R. James Barnard

Oxygen debt: Involvement of the Cori cycle

SummaryTryptophan and quinolinic acid, inhibitors of gluconeogenesis, were used to block the removal of lactate by the liver in order to investigate the involvement of the Cori cycle in oxygen debt. Five male, mongrel dogs were run on a treadmill at 4 mph with a 20 percent grade for 19 min. The mean exercise

The effect of training and various work loads on the lactacid-alactacid oxygen debt response of exercising dogs

\dot V_{O_2 }

Effect of a short-term diet and exercise intervention on inflammatory/anti- inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors

was 80.67±3.11 ml/kg/min for the control tests while peak arterial lactate values ranged from 3.83 to 4.98 mM/l. When removal of lactate by the liver was blocked, oxygen debt showed a mean reduction of 44 percent. Moreover, oxygen consumption during the last minute of exercise was reduced by 11 percent.Fasting (72 h) was used in 1 dog to prevent the accumulation of lactate during exercise. This procedure reduced oxygen debt to the same level as when the removal of lactate by the liver was blocked with tryptophan and quinolinic acid.The data show that the lactacid as well as the alactacid component is involved in oxygen debt when lactate is being removed by the liver during the recovery period following exercise.

Impaired insulin-receptor autophosphorylation is an early defect in fat-fed, insulin-resistant rats

SummaryCholinesterase activity in trained and nontrained rats was investigated in 50 male Sprague-Dawley rats. Half of this number had been trained in motor driven activity cages. Significant differences in resting heart rates and heart weights indicated that the program had been successful in producing a trained state. Atria and ventricular cholinesterase activities were appraised with a differential respirometer. Acetylcholine (ACH) was utilized as the universal substrate whereas acetyl-B-methylcholine (MCH) and butyrlcholine (BCH) were employed as substrates for Group I (ACHE) and Group II (CHE) type enzymes respectively. As noted by previous investigators, atria and ventricular CHE activity was significantly higher than ACHE. Moreover, the atria had higher ACHE and CHE activity than the ventricles. Training had no significant influence on myocardial cholinesterase (ACHE and CHE) activity.When atropine sulfate (1 mg/ml) was injected into unanesthetized rats, the trained animals demonstrated less cardiac acceleration than nontrained rats. This finding was in agreement with previous studies. Trained rats also exhibited lower resting heart rates after injections of neostigmine methylsulfate (300 μg/kg) than nontrained rats. These results supported the postulate that training produced a “cholinergic state.” Whether the difference was due primarily to neural or nonneural acetylcholine remains to be determined.

A high-fat, refined-carbohydrate diet affects renal NO synthase protein expression and salt sensitivity.

SummaryThe involvement of the lactacid and alactacid mechanisms in oxygen debt was examined in 2 dogs prior to and after a 6-week training program by using tryptophan and quinolinic acid to block the removal of lactate by the liver. The results show that the lactacid mechanism is involved at work loads resulting in sufficient elevation of blood lactate during the recovery period. It was further shown that training produced a significant decrease in both oxygen debt and blood lactate. Mechanisms responsible for the findings are discussed.