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Biomedical subjects

T J Angelopoulos

Publications and source records attributed to T J Angelopoulos.

6 recordsLinked to original sources

Endogenous opioids may modulate catecholamine secretion during high intensity exercise.

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake (VO2max)], nine fit men [mean (SE) VO2max, 63.9 (1.7) ml.kg-1.min-1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol.l-1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol.l-1 and 24 (2.2) versus 20 (1.7) nmol.l-1, respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol.l-1 and 6.9 (1.1) versus 5.3 (0.9) mmol.l-1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.

Adult

Exercise induces human lipoprotein lipase gene expression in skeletal muscle but not adipose tissue.

Lipoprotein lipase (LPL) is regulated by exercise in humans, but the effects of exercise on LPL expression in different tissues and the molecular mechanisms involved are unclear. We assessed the effects of 5-13 consecutive days of supervised exercise on tissue LPL expression as well as fasting plasma lipids and lipoproteins in 32 sedentary, weight-stable adult men. In skeletal muscle, exercise training increased the mean LPL mRNA level by 117% (P = 0.037), LPL protein mass by 53% (P = 0.038), and total LPL enzyme activity by 35% (P = 0.025). In adipose tissue, mean LPL mRNA, protein mass, and activity did not change. Exercise decreased triglycerides [from 172 +/- 4.3 to 127 +/- 3.2 (SE) mg/dl, P = 0.002], total cholesterol (from 188 +/- 1.2 to 181 +/- 1.0 mg/dl, P = 0.011), and very low-density lipoprotein-cholesterol (from 30.1 +/- 0.9 to 22.0 +/- 0.8, P = 0.004) and increased high-density lipoprotein cholesterol (HDL-C; from 43.4 +/- 0.35 to 45.0 +/- 0.37, P = 0.030) and HDL2-C (from 6.6 +/- 0.21 to 7.7 +/- 0.19, P = 0.021). Changes in muscle but not adipose tissue heparin-releasable LPL activity were inversely correlated (r = -0.435, P < 0.034) with changes in triglycerides. These data suggest the existence of an exercise stimulus intrinsic to skeletal muscle, which raises LPL activity in part by pretranslational mechanisms, a process that contributes to the improvement in circulating lipids seen with physical activity.

Adipose Tissue

Effect of repeated exercise bouts on high density lipoprotein-cholesterol and its subfractions HDL2-C and HDL3-C.

Nine sedentary men (mean age, 22.8 yrs) were studied during and after treadmill exercise at 65% VO2max to determine the number of repeated exercise bouts required to bring about a sustained elevation in HDL-cholesterol and its subfraction HDL2-C and HDL3-C. A Latin square counterbalanced design was used. Thirty minute exercise sessions were undertaken in the following patterns: (1) single bout, (2) two bouts on alternate days, and (3) three bouts on alternate days. The exercise bouts in patterns 2 and 3 were separated by 48 h. Patterns 1, 2 and 3 were conducted 7 days apart. Blood samples were obtained prior to each pattern and at 5 min, 24 and 48 h after the last session within each pattern. There were no significant differences in triglycerides and total cholesterol between the selected blood sampling points for all patterns. Total HDL-C remained higher (p < 0.05) than the pre-exercise level 5 min [pattern 1: 39.0 vs 41.2 mg.dl-1, pattern 2: 37.1 vs 39.2 mg.dl-1, pattern 3: 38.8 vs 42.7 mg.dl-1] and 24 h [pattern 1: 39.0 vs 39.4 mg.dl-1, pattern 2: 37.1 vs 39.1 mg.dl-1, pattern 3: 38.8 vs 42.6 mg.dl-1] post-exercise. Total HDL-C declined to pre-exercise values 48 h post-exercise in all patterns. HDL2-C was lower (p < 0.05) than pre-exercise 48 h for all exercise patterns. For all patterns, HDL3-C levels were higher (p < 0.05) at the 5 min and 48 h post-exercise time points than at the pre-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Short-term growth hormone treatment does not increase muscle protein synthesis in experienced weight lifters.

The purpose of this study was to determine whether recombinant human growth hormone (GH) administration enhances muscle protein anabolism in experienced weight lifters. The fractional rate of skeletal muscle protein synthesis and the whole body rate of protein breakdown were determined during a constant intravenous infusion of [13C]leucine in 7 young (23 +/- 2 yr; 86.2 +/- 4.6 kg) healthy experienced male weight lifters before and at the end of 14 days of subcutaneous GH administration (40 microgram.kg-1 x day-1). GH administration increased fasting serum insulin-like growth factor-I (from 224 +/- 20 to 589 +/- 80 ng/ml, P = 0.002) but did not increase the fractional rate of muscle protein synthesis (from 0.034 +/- 0.004 to 0.034 +/- 0.002%/h) or reduce the rate of whole body protein breakdown (from 103 +/- 4 to 108 +/- 5 mumol.kg-1 x h-1). These findings suggest that short-term GH treatment does not increase the rate of muscle protein synthesis or reduce the rate of whole body protein breakdown, metabolic alterations that would promote muscle protein anabolism in experienced weight lifters attempting to further increase muscle mass.

Adult

Effect of a single exercise bout on serum triglycerides in untrained men.

Seven sedentary men (mean age, 22.5 yrs) were studied during and after treadmill exercise at 65% VO2max to determine the effect of a typical acute exercise bout on serum triglycerides. A venous blood sample was drawn immediately prior to a 30 minute treadmill exercise session, 5 min, 24 and 48 h after exercise. There were no significant differences in triglycerides and total cholesterol between the selected blood sampling points. Total HDL-C was higher (p < 0.05) at 5 min (44.0 SE +/- 3.0 mg.dl-1) than pre-exercise (41.5, SE +/- 3.0 mg.dl-1). Total HDL-C did not differ between pre-exercise and both 24 and 48 h. Unlike prolonged heavy exercise, a typical exercise session does not bring about alterations in serum triglycerides.

Adult

Mechanisms of impaired exercise capacity in short duration experimental hyperthyroidism.

To investigate the mechanism of reduced exercise tolerance in hyperthyroidism, we characterized cardiovascular function and determinants of skeletal muscle metabolism in 18 healthy subjects aged 26 +/- 1 yr (mean +/- SE) before and after 2 wk of daily ingestion of 100 micrograms of triiodothyronine (T3). Resting oxygen uptake, heart rate, and cardiac output increased and heart rate and cardiac output at the same submaximal exercise intensity were higher in the hyperthyroid state (P less than 0.05). However, maximal oxygen uptake decreased after T3 administration (3.08 +/- 0.17 vs. 2.94 +/- 0.19 l/min; P less than 0.001) despite increased heart rate and cardiac output at maximal exercise (P less than 0.05). Plasma lactic acid concentration at an equivalent submaximal exercise intensity was elevated 25% (P less than 0.01) and the arteriovenous oxygen difference at maximal effort was reduced (P less than 0.05) in the hyperthyroid state. These effects were associated with a 21-37% decline in activities of oxidative (P less than 0.001) and glycolytic (P less than 0.05) enzymes in skeletal muscle and a 15% decrease in type IIA muscle fiber cross-sectional area (P less than 0.05). Lean body mass was reduced (P less than 0.001) and the rates of whole body leucine oxidation and protein breakdown were enhanced (P less than 0.05). Thus, exercise tolerance is impaired in short duration hyperthyroidism because of decreased skeletal muscle mass and oxidative capacity related to accelerated protein catabolism but cardiac pump function is not reduced.

Adult