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Biomedical subjects

J Trap-Jensen

Publications and source records attributed to J Trap-Jensen.

At least 109 records · Page 6Linked to original sources
PubMed1973

Utilization of acetate in the human forearm during exercise after ethanol ingestion.

The uptake of acetate in the human forearm was studied in five fasting (14 h) subjects during 10-min periods of ergometer work at 7 and 10 kilopond-meters per minute (kpm/min). A constant arterial acetate concentration was established by administration of a small quantity of alcohol (25 g) to the subjects after a control work period. Blood flow was measured by an indicator dilution technique. Acetate uptake varied linearly with the product of arterial acetate concentration and blood flow. Acetate metabolism was calculated to account for about 6.5% of the energy metabolism, assuming complete combustion to carbon dioxide and water. Oxygen uptake and blood flow did not change in the presence of acetate and ethanol. After administration of ethanol the arterial concentrations of FFA and glycerol decreased to about half, whereas the lactate concentration increased to about twice the control values, confirming other reports. Glucose utilization was increased and lactate output decreased during the ethanol periods, presumably a consequence of the changing arterial concentrations and increased insulin level. Measurements of the arterial and venous lactate/pyruvate concentration ratios indicate that the NAD-mediated cytoplasmic redox state in the muscle is not changed in the presence of acetate and ethanol.

Acetates↗
PubMed1970

Effects of training on the distribution of cardiac output in patients with coronary artery disease.

In nine patients with coronary artery disease, cardiac output distribution was evaluated at rest and during exercise by measurement of cardiac output and regional blood flow parameters (hepatic and muscle blood flow). In seven patients repeated values were obtained after a physical training program of 4 to 10 weeks' duration. After training, cardiac output was reduced at moderate work loads (13.1%) causing a change of the relation between oxygen uptake and cardiac output from hyperkinetic to normal. During heavy exercise the cardiac output was increased (5.5%) after training. Similar changes were observed in muscle blood flow, which was reduced at submaximal loads (14.9%) and increased at maximal (8.6%). Hepatic blood flow showed in contrast a less pronounced reduction at both work loads after training (difference, 7.2%). These effects of training could be explained as peripheral regulatory alterations without implying primary improvement in myocardial performance. They are consistent with the view that local changes in the trained muscles are important for the reduction in myocardial pressure-work caused by physical conditioning.

Cardiac Output↗