Jeb S. Orr

Arterial Destiffening With Weight Loss in Overweight and Obese Middle-Aged and Older Adults

We tested the hypothesis that weight loss via a hypocaloric diet would reduce arterial stiffness in overweight and obese middle-aged and older adults. Thirty-six individuals were randomly assigned to a weight loss (n=25; age: 61.2±0.8 years; body mass index: 30.0±0.6 kg/m2) or a control (n=11; age: 66.1±1.9 years; body mass index: 31.8±1.4 kg/m2) group. Arterial stiffness was measured via carotid artery ultrasonography combined with applanation tonometry and carotid-femoral pulse wave velocity via applanation tonometry at baseline and after the 12-week intervention. Body weight, body fat, abdominal adiposity, blood pressure, &bgr;-stiffness index, and carotid-femoral pulse wave velocity were similar in the 2 groups at baseline (all P>0.05). Body weight (−7.1±0.7 versus −0.7±1.1 kg), body fat, and abdominal adiposity decreased in the weight loss group but not in the control group (all P<0.05). Brachial systolic and diastolic blood pressures declined (P<0.05) only in the weight loss group. Central systolic and pulse pressures did not change significantly in either group. &bgr;-Stiffness index (−1.24±0.22 versus 0.52±0.37 U) and carotid-femoral pulse wave velocity (−187±29 versus 15±42 cm/s) decreased in the weight loss group but not in the control group (all P<0.05). The reductions in carotid-femoral pulse wave velocity were correlated with reductions in total body and abdominal adiposity (r=0.357–0.602; all P<0.05). However, neither total body nor abdominal adiposity independently predicted reductions in arterial stiffness indices. In summary, our findings indicate that weight loss reduces arterial stiffness in overweight/obese middle-aged and older adults, and the magnitudes of these improvements are related to the loss of total and abdominal adiposity.

Sympathetic nervous system behavior in human obesity.

The sympathetic nervous system (SNS) plays an essential role in the regulation of metabolic and cardiovascular homeostasis. Low SNS activity has been suggested to be a risk factor for weight gain and obesity development. In contrast, SNS activation is characteristic of a number of metabolic and cardiovascular diseases that occur more frequently in obese individuals. Until recently, the relation between obesity and SNS behavior has been controversial because previous approaches for assessing SNS activity in humans have produced inconsistent findings. Beginning in the early 1990s, many studies using state of the art neurochemical and neurophysiological techniques have provided important insight. The purpose of the present review is to provide an overview of our current understanding of the region specific alterations in SNS behavior in human obesity. We will discuss findings from our own laboratory which implicate visceral fat as an important depot linking obesity with skeletal muscle SNS activation. The influence of weight change on SNS behavior and the potential mechanisms and consequences of region specific SNS activation in obesity will also be considered.

Large Artery Stiffening With Weight Gain in Humans: Role of Visceral Fat Accumulation

We tested the hypothesis that weight gain would increase arterial stiffness in healthy nonobese adults. To address this, we overfed 14 nonobese men (age: 23±1 years) ≈1000 kcal/d for 6 to 8 weeks until a 5-kg weight gain was achieved. Carotid diameters (high-resolution ultrasound) and pressures (applanation tonometry), body composition (dual energy x-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 weeks of weight stability at each individual’s elevated body weight. Overfeeding increased body weight 5.1±0.1 kg and body fat 3.4±0.4 kg (both P<0.001) in 45±7 days. Total abdominal fat increased 46±7 cm2 with weight gain due to increases in both subcutaneous (30±6 cm2) and visceral fat (15±4 cm2; all P<0.01). As hypothesized, weight gain increased arterial stiffness 13±6% and decreased arterial compliance 21±4% (both P<0.05). Furthermore, those individuals above the median increase in abdominal visceral fat demonstrated a significantly greater increase in arterial stiffness (0.97±0.29 versus 0.06±0.36 U; P<0.05) compared with those below the median. Consistent with these observations, the only correlates of the changes in arterial stiffness with weight gain were the increases in total abdominal fat (r=0.794), abdominal visceral fat (r=0.651), and waist circumference (r=0.470; all P<0.05). Taken together, these findings suggest that modest weight gain is associated with increases arterial stiffness in nonobese men. The degree of large artery stiffening with weight gain seems to be determined, in part, by the amount of abdominal visceral fat gain. Importantly, this relation is independent of the amount of total body fat gained.

Arterial destiffening with atorvastatin in overweight and obese middle-aged and older adults.

We hypothesized that atorvastatin (ATOR) treatment would reduce arterial stiffness in overweight and obese middle-aged and older adults. Twenty-six (11 men and 15 women) overweight or obese (body mass index: 31.6±0.7 kg/m2) middle-aged and older adults (age: 54±2 years) were randomly assigned to receive either ATOR (80 mg/d) or placebo for 12 weeks. Arterial stiffness (&bgr;-stiffness and pulse wave velocity) was measured before and after the intervention. At baseline, the ATOR (n=16) and placebo (n=10) groups did not differ with respect to age, body mass index, blood pressure, serum lipid and lipoprotein concentrations, high-sensitivity C-reactive protein, indices of arterial stiffness, or compliance (all P>0.05). After the 12-week treatment period, the ATOR group experienced a 47% reduction in low-density lipoprotein cholesterol (149±6 to 80±8 mg/dL) and a 42% reduction in high-sensitivity C-reactive protein (3.6±0.8 to 2.1±0.5 mg/L; both P<0.05). In addition, &bgr;-stiffness (9.4±0.6 to 7.6±0.5 U) and aortic pulse wave velocity (1096±36 to 932±32 cm/s), but not brachial pulse wave velocity, decreased (both P<0.05) with ATOR. In contrast, there were no significant changes in &bgr;-stiffness (9.1±0.8 to 9.1±0.7 U) or aortic pulse wave velocity (1238±89 to 1191±90 cm/s; both P>0.05) in the placebo group. There were no relations between the reductions in arterial stiffness indices and any of the baseline cardiometabolic risk factors (all P>0.05). However, the reductions in arterial stiffness were correlated with the reduction in low-density lipoprotein cholesterol but not high-sensitivity C-reactive protein or any other cardiometabolic variables (all P<0.05). Taken together, these findings suggest that ATOR reduces arterial stiffness in overweight and obese middle-aged and older adults, and these favorable changes occur irrespective of baseline cardiometabolic risk factors.

Pre-meal water consumption reduces meal energy intake in older but not younger subjects

Objective: To determine whether the consumption of water 30 minutes before an ad libitum meal reduces meal energy intake in young and older adults.

Habitual physical activity differentially affects acute and short-term energy intake regulation in young and older adults

Background:Energy intake (EI) regulation is impaired in older adults, but it is not known if habitual physical activity affects accuracy of EI regulation in older compared with young adults.Objective:We hypothesized that the ability to compensate for a high-energy yogurt preload beverage at a subsequent ad libitum meal (i.e. acute compensation) and over the course of the testing day (i.e. short-term compensation) would decrease with age, but the magnitude of the decline would be smaller in physically active compared with sedentary older adults.Design:On two occasions, young active (n=15), young sedentary (n=14), older active (n=14) and older sedentary (n=11) subjects consumed either a high-energy yogurt preload beverage (YP: 500 ml, 1988 kJ, men; 375 ml, 1507 kJ, women), or no preload (NP), 30 min before an ad libitum test meal. EI at both ad libitum meals was measured, and total daily EI was determined on both testing days. Percent EI compensation for the YP was calculated for the test meal and testing day to determine acute and short-term compensation.Results:Percent EI compensation at the test meal was significantly lower in the older compared with the young subjects (65±4 vs 81±4%, P=0.005). There was no effect of habitual physical activity level on acute compensation, and no age by physical activity level interaction (P=0.60). In contrast, short-term compensation was not different with age (87±5 vs 93±6%, older vs young, P=0.45), but was more accurate in active vs sedentary subjects (100±5 vs 79±6%, P=0.01). As with acute compensation, there was no age by physical activity interaction (P=0.39).Conclusion:Acute EI regulation is impaired in older adults, which is not attenuated by physical activity status. However, EI regulation over the course of a day is more accurate in active vs sedentary adults, which may facilitate long-term energy balance. Future work is needed to determine if higher energy expenditure in older active vs older sedentary adults improves long-term EI regulation.

Sex differences in acute energy intake regulation.

The purpose of this investigation was to determine if energy intake compensation is more accurate in males compared to females matched for age, habitual physical activity, cardiorespiratory fitness, and dietary cognitive restraint. Healthy, nonobese young men (n=12) and women (n=12) were provided with an ad libitum lunch meal on two occasions. Thirty minutes prior to the lunch meals, subjects were given either a yogurt preload (YP; 500 mL, 1988 kJ, men; 375 mL, 1507 kJ, women) or no preload (NP). Energy intake at the two lunch meals was measured. Visual analog scales were used to assess changes in hunger and fullness. Blood glucose concentrations were also determined. Energy intake compensation for the YP was significantly more accurate in the male compared to the female subjects (86.2+/-5.0 vs. 73.6+/-4.8% compensation). There were no sex differences in perceptions of hunger and satiety. In the pooled sample, hunger ratings were significantly higher in the NP condition, but there were no significant differences in fullness ratings between test meals. In the YP condition, glycemic response to the preload and the ad libitum meal was significantly higher in males compared to females. These results suggest that under acute test meal conditions, energy intake regulation is more accurate in males. Relative inability to regulate energy intake may predispose females to gain weight over time.

Cardiorespiratory Fitness Influences the Blood Pressure Response to Experimental Weight Gain

Objective: We tested the hypothesis that with similar weight gain the increase in blood pressure (BP) would be smaller in men with higher cardiorespiratory fitness (HCRF) than in men with lower cardiorespiratory fitness (LCRF).

Large Artery Stiffening With Weight Gain in Humans

We tested the hypothesis that weight gain would increase arterial stiffness in healthy nonobese adults. To address this, we overfed 14 nonobese men (age: 23±1 years) ≈1000 kcal/d for 6 to 8 weeks until a 5-kg weight gain was achieved. Carotid diameters (high-resolution ultrasound) and pressures (applanation tonometry), body composition (dual energy x-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 weeks of weight stability at each individual’s elevated body weight. Overfeeding increased body weight 5.1±0.1 kg and body fat 3.4±0.4 kg (both P<0.001) in 45±7 days. Total abdominal fat increased 46±7 cm2 with weight gain due to increases in both subcutaneous (30±6 cm2) and visceral fat (15±4 cm2; all P<0.01). As hypothesized, weight gain increased arterial stiffness 13±6% and decreased arterial compliance 21±4% (both P<0.05). Furthermore, those individuals above the median increase in abdominal visceral fat demonstrated a significantly greater increase in arterial stiffness (0.97±0.29 versus 0.06±0.36 U; P<0.05) compared with those below the median. Consistent with these observations, the only correlates of the changes in arterial stiffness with weight gain were the increases in total abdominal fat (r=0.794), abdominal visceral fat (r=0.651), and waist circumference (r=0.470; all P<0.05). Taken together, these findings suggest that modest weight gain is associated with increases arterial stiffness in nonobese men. The degree of large artery stiffening with weight gain seems to be determined, in part, by the amount of abdominal visceral fat gain. Importantly, this relation is independent of the amount of total body fat gained.

LARGE ARTERY STIFFENING WITH EXPERIMENTAL WEIGHT GAIN IN HUMANS: ROLE OF VISCERAL FAT ACCUMULATION

We tested the hypothesis that weight gain would increase arterial stiffness in healthy nonobese adults. To address this, we overfed 14 nonobese men (age: 23±1 years) ≈1000 kcal/d for 6 to 8 weeks until a 5-kg weight gain was achieved. Carotid diameters (high-resolution ultrasound) and pressures (applanation tonometry), body composition (dual energy x-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 weeks of weight stability at each individual’s elevated body weight. Overfeeding increased body weight 5.1±0.1 kg and body fat 3.4±0.4 kg (both P<0.001) in 45±7 days. Total abdominal fat increased 46±7 cm2 with weight gain due to increases in both subcutaneous (30±6 cm2) and visceral fat (15±4 cm2; all P<0.01). As hypothesized, weight gain increased arterial stiffness 13±6% and decreased arterial compliance 21±4% (both P<0.05). Furthermore, those individuals above the median increase in abdominal visceral fat demonstrated a significantly greater increase in arterial stiffness (0.97±0.29 versus 0.06±0.36 U; P<0.05) compared with those below the median. Consistent with these observations, the only correlates of the changes in arterial stiffness with weight gain were the increases in total abdominal fat (r=0.794), abdominal visceral fat (r=0.651), and waist circumference (r=0.470; all P<0.05). Taken together, these findings suggest that modest weight gain is associated with increases arterial stiffness in nonobese men. The degree of large artery stiffening with weight gain seems to be determined, in part, by the amount of abdominal visceral fat gain. Importantly, this relation is independent of the amount of total body fat gained.