Plasma vasopressin, renin activity, and aldosterone responses to maximal exercise in active college females

The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p less than 0.05) from a pre-exercise concentration of 3.8 +/- 0.5 to 15.8 +/- 4.8 pg X ml-1 following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5 +/- 0.5 pg X ml-1 and increased to 16.7 +/- 5.9 pg X ml-1 after the exercise test. PRA increased (p less than 0.05) from a pre-exercise value of 1.6 +/- 0.6 to 6.8 +/- 1.7 ngAI X ml-1 X hr-1 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4 +/- 0.6 ngAI X ml- X hr-1), as was the elevation found after maximal exercise (8.3 +/- 1.9 ngAI X ml- X hr-1). Pre-season plasma ALDO increased (p less than 0.05) from 102.9 +/- 30.8 pg X ml-1 in the pre-exercise period to 453.8 +/- 54.8 pg X ml-1 after the exercise test. In the post-season the values were 108.9 +/- 19.4 and 365.9 +/- 64.4 pg X ml-1, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Plasma atriopeptin response to prolonged cycling in humans.

The exercise-induced increase in plasma atriopeptin (ANP) has been related to exercise intensity. The independent effect of duration on the ANP response to dynamic exercise remains incompletely documented. The purpose of this study was to describe the time course of plasma ANP concentration during a 90-min cycling exercise protocol and to examine this in light of concurrent variations in plasma arginine vasopressin (AVP), aldosterone (ALD), and catecholamine (norepinephrine and epinephrine) concentrations as well as plasma renin activity (PRA). Seven male and four female healthy college students (23 +/- 2 yr) completed a prolonged exercise protocol on a cycle ergometer at an intensity of 67% of maximal O2 uptake. Venous blood was sampled through an indwelling catheter at rest, after 15, 30, 45, 60, and 90 min of exercise, and after 30 min of passive upright recovery. Results (means +/- SE) indicate an increase in ANP from rest (22 +/- 2.6 pg/ml) at 15 min of exercise (45.3 +/- 7.4 pg/ml) with a further increase at 30 min (59.4 +/- 9.8 pg/ml) and a leveling-off thereafter until completion of the exercise protocol (51.7 +/- 10.7 pg/ml). In plasma ALD and PRA, a significant increase was found from rest (ALD, 21.4 +/- 6.4 ng/dl), PRA, 2.5 +/- 0.5 ng.ml-1.h-1 after 30 min of cycling, which continued to increase until completion of the exercise (ALD 46.6 +/- 8.7 ng/dl, PRA 9.5 +/- 0.9 ng.ml-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean +/- SEM showed that the ANF plasma level decreased significantly (p less than 0.05) from 32.5 +/- 4 to 28 +/- 6 pg.ml-1 after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60 +/- 13.6 pg.ml-1 and 53 +/- 13 pg.ml-1): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vascular fluid shifts and endocrine responses to exercise in the heat. Effect of rehydration

This study examines the relationships between vascular changes and endocrine responses to prolonged exercise in the heat, associated with dehydration and rehydration by fluids of different osmolarity. Five subjects were exposed, in a 34 degrees C environment for 4 h of intermittent exercise on a cycle ergometer at 85 +/- 12 Watts (SD). Fluid regulatory hormones and cortisol were analysed in 3 experimental sessions: one without any fluid supplement (NO FLUID), and two with progressive rehydration, either by spring water (WATER) or isotonic solution (ISO), given after 70 min of exercise. Results were expressed in terms of differences between the mean values observed at the end of the exercise and the first hour values taken as references. Dehydration (NO FLUID) elicited a 4.0 +/- 0.8% (SE) decrease in plasma volume (PV) and an increase in osmolarity (8.4 +/- 3.1 mosmol X l-1). Concomitantly, plasma aldosterone (PA), renin activity (PRA), arginin vasopressin (AVP) and cortisol (PC) levels increased greatly in response to exercise in the heat (PA: 37.2 +/- 10.8 ng. 100 ml-1; PRA: 13.4 +/- 2.5 ng X ml-1 X h-1; AVP: 3.8 +/- 1.3 pg X ml-1; PC: 12.2 +/- 2.7 micrograms X 100 ml-1). Rehydration with water led to decreased osmolarity (-8.2 +/- 2.1 mosmol X l-1) with no significant changes in PV. With ISO, PV increased by 6.0 +/- 1.3% and the decrease in osmolarity was-5.8 +/- 1.8 mosmol X l-1. With both modes of rehydration, the increases in PRA, AVP and cortisol were blunted; only ISO prevented the rise in PA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of angiotensin II on arterial pressure, renin and aldosterone during exercise

To evaluate the effect of isotonic exercise on the response to angiotensin II, angiotensin II in saline solution was infused intravenously (7.5 ng X kg-1 X min-1) in seven normal sodium replete male volunteers before, during and after a graded uninterrupted exercise test on the bicycle ergometer until exhaustion. The subjects performed a similar exercise test on another day under randomized conditions when saline solution only was infused. At rest in recumbency angiotensin II infusion increased plasma angiotensin II from 17 to 162 pg X ml-1 (P less than 0.001). When the tests with and without angiotensin II are compared, the difference in plasma angiotensin II throughout the experiment ranged from 86 to 145 pg X ml-1. The difference in mean intra-arterial pressure averaged 17 mmHg at recumbent rest, 12 mmHg in the sitting position, 9 mmHg at 10% of peak work rate and declined progressively throughout the exercise test to become non-significant at the higher levels of activity. Plasma renin activity rose with increasing levels of activity but angiotensin II significantly reduced the increase. Plasma aldosterone, only measured at rest and at peak exercise, was higher during angiotensin II infusion; the difference in plasma aldosterone was significant at rest, but not at peak exercise. In conclusion, the exercise-induced elevation of angiotensin II does not appear to be an important factor in the increase of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of 1-desamino-8-D-arginine vasopressin (DDAVP) on vasopressin release and blood pressure during hemorrhage.

Whether or not 1-desamino-8-D-arginine-vasopressin (DDAVP) reduces blood pressure or affects the release of arginine vasopressin (AVP) and renin is controversial, although evidence suggests AVP and renin are important in maintaining blood pressure during hemorrhage. We therefore investigated the effect of DDAVP on endogenous release of AVP and renin and on blood pressure during hemorrhage in dogs. In the control group the hemorrhage was performed at a rate of 0.4 ml.kg-1.min-1 for 40 min from the femoral artery. The plasma AVP concentration and renin activity (PRA) increased progressively in response to the hemorrhage, from 7.5 +/- 0.5 to 40.3 +/- 7.3 pg.ml-1, and from 11.8 +/- 1.5 to 20.5 +/- 4.2 ng.ml-1.h-1, respectively, while blood pressure decreased slightly. In the DDAVP group, intravenous infusion of DDAVP (2.5 ng.kg-1.min-1 for 40 min) and hemorrhage were simultaneously performed. The plasma DDAVP concentration increased progressively to 218 +/- 21.0 pg.ml-1. There was no significant difference, however, between the control and DDAVP groups in the response of AVP, PRA and blood pressure. The results suggested that DDAVP may not affect the release of AVP and renin or blood pressure during hemorrhage.     

Aldosterone response to angiotensin II during hypoxemia

Exercise in humans causes increases in plasma renin activity (PRA) and plasma aldosterone concentrations (PAC) except when performed at high altitude or while the subjects breathe hypoxic gas. Under those conditions, PRA increases with exercise but PAC does not. We speculated that the PAC suppression during hypoxemic exercise was due to hypoxemia-induced release of a circulating inhibitor of angiotensin II-mediated aldosterone secretion. To test this hypothesis, we measured the PAC response to graded infusions of angiotensin II during hypoxemia and normoxemia. Eight normal volunteers were given increasing doses of angiotensin II (first 2 ng X kg-1 X min-1 and then 4, 8, and finally 12 ng X kg-1 X min-1, each for 20-min periods) on 2 separate days, once while breathing room air and the other day while breathing hypoxic gas adjusted to maintain the subjects' hemoglobin saturation at 90%. The PAC response to different doses of angiotensin II did not significantly differ during hypoxemia from normoxemia. We conclude that our model of hypoxemia does not cause release of an inhibitor of angiotensin II-mediated aldosterone release.     

Neurohumoral and cardiopulmonary response to sustained submaximal exercise in the dog

Neurohumoral, cardiovascular, and respiratory parameters were evaluated during sustained submaximal exercise (3.2 km/h, 15 degrees elevation) in normal adult mongrel dogs. At the level of activity achieved (fivefold elevation of total body O2 consumption and threefold elevation of cardiac output), significant (P less than 0.05) increases in plasma norepinephrine and epinephrine concentration (from 150 +/- 23 to 341 +/- 35 and from 127 +/- 27 to 222 +/- 31 pg/ml, respectively) were present, as well as smaller but significant increases in plasma renin activity and plasma aldosterone concentration (from 2.2 +/- 0.3 to 3.1 +/- 0.6 ng X ml-1 X h-1 and from 98 +/- 8 to 130 +/- 6 pg/ml, respectively). Plasma arginine vasopressin increased variably and insignificantly. The cardiovascular response (heart rate, systemic arterial and pulmonary arterial pressures, left ventricular filling pressure, and calculated total peripheral and pulmonary arteriolar resistance) closely paralleled that of human subjects. Increased hemoglobin concentration was induced by exercise in the dogs. The ventilatory response of the animals was characterized by respiratory alkalosis. These data suggest similarities between canine and human subjects in norepinephrine, plasma renin activity, and plasma aldosterone responses to submaximal exercise. Apparent species differences during submaximal exertion include greater alterations of plasma epinephrine concentration and a respiratory alkalosis in dogs.     

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.     

Immersion diuresis without expected suppression of vasopressin

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20-35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersion experiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at the end of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed when there is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.     

Hormonal responses to exercise during moderate cold exposure in young vs. middle-age subjects.

The influence of moderate cold exposure on the hormonal responses of atrial natriuretic factor (ANF), arginine vasopressin (AVP), catecholamines, and plasma renin activity (PRA) after exhaustive exercise was studied in 9 young and 10 middle-aged subjects. Exercise tests were randomly performed in temperate (30 degrees C) and cold (10 degrees C) environments. Heart rate, oxygen consumption, and peripheral arterial blood pressure were measured at regular intervals. Blood samples were collected before and immediately after exercise at 30 or 10 degrees C. Plasma sodium and potassium concentrations as well as hemoglobin and hematocrit were measured, and the change in plasma volume was calculated. At rest and during exercise, oxygen consumption was similar during exposure to both temperate and cold temperatures. During submaximal exercise intensities, the rise in heart rate was blunted while the increase in systolic blood pressure was significantly greater at 10 than at 30 degrees C. The increases in plasma sodium and potassium concentrations after exhaustion were similar between environments, as was the decrease in plasma volume. In both groups, all plasma hormones were significantly elevated postexercise, with the AVP response similar at 10 and 30 degrees C. However, the norepinephrine and ANF responses were significantly greater while the PRA response was significantly reduced at 10 degrees C. In the middle-aged subjects the epinephrine response to exercise was higher at 10 than at 30 degrees C. The greater ANF and reduced PRA responses to exercise in the cold may have resulted from central hemodynamic changes caused by cold-induced cutaneous vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Training-overtraining: influence of a defined increase in training volume vs training intensity on performance, catecholamines and some metabolic parameters in experienced middle- and long-distance runners.

The influence of an increase in training volume (ITV; February 1989) vs intensity (ITI; February 1990) on performance, catecholamines, energy metabolism and serum lipids was examined in two studies on eight, and nine experienced middle- or long-distance runners; seven participated in both studies. During ITV, mean training volume was doubled from 85.9 km.week-1 (pretrial phase) to 174.6 km within 3 weeks. Some 96%-98% of the training was performed at 67 (SD 8)% of maximal performance. During ITI, speed-endurance, high-speed and interval runs increased within 3 weeks from 9 km.week-1 (pretrial phase) to 22.7 km.week-1 and the total training distance from 61.6 to 84.7 km.week-1. The ITV resulted in stagnation of running velocity at 4 mmol lactate concentration and a decrease in total running distance in the increment test. Heart rate, energy metabolic parameters, nocturnal urinary catecholamine excretion, low density, very low density lipoprotein-cholesterol and triglyceride concentrations decreased significantly; the exercise-related catecholamine plasma concentrations increased at an identical exercise intensity. The ITI produced an improvement in running velocity at 4 mmol lactate concentration and in total running distance in the increment test; heart rate, energy metabolic parameters, nocturnal catecholamine excretion, and serum lipids remained nearly constant, and the exercise-related plasma catecholamine concentrations decreased at an identical exercise intensity. The ITV-related changes in metabolism and catecholamines may have indicated an exhaustion syndrome in the majority of the athletes examined but this hypothesis has to be proven by future experimental studies.     

Plasma prostaglandins, renin, and catecholamines at rest and during exercise in hypertensive humans

Plasma prostaglandins (PGE and PGF alpha), catecholamine concentration, and plasma renin activity (PRA) were measured during an uninterrupted graded exercise test on the bicycle ergometer in 11 hypertensive patients. Blood was withdrawn from the brachial and pulmonary arteries after 30 min of recumbent rest, after 15 min of rest sitting, and at the final work load of the exercise test, which averaged 143 +/- 16.5 W. Exercise did not provoke a significant change in these plasma PGE or PGF alpha concentrations, whereas a rise (P less than 0.001) in arterial PRA and (nor)epinephrine concentration was observed. It is thus unlikely that PGE or PGF alpha is an important determinant of PRA release during exercise, although circulating levels of PGE and PGF alpha do not necessarily reflect release rate or activity in the kidney.     

Influence of endogenous opioids on atrial natriuretic factor release during exercise in man

To evaluate to what extent opioid secretion in exercise induces the release of atrial natriuretic factor (ANF), six healthy male volunteers who were trained subjects, were submitted to two maximal exercise tests with and without (control) opioid receptor blockade by Naltrexone. Blood samples were drawn before (rest) and after exercise (post-exercise) in order to measure human ANF (alpha h ANF), beta-endorphin, plasma aldosterone concentration (PAC) plasma renin activity (PRA) and adreno-cortico trophic hormone (ATCH) by radio-immunological methods. Expired gas was collected during exercise to measure oxygen consumption. On average, the same maximal oxygen consumption (VO2max) during exercise was reached by all subjects with and without treatment. Plasma ANF level at rest slightly decreased after administration of Naltrexone; the response to physical exercise was significantly reduced by Naltrexone. There was no statistical difference between plasma levels of beta-endorphin, PRA and ACTH at rest nor in the post-exercise situation under the influence of Naltrexone. The PAC increased significantly at rest after Naltrexone administration but there was no statistical difference between both values after exercise. These data demonstrate that: (1) ANF secretion during exercise is influenced by the level of beta-endorphin in the plasma; (2) the possible inhibitory role of ANF on aldosterone secretion during exercise is probably over-ruled by the increase in plasma ACTH and PRA.     

Effect of antigravity suit inflation on cardiovascular, PRA, and PVP responses in humans

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of normoxemic and hypoxemic exercise on renin and aldosterone

Five subjects (group 1) performed progressive treadmill exercise on 2 separate days, once while breathing room air (normoxemic) and the other time while breathing gas with a fractional inspired O2 of 17% (hypoxemic). Five other subjects (group 2) performed two progressive treadmill exercise tests on each of 2 separate days in a crossover design. On 1 day normoxemic exercise was first, followed by hypoxemic exercise, and on the other day the pattern was reversed. Plasma renin activity (PRA) increased to a similar extent with hypoxemic exercise as with normoxemic exercise. Plasma aldosterone concentrations (PAC) rose to a significantly higher level during normoxemic exercise than with hypoxemic exercise. Comparing changes in PRA to PAC with progressive exercise revealed dissociation of PAC from PRA during hypoxemic exercise. The PAC response remained depressed when normoxemic exercise followed hypoxemic exercise. These results indicate that hypoxemia interferes with PRA-mediated aldosterone secretions. The mechanism of this inhibition is unclear.     

Dissociated response of aldosterone from plasma renin activity during prolonged exercise under hypoxia

6 healthy male subjects on a fixed salt-diet performed 1 hour ergocycle exercise at 65% of VO2 max in normoxic (N) and hypoxic (H) conditions. Blood samples were taken at intervals for estimations of plasma aldosterone (PAC), angiotensin converting enzyme (ACE), adrenocorticotrophic hormone (ACTH) and catecholamine concentrations. Plasma volume reductions with exercise were similar in N (4.3 +/- 1%) and H (4.0 +/- 1%). PRA response to exercise was increased by hypoxia while PAC and plasma catecholamine rose to a similar extent in both conditions. Increases in ACTH concentration occurred at the end of exercise but no difference was found between high and low altitudes. Plasma ACE remained unchanged throughout exercise in either condition. These results indicate that hypoxemia interferes with PRA-mediated aldosterone secretion. The variations in plasma ACTH levels during exercise in hypoxia do not appear responsible for this interference.     

Renin, aldosterone, and converting enzyme during exercise and acute hypoxia in humans

The possibility that hypoxia might inhibit the secretion of angiotension-converting enzyme (ACE) would explain the low concentrations of aldosterone reported in humans at high altitude. To observe the effect of such a reduction in ACE concentration on the plasma aldosterone concentration (PAC) four subjects performed mild exercise throughout a 2-h study so as to elevate their plasma renin activity (PRA). After the first 60 min breathing air they were switched to breathing 12.8% O2 (4,000 an altitude equivalent). Venous samples were taken at intervals for hormone analysis. Results showed the expected rise of PRA and PAC both tending toward a plateau after about 45 min. There was no significant change in ACE activity (F = 0.065). Hypoxia produced a further 50% rise in PRA but a fall in PAC and a 30% reduction in ACE activity. Angiotensin I concentrations closely followed PRA throughout (r = 0.984). These results indicate that during exercise acute hypoxia changes the usual close relationship between PAC and PRA by reducing ACE activity.     

The effect of training on responses of beta-endorphin and other pituitary hormones to insulin-induced hypoglycemia

We studied whether the previously reported intensified beta-endorphin response to exercise after training might result from a training-induced general increase in anterior pituitary secretory capacity. Identical hypoglycemia was induced by insulin infusion in 7 untrained (VO2max 49 +/- 4 ml X (kg X min)-1, mean and SE) and 8 physically trained (VO2max 65 +/- 4 ml X (kg X min)-1) subjects. In response to hypoglycemia, levels of beta-endorphin and prolactin immunoreactivity in serum increased similarly in trained (from 41 +/- 2 pg X ml-1 and 6 +/- 1 pg X ml-1 before hypoglycemia to 103 +/- 11 pg X ml-1 and 43 +/- 9 pg X ml-1 during recovery, P less than 0.05) and untrained (from 35 +/- 7 pg X ml-1 and 7 +/- 2 pg X ml-1 to 113 +/- 18 pg X ml-1 and 31 +/- 8 pg X ml-1, P less than 0.05) subjects. Growth hormone (GH) was higher 90 min after glucose nadir in trained (61 +/- 13 mU X l-1) than in untrained (25 +/- 6 mU X l-1) subjects (P less than 0.05). Levels of thyrotropin (TSH) changed in neither of the groups. It is concluded that, in contrast to what has been formerly proposed, training does not result in a general increase in secretory capacity of the anterior pituitary gland. TSH responds to hypoglycemia neither in trained nor in untrained subjects. Finally, differences in beta-endorphin responses to exercise between trained and untrained subjects cannot be ascribed to differences in responsiveness to hypoglycemia.     

Plasma hormonal responses at graded hypohydration levels during exercise-heat stress

The effects of graded levels of hypohydration (3, 5, and 7% of body weight) on hormonal responses to exercise in the heat were examined in six heat-acclimated male volunteers. On the day following dehydration, subjects performed light (approximately 25% maximal O2 consumption, 1.03 1 X min-1) exercise in a hot (49 degrees C, 20% relative humidity) environment for four consecutive 25-min intervals interspaced by 10-min rests; blood was obtained before exercise and at approximately 10 min before completion of each exercise period. During euhydration, plasma cortisol (PC) levels manifested significant decrements over time (e.g., time 0, 14.2 micrograms X 100 ml-1 vs. time 2, 8.9 micrograms X 100 ml-1), probably related to its diurnal periodicity. However, during hypohydration, levels of PC were increased and correlated with hypohydration intensity (e.g., time 0, 0, 3, 5, and 7% hypohydration, 14.2, 16.5, 19.8, and 36.2 micrograms X 100 ml-1, respectively). Plasma renin activity (PRA) was increased significantly by hypohydration (e.g., time 0, euhydrated vs. 3%, 3.7 vs. 6.2 units) but was unaffected by exercise in the heat. Plasma aldosterone (ALD) levels were generally increased by exercise in the heat (e.g., time 0 vs. time 4, 3% hypohydration, 12.1 vs. 18.7 ng X 100 ml-1). Regression analysis illustrated that graded intensities of hypohydration were correlated with incremented PRA and ALD through 5% hypohydration. Conversely, PC was incrementally elevated through 7% hypohydration.(ABSTRACT TRUNCATED AT 250 WORDS)