The ventilatory (anaerobic) threshold for short-term exercise was defined as the work rate or O2 uptake (VO2) immediately below the work rate at which ventilation increased disproportionately relative to work rate or VO2, and the ventilatory threshold for long-term exercise as the work rate or VO2 immediately below the work rate at which ventilation continued to increase with time rather than attain a steady state. The purpose of the present study was to investigate how both thresholds relate to each other and how they relate to other measures of physical performance capacity. The subjects were eight healthy males, 20-53 yr of age. Maximal performance capacity was estimated by measurements of maximal O2 uptake (VO2 max) and by endurance performance during a 12-min distance run. A high interrelationship was found between the two thresholds (r = 0.84), and each threshold expressed in VO2 (ml X min-1 X kg-1) correlated highly with VO2 max (r = 0.87 and r = 0.75, for short-term and long-term exercise, respectively). When the two thresholds were expressed as a percentage of VO2 max, neither threshold showed a significant relationship with VO2 max. Endurance performance was significantly correlated with both the ventilatory threshold for short-term and long-term exercise (r = 0.73 and 0.82, respectively). A stepwise multiple regression analysis indicated that the distance run in 12 min was best predicted by VO2 max (R2 = 0.66) or the ventilatory threshold for long-term exercise (R2 = 0.63). It is concluded that the ventilatory threshold for long-term exercise is a more specific measure to explain running performance than is the threshold during graded exercise.

This double-blind placebo-controlled study investigated whether indomethacin-induced (500 mg/3 days) prostaglandin synthesis inhibition (PG inhibition) affected systemic hemodynamics and several humoral factors in nine sodium-replete normal humans, during exercise. Independent of the level of physical activity, PG inhibition was accompanied by small but significant (P less than 0.001) increases in systolic (+4.3 mmHg) and diastolic (+1.8 mmHg) intra-arterial pressure: the changes in cardiac output (determined noninvasively), systemic vascular resistance, and exercise capacity did not reach a level of statistical significance. After PG inhibition, plasma 13,14-dihydro-15-keto/prostaglandin F2 alpha, plasma renin, and aldosterone were reduced (P less than 0.001) at rest sitting and exercise, but PG inhibition did not prevent the exercise-induced stimulation of the plasma renin-aldosterone system. The urinary sodium excretion, averaging 156 meq/24 h during placebo, decreased (P less than 0.001) by 28 meq/24 h during PG inhibition: urinary aldosterone and kallikrein and the plasma catecholamines remained unchanged. In resting and exercising sodium-replete subjects, prostaglandins seem to exert a depressor effect on the systemic circulation and to increase plasma renin activity, but they are probably not involved in the exercise-related stimulation of the plasma renin-aldosterone system.

The systemic circulation at rest and during exercise was studied in ten normal male volunteers, after placebo on one occasion and after acute intravenous administration of the serotonergic antagonist ketanserin on another occasion. The effects of ketanserin on the components of the renin-angiotensin-aldosterone system, on plasma catecholamines and on exercise capacity for graded uninterrupted exercise were also investigated. At rest in recumbency rapid intravenous injection of 10 mg of ketanserin, followed by a continuous infusion of 2 mg/h, produced an acute but transient fall in mean intra-arterial pressure of 6 mmHg compared with placebo. After 15 min the mean arterial pressure with ketanserin was within 2 mmHg of the mean pressure with placebo. In the sitting position both at rest and up to 30% of maximal work rate, the mean arterial pressure during ketanserin did not differ from the pressure on placebo. However, at higher levels of physical activity the rise in mean arterial pressure was lower with ketanserin; the pressure achieved with placebo was 7.5 mmHg higher at maximal work rate. Heart rate and cardiac output were significantly higher during ketanserin. When the subjects were lying down and resting, plasma noradrenaline and adrenaline levels, plasma renin activity and angiotensin II concentration were not affected by ketanserin; however, these values were higher in the sitting position both at rest and during exercise. Plasma aldosterone was reduced by ketanserin during exercise and also when the subject was resting in the recumbent position.(ABSTRACT TRUNCATED AT 250 WORDS)

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