolic rate. By calculating the metabolic cost per Newton of reduced body weight, we deduced that generating force to support body weight comprises approximately 28% of the metabolic cost of normal walking. Similar to previous loading studies, we found that adding both weight and mass increased net metabolic rate in more than direct proportion to load. However, when we added mass alone by using a combination of simulated reduced gravity and added load, net metabolic rate increased about one-half as much as when we added both weight and mass. By calculating the cost per kilogram of added mass, we deduced that the work performed on the center of mass comprises approximately 45% of the metabolic cost of normal walking. Our findings support the hypothesis that force and work each incur a significant metabolic cost. Specifically, the cost of performing work to redirect and accelerate the center of mass is almost twice as great as the cost of generating force to support body weight.     

Blood pressure control during weight reduction in obese hypertensive men: separate effects of sodium and energy restriction.

The separate and combined effects of dietary energy and sodium restriction on regulation of blood pressure were investigated in 30 middle aged obese men with essential hypertension attending the outpatient department. In group 1 (n = 15) a basal period with no dietary restriction was followed by a period taking an energy reduced diet (5.1 MJ; 1230 kcal), the sodium intake being supplemented and hence unchanged (1:ErSn). In group 2 (n = 15) the basal period preceded a control period with no intervention, which was followed by taking a diet restricted in energy (5.1 MJ; 1220 kcal) and sodium (2:ErSr). During period 1:ErSn there were reductions in heart rate and urinary noradrenaline output but not in systolic or diastolic blood pressure. Body weight decreased by 4.9-11.7 kg and urinary sodium excretion did not change. In period 2:ErSr urinary sodium output was reduced by 81.4 (SEM 17.8) mmol(mEq)/24 h and there was a weight loss of 8.2 (SEM 0.7) kg. Systolic and diastolic blood pressures fell significantly, as did the heart rate and urinary noradrenaline excretion. These results show that in hypertensive obese men a moderate weight reducing diet decreases indices of sympathetic nervous system activity. Reduction of blood pressure to the normotensive range was observed only when there was a concomitant restriction of sodium intake.     

Leptin and metabolic syndrome in obese and non-obese children.

Metabolic syndrome is characterized by a clustering of metabolic abnormalities: insulin resistance - hyperinsulinemia, dyslipidemia (high triglycerides and low HDL - cholesterol serum concentrations), impaired glucose tolerance and/or type 2 diabetes, and hypertension. The aim of this study was to analyse the role of different variables of metabolic syndrome, including leptin, in 74 non-obese children and 68 children with non-syndromal obesity. As metabolic syndrome variables, we have included body mass index, waist circumference, trunk-to-total skinfolds (%), systolic blood pressure, diastolic blood pressure, glucose, uric acid, fasting insulin, triglycerides and high-density lipoprotein-cholesterol (HDL-C). Factor analysis showed 4 factors in each group. In non-obese children, waist circumference, BMI, fasting insulin, triglycerides, trunk-to-total skinfolds (%), leptin and uric acid loaded positively on factor 1, and HDL-C loaded negatively on this factor; systolic and diastolic blood pressure had high positive loadings in factor 2; HDL-C and leptin showed positive loadings and triglycerides and uric acid, negative loadings in factor 3; and, finally, glucose and insulin showed positive loadings in factor 4. These four factors explained 72.16 % of the total variance in the non-obese group. In obese children, BMI, waist circumference, leptin, diastolic blood pressure and systolic blood pressure loaded positively on factor 1; diastolic blood pressure, trunk-to-total skinfolds (%), uric acid and systolic blood pressure showed high positive loadings in factor 2; fasting insulin, glucose and triglycerides showed positive loadings in factor 3; and, finally, triglycerides showed positive loadings and HDL-C negative loadings in factor 4. These four factors explained 74.18 % of the total variance in the obese group. Our results point to a different homeostatic control of metabolic syndrome characteristics in obese and non-obese children. Leptin seems to play a key underlying role in metabolic syndrome, especially in the obese group.     

Metabolic effects of weight reduction in obese diabetics and nondiabetics.

A weight loss of about 10 kg was acheived by means of individual periods of total fasting, hypocaloric diets and physical activity in three groups of patients: maturity-onset diabetics, patients with pathological OGTT and overweight persons with normal OGTT. Adipocyte volume decreased in all groups, glucose tolerance improved. IRI curves showed a significant overall lowering and FFA concentrations during OGTT were dimished.     

PPAR-gamma2 Pro12Ala polymorphism in the population of obese and non-obese men of the city of Wroclaw

INTRODUCTION: The aim of this study was to examine the association of Pro12Ala PPARgamma2 polymorphism with anthropometric and biochemical parameters defining the risk for the development of metabolic syndrome in a healthy population of men. MATERIAL AND METHODS: The study group consisted of 176 healthy men, aged 25-65 years (average 54.16 years). Polymorphisms of the PPAR-g gene (Pro12Ala, Ala12Ala, Pro12Pro) were explored using the PCR-RFLP method. Plasma glucose, insulin, total cholesterol, LDL, HDL and TG were measured using commercially available kits. RESULTS: The genotypic distribution of the Pro12Ala polymorphism was as follows: Pro/Ala 69.8% (n = 123), Ala/Ala 28.4% (n = 50) and Pro/Pro 1.8% (n = 3). The Pro12Ala and Ala12Ala subjects did not differ in any of the measured variables. The non-obese (BMI < 30 kg/m(2), n = 117) and obese subpopulations (BMI > 30 kg/m(2), n = 56) did not significantly differ in the distribution of the genotypes. In the nonobese subpopulation, the homozygous Ala12 carriers (n = 38, 32.4%) had higher systolic blood pressure, plasma triglycerides, insulin levels and HOMA-IR. CONCLUSIONS: We conclude that despite the high frequency of the Ala allele at the PPAR-gamma2 gene in our population of Polish men, the Ala12 allele does not appear to improve insulin sensitivity or have an influence on the occurrence of obesity. It remains to be explained by larger studies if this polymorphism carries any risk of the development of metabolic abnormalities in non-obese men.     

Antihypertensive effect of diet compared with drug treatment in obese men with mild hypertension.

OBJECTIVE--To determine whether dietary treatment has a similar antihypertensive effect to conventional drug treatment while being superior to drugs in improving serum lipid concentrations in obese men with mild hypertension. DESIGN--Six week run in period followed by randomisation to either diet or drug treatment groups for one year. SETTING--Outpatient clinic in city hospital. PATIENTS--61 Men aged 40-69 years, body mass index greater than or equal to 26, diastolic blood pressure 90-104 mm Hg when untreated. Exclusion criteria were signs of organ damage secondary to hypertension and diseases that might have interfered with compliance or with interpretation of results. INTERVENTIONS--Dietary treatment was based on weight reduction, restriction of sodium, and decrease of excess alcohol intake (defined as greater than or equal to 250 g alcohol per week). Drug treatment used a stepped care approach with atenolol as drug of first choice. MAIN OUTCOME MEASURES--Diastolic blood pressure less than 90 mm Hg; absolute reductions in blood pressure and serum lipid concentrations. RESULTS--Mean body weight decreased 7.6 kg in the diet group and increased 0.9 kg in the drug treatment group (p less than 0.0001), and mean sodium excretion decreased 42 and 10 mmol/24 h respectively (p = 0.019). There was no difference in reported alcohol intake. Mean systolic blood pressure decreased 4 mm Hg in the diet group and 16 mm Hg in the drug group (p = 0.003) and diastolic blood pressure 3 and 11 mm Hg respectively (p = 0.002). Diastolic blood pressure of 90 mm Hg was attained by 29% of the diet group (nine men) and 73% (22) of those receiving drug treatment (mean difference 44%, 95% confidence interval 21 to 67%, p = 0.001). Dietary treatment produced decreases in mean serum concentrations of total and low density lipoprotein cholesterol as well as triglycerides and an increase in high density lipoprotein cholesterol concentration. In the drug treatment group the changes were in the opposite direction, and the groups differed significantly in all but total cholesterol. CONCLUSIONS--Dietary treatment was inferior to conventional drug treatment in controlling mild hypertension but superior in lowering serum concentrations of lipids.     

Direct genetic and postnatal maternal genetic effects on body composition in mice selected for body weight.

Line crossfostering techniques were used to study differences among selected and control lines of mice in direct genetic and postnatal maternal genetic influences on preweaning (day 12) body weight and composition. The lines were selected for high (H6) and low (L6) 6-week body weight and the control line (C2) was maintained by random selection. There were positive correlated responses to selection in both direct genetic and postnatal maternal genetic effects on body weight and weights of all body components (P less than 0.01) except for water and ash weight in H6. The correlated responses in postnatal maternal genetic effects were of the same order of magnitude as those in direct genetic effects. Correlated responses were greater in L6 than in H6. Correlated responses in direct genetic effects were positive (P less than 0.01) for water percent in H6 and ether extract percent in L6, and negative (P less than 0.01) for water percent and lean percent in L6. Correlated responses in postnatal maternal genetic effects were positive for ether extract percent and negative for water percent (P less than 0.01). Correlated responses were far greater in L6 than in H6 and were greater for postnatal maternal genetic effects than for direct genetic effects. Analyses of covariance results indicated line differences in the relative growth rates of the body components.     

Respective contribution of age, mean arterial pressure, and body weight on central arterial distensibility in SHR

In spontaneously hypertensive rats (SHR), carotid and aortic distensibilities measured at operational blood pressure (BP) are reduced. Increased body weight and mean arterial pressure (MAP) are both known to reduce distensibility independently. However, whether, after adjustment to body weight and mean BP, distensibility remains reduced in SHR has never been investigated. Carotid and abdominal aorta distensibilities were measured under anesthesia in SHR at 5, 12, 52, and 78 wk of age, and measurements were compared with age-matched normotensive Wistar rats. Each age group was composed of 9 or 10 animals. We determined distensibility using echo-tracking techniques of high resolution. Compared with Wistar rats, carotid and aortic distensibilities measured at operational MAP are reduced in SHR. This reduction is accentuated with age, particularly for the carotid artery. After adjustment to body weight and MAP, carotid and aortic distensibilities become identical in Wistar and SHR (or even slightly increased in SHR) but continue to be reduced with age, mainly for the carotid artery. In conclusion, in SHR, age and high BP do not have a parallel and similar influence on the reduction of arterial distensibility. Aging constantly reduces arterial distensibility, whereas MAP levels contribute to maintenance of arterial function.     

Effects of low calorie diet-induced weight loss on post-exercise heart rate recovery in obese men

[Purpose]

Heart Rate Recovery (HRR) after maximum exercise is a reactivation function of vagus nerve and an independent risk factor that predicts cardiovascular disease and mortality. Weight loss obtained through dietary programs has been employed as a therapy to reduce risks of cardiovascular disease and obesity.

[Methods]

Eighteen subjects of middle aged obese men (age 44.8 ± 1.6 yrs, BMI 29.7 ± 0.5 kg/m²) were selected for this study. As a weight loss direction, the nutritional direction of low-calorie diet mainly consisted of carbohydrate, protein, and fat has been conducted for 3 months. Blood pressure was measured after overnight fasting, and blood samples were collected from the antecubital vein before and after weight loss program. All the pre- and post-exercise ‘HRR decay constant’s were assessed by using values of HRR (heart recovery rate; 2 minutes) and HR measured after reached to the maximal oxygen uptake (VO₂max) exploited the bicycle ergometer.

[Results]

After the completion of weight loss program, body weight and BMI were significantly decreased, but the Heart Rate (HR) after maximum exercise and in steady state were not changed significantly (p > 0.05). The post-exercise HRR after the weight loss did not show significant changes in perspectives of 30 seconds (-16.6 ± 2.3 to -20.2 ± 2.1 beats/min, p > 0.05) and 60 seconds (-33.5 ± 3.4 to -34.6 ± 2.8 beats/min, p > 0.05) respectively but in perspectives of 90 seconds (-40.9 ± 2.6 to -48.1 ± 3.1 beats/min, p < 0.05) and 120 seconds (-48.6 ± 2.6 to -54.3 ± 3.5 beats/min, p < 0.05), they were decreased significantly. Pre-’HRR decay constant’s of 0.294 ± 0.02 %/second were significantly increased to post-values of 0.342 ± 0.03 %/second (p = 0.026). Changes in ‘HRR decay constant’ were significantly correlated with changes in blood glucose (r = -0.471, p < 0.05) and maximal oxygen consumption (VO₂max, r = 0.505, p < 0.05) respectively.

[Conclusions]

The low-calorie diet directed to obese middle aged men for 3 months significantly improved the HRR after maximum exercise, and this improvement in cardiovascular autonomic nerve system was estimated to be involved with improvements in blood glucose and maximal oxygen consumption.     

Fenofibrate prevents and reduces body weight gain and adiposity in diet-induced obese rats

Fibrates are hypolipidemic drugs that activate the peroxisome proliferator-activated receptors. Since fibrates may also increase energy expenditure, we investigated whether fenofibrate (FF) had this effect in diet-induced obese rats. A 2-month administration of a high-fat palatable diet to adult rats increased body weight by 25% and white adipose mass by 163% compared with a standard diet. These effects were prevented by FF, both when administered for the 2 months of high-fat feeding and when given for only the second month. Consequently, FF-treated rats had a final body weight and white adipose tissue mass similar to untreated animals on the standard diet. FF also increased resting metabolic rate, hepatic peroxisomal and mitochondrial palmitoyl-dependent oxygen uptake and mRNA levels of acyl-CoA oxidase and lipoprotein lipase. Finally, FF lowered mRNA levels of uncoupling protein-2 and did not affect mitochondrial respiration in skeletal muscle. Therefore, FF seems to act as a weight-stabilizer mainly through its effect on liver metabolism.