Richard B. Terry

Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise.

We studied separately the influence of two methods for losing fat weight on the levels of plasma lipids and lipoproteins in overweight sedentary men--decreasing energy intake without increasing exercise (diet), and increasing energy expenditure without altering energy intake (exercise, primarily running)--in a one-year randomized controlled trial. As compared with controls (n = 42), dieters (n = 42) had significant loss of total body weight (-7.8 +/- 0.9 kg [mean +/- SE]), fat weight (-5.6 +/- 0.8 kg), and lean (non-fat) weight (-2.1 +/- 0.5 kg) (P less than 0.001 for each variable), and exercisers (n = 47) had significant loss of total body weight (-4.6 +/- 0.8 kg) and fat weight (-3.8 +/- 0.7 kg) (P less than 0.001 for both variables) but not lean weight (-0.7 +/- 0.4 kg). Fat-weight loss did not differ significantly between dieters and exercisers. All subjects were discouraged from altering their diet composition; however, dieters and exercisers had slight reductions in the percentage of kilojoules derived from fat. As compared with the control group, both weight-loss groups had significant increases (P less than 0.01) in plasma concentrations of high-density lipoprotein (HDL) cholesterol (diet vs. exercise, 0.13 +/- 0.03 vs. 0.12 +/- 0.03 mmol per liter), HDL2 cholesterol (0.07 +/- 0.02 vs. 0.07 +/- 0.02 mmol per liter), and HDL3 cholesterol (0.07 +/- 0.02 vs. 0.06 +/- 0.02 mmol per liter) and significant decreases (P less than 0.05) in triglyceride levels (diet vs. exercise, -0.35 +/- 0.14 vs. -0.24 +/- 0.12 mmol per liter). Levels of total and low-density lipoprotein cholesterol were not significantly changed, relative to values in controls. None of these changes were significantly different between dieters and exercisers. Thus, we conclude that fat loss through dieting or exercising produces comparable and favorable changes in plasma lipoprotein concentrations.

AGING, HEALTH RISKS, AND CUMULATIVE DISABILITY

BACKGROUND Persons with lower health risks tend to live longer than those with higher health risks, but there has been concern that greater longevity may bring with it greater disability. We performed a longitudinal study to determine whether persons with lower potentially modifiable health risks have more or less cumulative disability. METHODS We studied 1741 university alumni who were surveyed first in 1962 (average age, 43 years) and then annually starting in 1986. Strata of high, moderate, and low risk were defined on the basis of smoking, body-mass index, and exercise patterns. Cumulative disability was determined with a health-assessment questionnaire and scored on a scale of 0 to 3. Cumulative disability from 1986 to 1994 (average age in 1994, 75 years) or death was the measure of lifetime disability. RESULTS Persons with high health risks in 1962 or 1986 had twice the cumulative disability of those with low health risks (disability index, 1.02 vs. 0.49; P<0.001). The results were consistent among survivors, subjects who died, men, and women and for both the last year and the last two years of observation. The onset of disability was postponed by more than five years in the low-risk group as compared with the high-risk group. The disability index for the low-risk subjects who died was half that for the high-risk subjects in the last one or two years of observation. CONCLUSIONS Smoking, body-mass index, and exercise patterns in midlife and late adulthood are predictors of subsequent disability. Not only do persons with better health habits survive longer, but in such persons, disability is postponed and compressed into fewer years at the end of life.

Contributions of regional adipose tissue depots to plasma lipoprotein concentrations in overweight men and women: Possible protective effects of thigh fat☆

Anthropometry and dual-photon absorptiometry (DPA) were used to examine associations of regional adiposity with plasma lipid, lipoprotein, and lipoprotein subfraction mass concentrations in moderately overweight men and women. Among 130 women, waist to thigh girth ratio (WTR) correlated with triglycerides (TG) (r = .33, P less than .0001) and negatively with high-density lipoprotein (HDL)-cholesterol (HDL-C) (r = -.37, P less than .0001) concentration, as expected. While WTR did not correlate with low-density lipoprotein (LDL)-cholesterol (LDL-C) it correlated positively with the mass subfraction of small (Sfo, 0 to 7) LDL (r = .38, P less than .0001), and negatively with large (Sfo, 7 to 12) LDL (r = -.31, P less than .01). Among 133 men, similar though weaker relationships were found. Thigh girth correlated positively with HDL and HDL2-C and mass, and with LDL particle size among women. Multivariate analysis suggests that association of WTR with lipoprotein values known to carry risk of coronary heart disease (CHD) are due at least as much to effects of thigh girth as to deleterious effects of waist girth. Estimates of fat weight in thigh and abdominal regions by DPA support thigh fat as contributing to these effects of thigh girth. Thigh fat may contribute to lipoprotein profiles that predict lower risk of cardiovascular disease.

Does weight loss cause the exercise-induced increase in plasma high density lipoproteins?

Studies showing an increase in plasma concentration of high density lipoprotein cholesterol (HDL-C) with moderate exercise have usually rejected the role of body weight change in the HDL-C raising process, ostensibly because the amount of weight lost has been negligible. To investigate HDL-C changes more thoroughly, we followed initially sedentary middle-aged men randomly assigned to either a moderate running (n = 36) or a sedentary control (n = 28) group for one year. Among runners, one-year changes in plasma HDL-C concentrations correlated strongly with their body weight changes (r = - 0.53, P less than 0.001). Curve-fitting procedures and regression analysis suggested that processes associated with weight change produce much of the plasma HDL-C changes induced by moderate exercise and that changes in HDL-C concentration predominantly reflect changes in the reputedly anti-atherogenic HDL2 sub-component. Further, the interaction between weight change and plasma HDL-C concentration was significantly different (P less than 0.001) in exercisers and controls suggesting that the metabolic consequences of exercise-induced weight change are different from the consequences of weight change in the sedentary state.

The effect of testosterone aromatization on high-density lipoprotein cholesterol level and postheparin lipolytic activity☆

Stanozolol, an oral 17 alpha-alkylated androgen, increases hepatic triglyceride lipase activity (HTGLA) and decreases high-density lipoprotein cholesterol (HDL-C) levels, whereas intramuscular testosterone has comparatively little effect. In the present study, we tested the hypothesis that aromatization of androgen to estrogen blunts the lipid and lipase effects of exogenous testosterone. Fourteen male weightlifters received testosterone enanthate (200 mg/wk intramuscularly), the aromatase inhibitor testolactone (250 mg four times per day), or both drugs together in a randomized cross-over design. Serum testosterone level increased during all three drug treatments, whereas estradiol level increased only with testosterone alone (+47%, P < .05), demonstrating that testolactone effectively inhibited testosterone aromatization. Testosterone decreased HDL-C(-16%, P < .05), HDL2-C(-23%, NS), and apoprotein (apo) A-I (-12%, P < .05) levels, effects that were consistently but not significantly greater with simultaneous testosterone and testolactone administration (HDL-C, -20%; HDL2-C, -30%; apo A-I, -15%; P < .05 for all). In contrast, both testosterone regimens decreased HDL3-C levels by 13% (P < .05 for both). HTGLA increased 21% during testosterone treatment and 38% during combined testosterone and testolactone treatment (P < .01 for both). Lipoprotein lipase activity (LPLA) increased only during combined testosterone and testolactone treatment (+31%, P < .01), suggesting that estrogen production may counteract the effects of testosterone on LPLA. Testolactone alone had little effect on any lipid, lipoprotein, apoprotein, or lipase concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of exercise-induced weight loss on low density lipoprotein subfractions in healthy men.

One-year changes in low density lipoprotein (LDL) peak flotation (Sf) rate and serum mass concentrations of LDL of Sf 0 to 7 (small LDL), LDL of Sf 7 to 12 (large LDL), intermediate density lipoprotein (IDL) of Sf 12 to 20, and very low density lipoprotein (VLDL) of Sf 20 to 400 were compared between men assigned at random to a 1-year exercise program (N = 48) or to a sedentary control condition (N = 31). Distance run among exercisers varied substantially (mean +/- SD: 12.7 +/- 8.9 km/week). Mean changes were not significantly different between the exercise and control groups for any of the low to very low density lipoprotein measurements. However, within the exercise group: 1) distance run correlated negatively with changes in the mass concentrations of small LDL; and 2) weight loss and reduced upper body obesity correlated positively with changes in small LDL, IDL, and VLDL mass and negatively with change in LDL peak flotation rate. Analyses with partial correlations suggest that weight loss may primarily affect LDL mass distributions through metabolic processes associated with high density lipoprotein2 or small VLDL (Sf 20 to 60). The decrease in small LDL concentrations and the increase in LDL peak flotation rate suggest that exercise-induced weight loss may be effective in reducing coronary heart disease risk in persons genetically predisposed to a high-risk lipoprotein profile.

Lipoprotein Lipase Activity and Plasma Triglyceride Clearance Are Elevated in Endurance-Trained Women

Numerous studies have examined factors regulating high-density lipoprotein cholesterol (HDL-C) levels in male endurance athletes, but few studies have examined HDL-C regulation in female athletes. The present study compared lipid and lipoprotein concentrations, postheparin lipolytic activities, and the clearance rate (K2) of triglycerides following an intravenous fat infusion in 12 female distance runners (aged 33 ± 9 years, mean ± SD) and 13 sedentary women (33 ± 9 years). Runners were leaner and had greater maximum oxygen uptake values than controls. Runners also had nonsignificantly lower triglyceride (53 ± 15 v 65 ± 13 mg/dL) and higher HDL-C (62 ± 14 v 52 ± 8 mg/dL, P = .06). Lipoprotein lipase activity (LPLA) was 33% greater (P < .05) and fat clearance (K2) was 27% faster (P < .01) in the trained women, and LPLA correlated directly with K2 (r = .61) and HDL-C (r = .62) in this group (P < .05 for both). K2 was directly related to HDL-C in the athletes (r = .57, P = .06), and also when the active and sedentary women were combined (r = .43, P < .05). These results suggest that increased LPLA and enhanced plasma triglyceride clearance may contribute to the HDL-C levels of physically active premenopausal women.

Exercise Fails to Improve Postprandial Glycemic Excursion in Women with Gestational Diabetes

The effect of an acute period of moderate intensity exercise on maternal glycemic excursion following a mixed nutrient meal was studied. Five normal (NL) and six gestational diabetic (GDM) subjects were enrolled. A randomized crossover design was used to compare fasting glucose and insulin levels, peak glucose and insulin levels and incremental area of the glycemic and insulin curves following a mixed nutrient meal with or without an exercise stress that took place 14 h earlier. Exercise consisted of upright stationary cycling for 30 min at a heart rate consistent with 60% VO2max. The clinical characteristics of normal and gestational diabetic subjects were comparable. Mean values (+/-SEM) with, versus without, exercise for fasting glucose (NL: 78.9 +/- 2.6 vs. 80.0 +/- 2.6 mg/dl; GDM: 86.4 +/- 2.0 vs. 82.1 +/- 3.5 mg/ dl), peak glucose (NL: 132.3 +/- 10.4 vs. 139.1 +/- 15.6 mg/dl; GDM: 165.8 +/- 5.5 vs. 160.3 +/- 7.8 mg/dl), the area under the glycemic curve (NL: 5758 +/- 1038 vs. 6393 +/- 1281 mg/dl.min; GDM: 8,178 +/- 890 vs. 8,331 +/- 563 mg/dl.min) did not differ. Similarly, plasma insulin levels did not differ between protocols for either group of subjects. Exercise has been proposed as a treatment to reduce glycemia in gestational diabetes. Results from this study indicate a single bout of exercise did not blunt the glycemic response observed following a mixed nutrient meal.

High-density apolipoprotein A-I and A-II kinetics in relation to regional adiposity

High-density lipoprotein (HDL) cholesterol and apolipoprotein (apo) A-I concentrations decrease with increasing central adiposity. The present study investigated possible mechanisms for these effects by examining the relationship between body mass index, regional adiposity, and HDL apo A-I and A-II metabolism. Fifteen sedentary men and 10 male endurance athletes aged 22 to 44 served as subjects. HDL apo A-I and A-II metabolism was examined using 125I-labeled autologous HDL. Chest and thigh skinfold thickness and the ratio of chest to thigh skinfold thickness were used as indices of regional adiposity. The relationship of adiposity to HDL metabolism was examined using correlational and multiple regression analysis. In both subject groups, the fractional catabolic rate of apo A-I and A-II increased with increasing chest skinfold thickness and chest to thigh skinfold ratio (.43 < r2 < .66). This effect was partially independent of triglyceride or HDL cholesterol concentrations. Apo A-I and A-II fractional catabolic rates increased with increasing body mass index only in the sedentary men. Concentrations and synthetic rates (mg.d-1.kg-1) of apo A-I and A-II were not consistently related to body mass index or regional adiposity. Peripheral adiposity assessed by thigh skinfold thickness was not correlated with any parameter of apo metabolism. We conclude that HDL apo A-I and A-II catabolism increases with increasing central adiposity.

Relationships of Changes in Postheparin Hepatic and Lipoprotein Lipase Activity to HDL-Cholesterol Changes Following Weight Loss Achieved by Dieting versus Exercise

Postheparin hepatic (HLA) and lipoprotein lipase activities (LPLA) were studied in moderately overweight (27.7 ± 0.47% body fat, mean ± S.E.) sedentary men aged 30–59 before and after randomization to control status (C.N = 41) or to a 1-year weight loss program by moderate dieting without exercise (D, N = 38) or exercise (running) without dieting (E, N = 44). After 6 weeks of weight stabilization at 1 year, both D and E had lost significant (P > 0.01) weight (-8.0 kg and -4.4 kg, respectively) relative to C. primarily as fat mass ( -6.0 kg and -3.8 kg), whereas only D lost nonfat mass (-2.0 kg). Compared to E, D lost more fat mass (P < 0.05) and nonfat mass (P < 0.01), but changes in percentage body fat did not differ between D and E, although these were significant relative to C ( -4.4% and -3.1%; P < 0.001). Both ΔHDL-cholesterol (HDL-C) and ΔHDL2-C were elevated (p < 0.01) in D and E versus C. but ΔHDL2-C correlated with loss of body fat in E only. Relative to C., HLA was reduced from base line (7.7 ± 0.3 mU/ml per min) in both D (-0.97 ± 0.31, P < 0.01) and E (-0.70 ± 0.30. P < 0.05). whereas increases in LPLA were not significant for D(P < 0.21) or E (P= 0.13) Both ΔHLA and ΔLPLA correlated (Spearman’s ρ) with changes in body composition and HDL-cholesterol and HDL-mass. In summary, at 1 year ΔHLA was closely associated with weight changes in D and E, whereas ΔLPLA correlated with these changes in E only. Furthermore, significant relationships for ΔHLA and ΔLPLA PLA versus ΔHDL-C and ΔHDL-mass were found only in E.