Cardiovascular fitness, body composition, and lipoprotein lipid metabolism in older men.

BACKGROUND: Lipoprotein lipids in older individuals are affected by family history of coronary artery disease (CAD), obesity, diet, and physical activity habits. METHODS: The relationship of obesity and physical fitness (VO2max) to lipoprotein lipids and postheparin lipases was examined in a cross-sectional study of 12 lean (LS) and 26 obese (OS) sedentary men and 18 master athletes (MAs) aged 65+/-1 years (mean +/- SE). The men were healthy, had no family history of CAD, and were weight stable on AHA diets at the time of study. RESULTS: VO2max was similar in LS and OS men but higher in the MAs. The OS men had a higher percentage of body fat (%BF), waist circumference, and waist:hip ratio (WHR) than the MA and LS men, but MA and LS men differed only in waist circumference. Total and LDL-C levels were comparable, but HDL-C, HDL2-C, and %HDL2b subspecies were higher in MAs than in OS and LS men, and in LS than in OS men. Triglyceride (TG) was similar in MAs and LS men but higher in OS men. Across groups, two multiple regression analyses models (VO2max, %BF, and WHR or waist circumference) showed that %BF and VO2max independently predicted HDL-C and HDL2, whereas WHR predicted TG (r2 = .45) more strongly than waist circumference (r2 = .39). Postheparin lipoprotein lipase activity (LPL) was comparable among groups and correlated independently with VO2max. Total postheparin lipolytic activity (PHLA), hepatic lipase activity (HL), and HL:PHLA ratio were similar in MAs and LS men but higher in OS men. In both multiple regression analysis models, only %BF predicted HL activity and the HL:PHLA ratio. The HL:PHLA ratio independently predicted HDL-C, HDL2-C, %HDL2b, %HDL3 subspecies, and the cholesterol:HDL-C ratio, whereas LPL activity predicted TG. CONCLUSIONS: Increased fitness and reduced total and abdominal fatness in MAs are associated with lower HL and higher LPL activities, which may mediate their higher HDL-C and lower TG levels relative to their sedentary peers.

Interrelationships of spontaneous growth hormone axis activity, body fat, and serum lipids in healthy elderly women and men.

Aging is associated with decreased growth hormone (GH) secretion and plasma insulin-like growth factor-I (IGF-I) levels, increased total and abdominal fat, total and low-density lipoprotein (LDL) cholesterol, and triglycerides, and reduced high-density lipoprotein (HDL) cholesterol. Similar changes in lipids and body composition occur in nonelderly GH-deficient adults and are reversed with GH administration. To examine whether GH/IGF-I axis function in the elderly is related to the lipid profile independently of body fat, we evaluated GH secretion, serum IGF-I and IGF binding protein-3 (IGFBP-3) levels, adiposity via the body mass index (BMI), waist to hip ratio (WHR), dual-energy x-ray absorptiometry (DEXA), and magnetic resonance imaging (MRI), and circulating lipids in 101 healthy subjects older than 65 years. Integrated nocturnal GH secretion (log IAUPGH) was inversely related (P < .005) to DEXA total and abdominal fat and MRI visceral fat in both genders. Log IAUPGH was inversely related to visceral fat in women (P < .005) and men (P < .0001), but was not significantly related to total fat in either gender. In women, log IAUPGH was related inversely to total and LDL cholesterol and positively to HDL cholesterol (P < .008). In men, log IAUPGH was inversely related to total cholesterol and triglycerides (P < .005). In women, HDL cholesterol was inversely related to the WHR (P < .005). In men, triglycerides were positively related (P < .001) to the WHR and DEXA abdominal and MRI visceral fat. Multivariate regression revealed log IAUPGH, but not DEXA total body fat, to be an independent determinant of total (P < .001 for women and P = .01 for men) and LDL (P < .007 and P = .05) cholesterol in both sexes and of HDL cholesterol (P < .005) and triglycerides (P < .03) in women. Log IAUPGH, but not DEXA abdominal fat, was related to total (P < .005 and P < .03) and LDL (P < .03 and P = .05) cholesterol in both genders and to HDL in women (P < .05). Log IAUPGH, but not MRI visceral fat, was related to total cholesterol (P < .03 and P = .05) in women and men. Age, IGF-I, and IGFBP-3 were not significantly related to any body fat or lipid measures, except for a positive correlation of IGF-I with triglycerides in men. Thus, endogenous nocturnal GH secretion predicts total, LDL, and HDL cholesterol levels independently of total or abdominal fat, suggesting that it is an independent cardiometabolic risk factor in healthy elderly people.

Predictors of adipose tissue lipoprotein lipase in middle-aged and older men: relationship to leptin and obesity, but not cardiovascular fitness.

The effects of long-term endurance exercise training, body composition, and cardiovascular fitness (VO2max) on the activity of adipose tissue lipoprotein lipase (AT-LPL) and lipoprotein lipids were examined in 66 healthy age-matched middle-aged and older men (mean +/- SE, 61 +/- 1 years). We compared subcutaneous abdominal (ABD) and gluteal (GLT) heparin-elutable AT-LPL activity in 19 master athletes (VO2max > 40 mL/kg/min) and 20 lean sedentary men (VO2max < 40 mL/kg/min) versus 27 obese sedentary men (VO2max < 40 mL/kg/min; body fat > 27%). Fasting insulin and leptin levels were similar in master athletes and lean sedentary men, but were lower than in obese sedentary men. There were no differences in fasting values for total cholesterol or low-density lipoprotein cholesterol (LDL-C) among the groups, but master athletes had lower triglyceride (TG) values (P < .05) and higher high-density lipoprotein cholesterol (HDL-C) and HDL2-C (P < .05) than obese and lean sedentary men. There were no regional (ABD v GLT) differences in the activity of AT-LPL in these groups, but obese sedentary men had higher levels of ABD AT-LPL (2.1 +/- 0.3 nmol/10(6) cells x min) than lean sedentary men (0.8 +/- 0.2) and master athletes (0.5 +/- 0.1, P = .01). Similar results were observed for GLT AT-LPL. Both ABD and GLT AT-LPL activity correlated positively with percent body fat (r = .46 to .54, P < .001), fasting insulin (r = .37 to .45, P < .001), and leptin (r = .61 to .65, P < .0001), but not with VO2max. In stepwise multiple regression analysis, leptin was the main independent predictor of ABD (R2 = .43, P < .0001) and GLT (R2 = .40, P < .0001) AT-LPL activity. Plasma TG correlated positively (r = .32, P < .01) and HDL-C correlated negatively (r = -.32, P = .02) with ABD AT-LPL activity, but these relationships were not significant after controlling for percent body fat or leptin. The results of this study indicate that in healthy middle-aged and older men, the major determinants of AT-LPL activity are obesity and its major associated hormones, leptin and insulin, not cardiovascular fitness, and also suggest that the higher HDL-C levels observed in endurance-trained men are not associated with increased AT-LPL activity.

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.

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.

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.

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.

Reduced adipose tissue lipoprotein lipase responses, postprandial lipemia, and low high-density lipoprotein-2 subspecies levels in older athletes with silent myocardial ischemia.

Healthy older (64 +/- 1 years, mean +/- SEM) athletic (maximal oxygen consumption [VO2max] > 40 mL/kg/min) normocholesterolemic men with no prior history of coronary artery disease (CAD) were recruited for cardiovascular and metabolic studies. Thirty-three percent had asymptomatic exercise-induced ST segment depression on their exercise electrocardiogram (ECG), consistent with silent myocardial ischemia (SI). We hypothesized that abnormalities in high-density lipoprotein (HDL) and postprandial triglyceride (TG) metabolism may increase their risk for CAD. Compared with 12 nonischemic controls of comparable age, percent body fat, and VO2max, the 13 men with SI had decreased fasting HDL cholesterol ([HDL-C] 41 +/- 2 v 50 +/- 2 mg/dL, P < .001) and %HDL2b subspecies levels as measured by gradient gel electrophoresis (22 +/- 2 v 34 +/- 3, P < .001). Fasting plasma TG and low-density lipoprotein cholesterol (LDL-C) levels were the same in both groups. Although plasma glucose levels during an oral glucose tolerance test (OGTT) were similar in both groups, the total insulin area was higher in men with SI (P < .05). After consumption of a standard high-fat meal (680 kcal/m2 body surface area of a formula in which 86% of the calories were derived from fat), postprandial plasma TG, chylomicron-TG, and very-low-density lipoprotein (VLDL)-TG levels and postprandial areas were higher in men with SI (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

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.