Metabolic syndrome and endothelial fibrinolytic capacity in obese adults

The metabolic syndrome (MetS) often accompanies obesity and contributes to the increased risk of atherothrombotic events with increased body fatness. Indeed, the risks for coronary artery disease and acute vascular events are greater with obesity combined with MetS compared with obesity alone. Endothelial release of tissue-type plasminogen activator (t-PA) is a key defense mechanism against thrombosis and has been shown to be impaired with obesity. The aim of the present study was to determine whether the presence of MetS exacerbates endothelial fibrinolytic dysfunction in obese adults. Net endothelial release of t-PA was determined in vivo in response to intrabrachial infusions of bradykinin and sodium nitroprusside in 47 sedentary adults: 15 normal weight (age 57 +/- 2 yr; body mass index 22.9 +/- 0.5 kg/m(2)), 14 obese but otherwise healthy (55 +/- 1 yr; 29.4 +/- 0.3 kg/m(2)), and 18 obese with MetS (55 +/- 2 yr; 32.3 +/- 1 kg/m(2)). MetS was established according to National Cholesterol Education Program ATP III criteria. Net release of t-PA antigen to bradykinin was approximately 50% lower (P < 0.01) in the obese (from 2.5 +/- 1.9 to 37.1 +/- 5.3 ng.100 ml tissue(-1).min(-1)) and obese with MetS (from 0.4 +/- 0.8 to 32.5 +/- 3.8 ng.100 ml tissue(-1).min(-1)) compared with normal-weight (from 0.9 +/- 1.0 to 74.3 +/- 8.1 ng.100 ml tissue(-1).min(-1)) subjects. However, there were no significant differences in the capacity of the endothelium to release t-PA in the obese and obese with MetS adults. These results indicate that the presence of the MetS does not worsen the obesity-related endothelial fibrinolytic dysfunction.     

Influence of abdominal obesity on vascular endothelial function in overweight/obese adult men

It has been suggested that body fat distribution may be an important determinant of the impact of adiposity on endothelial function. We tested the hypothesis that overweight/obese adults with abdominal adiposity exhibit worse endothelial vasodilator and fibrinolytic function than overweight/obese adults without abdominal adiposity. Sixty adult men were studied: 20 normal weight (BMI: 22.3 ± 0.7 kg/m2; waist circumference (WC): 84.9 ± 2.0 cm); 20 overweight/obese with WC <102 cm (29.2 ± 0.3 kg/m2; 98.1 ± 0.7 cm); and 20 overweight/obese with WC ≥102 cm (30.0 ± 0.4 kg/m2; 106.7 ± 1.0 cm). Forearm blood flow (FBF) responses to intra-arterial acetylcholine and sodium nitroprusside (SNP) were measured. Additionally, net endothelial release of tissue-type plasminogen activator (t-PA) was determined in response to bradykinin (BK) and SNP. Overweight/obese men demonstrated lower (~30%; P < 0.01) FBF responses to acetylcholine compared with normal weight controls. However, there were no differences in FBF responses to acetylcholine between overweight/obese men with (4.1 ± 0.3-10.8 ± 1.3 ml/100 ml tissue/min) and without (4.5 ± 0.3-11.6 ± 0.8 ml/100 ml tissue/min) abdominal adiposity. Similarly, endothelial t-PA release to BK was lower (~40%; P < 0.05) in the overweight/obese men compared with normal weight controls; however, t-PA release was not different between the overweight/obese men with (-0.7 ± 0.4-40.4 ± 6.2 ng/100 ml tissue/min) and without (-0.3 ± 0.6-48 ± 7.5 ng/100 ml tissue/min) abdominal adiposity. These results indicate that abdominal obesity is not associated with greater impairment in endothelial vasodilation and fibrinolytic capacity in overweight/obese men. Excess adiposity, regardless of anatomical distribution pattern, is associated with impaired endothelial function.     

Influence of oral contraceptive use on endothelial t-PA release in healthy premenopausal women

We determined the influence of oral contraceptives (OC) on the capacity of the endothelium to release tissue-type plasminogen activator (t-PA). Twenty-three healthy premenopausal women were studied: 12 nonusers and 11 users of OC. Net endothelial release rates of t-PA were calculated as the product of the arteriovenous concentration gradient and forearm plasma flow in response to intra-arterial bradykinin (BK: 12.5-50 ng. 100 ml tissue(-1) x min(-1)) and sodium nitroprusside (SNP: 1.0-4.0 microg x 100 ml tissue(-1) x min(-1)). Net release of t-PA antigen and increment in t-PA activity across the forearm to BK increased (P < 0.01) in a dose-dependent fashion and to similar extents in the nonusers and users of OC. At the highest BK dose, net release of t-PA antigen was 64.5 +/- 8.2 and 66.2 +/- 15.4 ng x 100 ml tissue(-1) x min(-1) in the nonusers and users of OC, whereas the net increment in t-PA activity was 18.6 +/- 3.0 and 16.0 +/- 2.0 IU. 100 ml tissue(-1) x min(-1), respectively. There was no effect of SNP on t-PA release in either group. These results indicate that endothelial t-PA release is not altered in premenopausal women who use oral contraception.     

Impaired endothelium-dependent vasodilation in overweight and obese adult humans is not limited to muscarinic receptor agonists

Muscarinic receptor agonists have primarily been used to characterize endothelium-dependent vasodilator dysfunction with overweight/obesity. Reliance on a single class of agonist, however, yields limited, and potentially misleading, information regarding endothelial vasodilator capacity. The aims of this study were to determine 1) whether the overweight/obesity-related reduction in endothelium-dependent vasodilation extends beyond muscarinic receptor agonists and 2) whether the contribution of nitric oxide (NO) to endothelium-dependent vasodilation is reduced in overweight/obese adults. Eighty-six middle-aged and older adults were studied: 42 normal-weight (54 +/- 1 yr, 21 men and 21 women, body mass index = 23.4 +/- 0.3 kg/m(2)) and 44 overweight/obese (54 +/- 1 yr, 28 men and 16 women, body mass index = 30.3 +/- 0.6 kg/m(2)) subjects. Forearm blood flow (FBF) responses to intra-arterial infusions of acetylcholine in the absence and presence of the endothelial NO synthase inhibitor N(G)-monomethyl-l-arginine, methacholine, bradykinin, substance P, isoproterenol, and sodium nitroprusside were measured by strain-gauge plethysmography. FBF responses to each endothelial agonist were significantly blunted in the overweight/obese adults. Total FBF (area under the curve) to acetylcholine (50 +/- 5 vs. 79 +/- 4 ml/100 ml tissue), methacholine (55 +/- 4 vs. 86 +/- 5 ml/100 ml tissue), bradykinin (62 +/- 5 vs. 85 +/- 4 ml/100 ml tissue), substance P (37 +/- 4 vs. 57 +/- 5 ml/100 ml tissue), and isoproterenol (62 +/- 4 vs. 82 +/- 6 ml/100 ml tissue) were 30%-40% lower in the overweight/obese than normal-weight adults. N(G)-monomethyl-l-arginine significantly reduced the FBF response to acetylcholine to the same extent in both groups. There were no differences between the groups in the FBF responses to sodium nitroprusside. These results indicate that agonist-stimulated endothelium-dependent vasodilation is universally impaired with overweight/obesity. Moreover, this impairment appears to be independent of NO.     

Regular Aerobic Exercise,Without Weight Loss,Improves Endothelium‐dependent Vasodilation in Overweight and Obese Adults

Lifestyle modification in the form of weight reduction by caloric restriction alone or in combination with regular aerobic exercise significantly improves endothelium‐dependent vasodilation in overweight and obese adults. We determined whether regular aerobic exercise, independent of weight loss, improves endothelium‐dependent vasodilation in overweight and obese adults. Twenty overweight and obese adults (age 53 ± 1 years; BMI: 30.2 ± 0.8 kg/m²) were studied before and after a 3‐month aerobic exercise training intervention. Forearm blood flow (FBF) responses were determined (via plethysmography) in response to intra‐arterial infusion of acetylcholine and sodium nitroprusside. There were no changes in body mass or composition with the intervention. FBF responses to acetylcholine were ～35% higher (P < 0.01) after (4.1 ± 0.9 to 14.7 ± 4.3 ml/100 ml tissue/min) compared with before (4.2 ± 0.8 to 11.0 ± 3 ml/100 ml tissue/min) exercise training. FBF responses to sodium nitroprusside were unchanged. These results indicate that regular aerobic exercise improves endothelium‐dependent vasodilation in overweight and obese adults, independent of changes in body mass or composition.     

Skeletal muscle lipid metabolism with obesity

The objectives of this study were to 1). examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity and 2). determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long-chain fatty acyl-CoAs. Muscle was obtained from normal-weight [n = 8; body mass index (BMI) 23.8 +/- 0.58 kg/m(2)], overweight/obese (n = 8; BMI 30.2 +/- 0.81 kg/m(2)), and extremely obese (n = 8; BMI 53.8 +/- 3.5 kg/m(2)) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long-chain fatty acyl-CoA concentrations were measured in a separate portion of the same muscle tissue in which fatty acid oxidation was determined. Palmitate oxidation was 58 and 83% lower in skeletal muscle from extremely obese (44.9 +/- 5.2 nmol x g(-1) x h(-1)) patients compared with normal-weight (71.0 +/- 5.0 nmol x g(-1) x h(-1)) and overweight/obese (82.2 +/- 8.7 nmol x g(-1) x h(-1)) patients, respectively. Palmitate oxidation was negatively (R = -0.44, P = 0.003) associated with BMI. Long-chain fatty acyl-CoA content was higher in both the overweight/obese and extremely obese patients compared with normal-weight patients, despite significantly lower fatty acid oxidation only in the extremely obese. No associations were observed between long-chain fatty acyl-CoA content and palmitate oxidation. These data suggest that there is a defect in skeletal muscle fatty acid oxidation with extreme obesity but not overweight/obesity and that the accumulation of intramyocellular long-chain fatty acyl-CoAs is not solely a result of reduced fatty acid oxidation.     

Leptin production during early starvation in lean and obese women

We evaluated abdominal adipose tissue leptin production during short-term fasting in nine lean [body mass index (BMI) 21 +/- 1 kg/m(2)] and nine upper body obese (BMI 36 +/- 1 kg/m(2)) women. Leptin kinetics were determined by arteriovenous balance across abdominal subcutaneous adipose tissue at 14 and 22 h of fasting. At 14 h of fasting, net leptin release from abdominal adipose tissue in obese subjects (10.9 +/- 1.9 ng x 100 g tissue x (-1) x min(-1)) was not significantly greater than the values observed in the lean group (7.6 +/- 2.1 ng x 100 g(-1) x min(-1)). Estimated whole body leptin production was approximately fivefold greater in obese (6.97 +/- 1.18 microg/min) than lean subjects (1.25 +/- 0.28 microg/min) (P < 0.005). At 22 h of fasting, leptin production rates decreased in both lean and obese groups (to 3.10 +/- 1.31 and 10.5 +/- 2.3 ng x 100 g adipose tissue(-1) x min(-1), respectively). However, the relative declines in both arterial leptin concentration and local leptin production in obese women (arterial concentration 13.8 +/- 4.4%, local production 10.0 +/- 12.3%) were less (P < 0.05 for both) than the relative decline in lean women (arterial concentration 39.0 +/- 5.5%, local production 56.9 +/- 13.0%). This study demonstrates that decreased leptin production accounts for the decline in plasma leptin concentration observed after fasting. However, compared with lean women, the fasting-induced decline in leptin production is blunted in women with upper body obesity. Differences in leptin production during fasting may be responsible for differences in the neuroendocrine response to fasting previously observed in lean and obese women.     

Enhanced endothelin-1 system activity with overweight and obesity

Endothelin (ET)-1-mediated vasoconstrictor tone contributes to the development and progression of several adiposity-related conditions, including hypertension and atherosclerotic vascular disease. The aims of the present study were to determine 1) whether endogenous ET-1 vasoconstrictor activity is elevated in overweight and obese adults, and, if so, 2) whether increased ET-1-mediated vasoconstriction contributes to the adiposity-related impairment in endothelium-dependent vasodilation. Seventy-nine adults were studied: 34 normal weight [body mass index (BMI) < 25 kg/m(2)], 22 overweight (BMI ≥ 25 and < 30 kg/m(2)), and 23 obese (BMI ≥ 30 kg/m(2)). Forearm blood flow (FBF) responses to intra-arterial infusion of ET-1 (5 pmol/min for 20 min) and selective ET-1 receptor blockade (BQ-123, 100 nmol/min for 60 min) were determined. In a subset of the study population, FBF responses to ACh (4.0, 8.0, and 16.0 μg·100 ml tissue(-1)·min(-1)) were measured in the absence and presence of selective ET-1 receptor blockade. The vasoconstrictor response to ET-1 was significantly blunted in overweight and obese adults (～ 70%) compared with normal weight adults. Selective ET-1 receptor blockade elicited a significant vasodilator response (～ 20%) in overweight and obese adults but did not alter FBF in normal weight adults. Coinfusion of BQ-123 did not affect FBF responses to ACh in normal weight adults but resulted in an ～ 20% increase (P < 0.05) in ACh-induced vasodilation in overweight and obese adults. These results demonstrate that overweight and obesity are associated with enhanced ET-1-mediated vasoconstriction that contributes to endothelial vasodilator dysfunction and may play a role in the increased prevalence of hypertension with increased adiposity.     

Basal Endothelial Nitric Oxide Release Is Preserved in Overweight and Obese Adults

Objective: Impaired basal nitric oxide release is associated with a number of cardiovascular disorders including hypertension, arterial spasm, and myocardial infarction. We determined whether basal endothelial nitric oxide release is reduced in otherwise healthy overweight and obese adult humans. Research Methods and Procedures: Seventy sedentary adults were studied: 32 normal weight (BMI <25 kg/m²), 24 overweight (BMI ≥ 25 < 30 kg/m²), and 14 obese (BMI ≥ 30 kg/m²). Forearm blood flow (FBF) responses to intra‐arterial infusions of N^g‐monomethyl‐l ‐arginine (5 mg/min), a nitric oxide synthase inhibitor, were used as an index of basal nitric oxide release. Results: N^g‐monomethyl‐l ‐arginine elicited significant reductions in FBF in the normal weight (from 4.1 ± 0.2 to 2.7 ± 0.2 mL/100 mL tissue/min), overweight (4.1 ± 0.1 to 2.8 ± 0.2 mL/100 mL tissue/min), and obese (3.9 ± 0.3 to 2.7 ± 0.2 mL/100 mL tissue/min) subjects. Importantly, the magnitude of reduction in FBF (～30%) was similar among the groups. Discussion: These results indicate that the capacity of the endothelium to release nitric oxide under basal conditions is not compromised in overweight and obese adults.     

Effects of aerobic exercise on serum leptin levels in obese women

It has been demonstrated that leptin concentrations in obese patients may be altered by weight loss. We examined the effects of a 9-week aerobic exercise program on serum leptin concentrations in overweight women (20-50% above ideal body mass) under conditions of weight stability. Sixteen overweight women, mean (SE) age 42.75 (1.64) years, comprised the exercise group which adhered to a supervised aerobic exercise program. A graded exercise treadmill test was conducted before and after the exercise program to determine maximal oxygen uptake (VO2max) using open-circuit spirometry. The women demonstrated improved aerobic fitness (VO2max increased 12.29%), however, body fat and the body mass index did not change significantly [42.27 (1.35)-41.87 (1.33)%]. Fourteen women, age 40.57 (2.80) years, did not exercise over the same time period and served as a control group. Serum leptin levels were not significantly altered for either the exercise [28.00 (2.13)-31.04 (2.71) ng x ml(-1)] or the control group [33.24 (3.78)-34.69 (3.14) ng x mg(-1)]. The data indicate that 9 weeks of aerobic exercise improves aerobic fitness, but does not affect leptin concentrations in overweight women.     

Regional muscle and adipose tissue amino acid metabolism in lean and obese women

The effect of obesity on regional skeletal muscle and adipose tissue amino acid metabolism is not known. We evaluated systemic and regional (forearm and abdominal subcutaneous adipose tissue) amino acid metabolism, by use of a combination of stable isotope tracer and arteriovenous balance methods, in five lean women [body mass index (BMI) <25 kg/m(2)] and five women with abdominal obesity (BMI 35.0-39.9 kg/m(2); waist circumference >100 cm) who were matched on fat-free mass (FFM). All subjects were studied at 22 h of fasting to ensure that the subjects were in net protein breakdown during this early phase of starvation. Leucine rate of appearance in plasma (an index of whole body proteolysis), expressed per unit of FFM, was not significantly different between lean and obese groups (2.05 +/- 0.18 and 2.34 +/- 0.04 micromol x kg FFM(-1) x min(-1), respectively). However, the rate of leucine release from forearm and adipose tissues in obese women (24.0 +/- 4.8 and 16.6 +/- 6.5 nmol x 100 g(-1) x min(-1), respectively) was lower than in lean women (66.8 +/- 10.6 and 38.6 +/- 7.0 nmol x 100 g(-1) x min(-1), respectively; P < 0.05). Approximately 5-10% of total whole body leucine release into plasma was derived from adipose tissue in lean and obese women. The results of this study demonstrate that the rate of release of amino acids per unit of forearm and adipose tissue at 22 h of fasting is lower in women with abdominal obesity than in lean women, which may help obese women decrease body protein losses during fasting. In addition, adipose tissue is a quantitatively important site for proteolysis in both lean and obese subjects.     

Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats.

We hypothesized that nitric oxide (NO) opposes ANG II-induced increases in arterial pressure and reductions in renal, splanchnic, and skeletal muscle vascular conductance during dynamic exercise in normal and heart failure rats. Regional blood flow and vascular conductance were measured during treadmill running before (unblocked exercise) and after 1) ANG II AT(1)-receptor blockade (losartan, 20 mg/kg ia), 2) NO synthase (NOS) inhibition [N(G)-nitro-L-arginine methyl ester (L-NAME); 10 mg/kg ia], or 3) ANG II AT(1)-receptor blockade + NOS inhibition (combined blockade). Renal conductance during unblocked exercise (4.79 +/- 0.31 ml x 100 g(-1) x min(-1) x mmHg(-1)) was increased after ANG II AT(1)-receptor blockade (6.53 +/- 0.51 ml x 100 g(-1) x min(-1) x mmHg(-1)) and decreased by NOS inhibition (2.12 +/- 0.20 ml x 100 g(-1) x min(-1) x mmHg(-1)) and combined inhibition (3.96 +/- 0.57 ml x 100 g(-1) x min(-1) x mmHg(-1); all P < 0.05 vs. unblocked). In heart failure rats, renal conductance during unblocked exercise (5.50 +/- 0.66 ml x 100 g(-1) x min(-1) x mmHg(-1)) was increased by ANG II AT(1)-receptor blockade (8.48 +/- 0.83 ml x 100 g(-1) x min(-1) x mmHg(-1)) and decreased by NOS inhibition (2.68 +/- 0.22 ml x 100 g(-1) x min(-1) x mmHg(-1); both P < 0.05 vs. unblocked), but it was unaltered during combined inhibition (4.65 +/- 0.51 ml x 100 g(-1) x min(-1) x mmHg(-1)). Because our findings during combined blockade could be predicted from the independent actions of NO and ANG II, no interaction was apparent between these two substances in control or heart failure animals. In skeletal muscle, L-NAME-induced reductions in conductance, compared with unblocked exercise (P < 0.05), were abolished during combined inhibition in heart failure but not in control rats. These observations suggest that ANG II causes vasoconstriction in skeletal muscle that is masked by NO-evoked dilation in animals with heart failure. Because reductions in vascular conductance between unblocked exercise and combined inhibition were less than would be predicted from the independent actions of NO and ANG II, an interaction exists between these two substances in heart failure rats. L-NAME-induced increases in arterial pressure during treadmill running were attenuated (P < 0.05) similarly in both groups by combined inhibition. These findings indicate that NO opposes ANG II-induced increases in arterial pressure and in renal and skeletal muscle resistance during dynamic exercise.     

Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans?

Aerobic exercise increases whole body adipose tissue lipolysis, but is lipolysis higher in subcutaneous adipose tissue (SCAT) adjacent to contracting muscles than in SCAT adjacent to resting muscles? Ten healthy, overnight-fasted males performed one-legged knee extension exercise at 25% of maximal workload (W(max)) for 30 min followed by exercise at 55% W(max) for 120 min with the other leg and finally exercised at 85% W(max) for 30 min with the first leg. Subjects rested for 30 min between exercise periods. Femoral SCAT blood flow was estimated from washout of (133)Xe, and lipolysis was calculated from femoral SCAT interstitial and arterial glycerol concentrations and blood flow. In general, blood flow and lipolysis were higher in femoral SCAT adjacent to contracting than adjacent to resting muscle (time 15-30 min; blood flow: 25% W(max) 6.6 +/- 1.0 vs. 3.9 +/- 0.8 ml x 100 g(-1) x min(-1), P < 0.05; 55% W(max) 7.3 +/- 0.6 vs. 5.0 +/- 0.6 ml x 100 g(-1) x min(-1), P < 0.05; 85% W(max) 6.6 +/- 1.3 vs. 5.9 +/- 0.7 ml x 100 g(-1) x min(-1), P > 0.05; lipolysis: 25% W(max) 102 +/- 19 vs. 55 +/- 14 nmol x 100 g(-1) x min(-1), P = 0.06; 55% W(max) 86 +/- 11 vs. 50 +/- 20 nmol x 100 g(-1) x min(-1), P > 0.05; 85% W(max) 88 +/- 31 vs. -9 +/- 25 nmol x 100 g(-1) x min(-1), P < 0.05). In conclusion, blood flow and lipolysis are generally higher in SCAT adjacent to contracting than adjacent to resting muscle irrespective of exercise intensity. Thus specific exercises can induce "spot lipolysis" in adipose tissue.     

Regional blood flow during exercise in humans measured by near-infrared spectroscopy and indocyanine green.

Using near-infrared spectroscopy (NIRS) and the tracer indocyanine green (ICG), we quantified blood flow in calf muscle and around the Achilles tendon during plantar flexion (1-9 W). For comparison, blood flow in calf muscle was determined by dye dilution in combination with magnetic resonance imaging measures of muscle volume, and, for the peritendon region, blood flow was measured by (133)Xe washout. From rest to a peak load of 9 W, NIRS-ICG blood flow in calf muscle increased from 2.4+/-0.2 to 74+/-5 ml x 100 ml tissue(-1) x min(-1), similar to that measured by reverse dye (77+/-6 ml x 100 ml tissue(-1) x min(-1)). Achilles peritendon blood flow measured by NIRS-ICG rose with exercise from 2.2+/-0.5 to 15.1+/-0.2 ml x 100 ml(-1) x min(-1), which was similar to that determined by (133)Xe washout (2.0+/-0.6 to 14.6+/-0.3 ml x 100 ml tissue(-1) x min(-1)). This is the first study using NIRS and ICG to quantify regional tissue blood flow during exercise in humans. Due to its high spatial and temporal resolution, the technique may be useful for determining regional blood flow distribution and regulation during exercise in humans.     

Sympathetic activity and the heterogenous blood pressure response to exercise training in hypertensives.

To test whether changes in sympathetic nervous system (SNS) activity or insulin sensitivity contribute to the heterogeneous blood pressure response to aerobic exercise training, we used compartmental analysis of [3H]norepinephrine kinetics to determine the extravascular norepinephrine release rate (NE2) as an index of systemic SNS activity and determined the insulin sensitivity index (S(I)) by an intravenous glucose tolerance test, before and after 6 mo of aerobic exercise training, in 30 (63 +/- 7 yr) hypertensive subjects. Maximal O2 consumption increased from 18.4 +/- 0.7 to 20.8 +/- 0.7 ml x kg(-1) x min(-1) (P = 0.02). The average mean arterial blood pressure (MABP) did not change (114 +/- 2 vs. 114 +/- 2 mmHg); however, there was a wide range of responses (-19 to +17 mmHg). The average NE2 did not change significantly (2.11 +/- 0.15 vs. 1.99 +/- 0.13 microg x min(-1) x m(-2)), but there was a significant positive linear relationship between the change in NE2 and the change in MABP (r = 0.38, P = 0.04). S(I) increased from 2.81 +/- 0.37 to 3.71 +/- 0.42 microU x 10(-4) x min(-1) x ml(-1) (P = 0.004). The relationship between the change in S(I) and the change in MABP was not statistically significant (r = -0.03, P = 0.89). When the changes in maximal O2 consumption, percent body fat, NE2, and S(I) were considered as predictors of the change in MABP, only NE2 was a significant independent predictor. Thus suppression of SNS activity may play a role in the reduction in MABP and account for a portion of the heterogeneity of the MABP response to aerobic exercise training in older hypertensive subjects.     

Influence of aerobic fitness and body fatness on tolerance to uncompensable heat stress.

This study examined the independent and combined importance of aerobic fitness and body fatness on physiological tolerance and exercise time during weight-bearing exercise while wearing a semipermeable protective ensemble. Twenty-four men and women were matched for aerobic fitness and body fatness in one of four groups (4 men and 2 women in each group). Aerobic fitness was expressed per kilogram of lean body mass (LBM) to eliminate the influence of body fatness on the expression of fitness. Subjects were defined as trained (T; regularly active with a peak aerobic power of 65 ml x kg LBM(-1) x min(-1)) or untrained (UT; sedentary with a peak aerobic power of 53 ml x kg LBM(-1) x min(-1)) with high (High; 20%) or low (Low; 11%) body fatness. Subjects exercised until exhaustion or until rectal temperature reached 39.5 degrees C or heart rate reached 95% of maximum. Exercise times were significantly greater in T(Low) (116 +/- 6.5 min) compared with their matched sedentary (UT(Low); 70 +/- 3.6 min) or fatness (T(High); 82 +/- 3.9 min) counterparts, indicating an advantage for both a high aerobic fitness and low body fatness. However, similar effects were not evident between T(High) and UT(High) (74 +/- 4.1 min) or between the UT groups (UT(Low) and UT(High)). The major advantage attributed to a higher aerobic fitness was the ability to tolerate a higher core temperature at exhaustion (the difference being as great as 0.9 degrees C), whereas both body fatness and rate of heat storage affected the exercise time as independent factors.     

Aerobic exercise training reduces epicardial fat in obese men

The purpose of this study was to determine the effects of exercise training on ventricular epicardial fat thickness in obese men and to investigate the relationship of the change in epicardial fat thickness to changes in abdominal fat tissue following exercise training. Twenty-four obese middle-aged men [age, 49.4 +/- 9.6 yr; weight, 87.7 +/- 11.2 kg; body mass index (BMI), 30.7 +/- 3.3 kg/m(2); peak oxygen consumption, 28.4 +/- 7.2 ml.kg(-1).min(-1); means +/- SD] participated in this study. Each participant completed a 12-wk supervised exercise training program (60-70% of the maximal heart rate; 60 min/day, 3 days/wk) and underwent a transthoracic echocardiography. The epicardial fat thickness on the free wall of the right ventricle was measured from both parasternal long- and short-axis views. The visceral adipose tissue (VAT) and subcutaneous adipose tissues were measured by computed tomography. Following exercise training, the epicardial fat thickness was significantly decreased (P < 0.001). The percentage change of epicardial fat thickness was twice as high compared with those of waist, BMI, and body weight of original values (P <0.05). There was a significant relationship (r = 0.525, P = 0.008) between changes in the epicardial fat thickness and VAT with exercise training. Stepwise multiple regression analysis revealed that the change in VAT, change in systolic blood pressure, and change in quantitative insulin sensitivity check index were independently related to the change epicardial fat thickness (P < 0.05). The ventricular epicardial fat thickness is reduced significantly after aerobic exercise training and is associated with a decrease in VAT. These results suggest that aerobic exercise training may be an effective nonpharmacological strategy for decreasing the ventricular epicardial fat thickness and visceral fat area in obese middle-aged men.     

Acute changes in dietary omega-3 fatty acid intake lowers soluble interleukin-6 receptor in healthy adult normal weight and overweight males

OBJECTIVE: To determine the effect of a short-term isocaloric exchange of alpha-linolenic acid (ALA, 18:3n3) for linoleic acid (LA, 18:2n6) on fasting levels of soluble interleukin-6 receptor (sIL6R), and soluble tumor necrosis factor-alpha receptors 1 and 2 (sTNFR1 and sTNFR2) in healthy normal weight and overweight/obese adult males. DESIGN: Four-day clinical intervention study with 0.5% or 5% of total energy from ALA. Fasting (10 h) blood samples were obtained on the morning of day 5 in both diet treatments to measure sTNFR1, sTNFR2, and sIL6R. SUBJECTS: Nine normal weight (BMI < 25 kg/m2) and seven overweight (BMI > or = 25 kg/m2) healthy males. RESULTS: Fasting sIL6R decreased significantly from the control (C) diet following four days on the high ALA isocaloric (ISO) diet in normal weight and overweight/obese subjects (normal weight: C = 34.89 +/- 3.17 ng/ml, ISO = 30.91 +/- 2.24 ng/ml, p < 0.05; overweight/obese: C = 38.19 +/- 3.92 ng/ml, ISO = 33.57 +/- 2.47 ng/ml, p , 0.05). The dietary intervention did not have a significant effect on fasting sTNFR1 or sTNFR2. CONCLUSIONS: The results suggest that an isocaloric exchange of ALA for LA can reduce fasting sIL6R concentration by approximately 11% after a four-day dietary intervention in both overweight/obese and normal weight subjects. The data also suggest that longer exposure to a similar diet may have the potential to reduce inflammatory burden and thus lower the risk of both cardiovascular disease as well as diabetes.