Background-Muscle sympathetic nerve activity (MSNA) is elevated in obese humans. However, the potential role of abdominal visceral fat as an important adipose tissue depot linking obesity to elevated MSNA has not been explored.

Water consumption acutely reduces meal energy intake (EI) among middle‐aged and older adults. Our objectives were to determine if premeal water consumption facilitates weight loss among overweight/obese middle‐aged and older adults, and to determine if the ability of premeal water consumption to reduce meal EI is sustained after a 12‐week period of increased water consumption. Adults (n = 48; 55–75 years, BMI 25–40 kg/m2) were assigned to one of two groups: (i) hypocaloric diet + 500 ml water prior to each daily meal (water group), or (ii) hypocaloric diet alone (nonwater group). At baseline and week 12, each participant underwent two ad libitum test meals: (i) no preload (NP), and (ii) 500 ml water preload (WP). Meal EI was assessed at each test meal and body weight was assessed weekly for 12 weeks. Weight loss was ∼2 kg greater in the water group than in the nonwater group, and the water group (β = −0.87, P < 0.001) showed a 44% greater decline in weight over the 12 weeks than the nonwater group (β = −0.60, P < 0.001). Test meal EI was lower in the WP than NP condition at baseline, but not at week 12 (baseline: WP 498 ± 25 kcal, NP 541 ± 27 kcal, P = 0.009; 12‐week: WP 480 ± 25 kcal, NP 506 ± 25 kcal, P = 0.069). Thus, when combined with a hypocaloric diet, consuming 500 ml water prior to each main meal leads to greater weight loss than a hypocaloric diet alone in middle‐aged and older adults. This may be due in part to an acute reduction in meal EI following water ingestion.

The association between obesity and hypertension is well documented, although the exact nature of this relation remains unclear. Sympathetic nervous and renin-angiotensin-aldosterone system activation appear to play an important role in the sodium and water retention, rightward shift in the pressure-natriuresis, and blood pressure elevation observed in obese individuals. Visceral obesity and the ectopic deposition of adipose tissue may be important in the activation of these systems and in the target organ damage that ensues. Weight loss is critical in the effective management of obesity hypertension and the accompanying target organ damage, although recidivism rates are high. However, prevention of weight gain should be the major priority for combating hypertension and its consequences in the future. The present review will provide an overview of our understanding of the etiology, pathophysiology, and treatment of obesity hypertension. Our focus is on the state of knowledge in humans. The potential role of abdominal obesity is considered throughout our review. We refer to relevant animal literature for supportive evidence and where little or no data in humans are available.

Abstract-Based on observations of smaller increases in limb vascular resistance during acute incremental hypovolemia in older adults, cardiopulmonary and integrative (combined cardiopulmonary and arterial) baroreflex control of sympatho-circulatory function is thought to be impaired with aging in humans. We tested this hypothesis directly by making intraneural measurements of skeletal muscle sympathetic nerve activity (MSNA; peroneal microneurography) in groups of young (23Ϯ1 years; nϭ11) and older (64Ϯ1 years; nϭ12) healthy adult men during progressive hypovolemia produced by graded (Ϫ5 to Ϫ40 mm Hg) lower body negative pressure (LBNP). Baseline levels of MSNA and arterial blood pressure were higher and heart rate was lower in the older subjects (PϽ0.05). Lower levels of LBNP (Ϫ5 to Ϫ20 mm Hg) did not affect arterial blood pressure or heart rate in either group; systolic and pulse pressures declined during higher levels of LBNP (Ϫ30 and Ϫ40 mm Hg) but only in the young subjects (PϽ0.05). Graded LBNP evoked progressive, linear reductions in peripheral venous pressure (PVP) and increases in MSNA, plasma norepinephrine concentration (PNE), and forearm vascular resistance (FVR) in both groups (all PϽ0.05). ⌬MSNA/ ⌬PVP was Ϸ150% greater in the older versus young men during both lower and higher levels of hypovolemia (PϽ0.01); however, ⌬FVR/⌬PVP was Ϸ50% smaller in the older men (PϽ0.05). There was no difference in the MSNA-PNE relation with age, but ⌬FVR/⌬MSNA was Ϸ65% to 70% smaller in the older subjects (PϽ0.05). Our findings indicate that cardiopulmonary and integrative baroreflex control of central sympathetic outflow during hypovolemia is augmented, not impaired, with age in healthy humans. However, the reflex-mediated increases in limb vascular resistance during hypovolemia are smaller in older adults because of attenuated vasoconstrictor responsiveness to sympathetic stimulation. (Hypertension. 1998;32:298-304.)Key Words: hypovolemia Ⅲ aging Ⅲ blood pressure T he cardiopulmonary and arterial baroreflexes play a critical role in maintaining circulatory homeostasis, in large part through their tonic inhibition of SNA.1,2 In humans, baroreflex control of SNA often has been studied using graded hypovolemia.1,2 Low levels of hypovolemia at which heart rate and arterial blood pressure are unaffected are thought to preferentially deactivate cardiopulmonary baroreflexes and evoke increases in skeletal MSNA, PNE concentration, and limb vascular resistance. [1][2][3][4][5][6][7] More severe levels of hypovolemia that cause tachycardia and, at least in healthy young adults, reductions in arterial blood pressure are thought to unload both cardiopulmonary and arterial baroreceptors, resulting in a greater and more systemic "integrative" baroreflex stimulation of SNA. 1,2,4,5 Primary aging produces a number of changes in cardiovascular structure and function in humans. 8,9 It has been proposed that among these changes is an impairment in cardiopulmonary and integrative baroreflex sympatho-circulatory control. 10,11 This id...

Using a meta-analytic approach, we recently reported that the rate of decline in maximal oxygen uptake (VO2 max) with age in healthy women is greatest in the most physically active and smallest in the least active when expressed in milliliters per kilogram per minute per decade. We tested this hypothesis prospectively under well-controlled laboratory conditions by studying 156 healthy, nonobese women (age 20-75 yr): 84 endurance-trained runners (ET) and 72 sedentary subjects (S). ET were matched across the age range for age-adjusted 10-km running performance. Body mass was positively related with age in S but not in ET. Fat-free mass was not different with age in ET or S. Maximal respiratory exchange ratio and rating of perceived exertion were similar across age in ET and S, suggesting equivalent voluntary maximal efforts. There was a significant but modest decline in running mileage, frequency, and speed with advancing age in ET. VO2 max (ml . kg-1 . min-1) was inversely related to age (P < 0.001) in ET (r = -0.82) and S (r = -0.71) and was higher at any age in ET. Consistent with our meta-analysic findings, the absolute rate of decline in VO2 max was greater in ET (-5.7 ml . kg-1 . min-1 . decade-1) compared with S (-3.2 ml . kg-1 . min-1 . decade-1; P < 0. 01), but the relative (%) rate of decline was similar (-9.7 vs -9. 1%/decade; not significant). The greater absolute rate of decline in VO2 max in ET compared with S was not associated with a greater rate of decline in maximal heart rate (-5.6 vs. -6.2 beats . min-1 . decade-1), nor was it related to training factors. The present cross-sectional findings provide additional evidence that the absolute, but not the relative, rate of decline in maximal aerobic capacity with age may be greater in highly physically active women compared with their sedentary healthy peers. This difference does not appear to be related to age-associated changes in maximal heart rate, body composition, or training factors.

Moderate SR lowers SBP and PP in postmenopausal women with elevated baseline levels more than does daily walking. The greater blood pressure reductions with SR may be mediated in part by a decrease in the stiffness of the large elastic arteries.

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 1990's, 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 regional 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.

Abstract-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 (nϭ25; age: 61.2Ϯ0.8 years; body mass index: 30.0Ϯ0.6 kg/m 2 ) or a control (nϭ11; age: 66.1Ϯ1.9 years; body mass index: 31.8Ϯ1.4 kg/m 2 ) 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, ␤-stiffness index, and carotid-femoral pulse wave velocity were similar in the 2 groups at baseline (all PϾ0.05). Body weight (Ϫ7.1Ϯ0.7 versus Ϫ0.7Ϯ1.1 kg), body fat, and abdominal adiposity decreased in the weight loss group but not in the control group (all PϽ0.05). Brachial systolic and diastolic blood pressures declined (PϽ0.05) only in the weight loss group. Central systolic and pulse pressures did not change significantly in either group. ␤-Stiffness index (Ϫ1.24Ϯ0.22 versus 0.52Ϯ0.37 U) and carotid-femoral pulse wave velocity (Ϫ187Ϯ29 versus 15Ϯ42 cm/s) decreased in the weight loss group but not in the control group (all PϽ0.05). The reductions in carotid-femoral pulse wave velocity were correlated with reductions in total body and abdominal adiposity (rϭ0. all PϽ0.05). 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.