Acute metabolic effects of exercise in bodybuilders using anabolic steroids.

Four male bodybuilders who had started taking anabolic steroids were monitored during exercise. Most metabolic indicators were similar to bodybuilders not taking steroids; i.e. metabolic acidosis with little change in glucose. However, there is a marked elevation of creatine kinase.

Current clinical laboratory practice: investigation of plasma lipids--which tests and when?

Clinical interest in the lipoproteins stems mainly from the association between serum cholesterol concentrations and coronary heart disease. Investigations of lipoproteins should be performed in patients with premature coronary heart disease, with a strong family history of coronary heart disease, or with certain cutaneous stigmata of hyperlipoproteinaemia and when fasting serum samples are seen to be lipaemic. Family studies should be performed in appropriate cases to identify relatives at increased risk of developing coronary heart disease. Patients with conditions known to cause secondary hyperlipoproteinaemia should be investigated if they fall into one of these categories but only after treatment of the underlying condition. Non-specialist laboratories should be able to measure total cholesterol and triglyceride concentrations and high density lipoprotein cholesterol concentrations. Lipoprotein electrophoresis has a limited role in such laboratories and is not necessary as a routine procedure. Specialist laboratories should in addition be able to measure individual lipoproteins and identify apolipoprotein E phenotypes.

Thiazides, beta blockers and lipoproteins.

Some of the more important recent studies on the effect of thiazides and beta-adrenoceptor blocking agents is conflicting, possibly because of differences in patient compliance and in lipoprotein methodology and quality assurance between studies. It is likely that in the short-term, thiazide diuretics produce an increase in plasma triglyceride and cholesterol and in LDL-cholesterol. No consistent effect of monotherapy with beta-adrenoceptor blocking agents was seen. Further long-term studies of monotherapy with both of these classes of drugs are required. Combined therapy with thiazides or beta-adrenoceptor blocking agents consistently increased plasma triglyceride concentrations, but their effect on VLDL, LDL and HDL concentrations is uncertain. Further research required into the effect of these drugs on apolipoproteins which may be useful discriminators for patients with coronary heart disease (Avogaro et al., 1979) and on HDL subfractions.

High-density lipoprotein subfractions as measured by differential polyanionic precipitation and rate zonal ultracentrifugation.

Recent interest in the putative protective role of high-density lipoprotein (HDL) and its subfractions against atherosclerosis has highlighted the need for a rapid, simple subfractionation procedure. Here we compared HDL subfractionation by two recently developed polyanionic-precipitation methods with the values obtained by rate zonal ultracentrifugation. A similar result for total HDL cholesterol was obtained by all three methods. However, HDL2 cholesterol as measured by the precipitation procedures was significantly higher than the zonal value, and HDL3 was lower. This reflects the different underlying principles involved in the separations and highlights the need for a clearer understanding of the functional roles of the HDL fractions.

The effect of moderate physical exercise on the plasma lipoprotein subfractions of male survivors of myocardial infarction.

The effect of regular, moderate exercise on the lipoprotein subfractions of male survivors of myocardial infarction was studied. Nineteen men were randomly allocated to an incremental exercise program and 23 to a control group. Both groups were studied for 6 months. No change occurred in any lipoprotein class in the control group. In the trained group, total triglyceride and low-density lipoprotein (LDL) cholesterol concentrations decreased significantly (0.01 greater than p greater than 0.001 and 0.05 greater than p greater than 0.01, respectively) and high-density lipoprotein (HDL) cholesterol and apolipoprotein A-1 rose (both p less than 0.001). The concentration of the HDL2 subfraction increased with training (0.01 greater than p greater than 0.001) and HDL2 did not change. No relationship was found between changes in lipoproteins and treadmill exercise test performance. Thus, in survivors of myocardial infarction, exercise may alter plasma lipoprotein values beneficially.

High density and low density lipoprotein subfractions in survivors of myocardial infarction and in control subjects.

The major lipoprotein classes (very low, low and high density lipoproteins, VLDL, LDL and HDL) and three lipoprotein subfractions (HDL2, HDL3 and LDL2) of 31 male survivors of myocardial infarction (MI) have been compared with those of 24 ostensibly normal subjects. The two groups had similar ages, relative weights, smoking and dietary habits, and physical activities. The MI survivors had significantly higher concentrations of total and VLDL-triglyceride and total and LDL-cholesterol than the control subjects. The differences in HDL-cholesterol, and total apolipoproteins A-1 and B were of borderline significance. HDL2 was significantly lower and LDL2 was higher in the MI survivors. There was no difference in HDL3. The differences in lipoprotein subfractions could be ascribed to differences in cholesterol, phospholipid and proteins, but not in triglyceride. The data suggest that the minor HDL2 subfraction shows a closer association with established coronary heart disease than does total HDL-cholesterol. The increased LDL-cholesterol concentration in the MI survivors can be ascribed at least partly to an increase in the major subfraction, LDL2.

Effect of slow oxprenolol and a combination of slow oxprenolol and cyclopenthiazide on plasma lipoproteins.

The effect of slow oxprenolol on plasma lipoprotein concentrations was compared to that of combined therapy with slow oxprenolol and cyclopenthiazide. The design of the study was a double blind between patient investigation in which 9 subjects with mild hypertension received slow oxprenolol and 11 slow oxprenolol and cyclopenthiazide. Plasma lipoproteins were analysed at 0, 2, 4, 8, 12 and 16 weeks. Slow oxprenolol given alone resulted in a significant rise in plasma and low density lipoprotein (LDL) cholesterol concentration whereas combined therapy with slow oxprenolol and cyclopenthiazide produced significant rises in plasma and very low density lipoprotein (VLDL) triglyceride. If one accepts that a rise in plasma or LDL cholesterol increases atherogenic risk more than a rise in plasma or VLDL triglyceride combined therapy is preferable.

Comparison of immunonephelometry and electroimmunoassay for estimation of plasma apolipoprotein A-I.

Immunonephelometry using a helium-neon laser as light-sources has been compared with the established technique of electroimmunoassay for estimation of plasma apolipoprotein A-I (apoA-I), the major protein component of high density lipoproteins (HDL). The within-batch coefficient of variation for immunonephelometry was 6.7% and for electroimmunoassay was 4.7%, but both methods showed similar between-batch precisions (6.9% and 7.0% respectively). Plasma from 122 subjects (62 male, 60 female) were analysed by both methods. Results showed good correlation but immunonephelometry gave consistently lower apoA-I values (mean +/- 1 S.D. = 1.32 +/- 0.25 g/l) than did electroimmunoassay (1.56 +/- 0.33 g/l). Plasma apoA-I concentrations obtained by both procedures were significantly higher (P less than 0.002) in females than in males. Both assays gave results which were highly correlated with high density lipoprotein cholesterol. Immunonephelometry is therefore considered to be satisfactory for estimation of plasma apoA-I concentration.