Kevin P. Davy

Sympathetic neural activation in visceral obesity

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. Accordingly, we tested the hypothesis that MSNA would be increased in men (age=18 to 40 years, body mass index ≤35 kg/m2) with higher abdominal visceral fat (HAVF; n=13, abdominal visceral fat=118.1±15.8 cm2) compared with their age- (28.7±2.4 versus 25.5±2.0 years, P >0.05), total fat mass-matched (20.6±2.1 versus 20.8±2.4 kg, P >0.05) and abdominal subcutaneous fat-matched (230.6±24.9 versus 261.4±34.8 cm2, P >0.05) peers with lower abdominal visceral fat levels (LAVF; n=13, visceral fat= 73.0±6.0 cm2). Methods and Results—MSNA (microneurography), body composition (dual energy x-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) were measured in 37 sedentary men across a wide range of adiposity. MSNA was ≈55% higher in men with HAVF compared with men with LAVF (33±4 versus 21±2 bursts/min, P <0.05). Furthermore, MSNA was more closely associated with the level of abdominal visceral fat (r =0.65, P <0.05) than total fat mass (r =0.323, P <0.05) or abdominal subcutaneous fat (r =0.27, P =0.05). The relation between MSNA and abdominal visceral fat was independent of total body fat (r =0.61, P <0.05). Conclusions—The results of our study indicate that MSNA is elevated in men with visceral obesity. Our observations are consistent with the idea that abdominal visceral fat is an important adipose tissue depot linking obesity with sympathetic neural activation in humans. Furthermore, these findings may have important implications for understanding the increased risk of developing cardiovascular diseases in individuals with visceral obesity.

Blood pressure reductions with exercise and sodium restriction in postmenopausal women with elevated systolic pressure: Role of arterial stiffness

OBJECTIVESnThis study determined the relative efficacy of aerobic exercise (daily walking) and moderate dietary sodium restriction (sodium intake <100 mmol/day) for reducing systolic blood pressure (SBP) and pulse pressure (PP) in postmenopausal women with elevated initial levels, and the potential role of reductions in large artery stiffness in these changes.nnnBACKGROUNDnLifestyle behaviors are recommended for lowering blood pressure (BP) in adults with elevated baseline levels, but there is little information as to the relative efficacy of different interventions or the mechanisms underlying their potential beneficial effects.nnnMETHODSnAfter baseline measurements and random assignment, 35 nonmedicated healthy postmenopausal women with SBP between 130 and 159 mm Hg completed three months of either aerobic (walking) exercise (n = 18; 62 +/- 9 years, mean +/- SD) or moderate dietary sodium restriction (SR) (n = 17; 65 +/- 10 years, mean +/- SD).nnnRESULTSnBody mass and composition, plasma volume, and fasting concentrations of metabolic coronary risk factors did not differ between the groups at baseline or change with intervention. Systolic BP and PP at rest decreased with both exercise and SR (p < 0.05); however, the reductions were three- to fourfold greater with SR (p < 0.05). Sodium restriction, but not exercise, also reduced 24-h SBP and PP (p < 0.05). Aortic pulse wave velocity (PWV) and carotid augmentation index were reduced only with SR (p < 0.05). Changes in SBP and PP at rest and over 24 h correlated with the corresponding changes in aortic PWV (r = 0.53 to 0.61, p < 0.01).nnnCONCLUSIONSnModerate 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.

Low-frequency arterial pressure fluctuations do not reflect sympathetic outflow : gender and age differences

Low-frequency arterial pressure oscillations (Mayer waves) have been proposed as an index of vascular sympathetic outflow. However, cross-sectional differences in these pressure oscillations may not reflect different levels of sympathetic nervous outflow in humans. Three groups of healthy subjects with characteristically different sympathetic nervous outflow were studied: young females (n = 10, 18-28 yr), young males (n = 11, 18-29 yr), and older males (n = 13, 60-72 yr). Average R-R interval, arterial pressures, and systolic pressure variability at the Mayer wave frequency (0.05-0.15 Hz) did not differ among the three groups. Diastolic pressure Mayer wave variability was similar in young females vs. young males (39 +/- 10 vs. 34 +/- 5 mmHg2) and lower in older males vs. young males (14 +/- 2 mmHg2; P < 0.05). In contrast, muscle sympathetic activity was lowest in young females (892 +/- 249 total activity/min) and highest in older males (3,616 +/- 528 total activity/min; both P < 0.05 vs. young males: 2,505 +/- 285 total activity/min). Across the three groups, arterial pressure Mayer wave variability did not correlate with any index of sympathetic activity. Our results demonstrate that arterial pressure Mayer wave amplitude is not a surrogate measure of vascular sympathetic outflow.Low-frequency arterial pressure oscillations (Mayer waves) have been proposed as an index of vascular sympathetic outflow. However, cross-sectional differences in these pressure oscillations may not reflect different levels of sympathetic nervous outflow in humans. Three groups of healthy subjects with characteristically different sympathetic nervous outflow were studied: young females ( n = 10, 18-28 yr), young males ( n = 11, 18-29 yr), and older males ( n = 13, 60-72 yr). Average R-R interval, arterial pressures, and systolic pressure variability at the Mayer wave frequency (0.05-0.15 Hz) did not differ among the three groups. Diastolic pressure Mayer wave variability was similar in young females vs. young males (39 ± 10 vs. 34 ± 5 mmHg2) and lower in older males vs. young males (14 ± 2 mmHg2; P < 0.05). In contrast, muscle sympathetic activity was lowest in young females (892 ± 249 total activity/min) and highest in older males (3,616 ± 528 total activity/min; both P < 0.05 vs. young males: 2,505 ± 285 total activity/min). Across the three groups, arterial pressure Mayer wave variability did not correlate with any index of sympathetic activity. Our results demonstrate that arterial pressure Mayer wave amplitude is not a surrogate measure of vascular sympathetic outflow.

Influence of age on arterial baroreflex inhibition of sympathetic nerve activity in healthy adult humans

Resting levels of muscle sympathetic nerve activity (MSNA) increase markedly with age in healthy adult humans. An age-related reduction in arterial baroreflex inhibition of MSNA could contribute to these elevations. To test this hypothesis, we measured MSNA using peroneal microneurography in young (age, 25 +/- 1 yr; n = 8) and older (69 +/- 1 yr; n = 7) healthy normotensive men before (baseline control) and during graded constant infusion of phenylephrine hydrochloride (0.5-2.0 microgram . kg-1. min-1) that produced a sustained approximately 10-mmHg increase in arterial blood pressure. Central venous pressure was controlled at baseline levels (+/-1 mmHg) using lower body negative pressure. Resting MSNA was approximately 95% higher in the older compared with the young subjects (43 +/- 5 vs. 22 +/- 3 bursts/min; P < 0.05). However, arterial baroreflex MSNA inhibitory responsiveness was similar in the older compared with the young subjects (254 +/- 112 vs. 259 +/- 40 arbitrary integration units/mmHg, respectively), although the percent reduction in MSNA was smaller in the older men (8.9 +/- 0.7 vs. 5.2 +/- 1.1%/mmHg), due to their elevated baseline levels. The reflex increase in the R-R interval was not different in the two groups (13 +/- 10 vs. 16 +/- 7 ms/mmHg). In summary, our findings suggest that arterial baroreflex inhibition of MSNA is preserved with age in healthy normotensive adult humans. As such, this mechanism does not appear to contribute to the age-related rise in tonic MSNA.Resting levels of muscle sympathetic nerve activity (MSNA) increase markedly with age in healthy adult humans. An age-related reduction in arterial baroreflex inhibition of MSNA could contribute to these elevations. To test this hypothesis, we measured MSNA using peroneal microneurography in young (age, 25 ± 1 yr; n = 8) and older (69 ± 1 yr; n = 7) healthy normotensive men before (baseline control) and during graded constant infusion of phenylephrine hydrochloride (0.5-2.0 μg ⋅ kg-1 ⋅ min-1) that produced a sustained ∼10-mmHg increase in arterial blood pressure. Central venous pressure was controlled at baseline levels (±1 mmHg) using lower body negative pressure. Resting MSNA was ∼95% higher in the older compared with the young subjects (43 ± 5 vs. 22 ± 3 bursts/min; P < 0.05). However, arterial baroreflex MSNA inhibitory responsiveness was similar in the older compared with the young subjects (254 ± 112 vs. 259 ± 40 arbitrary integration units/mmHg, respectively), although the percent reduction in MSNA was smaller in the older men (8.9 ± 0.7 vs. 5.2 ± 1.1%/mmHg), due to their elevated baseline levels. The reflex increase in the R-R interval was not different in the two groups (13 ± 10 vs. 16 ± 7 ms/mmHg). In summary, our findings suggest that arterial baroreflex inhibition of MSNA is preserved with age in healthy normotensive adult humans. As such, this mechanism does not appear to contribute to the age-related rise in tonic MSNA.

TOTAL BLOOD VOLUME IN ENDURANCE-TRAINED POST-MENOPAUSAL FEMALES: RELATION TO EXERCISE MODE AND MAXIMAL AEROBIC CAPACITY 626

We have recently shown that postmenopausal female distance runners demonstrate elevated levels of blood volume compared with sedentary healthy peers. We also found a strong positive relation between blood volume and maximal oxygen consumption. In young adult males, endurance exercise training increases blood volume when performed in the upright, but not in the supine body position. Based on these observations, we hypothesized that among postmenopausal females, the elevation in blood volume would be absent or attenuated in women who train in the horizontal vs. upright body position, and that the lower blood volume in the former would be associated with lower maximal aerobic capacity. Thus, we measured supine resting plasma and total blood volumes (Evans blue dye) and maximal oxygen consumption in postmenopausal women: 10 sedentary controls, 10 swimmers and 10 runners matched for age (60 +/- 2; 59 +/- 2; 58 +/- 2 years, mean +/- SE) and hormone replacement use (5 per group). The swimmers and runners were further matched for training volume (4.5 +/- 0.2 vs. 4.8 +/- 0.6 h week-1), relative performance (78 +/- 5 vs. 75 +/- 3% of age-group world record) and fat-free mass (45.5 +/- 0. 8 vs. 44.9 +/- 1.5 kg). Total blood volume and maximal oxygen consumption were highest in the runners (81.2 +/- 4; 52.4 +/- 3 mL kg-1, respectively) and progressively lower in the swimmers (68.8 +/- 3; 44.2 +/- 2) and controls (59.2 +/- 2; 37.9 +/- 2; all P < 0. 05). In the pooled population, blood volume was positively related to maximal oxygen consumption (r = 0.72, P < 0.0001). We conclude that in endurance-trained postmenopausal females matched for training volume and competitive performance: (1) blood volume is lower in those who train in the horizontal (swimmers) compared with the upright position (runners); (2) the lower blood volume is associated with a lower maximal aerobic capacity. Nevertheless, blood volume and maximal oxygen consumption are higher in postmenopausal women who train in the horizontal position than in sedentary controls.