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Objectives: The objectives of the present study were (1) to evaluate the pressor response to an isometric handgrip exercise in normotensive black and white males; (2) to measure plasma catecholamine levels pre- and post-exercise, as an index of sympathetic nervous system activity; and (3) to quantify the pressor response to bolus intravenous injections of phenylephrine (an alpha-specific agonist)., Methods: Cardiovascular and catecholamine responses to an isometric handgrip exercise (3 minutes at 30% MVC) were measured in 15 normotensive blacks and whites. In another phase of the study, pressor responses to bolus injections of phenylephrine were assessed to evaluate alpha-adrenergic sensitivity., Results: The blood pressure in the blacks increased from 119/69 to 160/120 mm HG during isometric exercise, while in the whites it increased from 118/67 to 153/110 mm HG. The blacks exhibited a greater diastolic blood pressure reactivity, as evidenced by a significant race x time interaction (p < 0.05). The heart rate responses were not significantly different between the two groups. The plasma levels of norepinephrine were similar at rest, but were 25% lower in the blacks than in the whites following isometric exercise (p < 0.01). Black subjects also demonstrated an increased pressor response to intravenous injections of phenylephrine at rest (p < 0.05)., Conclusions: The enhanced vascular sensitivity to norepinephrine may have contributed to the greater exercise pressor response in the blacks.

This study has shown, for the first time, that the change in plasma adenosine 3',5' cyclic monophosphate (cAMP), from accommodation or trough levels, correlates highly in both progressive and continuous work stress experiments with epinephrine (E) at 0.990 and 0.898, and norepinephrine (NE) at 0.954 and 0.927, respectively, in men subjected to the same relative, rather than absolute, stress levels. All three analytes increased significantly (p less than 0.05) by the time each subject had reached 80% of their Vo2 max in the progressive experiments and after working at 80% of their Vo2 max continuously for 10 min. In no case did plasma cAMP rise before the catecholamines. The possible significance of these observations to net perceived relative physiological stress are discussed.

Plasma catecholamines (Ca) increase over time during prolonged exercise at a constant work rate. Possible reasons for this include hypoglycemia, dehydration, increased perceived exertion, and rising body temperature. In an effort to ascertain the contribution of elevated core temperature on the plasma Ca response to prolonged exercise four trained men were studied under two thermal conditions during 45 min of bicycle exercise (approximately 60% Vo2max) and during passive heating. On one testing day each subject was heat-stressed during exercise wearing a nylon pullover shell and cotton pants, (heat stress treatment); on the second day fans were directed on the subjects exercising in a thermoneutral environment (fan treatment). The passive heating experiment was conducted in a hot water bath (41 degrees C). The exercise heat stress treatment produced a higher plasma norepinephrine (NE) concentration (P less than 0.05) in all subjects than the fan treatment. The plasma epinephrine (E) concentration was not significantly (P greater than 0.05) different during exercise in the heat stress treatment from that found during fan treatment. A rise in rectal temperature (Tre) during passive heating resulted in quantitatively small changes in plasma E and NE. The heat load combined with the exercise task produced an increase in plasma NE concentration greater than the sum of the values measured during exercise in the thermoneutral environment and passive heating. This suggested that the combination of stressors caused an augmentation of the sympathetic nervous system's response. Finally, the added heat load caused changes in plasma NE and little change in plasma E, suggesting a differential Ca response with heat stress.

Anticipation of a potentially stressful situation can alter the activity of the sympathetic nervous system. The purpose of this study was to measure the effect of three different intensities of exercise on epinephrine (E) and norepinephrine (NE) excretion when the work test order was randomly assigned and the subjects were not informed of the test order. Six subjects exercised at work loads which averaged 49%, 65%, and 82% Vo2max. Each subject showed an increased rate of NE excretion as the work load increased. The differences among work loads were significant (P less than 0.01). The E response was less consistent. Two subjects showed the greatest rate of excretion at the lowest work load, and one subject showed no increase above his pre-exercise resting value. While NE excretion was closely related to the work load, factors other than exercise appeared to exert considerable influence on the rate of E excretion during exercise.

The purpose of this study was to investigate the relationship between hypoxia and heart rate (HR), pulmonary ventilation, plasma epinephrine (E) and norepinephrine (NE) at rest and during exercise at 40% of maximal oxygen uptake. Six subjects were exposed to inspired gas mixtures containing 21%, 19%, 17%, 15%, and 13% O2. The duration of exposure to each mixture was 10 continuous min at rest, followed by 10 continuous min during exercise. The order of the inspired gas mixtures was randomized. During the exercise test, HR was elevated with exposure to 15% and 13% O2 (p less than 0.001). Pulmonary ventilation was higher at 13% O2 than at the higher O2 percents (p less than 0.001). There were no significant changes in plasma E or NE at rest or during exercise in response to the gas treatments. These results indicate that acute exposure to hypoxic gas mixtures at rest and during light work does not result in significant increases in sympathetic nervous system activity, as judged by the plasma E and NE response.

The use of inspired gas mixtures with an oxygen fraction in excess of 0.3 has been associated with a decrease in the gas exchange ratio (R) during prolonged work in humans. It had been hypothesized that the lower R was due to a lower plasma catecholamine concentration caused by the hyperoxia (Med. Sci. Sports 10: 167-170, 1978). We tested this hypothesis by measuring changes in plasma epinephrine and norepinephrine when the subjects were switched from breathing air to 60% O2 (and vice versa) during 40 min of cycle ergometer exercise at 67% maximal oxygen uptake (VO2max). The subject breathed one gas mixture for the first 30 min and was switched to the other in the last 10 min. The order was reversed in the second test. The switch in gas mixtures from air to 60% O2 resulted in a significant reduction in R, heart rate, minute ventilation, blood lactate concentration, and plasma epinephrine concentration (P less than 0.05). The plasma norepinephrine concentration (0.1 greater than P greater than 0.05) and the plasma free fatty acid concentration were not significantly changed. Although the direction of the epinephrine change was consistent with the change in R, the epinephrine change was quantitatively small (20 pg/ml) and of questionable physiological significance. This suggests a direct effect of PO2 on cellular metabolism as one cause of the change in R when the subjects were switched from air to 60% O2.