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This study was designed to determine changes in metabolic and cardiovascular risk factors following normobaric hypoxic exercise training in healthy men.Following a randomized baseline maximal exercise test in hypoxia and/or normoxia, 34 physically active subjects were randomly assigned to either a normoxic (N = 14) or a hypoxic (N = 18) training group. Training involved 4 wk of cycling exercise inspiring either a normobaric normoxic (F(IO2) = approximately 20.9%) or a normobaric hypoxic (F(IO2) = approximately 16.0%) gas, respectively, in a double-blind manner. Cycling exercise was performed three times per week for 20-30 min at 70-85% of maximum heart rate determined either in normoxia or hypoxia. Resting plasma concentrations of blood lipids, lipoproteins, total homocysteine, and auscultatory arterial blood pressure responses at rest and in response to submaximal and maximal exercise were measured before and 4 d after physical training.Total power output during the training period was identical in both normoxic and hypoxic groups. Lean body mass increased by 1.4 +/- 1.5 kg following hypoxic training only (P0.001). While dietary composition and nutrient intake did not change during the study, both normoxic and hypoxic training decreased resting plasma concentrations of nonesterified fatty acids, total cholesterol, high density lipoprotein (HDL), and low density lipoprotein (LDL) (P0.05 -0.001). Apolipoproteins AI and B decreased following normoxic training only (Por = 0.001). Plasma concentrations of resting total homocysteine decreased by 11% following hypoxic training (Por = 0.05) and increased by 10% (P0.05) following normoxic training. These changes were independent of changes in serum vitamin B12 and red cell folate which remained stable throughout. A decreased lactate concentration during submaximal exercise was observed in response to both normoxic and hypoxic training. Hypoxic training decreased maximal systolic blood pressure by 10 +/- 9 mm Hg (P0.001) and the rate pressure product by 14 +/- 23 mm Hg x beats x min(-1)/100 (Por = 0.001) and increased maximal oxygen uptake by 0.47 +/- 0.77 L x min(-1) (P0.05).Normoxic and hypoxic training was associated with significant improvements in selected risk factors and exercise capacity. The stimulus of intermittent normobaric hypoxia invoked an additive cardioprotective effect which may have important clinical implications.

Aim To examine differences in resting blood lipid and lipoprotein concentrations in male subjects of varying degrees of cardiovascular fitness ranging from the healthy elite athlete to the sedentary subject either with or without angiographically confirmed evidence of coronary artery disease (CAD). Methods Two-hundred-and-eighty-four clinically asymptomatic male subjects were selected from a group of Olympic distance runners (n = 1 7), physical education athletes (n = 44), and industrial executives (n = 223). Each subject received a detailed physical examination and provided a venous blood sample after fasting, which was analysed for lipid and lipoprotein concentrations. Maximum oxygen uptake was determined using on-line computerised respiratory analysis during a functional diagnostic test. The industrial executive group was further divided according to their electrocardiographic (ECG) response to exercise; negative ECG (n = 138), positive (abnormal) ECG but no angiographic evidence of CAD (n = 18) and positive ECG with angiographic evidence of significant CAD (n=67). Results Lipid-lipoprotein profiles were consistently abnormal in subjects with a positive ECG and documented evidence of CAD, whereas those subjects who tested negative or false-positive were less affected. The lipid-lipoprotein profiles observed between Olympic distance runners and an age-matched group of physically active students were not significantly different despite clear differences in physical activity patterns. Conclusions In addition to the abnormal lipid-lipoprotein profile in subjects with CAD, the present data also suggest that while physical activity confers metabolic cardioprotection, a threshold stimulus exists beyond which no further benefits can be gained.

Twenty five subjects were divided into experimental (N = 13, 7 male and 6 female, age 32.1 +/- 6.4 yr) and control groups (N = 12, 6 male and 6 female, age 33.4 +/- 5.4 yr) in order to examine the effect of a conditioning program on fibrinogen concentration. Before and after conditioning, VO2max was determined in all subjects. The experimental group (E) exercised for 30 min, 3 d.wk-1 for 12 wk at 70% (initial 6 wk) and 80% (latter 6 wk) of maximum heart rate. The control group (C) maintained normal activity pattern. After conditioning, subjects in E, but not in C, increased (P 0.05) after conditioning. Although RFC showed a 6% decrease in the E group post conditioning (249.1 +/- 21.5 mg.dl-1 vs 236.4 +/- 34.6 mg.dl-1), this decrease was not significant (P > 0.05). A significant increase (P 0.05) when data were corrected for hemoconcentration. These results suggest that after conditioning the 6% decrease in RFC was not statistically significant, but the possibility of Type II error is high.

It has been reported that catecholamine release is associated with stressful events and that adrenaline administration induces hyperfibrinolysis. To examine the possible involvement of the adrenoreceptor mechanism in the regulation of fibrinolytic activity at rest and to maximum exercise, 12 healthy volunteers (six males and six females, age range 19-21 yr) were orally medicated with two formulations of a beta blocker. The drug treatments consisted of 1) a single dose of OM756 alpha 10 mg propranolol "Inderal" tablet, 2) a single dose of a generic 10 mg propranolol tablet, and 3) a single dose of generic placebo. The drug administrations were assigned to the subjects using a complete Latin square design and double-blind procedure and were separated by 7 d. Two hours after the administration of the respective drug treatment, subjects exercised to maximal capacity using a graded exercise protocol on a bicycle ergometer. Prior to and 2 h after the drug administration and immediately after maximum exercise, heart rate, blood pressure, and oxygen consumption were measured and venous blood was removed and analyzed for fibrinolytic activity using a standard fibrin plate method. ANOVA showed that the resting and maximum heart rates were significantly reduced (P less than 0.05) following oral premedication with either of the two formulations of beta blocker, while blood pressure and oxygen consumption were unaffected. ANOVA also showed no difference in the resting fibrinolytic activity 2 h post-administration of the drug treatments but a significant decrease (P less than 0.05) in the normal fibrinolytic response to maximum exercise. It was concluded, therefore, that the resting level of fibrinolytic activity is not mediated via an adrenergic pathway but that the enhanced fibrinolytic activity to maximum exercise is partially regulated via an adrenoreceptor mechanism.