Association of fasting glucose with subclinical cerebrovascular disease in older adults without Type 2 diabetes.

AIMS: To examine how fasting glucose and glucose tolerance are related to magnetic resonance imaging-assessed indicators of subclinical cerebrovascular disease and brain atrophy and their variation according to age, sex and education. METHODS: Participants in the present study were 172 healthy, community-dwelling older adults. An oral glucose tolerance test was administered and magnetic resonance imaging performed. Fasting, 2-h, and 2-h area-under-the-curve glucose levels, their associations with subclinical cerebrovascular disease and brain atrophy, and their respective interactions with age, sex and education were examined. RESULTS: A positive association between fasting glucose and subclinical cerebrovascular disease (but not brain atrophy) emerged; this association was more pronounced for participants with < 12 years of education; however, glucose tolerance was not related to subclinical cerebrovascular disease or brain atrophy. CONCLUSIONS: Findings revealed a potential link between fasting glucose levels and the presence of subclinical cerebrovascular disease indicators - white matter hyperintensities and silent brain infarction - in older adults without diabetes and with an education level below high school. Additional research is needed to confirm these associations and to determine the need for interventions aimed at closely monitoring and preventing elevated glucose levels in this population to reduce the prevalence of subclinical cerebrovascular disease.

Reduced aerobic capacity and physical functioning in older HIV-infected men.

Aerobic capacity and physical functioning decline with age and chronic illness. The extent of physical disability is unknown in older HIV-infected adults, who represent a rapidly growing proportion of HIV/AIDS patients in the United States. We performed functional performance testing including treadmill testing in 32 HIV-infected male veterans aged 40-69 years. Controls were 47 healthy male subjects tested previously in the same exercise laboratory. HIV-infected subjects were classified as younger (40-49 years, n = 12) or older age (50+ years, n = 20). Peak aerobic capacity (VO2peak) was significantly reduced in the older vs. younger HIV subjects [19.1 mL/kg/min +/- 5.7 (mean, SD) vs. 25.2 +/- 4.2, p = 0.01]. VO2peak was reduced 41% +/- 15% (mean, SD) in HIV-infected subjects compared to expected values from age-matched healthy controls. Regression analyses show a similar decline in VO2peak with age in HIV-infected and healthy controls. Mean 6-min walk distance was not significantly different between the HIV-infected age groups, and was reduced only 8% compared to expected values for healthy adults. Current CD4 count and HAART exposure were similar in the two age groups and were not significantly associated with VO2peak. Anemia (HCT <35%) was significantly associated with reduced VO2peak (p = 0.02), but this association was not independent of the effect of age (p = 0.1). We conclude that older HIV-infected adults have markedly impaired aerobic capacity but maintain the capacity to undertake day-to-day activities. Additional physiologic and metabolic testing is needed to measure the effect of HAART toxicity and primary aging on aerobic capacity, and to determine if older HIV-infected adults are at greater risk.

Effect of an American Heart Association diet, with or without weight loss, on lipids in obese middle-aged and older men.

Forty-two obese [body mass index (kg/m2): 30 +/- 5; weight: 92.9 +/- 10.1 kg] men aged 60 +/- 9 y were recruited to determine the effects of an American Heart Association (AHA) diet, with and without weight loss, on lipoprotein lipids. All subjects entered a 3-mo, weight-maintaining AHA diet followed by either a 9-mo weight-loss (AHA + WL, n = 28) or a 9-mo AHA plus weight-maintenance (AHA + WM, n = 14) intervention. Baseline diets were high in fat (35 +/- 6% of energy) and cholesterol (380 +/- 158 mg/d), and low in dietary fiber (18 +/- 5 g/d). The 3-mo AHA diet resulted in an 11% decrease in plasma triacylglycerol (1.83 +/- 0.15 to 1.47 +/- 0.08 mmol/L, P < 0.05), a 16% decrease in plasma cholesterol (5.39 +/- 0.96 to 4.56 +/- 0.91 mmol/L, P = 0.0001), a 17% decrease in high-density-lipoprotein (HDL) cholesterol (1.09 +/- 0.23 to 0.91 +/- 0.18 mmol/L, P = 0.0001), and a 14% decrease in low-density-lipoprotein (LDL) cholesterol (3.47 +/- 0.83 to 2.98 +/- 0.78 mmol/L, P = 0.0001) The AHA + WL group lost 9.8 +/- 4.3 kg (P < 0.001, n = 28) and further reduced plasma triacylglycerol by 17% (P < 0.05), total cholesterol by 4% (P < 0.05), LDL cholesterol by 7% (P < 0.05), and significantly increased HDL cholesterol by 15% (P < 0.05) when compared with their 3-mo AHA-intervention values. These changes were significant (P < 0.05) when compared with the AHA + WM group, in whom lipoprotein lipids did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of an American Heart Association diet and weight loss on lipoprotein lipids in obese, postmenopausal women.

The sequential effects of an American Heart Association (AHA) Step 1 diet and subsequent weight loss on lipoprotein lipids in obese [body mass index (in kg/m2) > 27], postmenopausal women (n = 48) were determined. Subjects followed a euenergetic AHA Step 1 diet for 2 mo, followed by a weight-loss diet (deficit of 1.0-1.5 MJ/d) for 6 mo. The AHA diet lowered concentrations of total (7%), low-density-lipoprotein (LDL) (6%), and high-density-lipoprotein (HDL) (14%) cholesterol (P < 0.01). Weight loss (-5.6 +/- 0.7 kg; P < 0.01) increased plasma triacylglycerol concentrations (9%; P < 0.01) and increased HDL-cholesterol concentrations (8%; P < 0.01) compared with changes after the AHA diet, but there were no changes in total or LDL cholesterol. The combined AHA diet and weight-loss interventions lowered triacylglycerol (10%) and total (6%), LDL (6%), and HDL (7%) cholesterol. These changes correlated indirectly with the baseline concentration for each lipid. When the women were divided on the basis of initial LDL-cholesterol concentration, the AHA diet and weight-loss interventions reduced (P < 0.01) triacylglycerol (19%), total cholesterol (13%), and LDL cholesterol (14%) in the women with hypercholesterolemia but not in normocholesterolemic or midly hypercholesterolemic women. Thus, an AHA Step 1 diet and subsequent weight loss improve lipoprotein lipid profiles of obese, postmenopausal women with hypercholesterolemia. However, because it lowers HDL cholesterol, a low-fat diet without substantial weight loss may not be beneficial for improving lipoprotein lipid risk factors for coronary artery disease in obese, postmenopausal women with normal lipid profiles.

Energy requirements of middle-aged men are modifiable by physical activity.

BACKGROUND: Energy requirements for weight maintenance decrease with age. Often, this decline is not proportionately matched by reduced energy intake, resulting in weight gain. OBJECTIVE: We hypothesized that energy requirements for total daily weight maintenance in healthy, sedentary, middle-aged men would increase after regular aerobic exercise or aerobic exercise plus weight loss to levels comparable with those in middle-aged athletes. DESIGN: Weight-maintenance energy requirements were determined during weight stability (+/- 0.25 kg) in 14 lean, sedentary (LS) men; 18 obese, sedentary (OS) men; and 10 male athletes of comparable ages (x +/- SEM: 58 +/- 1 y). Studies were done at baseline and after 6 mo of aerobic exercise (LS men) or aerobic exercise plus weight loss (OS men) or 3 mo of deconditioning (athletes). RESULTS: The interventions raised maximal oxygen uptake (VO2max) by 15% in the LS men and by 13% in the OS men and decreased it by 14% in athletes (all P < 0.01), eliminating the differences among groups at baseline. Body fat was reduced significantly in LS and OS men; fat-free mass decreased in OS men. Average daily energy requirements increased by 8% in LS men and by 5% in OS men (both P < 0.01) to levels comparable with the baseline requirements of athletes and correlated with VO2max (r2 = 0.22, P < 0.0001) and fat-free mass (r2 = 0.05, P < 0.02) across the range of VO2max achieved by all subjects. CONCLUSIONS: Under free-living conditions, aerobic exercise eliminated the difference in weight-maintenance energy requirements between middle-aged sedentary and athletic men, suggesting that energy requirements of healthy, middle-aged men are modifiable by regular physical activity.

Relationship between physical activity and HDL-cholesterol in healthy older men and women: a cross-sectional and exercise intervention study.

We used cross-sectional and exercise intervention studies to examine whether physical activity levels or increases in peak aerobic capacity (peak VO2) explain variation in high density lipoprotein cholesterol (HDL-C) levels in older men and women. In the cross-sectional study, 307 older individuals (169 men; 138 women; 67 +/- 7 years) were characterized for HDL-C, leisure time physical activity, peak VO2, body composition, body fat distribution and dietary intake. HDL-C was 19% higher (P < 0.001) in women (57 +/- 14 mg/dl) versus men (48 +/- 14 mg/dl). Thirty-two percent of the variation in HDL-C in older men was explained by the waist circumference (r2 = 16%), percent dietary intake of alcohol (r2 = 11%), and carbohydrate (r2 = 6%). Waist circumference was also the best predictor of HDL-C in older women, (r2 = 7%); with percent dietary intake of carbohydrate adding an additional 6% to the model. Neither peak VO2 nor leisure time physical activity were independent predictors of HDL-C. Statistical control for the aforementioned variables diminished, but did not abolish gender differences in HDL-C. Thirty-seven older individuals (23 men; 14 women) participated in a 2-month exercise program in which individuals by week eight were expending approximately 900 kcal per week in exercise energy expenditure. Subjects were maintained in energy balance throughout the exercise program. Endurance training significantly increased peak VO2 by 15% in both men and women, and by design, body composition and body fat distribution did not change. No changes in HDL-C levels were noted. In conclusion, variations in leisure time physical activity or increases in peak VO2 are not independent predictors of HDL-C levels in healthy older men and women. Instead, central adiposity, as estimated by the waist circumference, and to a lesser extent, dietary intake of carbohydrate and alcohol, are significant predictors of variation in plasma HDL-C levels. Furthermore, short-term exercise training, generating less than 900 kcal per week in exercise energy expenditure, in the absence of weight loss, fails to influence HDL-C levels.

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.

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.

Effects of exercise rehabilitation on endothelial reactivity in older patients with peripheral arterial disease.

Peripheral arterial disease (PAD) is a major cause of morbidity and mortality. Endothelial function, which is a measure of vascular health, is impaired in patients with PAD. We examined the effects of 6 months of aerobic exercise rehabilitation on brachial artery endothelial function, assessed using high-frequency ultrasonography, and calf blood flow in 19 older PAD patients (age 69 +/- 1 years, mean +/- SEM) with intermittent claudication (ankle to brachial artery index of 0.73 +/- 0.04). After exercise, the time to onset of claudication pain increased by 94%, from 271 +/- 49 to 525 +/- 80 seconds (p <0.01), and the time to maximal claudication pain increased by 43%, from 623 +/- 77 to 889 +/- 75 seconds (p <0.05). Exercise rehabilitation increased the flow-mediated brachial arterial diameter by 61%, from 0.18 +/- 0.03 to 0.29 +/- 0.04 mm (p <0.005), as well as the relative change in brachial arterial diameter from the resting state by 60%, from 4.81 +/- 0.82% to 7.97 +/- 1.03% (p <0.005). Maximal calf blood flow (14.2 +/- 1.0 vs 19.2 +/- 2.0 ml/100 ml/min; p = 0.04), and postocclusive reactive hyperemic blood flow (9.8 +/- 0.8 vs 11.3 +/- 0.7 ml/100 ml/min; p = 0.1) increased 35% and 15%, respectively. In conclusion, exercise rehabilitation improved ambulatory function, endothelial-dependent dilation, and calf blood flow in older PAD patients with intermittent claudication.

Exercise-induced silent myocardial ischemia in master athletes.

High-physical activity levels are associated with reduced risk of symptomatic coronary artery disease (CAD). However, there are a number of reports of exercise-related sudden death and myocardial infarction in aerobically trained athletes. This study compared the prevalence of exercise-induced silent myocardial ischemia on maximum graded exercise tests with tomographic thallium scintigraphy in 70 master male athletes (63 +/- 6 years, mean +/- SD) (maximum aerobic capacity, VO2max >40 ml/kg/min) and in 85 healthy untrained men (61 +/- 7 years) with no history of CAD. The prevalence of silent ischemia (exercise-induced ST-segment depression on electrocardiogram and perfusion abnormalities on thallium scintigraphy) was similar in athletes and untrained men; 16% of the athletes (11 of 70) had silent ischemia compared with 21% of the untrained men (chi-square = 0.81, p = 0.36). No athletes had hyperlipidemia, systemic hypertension, or diabetes mellitus. However, the apolipoprotein E4 allele was present in 9 of the 11 athletes with silent ischemia compared with 2 of 32 athletes with normal exercise tests (chi-square = 24, p = 0.0001). These results suggest that older male athletes with the apolipoprotein E4 allele are at increased risk for the development of exercise-induced silent ischemia.

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.

Adverse effects of abdominal obesity on lipoprotein lipids in healthy older men.

Individuals with abdominal obesity are at increased risk for the development of coronary artery disease (CAD). This study examines whether an abdominal fat distribution, indexed by the waist to hip ratio (WHR), is associated with an atherogenic lipoprotein lipid profile independent of the degree of obesity (percent body fat) and maximal aerobic capacity (VO2max) in 127 older (60 +/- 8 years, mean +/- SD) normotensive, nonsmoking, nondiabetic men. Compared to men with WHR below the population mean (< 0.96, low WHR), men with high WHR (> 0.96) had higher triglycerides (TG) (124 +/- 47 vs. 93 +/- 48 mg/dl, p < 0.001) and lower high density lipoprotein cholesterol (HDL-C) (34 +/- 7 vs 41 +/- 9 mg/dl, p < 0.001) levels with no difference in low density cholesterol (LDL-C) levels. Plasma TG levels were positively associated with both percent body fat (r = 0.50, p < 0.0001) and WHR (r = 0.49, p < 0.0001), and negatively with VO2max (r = -0.36, p < 0.0001), whereas plasma HDL-C levels were negatively associated with percent body fat (r = -0.50, p < 0.0001) and WHR (r = -0.54, p < 0.0001), and positively with VO2max (r = 0.45, p < 0.0001). Independent relationships between WHR and both plasma TG (r = 0.30, p < 0.001) and HDL-C (r = -0.34, p < 0.0001) remained after correction for both percent body fat and VO2max. Using analysis of covariance, the differences in TG and HDL-C between groups remained after adjustment for percent body fat and VO2max. These results suggest that in older men, an abdominal distribution of body fat, independent of both percent body fat and VO2max, is associated with elevated TG and low HDL levels, thus increasing the risk for CAD.

The role of obesity and cardiovascular fitness in the impaired glucose tolerance of aging.

The prevalence of impaired glucose tolerance (IGT) increases with aging. Although some data suggest that age is independently associated with IGT, other studies suggest that age-associated changes in body composition and reduced cardiovascular fitness are responsible for the development of IGT. We, therefore, examined the relationship of age, total and regional adiposity, and level of fitness (VO2max) to the presence of IGT in 155 healthy, nondiabetic, nonsmoking, older community dwelling men. Sixty-two of 155 men (40%) had IGT, while 93 men (60%) had normal glucose tolerance (WHO criteria). The subjects with IGT were of similar age (61.0 +/- 1.0 vs. 59.0 +/- 0.7 years, p = 0.49) and had the same maximal aerobic capacity, (VO2max) (42.0 +/- 1.0 vs. 44.0 +/- 0.8 mL/kg ffm/min, p = 0.42), but had a higher waist to hip ratio (WHR) (0.98 +/- 0.01 vs. 0.96 +/- 0.01, p = 0.005) and percent body fat (30.0 +/- 0.4 vs. 26.0 +/- 0.6, p = 0.004) than the men with normal glucose tolerance. In univariate analysis, the 2-h glucose level correlated positively with percent body fat (r = 0.30, p = 0.0002), WHR (0.24, p = 0.002), and age (r = 0.17, p = 0.03) and negatively with VO2max (r = -0.23, p = 0.005). In both multiple logistic and linear regression analyses, percent body fat was the only independent predictor of IGT (p = 0.002). These results suggest that the age-associated increase in total adiposity is a major contributor to the development of IGT in middle-aged and older men. Thus, lifestyle modifications that reduce body fat should reduce the risk for IGT and the development of noninsulin-dependent diabetes mellitus in the elderly.

Silent ischemia during voluntary detraining and future cardiac events in master athletes.

OBJECTIVES: To determine whether exercise-induced silent ischemia in older master athletes following a 3-month period of deconditioning is a predictor of future cardiovascular events. DESIGN: A longitudinal study of a cohort of master athletes. SETTING: The Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland. PARTICIPANTS: Ten older (59 +/- 8 years, mean +/- SD), highly conditioned (maximal aerobic capacity VO2max 50 +/- 5 mL/kg/min), aerobically trained athletes. INTERVENTION: Five to eight years of longitudinal follow-up of athletes who had previously participated in a 3-month-long detraining intervention. MEASUREMENTS: At baseline, all 10 athletes had their history taken and underwent physical examinations, metabolic testing, electrocardiogram at rest, exercise treadmill tests, exercise thallium scintigrams, and exercise multigated acquisition scans. After 3 months of deconditioning, they had repeat maximal exercise stress tests. After 5 to 8 years of follow-up, they were re-evaluated, including history and physical examination and measurement of their VO2max. RESULT: All 10 master athletes had normal studies at baseline. At the end of 3 months of detraining, three of these athletes had exercise-induced silent ischemia, which disappeared after retraining in two subjects and persisted at a higher heart rate in one subject. Over a 5- to 8-year period of observation, two of these three athletes with silent ischemia experienced major cardiac events (sudden death, cardiac bypass surgery). The other seven athletes did not have any cardiovascular events. CONCLUSIONS: Exercise-induced silent ischemia after a short period of detraining in highly trained older athletes may be a predictor of future cardiac events. A study with a larger cohort is warranted.

Exercise-induced silent myocardial ischemia and future cardiac events in healthy, sedentary, middle-aged and older men.

OBJECTIVES: Before men older than age 45 participate in vigorous exercise programs, the American Heart Association and the American College of Sports Medicine recommend they undergo a screening maximal exercise treadmill test. We examined the predictive value for subsequent cardiac events of exercise-induced silent myocardial ischemia (SI) during the exercise treadmill test in healthy, sedentary, obese, middle-aged and older men recruited for research studies. DESIGN: A cohort study with 7 years of follow-up. SETTING: Out-patient research at a tertiary hospital. PARTICIPANTS: 170 healthy, sedentary, obese, middle-aged and older (ages 45-79 years) men with no prior history of coronary artery disease (CAD) recruited for research studies. MEASUREMENTS: Cardiac risk factors, exercise-induced SI (ST segment depression on the electrocardiogram during a maximal exercise treadmill test), maximal aerobic capacity (VO2max), and 7- year follow-up data on incident CAD. RESULTS: At baseline, 37 of the men (22%) had exercise-induced SI on their treadmill tests. Seven-year follow-up data was obtained in 97% of the patients. In the interim, 31 men had cardiac endpoints (sudden cardiac death, myocardial infarction, angioplasty, coronary artery bypass graft surgery, angina), and four had noncardiac deaths. Seventeen of the 37 men (46%) with exercise-induced SI on their baseline exercise tests had cardiac endpoints compared with 14 of 133 (11%) men with normal exercise tests (P < .001). Compared with the men with no cardiac endpoints, the men with subsequent cardiac endpoints were older (63 +/- 1 vs 58 +/- 1 years, mean +/- SEM, P < .001) and had a lower maximal aerobic capacity (VO2max) (24 +/- 1 vs 29 +/- 1 mL/kg/min, P < .001). In Cox proportional hazards analysis, exercise-induced SI and a low VO2max were independent predictors of subsequent cardiac endpoints. CONCLUSION: In a healthy population of obese, sedentary, middle-aged and older men, exercise-induced SI and low VO2max were predictors of incident CAD. This suggests that exercise treadmill testing is beneficial in assessing risk for future cardiac events in obese, sedentary individuals.

A comparison of longitudinal changes in aerobic fitness in older endurance athletes and sedentary men.

OBJECTIVES: To compare the longitudinal changes in maximal aerobic capacity (VO2max) in healthy middle aged and older athletes and sedentary men. DESIGN: A cohort study with mean follow-up of 8.7 years (range 4.0-12.8). SETTING: Outpatient research at a tertiary hospital. PARTICIPANTS: Forty-two healthy, middle aged, and older athletes (initial age 64 +/- 1 year) and 47 healthy sedentary men of comparable age recruited for research studies. MEASUREMENTS: VO2max during a maximal treadmill test. RESULTS: At baseline, the cross-sectional rates of decline in VO2max with age (slope) were virtually identical in the athletes and sedentary men (-0.42 versus -0.43 mL x kg(-1) x min(-1) x year(-1)). At follow-up, the VO2max had declined by 11.9 +/- 1.1 mL x kg(-1) x min(-1) (22%) in the athletes, a crude average rate of -1.4 +/- 0.14 mL x kg(-1)x min(-1) x year(-1). By comparison, the VO2max declined by 4.4 +/- 0.6 mL x kg(-1) x min(-1) (14%) in the sedentary men, a crude average rate of change of -0.48 +/- 0.07 mL x kg(-1) x min(-1) x year(-1). Therefore, the observed absolute rate of longitudinal decline in VO2max in the athletes was triple that of the sedentary men (P= .001) and significantly greater than the decline predicted by their baseline cross-sectional data (P= .001). Post hoc analyses of the longitudinal data in the athletes based on the training regimens over the follow-up period demonstrated that the seven individuals who continued to train vigorously ("high training") had no significant decline in VO2max (0.28% change in VO2max per year). By contrast, the VO2max declined by 2.6% per year in the "moderate training" group (N=21), 4.6% per year in the "low training" group (N=13), and 4.7% per year in the two individuals who developed cardiovascular disease. CONCLUSION: The longitudinal decline in VO2max in older male endurance athletes is highly dependent upon the continued magnitude of the training stimulus. The majority of the athletes reduced their training levels over time, resulting in longitudinal reductions in VO2max two to three times as large as those predicted by cross-sectional analyses or those observed longitudinally in their sedentary peers.

Abnormal exercise electrocardiograms in master athletes after three months of deconditioning.

OBJECTIVE: To determine the effects of 3 months of voluntary deconditioning on cardiac function in master athletes. DESIGN: A prospective study. SETTING: Research participants at the University of Maryland School of Medicine and Johns Hopkins Bayview Medical Center. PARTICIPANTS: Ten older (59 +/- 8 years, mean +/- SD), highly conditioned (maximal aerobic capacity VO2 max 50 +/- 5 mL/kg/min), aerobically trained athletes. MEASUREMENTS AND RESULTS: Three months after the cessation of training, three of the 10 athletes had unexpected, new, markedly asymptomatic, ischemic-appearing, exercise-induced ST-segment depression on their maximal exercise tests. After retraining, the ST-segment changes disappeared in two of the subjects, but it persisted, although at a higher work load, in one of the athletes. CONCLUSION: In three master athletes, voluntary cardiopulmonary deconditioning was associated with the development of new, asymptomatic, exercise-induced ST-segment depression on exercise ECG. The mechanisms underlying these new ischemic-appearing ST-segment changes accompanying detraining and their clinical significance are not known and warrant further investigation.

Exercise rehabilitation improves functional outcomes and peripheral circulation in patients with intermittent claudication: a randomized controlled trial.

OBJECTIVE: To determine the effects of a 6-month exercise program on ambulatory function, free-living daily physical activity, peripheral circulation, and health-related quality of life (QOL) in disabled older patients with intermittent claudication. DESIGN: Prospective, randomized controlled trial. SETTING: University Medical (Center and Veterans Affairs Medical Center, Baltimore, Maryland. PARTICIPANTS: Thirty-one of 61 patients with Fontaine stage II peripheral arterial occlusive disease (PAOD) were randomized to exercise rehabilitation and 30 to usual-care control. Three patients from the exercise group and six patients from the control group dropped out, leaving 28 and 24 patients, respectively, completing the study in each group. INTERVENTION: Six months of exercise rehabilitation. MEASUREMENTS: Treadmill distance walked to onset of claudication and to maximal claudication, ambulatory function, peripheral circulation, perceived QOL, and daily physical activity. RESULTS: Compliance with the exercise program was 73% of the possible sessions. Exercise rehabilitation increased treadmill distance walked to onset of claudication by 134% (P < .001) and to maximal claudication by 77% (P < .001), walking economy by 12% (P = .003), 6-minute walk distance by 12% (P < .001), and maximal calf blood flow by 30% (P < .001). Changes in distance walked to maximal pain correlated with changes in walking economy (r = -.50, P = .013) and changes in maximal calf blood flow (r = .38, P = .047). Exercise rehabilitation increased accelerometer-derived daily physical activity by 38% (P < .001); this change correlated with the change in distance walked to maximal pain (r = .45, P = .020). These improvements were significantly better than the changes in the control group (P < .05). CONCLUSION: Improvements in claudication following exercise rehabilitation in older PAOD patients are dependent on improvements in peripheral circulation and walking economy. Improvement in treadmill claudication distances in these patients translated into increased accelerometer-derived physical activity in the community, which enabled the patients to become more functionally independent.

Determinants of peak V(O2) in peripheral arterial occlusive disease patients.

Peripheral arterial occlusive disease (PAOD) patients with intermittent claudication are functionally limited and deconditioned. This study examined whether peak aerobic capacity (V(O2) peak) was associated with PAOD severity, muscle mass, and comorbidities in 109 PAOD patients (93 men and 16 women) aged 48-86 years. The V(O2) peak (1.12+/-0.34 L/min), percentage body fat (30.6+/-8.3%), lean tissue mass of the total body (51.4+/-8.4 kg), lean tissue mass of the legs (16.6+/-3.0 kg), and appendicular skeletal mass (22.8+/-4.2 kg) were determined. The lean tissue mass of the total body (r = .44), lean tissue of the legs (r = .43) and resting ankle/brachial systolic pressure index (ABI; r = .41) correlated with peak V(O2) (all p < .001). None of the comorbidity variables (obesity, arthritis, coronary artery disease, hypertension, diabetes, and smoking history) were significantly associated with peak V(O2) except smoking status. The final model for the prediction of peak V(O2) included lean tissue mass of the legs, resting ABI, smoking status, and ABI x smoking status (r2 = .37,p < .001). In older patients with intermittent claudication, lean tissue mass is an important determinant of physical performance independent of PAOD severity and smoking status. Prevention of muscle atrophy may preserve ambulatory function and peak exercise capacity in older PAOD patients.

Weight loss, not aerobic exercise, improves pulmonary function in older obese men.

BACKGROUND: We evaluated the effect of weight loss (WL) or aerobic exercise (AEX) on pulmonary function in middle-aged and older (46-80 years) obese, sedentary men to determine the effect of reductions in body weight and increases in cardiorespiratory fitness on pulmonary function. METHODS: Subjects were randomly assigned to WL (n = 73), AEX (n = 71), or control (n = 26) groups. Maximal oxygen uptake (VO2max), body composition and anthropometrics, pulmonary function, and arterial blood gases were measured at baseline and after interventions. RESULTS: The 35 subjects who completed WL decreased weight by 11%, body fat percentage by 21% (p < .001), waist circumference by 8%, waist-hip ratio by 2%, and fat-free mass by 3% (p < .05). This resulted in a 3% increase in forced vital capacity (FVC) (4.08 +/- 0.71 L vs 4.21 +/- 0.76 L), a 5% increase in total lung capacity (6.62 +/- 0.99 L vs 6.94 +/- 0.99 L), an 18% increase in functional residual capacity (3.09 +/- 0.58 L vs 3.66 +/- 0.79 L), and an 8% increase in residual volume (2.20 +/- 0.44 L vs 2.37 +/- 0.52 L), with no change in forced expiratory volume in one second (FEV1), FEV1/FVC ratio, or carbon monoxide diffusing capacity. The change in FVC correlated with change in body weight (r = -.34, p < .05). The 38 subjects who completed AEX increased VO2max by 14%, with no change in pulmonary function. There were no changes in 8 control subjects. CONCLUSIONS: WL changes static lung volumes, not dynamic pulmonary function, in middle-aged and older, moderately obese, sedentary men. Some of the alterations in static lung function associated with aging may be due to the development of obesity and are modifiable by WL.