Plasma renin activity and plasma catecholamines in intact and splenectomized running and swimming beagle dogs

Summary The influence of splenectomy in the dog on plasma catecholamine levels and plasma renin activity during treadmill running and swimming was investigated. Plasma catecholamines were measured by a radioenzymatic assay and plasma renin activity by a radioimmunoassay. Exercise consistently increased plasma catecholamine levels before and after splenectomy (range of increase:3–38 pmol·ml^–1). Swimming, however, was a stronger stimulus than running. No change in the ratio between noradrenaline and adrenaline was found. In intact dogs exercise results in a marked increase in hematocrit due to splenic contraction (range of increase 3–8 volume %), while renal blood flow and plasma renin activity remain virtually constant. In splenectomized dogs, exercise has been reported to induce a decrease in renal blood flow. In contrast to this known effect on renal blood flow, splenectomy did not affect plasma renin activity in treadmill running dogs. In swimming dogs, however, plasma renin activity was increased after splenectomy (range of increase 3.3–6.9 ng·Ang I·ml^–1·h^–1). Possibly, a threshold in sympathetic tone is required to increase renin release in the dog.     

Vascular fluid shifts and endocrine responses to exercise in the heat

Summary 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 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 · 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 · ml^–1 · h^–1; AVP: 3.8±1.3 pg · ml^–1; PC: 12.2±2.7 g · 100 ml^–1). Rehydration with water led to decreased osmolarity (–8.2±2.1 mosmol · 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 · l^–1. With both modes of rehydration, the increases in PRA, AVP and cortisol were blunted; only ISO prevented the rise in PA.These data indicate that prolonged exercise in moderate heat is extremely effective in increasing cortisol and fluid-electrolyte regulatory hormones in dehydrated subjects. Progressive rehydration with water or isotonic solution, in the absence of osmotic and volemic stimuli, prevents the hormonal increases.     

Plasma renin activity and serum aldosterone during prolonged physical strain

Summary Plasma renin activity (PRA), serum aldosterone and the serum and urinary levels of sodium and potassium have been investigated in 24 young men participating in a 5-day military training course with heavy continuous physical exercise, energy and sleep deprivation. The subjects were divided into three groups. Group 1 did not get any extra sleep or food, group 2 were compensated for the energy deficiency, and group 3 slept 3 h each night. The basic diet given to all the subjects was about 5,000 kJ and 2 g NaCl·24 h^–1·cadet^–1. The high calorie diet contained approximately 25,000–35,000 kJ and 20 g of NaCl·24 h^–1·cadet^–1.The study showed that serum aldosterone and PRA were extremely activated during such prolonged physical strain combined with lack of food and salt, whereas sleep deprivation did not seem to have any large influence. Only small variations were found in the serum levels of sodium and potassium and the urinary level of potassium during the course, whereas a decrease was seen in urinary sodium concentration. The fairly good correlations between the decrease in urinary sodium levels and the increase in PRA (r=0.7) and further between PRA and serum aldosterone (r=0.8) during the course indicate that there is a causal connection between the decrease in urinary sodium excretion and the increase in PRA and serum aldosterone. An increased response was seen during a short term exercise test in groups 1 and 3, whereas no such increase was seen in the subjects of group 2, probably because the higher salt intake abolishes the renin-aldosterone response to exercise. In spite of high catecholamine levels during the course, the serum potassium response to physical exercise was unchanged. The circulating catecholamines did not seem to have any significance for renin secretion and sodium reabsorption during the course. Further, there was no sign of exhaustion in Na/K homeostasis during the experiment.     

Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

This study was designed to examine whether macula densa function is involved in the changes of renal renin gene expression upon acute hypoperfusion of one kidney. To block macula densa function, rats with free access to salt and water were subcutaneously infused with furosemide (12 mg/day) for 6 days. Then, 4 days after the start of the infusion, the left renal arteries were clipped with 0.2-mm silver clips and renin mRNA levels in ipsilateral and contralateral kidneys, as well as plasma renin activities (PRA), were determined 48 h after clipping. In non-clipped animals furosemide increased PRA from 10 to 47 ng angiotensin I · h^–1 · ml^–1 and raised renin mRNA levels in both kidneys 2.5-fold. In vehicle-infused animals, clipping of the left renal artery increased PRA to 37 ng angiotensin I · h^–1 · ml^–1 and led to a 5-fold rise of renin mRNA levels in the ipsilateral kidneys and to a suppression to 20% of the control values in the contralateral kidneys. PRA values in clipped and furosemide-infused animals were 45 ng angiotensin I · h^–1 · ml^–1. In these animals renin mRNA levels increased in the ipsilateral kidneys to similar absolute values as in vehicle-infused rats, whilst contralateral renin mRNA levels fell to about 25% of the respective controls. These findings indicate that the stimulations of renin gene expression by inhibition of macula densa salt transport and by renal artery clipping are not additive, suggesting that the macula densa mechanism may participate in the stimulation of renin gene expression upon hypoperfusion. The macula densa mechanism, however, appears to be not essentially involved in the suppression of renin gene expression in the contralaterals to stenosed kidneys.     

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

Summary 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<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. PAC was not influenced by postural change but significantly increased in all exercise tests. ACTH increased to the same extent in both exercise tests. The plasma catecholamine level increased during upright posture and both physical exercise procedures. These results indiate that enhanced venous return during anti-G suit inflation increases ANF secretion at rest in an upright posture and that physical exercise greatly increases plasma ANF level independently of the anti-G suit inflation. They suggest that ANF release during exercise could be influenced by factors other than haemodynamic stimuli. The comparison between ANF and PRA changes during arm-cranking indicates that PRA is influenced more than ANF by blood volume displacement. The ANF increase during exercise does not inhibit aldosterone secretion.     

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

Summary 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<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · 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 · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · 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.     

The interaction between short-term exercise training and a diuretic-induced hypovolemic stimulus

Nine healthy untrained males [mean (SEM) age, 20.2 (1) years; peak oxygen uptake (VO_2max, 48.2 (2) ml · kg^–1 · min^–1] took part in a study to examine whether short-term exercise training (cycle exercise 2 h · day^–1 for 3 days at 60% ), which normally results in an expansion of plasma volume (PV), can counteract a diuretic-induced hypovolemic stimulus (100 mg triamterene + 50 mg hydrochlorothiazide day^–1 for 5 days concurrent with exercise training) and restore PV to control levels. Resting and exercise responses (90 min, 60% ) in the diuretic plus exercise training condition (D + E) were compared to a control (C) and a diuretic (D) condition in which no exercise was performed. Following the short-term training, PV was still decreased (P < 0.05) below C by –8.3 (3)% in D + E and was similar (P > 0.05) to the reduction in D [–12.4 (2)%]. The reduced PV in response to the diuretic was associated with similar (P > 0.05) elevations in resting aldosterone (ALDO) and norepinephrine (NOREPI) levels (ng · 100 ml^–1) in D [101 (12), 61 (4)] and D + E [85 (16), 60 (10)] above (P < 0.05) C [22 (5), 37 (4)]. During exercise, ALDO levels were increased (P < 0.05) by 66 (5) and 70 (10) ng · 100 ml^–1 in D and D + E, respectively, and the increase was greater (P < 0.05) than C [44 (8) ng · 100 ml^–1]. The rise in NOREPI during exercise was lower (P < 0.05) in D + E [164 (44) ng · 100 ml^–1] than in D [244 (24) ng · 100 ml^–1] with levels similar to C [176 (25) ng · 100 ml^–1]. Thus, the ALDO response to the diuretic was heightened at rest and during exercise but was not additionally affected by the short-term training session. Results suggest that 3 days of exercise training are unable to counteract the hypovolemic effects of a diuretic and restore PV to control levels despite chronic elevations in NOREPI and ALDO.     

Effects of exercise training on plasma catecholamines and blood pressure in labile hypertensive subjects

Summary Plasma catecholamine concentrations (norepinephrine, NE; epinephrine, E) were measured along with heart rate (HR) and blood pressure (BP) at rest in supine (20 min) and standing (10 min) positions and in response to cycle ergometer exercise (5 min; 60% estimated maximal aerobic power) in 12 hypertensive patients before and after 20 weeks of aerobic training on cycle ergometer (six males, one female) or by jogging (five males). In a control group of labile hypertensive patients (five males, two females), estimated maximal aerobic power as well as HR and BP at rest in the supine and standing positions and in response to exercise were not modified from the first to the second evaluation (43±4 vs 43±5 ml·kg^–1·min^–1). In comparison estimated maximal aerobic power significantly increased in both training groups (cycle: 38±4 to 43±4; jogging: 38±3 to 46±4 ml·kg^–1·min^–1). However HR and BP were not modified following training, except for small reductions in systolic (18.9 to 18 kPa: 142 to 135 mmHg) and diastolic pressures (13.3 to 12 kPa: 100 to 90 mmHg) (p<0.05) at standing rest in the cycle group. Changes in plasma E and NE concentrations at rest and in response to exercise were small and not consistent: plasma NE was lower at standing rest following cycle training, (559±95 vs 462±108 pg·ml^–1) but a similar reduction was observed in the control group (428±45 vs 321±28 pg·ml^–1); plasma E was lower at rest following cycle training (29±7 vs 12±8 pg·ml^–1), but was higher in response to exercise (137±24 vs 419±113 pg·ml^–1). These results are in accordance with previous reports which do not clearly demonstrate that physical training in hypertensive patients lowers BP and the activity or reactivity of the sympathetic system.     

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

Summary 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.     

Endothelium derived relaxing factor is involved in the pressure control of renin gene expression in the kidney

To study the influence of endothelium derived relaxing factor/nitric oxide (EDNO) on renin gene expression, the effects of a 2-day treatment with the NO-synthase inhibitor nitro-L-arginine-methylester (L-NAME, 40 mg/kg twice a day) on plasma renin activity (PRA) and renal and adrenal renin m-RNA levels were examined in conscious rats with and without unilateral renal clips (0.2 mm). In sham-clipped animalsL-NAME led to a decrease of PRA from 7.5 to 2.5 ng angiotensin I (ANGI) · h^–1 · ml^–1 and to a 35% decrease of renal renin m-RNA levels. Unilateral renal artery clipping increased PRA to 35 and to 13 ng ANGI · h^–1 · ml^–1 in vehicle and inL-NAME-treated rats, respectively. In the clipped kidneys renin m-RNA levels increased to 450% of control values in vehicle-treated animals and to 220% of control values inL-NAME-treated animals. In the contralaterals as opposed to clipped kidneys, renin m-RNA levels decreased to 16% and 50% of the control values in vehicle- and inL-NAME-treated animals, respectively. In the adrenal glands renin m-RNA levels were not significantly changed either by clipping of one renal artery or by treatment of animals withL-NAME. The NO-donor sodium nitroprusside (100 M) was found to increase renin secretion and renin m-RNA levels in primary cultures of renal juxtaglomerular cells. These findings suggest that EDNO is involved in the control of the renin gene by the renal perfusion pressure.     

Left ventricular performance during prolonged exercise and early recovery in healthy subjects

The effect of semi-supine long lasting exercise to exhaustion [61 (SD 10) min] on left ventricular systolic performance was studied by echocardiography in 16 young healthy volunteers. During the incremental phase of exercise, the ejection fraction increased from 65.2 (SD 4.1)% to 80.1 (SD 4.8)% (P<0.0001), then it levelled off up to the end of exercise [81.7 (SD 4.4)%,P<0.0001 vs rest]. During recovery, the ejection fraction rapidly and steadily decreased to a value similar to that at rest [66.1 (SD 5.0)%, n.s.). A similar pattern was shown by the systolic blood pressure/end-systolic volume coefficient, which rose from 3.2 (SD 0.8) mmHg · ml^–1 to 7.5 (SD 2.7) mmHg · ml^–1 (P < 0.0001) in the initial phase and subsequently did not change until the end of exercise [7.0 (SD 2.2) mmHg · ml^–1,P<0.0001 vs rest], to fall sharply after the cessation of exercise [2.9 (SD 1.1) mmHg · ml^–1 at the 10th min, n.s. vs rest]. Exercise and recovery indices of left ventricular performance were not correlated with exercise duration, maximal heart rate and increase in free fatty acids. The present results indicated that, after the initial increase, left ventricular performance remained elevated during prolonged high intensity exercise and that conclusions on exercise cardiac performance drawn from postexercise data can be misleading.     

Influence of angiotensin II blockade during exercise in the heat

The effect of the blockade of the renin angiotensin system (RAS) on thermorgulatory, cardiovascular and renal function during moderate exercise in a hot [mean (SEM) 34.4 (0.1)°C] environment was evaluated. Six men and three women cycled at 60% peak oxygen uptake for 45 min following acute administration of a placebo (PLAC) or enalapril (ENAL), an angiotensin converting enzyme inhibitor (ACE-I). Resting mean arterial pressure (MAP) was reduced by ENAL, but the pressor response to exercise was unaffected [MAP = 7.8 (1.4) mmHg for both trials (P > 0.05)]. Peak esophageal temperature [T _es = 38.7 (1.0)°C (PLAC) vs 38.4 (0.2)°C (ENAL)] and mean skin temperatures [ _sk = 36.5 (0.1)°C (PLAC) vs 36.6 (0.1)°C (ENAL)] were similar for both drug treatments during the exercise. Both aldosterone and plasma renin activity (PRA) increased five fold above resting values during exercise; however, only the PRA response [16.7 (3.2) ng angiotensin I (Ang I) · ml^–1 · h^–1 (ENAL) vs 7.4 (1.2) ng Ang I · ml^–1 · h^–1 (PLAC)] was significantly altered by ENAL treatment (P < 0.05). Urine flow, sodium excretion and glomerular filtration rates, determined from creatinine clearance, were similarly reduced following exercise for both ENAL and PLAC treatments. These results suggest acute administration (5 mg) of ACE-I does not impair thermoregulatory, cardiovascular or renal responses during moderate exercise in the heat.     

Control of mineralocorticoid substitution in Addison's disease by plasma renin measurement

Summary In 7 out-patients with Addison's disease, plasma renin activity (PRA), plasma concentrations of angiotensin II (AT II), renin substrate (PRS), potassium, sodium and total protein, hematocrit, blood pressure, heart rate and body weight were studied after 2 weeks each on 2 mg of dexamethasone, 25 mg hydrocortisone (HC), 25 mg HC+0.05 mg 9--fluorohydrocortisone (FC), 25 mg HC+0.1 mg FC and 25 mg HC+0.2 mg FC. Four further patients were less extensively studied. Mean PRA (upper normal limit, ambulatory: 12 ng AT I·ml^–1·h^–1) after the 5 steps of incremental substitution, starting with dexamethasone, was 192, 59, 38, 24 and 9 ng AT I·ml^–1·h^–1 rsp. PRS did not change with increasing substitution. PRA and AT II were significantly correlated (r=0.91;p<0.0001) and proved to be the most sensitive parameters of insufficient mineralocorticoid substitution. With decreasing significance, PRA also correlated with plasma protein concentration, plasma sodium concentration (negative), body weight (negative), heart rate, mean blood pressure (negative) and plasma potassium concentration.PRA or AT II measurements are useful clinical tools to control mineralocorticoid substitution in Addisonian patients. Inappropriately high substitution can be prevented by keeping PRA in the upper normal range.Presented in part to the 21st Symposium of the Deutsche Gesellschaft für Endokrinologie, Munich, February 1975     

Finger and forearm vasodilatatory changes after local cold acclimation

Summary To determine the vascular changes induced by local cold acclimation, post-ischaemia and exercise vasodilatation were studied in the finger and the forearm of five subjects cold-acclimated locally and five non-acclimated subjects. Peak blood flow was measured by venous occlusion plethysmography after 5 min of arterial occlusion (PBF_isc), after 5 min of sustained handgrip at 10% maximal voluntary contraction (PBF_exe), and after 5 min of both treatments simultaneously (PBF_isc+exe). Each test was performed at room temperature (25° C, SE 1 C) (non-cooled condition) and after 5 min of 5'C cold water immersion (cooled condition). After the cold acclimation period, the decrease in skin temperature was more limited in the cold-acclimated compared to the non-acclimated (P<0.01). The PBF_isc was significantly reduced in the cooled condition only in the cold-acclimated subjects (finger: 8.4 ml · 100 ml^–1 · min^–1, SE 1.1,P<0.01; forearm: 5.8 ml · 100 ml^–1 · min^–1, SE 1.5,P<0.01) compared to the non-cooled condition. Forearm PBF_exe was significantly decreased in the cooled condition only in the cold-acclimated subjects (non-cooled: 7.4 ml · 100 ml^–1 · min^–1, SE 1.2; cooled: 3.9 ml · 100 ml^–1 ·min^–1, SE 2.6,P<0.05) indicating that muscle blood flow was also reduced. The application of PBF_isc+exe elicited an increase in peak blood flow only in the forearm of the non-acclimated subjects (non-cooled: 10.4 ml· 100 ml^–1 · min^–1, SE 2.0; cooled: 14.3 ml · 100 ml^–1 · min^–1, SE 2.6,P<0.05) and conversely only in the finger of the cold-acclimated (non-cooled finger: 25.7 ml · 100 ml^–1 · min^–1, SE 4.4; cooled finger: 19.2 ml · 100 ml^–1 · min^–1, SE 3.3,P<0.01). Therefore, subjects cold-acclimated locally showed decreased vasodilatatory responses only when exposed to cold.     

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

Summary We studied whether the previously reported intensified -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 (Skeletal muscle enzyme activity, fiber composition and in relation to distance running performance 49±4 ml · (kg · min)^–1, mean and SE) and 8 physically trained (Skeletal muscle enzyme activity, fiber composition and in relation to distance running performance 65±4 ml · (kg · min)^–1) subjects. In response to hypoglycemia, levels of -endorphin and prolactin immunoreactivity in serum increased similarly in trained (from 41±2 pg · ml^–1 and 6±1 pg · ml^–1 before hypoglycemia to 103±11 pg · ml^–1 and 43±9 pg · ml^–1 during recovery, P<0.05) and untrained (from 35±7 pg · ml^–1 and 7±2 pg · ml^–1 to 113±18 pg · ml^–1 and 31±8 pg · ml^–1 P<0.05) subjects. Growth hormone (GH) was higher 90 min after glucose nadir in trained (61±13 mU · l^–1) than in untrained (25±6 mU · l^–1) subjects (P<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 -endorphin responses to exercise between trained and untrained subjects cannot be ascribed to differences in responsiveness to hypoglycemia.     

Sustained noradrenaline sulphate response in long-distance runners and untrained subjects up to 2 h after exhausting exercise

Summary We investigated the response of plasma and platelet free catecholamine ([CA]) and sulphated catecholamine ([CA-S]) concentrations after an incremental treadmill test to exhaustion and during recovery. In triathletes (n = 9) plasma and platelet [CA] and [CA-S] were measured before, immediately after and 0.5 and 24 h after exercise. In long-distance runners (n = 9) and in controls (n = 10) plasma [CA] and [CA-S] were determined 2 h instead of 24 h after exercise. Platelet [CA] and [CA-S] remained unchanged throughout the study. Plasma [CA] increased after exercise in all groups (P<0.05) and returned to pre-exercise values within 0.5 h of recovery. Plasma sulphoconjugated noradrenaline concentration ([NA-S]) was elevated after exercise in the triathletes, long-distance runners and in controls [9.96 (SEM 0.84) nmol·1^–1, 11.8 (SEM 1.19) nmol·1^–1, 9.53 (SEM 1.10) nmol·l^–1, respectively;P<0.05] compared with resting values [7.13 (SEM 1.04) nmol·l^–1, 6.19 (SEM 0.56) nmol·l^–1, 6.76 (SEM 0.67) nmol·1^–1, respectively] and remained elevated after 0.5 h of recovery [9.94 (SEM1.14) nmol·l^–1, 10.96 (SEM 0.80) nmol·l^–1, 8.95 (SEM 0.99) nmol·l^–1, respectively;P<0.05]. In the long-distance runners and controls plasma [NA-S] remained elevated during 2 h of recovery [9.96 (SEM 0.76) nmol·l^–1, 9.03 (SEM 0.88) nmol·l^–1, respectively]. These results would indicate that plasma [NA-S] increases after sympathetic nervous system activation by an exhausting incremental exercise test and remain elevated up to 2 h after exercise.     

Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity

The calf and forearm blood flows (Q _calf and Q _forearm respectively), blood pressure, heart rate and oxygen uptake of six men and women were studied during combined leg and handgrip exercise to determine whether a reduction of exercise-induced hyperaemia would occur in the active leg when exhausting rhythmic handgrip exercise at 50% maximal voluntary contraction (MVC) was superimposed upon rhythmic plantar flexion lasting for 10 min at 10% MVC (P₁₀) prior to this combined exercise. The Q _calf and Q _forearm were measured by venous occlusion plethysmography during 5-s rests interposed during every minute of P₁₀ exercise and immediately after combined exercise. The muscle sympathetic nerve activity (MSNA) changes were also recorded during leg exercise alone and combined exercise. During plantar flexion performed 60 times · min^–1 with a load equal to 10% MVC (P₁₀), Q _calf was maintained at a constant level, which was significantly higher than the resting value (P < 0.001). When rhythmic handgrip contraction at 50% MVC (H₅₀) and P₁₀ were performed simultaneously, the combined exercise was concluded due to forearm exhaustion after a mean of 51.2 (SEM 5.5) s. At exhaustion, Q _calf had decreased significantly from 20.6 (SEM 3.0) ml · 100 ml^–1 · min^–1 (10th min during P₁₀ exercise) to 15.3 (SEM) ml · 100 ml^–1 · min^–1 (P = 0.001), whereas Q _forearm had increased significantly (0.001 < P < 0.01) from 8.6 (SEM 1.9) ml · 100 ml^–1 · min^–1 (10th min of P₁₀ exercise) to 26.2 (SEM 3.2) ml · 100 ml^–1 · min^–1. The mean blood pressure remained at an almost constant level during the 3rd to 10th min of P₁₀ exercise and increased markedly when H₅₀ was added. The calf vascular conductance during combined exercise decreased significantly (0.001 < P < 0.01) compared with that at the 10th min of P₁₀ alone. Although the MSNA (expressed as burst rate) remained unchanged during P₁₀ exercise for 10 min, it increased markedly when exhausting H₅₀ and P₁₀ exercise were performed simultaneously. These findings indicated that superimposition of exhausting handgrip exercise at 50% MVC caused a vasoconstriction in the exercising calf due to increased MSNA, which counteracted the vasodilatation in this active muscle.     

Effect of heat stress on muscle blood flow during dynamic handgrip exercise

Summary During exercise in a hot environment, blood flow in the exercising muscles may be reduced in favour of the cutaneous circulation. The aim of our study was to examine whether an acute heat exposure (65–70°C) in sauna conditions reduces the blood flow in forearm muscles during handgrip exercise in comparison to tests at thermoneutrality (25° C). Nine healthy men performed dynamic handgrip exercise of the right hand by rhythmically squeezing a water-filled rubber tube at 13% (light), and at 34% (moderate) of maximal voluntary contraction. The left arm served as a control. The muscle blood flow was estimated as the difference in plethysmographic blood flow between the exercising and the control forearm. Skin blood flow was estimated by laser Doppler flowmetry in both forearms. Oesophageal temperature averaged 36.92 (SEM 0.08) ° C at thermo-neutrality, and 37.74 (SEM 0.07) ° C (P<0.01) at the end of the heat stress. The corresponding values for heart rate were 58 (SEM 2) and 99 (SEM 5) beats -min^–1 (P<0.01), respectively. At 25° C, handgrip exercise increased blood flow in the exercising forearm above the control forarm by 6.0 (SEM 0.8) ml · 100 ml^–1 · min^–1 during light exercise, and by 17.9 (SEM 2.5) ml · 100 ml^–1 · min^–1 during moderate exercise. In the heat, the increases were significantly higher: 12.5 (SEM 2:2) ml · 100 ml^–1 · min^–1 at the light exercise level (P<0.01), and 32.2 (SEM 5.9) ml · 100 ml^–1·min^–1 (P<0.05) at the moderate exercise level. Skin blood flow was not significantly different in any of the test conditions between the two forearms. These results suggested that hyperthermia of the observed magnitude did not reduce blood flow in active muscles during light or moderate levels of dynamic handgrip exercise.     

Influence of acute maximal exercise on lecithin: cholesterol acyltransferase activity in healthy adults of differing aerobic performance

Summary To document the possible influence of a single episode of maximal aerobic stress on the serum lecithin: cholesterol acyltransferase (LCAT) activity in subjects with differing histories of training, two groups of healthy male adults [controls (C),n = 18, 28.6 years, SD 5.2, 50.1 ml · kg^–1 · min^–1 maximal O₂ uptake (VO_2max), SD 5.3; endurance trained athletes (T),n = 18, 31.4 years, SD 8.8, 65.0 ml · kg^–1 · min^–1 VO_2max, SD 2.8] were examined in a maximal aerobic stress test. In addition to the routine assessment of lipid status, LCAT activity was measured immediately before and after exercise. At rest nearly identical LCAT activity values were found in both groups: C 64.4 nmol · ml^–1 · h^–1, SD 16.7 vs T 65.0 nmol · ml^–1 · h^–1, SD 20.9. The post-exercise LCAT values induced by the maximal stress test increased significantly to (C) 95.7 nmol · ml^–1 · h^–1, SD 23.5, +48.6%,P<0.001; (T) 83.5 nmol · ml^–1 · h^–1, SD 24.3, +29.1%,P<0.01. Neither the pre nor the post-exercise individual LCAT activity values showed any significant correlation to the corresponding data on physical performance.     

The monitoring of the menstrual status of female athletes by salivary steroid determination and ultrasonography

Summary This study was designed to evaluate whether traditional plasma hormone determinations can be adequately replaced by measurements of salivary hormones. Eleven young sportswomen with menstrual irregularities attributed to strenuous physical exercise participated in this study. Mean body weight expressed as a percentage of ideal body weight was 92%, SD 4%. Their mean weekly training distance was 35 km, SD 15. Basal plasma endocrinological measurements revealed a hypo-oestrogenic status (mean plasma oestradiol values: 22pg-ml^–1, SD 8.8), and a deficient luteal phase (mean plasma progesterone: 2.9 ng · ml^–1, SD 2.1). Preexercise salivary sex steroids were low. Salivary progesterone levels were 39.3 pg · ml^–1, SD 9.5 (normal ranges in saliva: 25–60 pg· ml^–1), salivary oestrone (E₁) was 12.2 pg · ml^–1, SD 2.3 (normal ranges in saliva: 7.5–25 pg·ml^–1), and salivary oestradiol (E₂) < 1.9 pg · ml^–1, SD 1.1 (normally 1.0–10.0 pg · ml^–1). After a 21-km run, all salivary steroids appeared to increase. Mean salivary testosterone levels increased by 15.2% and salivary progesterone by 14.8%. Mean salivary oestrogens also increased (E₁: + 13.9%; E₂: +21.1%). These findings confirm the results of earlier studies which found higher post-exercise plasma sex steroid levels. Since salivary measurements are believed to reflect non-protein-bound, thus free steroid levels, the results obtained by these techniques may provide a more realistic picture of the hormonal effects of physical exercise. In future, more accurate, cost-effective and easier techniques for salivary measurements may offer additional advantages.