Continuum of cardiovascular performance across a broad range of fitness levels in healthy older men.

BACKGROUND: Although it has become clear that habitual exercise in older individuals can partially offset age-associated cardiovascular declines, it is not known whether the beneficial effects of exercise training in older individuals depend on their prior fitness level. METHODS AND RESULTS: Ten sedentary men (S), age 60.0 +/- 1.6 years (mean +/- SEM), who were carefully screened to exclude cardiac disease underwent exercise training for 24 to 32 weeks, and eight age-matched endurance-trained men (ET) stopped their exercise training for 12 weeks. All underwent treadmill exercise and rest and maximal cycle exercise upright gated blood pool scans at baseline and after the lifestyle intervention. Before the intervention, the treadmill maximum rate of oxygen consumption (Vo2max) was 49.9 +/- 1.9 and 32.1 +/- 1.4 mL.kg-1.min-1 in ET and S, respectively. During upright cycle exercise at exhaustion, although heart rate did not differ between groups, cardiac index, stroke volume index, ejection fraction, and left ventricular contractility index (systolic blood pressure/end-systolic volume index) all were significantly higher, and end-systolic volume index, diastolic blood pressure, and total systemic vascular resistance all were significantly lower in ET versus S. After the partial deconditioning of ET men, Vo2max fell to 42 +/- 2.2 mL.kg-1.min-1, and training of S increased Vo2max to 36.2 +/- 1.6 mL.kg-1.min-1. Training of S had effects on cardiovascular function that were similar in magnitude but directionally opposite those of detraining ET. All initial differences in cardiovascular performance at peak work rate between S and ET were abolished with the intervention. Across the broad range of fitness levels encountered before and after change in training status (Vo2max of 26 to 58 mL.kg-1.min-1), cardiac index, stroke volume index, end-systolic volume index, ejection fraction, and the left ventricular contractility index were all linearly correlated with Vo2max. CONCLUSIONS: Exercise training or detraining of older men results in changes in left ventricular performance that are qualitatively and quantitatively similar, regardless of the initial level of fitness before the intervention.

Risk factors for exercise-induced silent myocardial ischemia in healthy volunteers.

This study determined the risk factors for exercise-induced silent ischemia (SI) in 281 apparently healthy volunteers aged 40 to 87 years and compared their risk factor profiles with those of 132 patients with overt coronary artery disease (CAD). SI (concordant exercise-induced asymptomatic ST-segment depression on electrocardiography and perfusion defects on tomographic thallium-201 scintigraphy) was detected in 37 of 225 men (16%), versus 2 of 56 women (4%, p < 0.05). The prevalence of SI increased with age from 6% in men aged < 55 years to 18% in men aged 55 to 70 years, and to 25% in men aged > 70 years (p < 0.001). Compared with the 118 men with concordant normal exercise electrocardiogram and thallium scan (normals), men with SI were older (p < 0.001), and had a higher waist-to-hip ratio (p < 0.005), higher plasma triglyceride levels (p < 0.001), and lower high-density lipoprotein (HDL) cholesterol levels (p < 0.001). In stepwise logistic regression analysis, age, waist-to-hip ratio, and HDL levels were independent predictors of SI in men. Compared with 108 men with overt CAD, men with SI were younger (67 +/- 2 vs 73 +/- 1 years, p < 0.001) but had similar plasma lipids and waist-to-hip ratio. Thus, older age, male gender, abdominal obesity, and reduced HDL levels--all well-established risk factors for overt CAD--were risk factors for exercise-induced SI in these asymptomatic volunteers.

Effects of age and aerobic capacity on arterial stiffness in healthy adults.

BACKGROUND: It has been well established that arterial stiffness, manifest as an increase in arterial pulse wave velocity or late systolic amplification of the carotid artery pressure pulse, increases with age. However, the populations studied in prior investigations were not rigorously screened to exclude clinical hypertension, occult coronary disease, or diabetes. Furthermore, it is unknown whether exercise capacity or chronic physical endurance training affects the age-associated increase in arterial stiffness. METHODS AND RESULTS: Carotid arterial pressure pulse augmentation index (AGI), using applanation tonometry, and aortic pulse wave velocity (APWV) were measured in 146 male and female volunteers 21 to 96 years old from the Baltimore Longitudinal Study of Aging, who were rigorously screened to exclude clinical and occult cardiovascular disease. Aerobic capacity was determined in all individuals by measurement of maximal oxygen consumption (VO2max) during treadmill exercise. In this healthy, largely sedentary cohort, the arterial stiffness indexes AGI and APWV increased approximately fivefold and twofold, respectively, across the age span in both men and women, despite only a 14% increase in systolic blood pressure (SBP). These age-associated increases in AGI and APWV were of a similar magnitude to those in prior studies of less rigorously screened populations. Both AGI and APWV varied inversely with VO2max, and this relationship, at least for AGI, was independent of age. In endurance trained male athletes, 54 to 75 years old (VO2max = 44 +/- 3 mL.kg-1.min-1), the arterial stiffness indexes were significantly reduced relative to their sedentary age peers (AGI, 36% lower; APWV, 26% lower) despite similar blood pressures. CONCLUSIONS: Even in normotensive, rigorously screened volunteers in whom SBP increased an average of only 14% between ages 20 and 90 years, major age-associated increases of arterial stiffness occur. Higher physical conditioning status, indexed by VO2max, was associated with reduced arterial stiffness, both within this predominantly sedentary population and in endurance trained older men relative to their less active age peers. These findings suggest that interventions to improve aerobic capacity may mitigate the stiffening of the arterial tree that accompanies normative aging.