Enhanced endothelial vasoreactivity in endurance-trained older men.

Using external vascular ultrasound, we measured brachial artery diameter (Diam) at rest, after release of 4 min of limb ischemia, i. e., endothelium-dependent dilation (EDD), and after sublingual nitroglycerin, i.e., non-endothelium-dependent dilation (NonEDD), in 35 healthy men aged 61-83 yr: 12 endurance athletes (A) and 23 controls (C). As anticipated, treadmill exercise maximal oxygen consumption (VO(2 max)) was significantly higher in A than in C (40. 2 +/- 6.6 vs. 27.9 +/- 3.8 ml. kg(-1). min(-1); respectively, P < 0. 0001). With regard to arterial physiology, A had greater EDD (8.9 +/- 4.2 vs. 5.7 +/- 3.5%; P = 0.02) and a tendency for higher NonEDD (13.9 +/- 6.7 vs. 9.7 +/- 4.2%; P = 0.07) compared with C. By multiple linear regression analysis in the combined sample of older men, only baseline Diam (beta = -2.0, where beta is the regression coefficient; P = 0.005) and VO(2 max) (beta = 0.23; P = 0.003) were independent predictors of EDD; similarly, only Diam (beta = -4.0; P = 0.003) and VO(2 max) (beta = 0.27; P = 0.01) predicted NonEDD. Thus endurance-trained older men demonstrate both augmented EDD and NonEDD, consistent with a generalized enhanced vasodilator responsiveness, compared with their sedentary age peers.

Acute reduction in ankle/brachial index following smoking in chronic smokers with peripheral arterial occlusive disease.

The ankle-brachial systolic pressure index (ABI), a noninvasive measure of peripheral arterial occlusive disease (PAOD) severity, is considered a marker of atherosclerosis and an independent predictor of mortality. However, it is not known whether factors other than PAOD severity, such as cigarette smoking, have an effect on ABI measurement. Therefore, the authors examined the acute effects of cigarette smoking on ABI and the peripheral circulation in 10 older (63 +/- 10 years) chronic smokers (39 +/- 37 pack-years) with PAOD (ABI=0.64 +/- 0.14). The patients were instructed to refrain from smoking and from consuming caffeine-containing beverages for at least 12 hours before the tests. The patients were randomly assigned to 2 days of testing consisting of a nonsmoking and a smoking day. Resting heart rate, blood pressure, ABI, and calf blood flow by plethysmography were obtained on both testing days. The smoking day consisted of smoking two filter cigarettes over a period of 10 minutes before the measurement of ABI and calf blood flow. The ABI on the smoking day (0.55 +/- 0.11) was lower (p=0.008) than on the nonsmoking day (0.64 +/- 0.14) owing to a lower (p=0.020) ankle systolic blood pressure (81 +/- 28 vs 93 +/- 28 mmHg). Brachial systolic blood pressures, heart rate, and calf blood flow were not altered by smoking (p>0.05). These results demonstrate that the acute effect of cigarette smoking lowers the ABI in chronic smokers with intermittent claudication, thereby yielding evidence of a transient deleterious effect of cigarette smoking on the peripheral circulation in chronic smokers.

Endothelial reactivity and cardiac risk factors in older patients with peripheral arterial disease.

Peripheral arterial disease (PAD) is a major cause of morbidity and mortality. Endothelium-dependent vasoreactivity, which is advocated as a measure of vascular health, is impaired in persons with cardiac risk factors and coronary artery disease. Few studies have examined the degree of endothelial dysfunction in patients with PAD. Using high-resolution external vascular ultrasound, we measured brachial artery diameter and flow at rest, and in response to reactive hyperemia (flow-mediated dilation) in 50 older patients (age 69 +/- 1 year) with PAD (ankle-to-brachial artery index of 0.67 +/- 0.03), and 50 age-matched non-PAD patients. Coronary artery disease was more prevalent in PAD than in non-PAD patients (40% vs 4%, p <0.001). Systolic blood pressure (153 +/- 4 vs 141 +/- 3 mm Hg, p <0.01), fasting glucose (129 +/- 6 vs 109 +/- 5 mg/dl, p <0.001), and pack-years smoked (54 +/- 7 vs 25 +/- 3, p <0.01) were higher in the PAD than in non-PAD patients. There were no differences in baseline brachial artery diameter, blood velocity, or flow between the 2 groups. However, the 1-minute postocclusion percent change in diameter (6.5 +/- 0.7% vs 9.8 +/- 0.7%, p <0.001) and the change in diameter (0.22 +/- 0.02 vs 0.33 +/- 0.02 mm, p <0.001) were lower in PAD than in non-PAD patients, suggesting impaired endothelium-dependent dilation. The postocclusion hyperemic velocity and blood flow were also lower in PAD than in non-PAD patients. In multiple regression analyses the low-density lipoprotein-to-high-density lipoprotein cholesterol ratio, elevated fasting glucose, and high systolic blood pressure were independent predictors of percent change in brachial artery diameter (r2 = 0.37, p <0.001). Thus, older patients with PAD had impaired endothelial dependent vasodilation compared with controls that was associated with the presence of cardiac risk factors. The effect of cardiac risk factor intervention on endothelial function in patients with PAD remains to be determined.

Heart rate variability and cardiovascular fitness in senior athletes.

To determine if the age-associated decline in heart rate variability is due in part to decreases in fitness levels, we compared heart rate variability parameters in older athletes and age-matched sedentary persons. All heart rate variability parameters were superior in the athletes, consistent with an enhanced cardiac vagal modulation in the athlete.

Relationship of body composition and cardiovascular fitness to lipoprotein lipid profiles in master athletes and sedentary men.

A number of studies demonstrate that highly conditioned older athletes are leaner than their sedentary counterparts, and have lipoprotein profiles similar to that of young individuals. It is not clear whether the high maximal aerobic capacity (VO2max) or lean body habitus is the major determinant of the favorable lipoprotein lipid profiles present in older athletes. The objective of this study was to determine whether body composition or VO2max was the major determinant of lipoprotein lipid profiles among 61 master (age 63 +/- 6 years, mean +/- SD) athletes (VO2max > 40 mL/kg/min), 39 age-matched lean (% body fat < 25%), and 51 obese (% body fat > 25%) sedentary men. Plasma high density lipoprotein cholesterol (HDL-C) concentrations were 25% higher in that athletes than in the lean sedentary men, and 42% higher than in the obese sedentary men. Triglyceride (TG) concentrations were 24% lower in the master athletes than in the lean sedentary men, and 51% lower than in the obese sedentary group. Plasma low density lipoprotein cholesterol (LDL-C) levels were 9% lower in the athletes than in the other groups of sedentary individuals. In stepwise multiple regression analysis the percent body fat was the major independent predictor of HDL-C and TG levels accounting for 29% and 41% of the variation in these levels, respectively. The VO2max accounted for an additional 6% of the variance in HDL-C levels and 2% of the variance in TG levels. These cross-sectional results suggest that the favorable lipoprotein profile of master athletes is largely due to their lean body habitus, with a small independent contribution from their higher levels of cardiovascular fitness. Thus, regular vigorous aerobic exercise and maintenance of low body fat may prevent the commonly observed age-associated deterioration in lipoprotein concentrations.