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.     

Effect of acute mild hypoxia during exercise on plasma free and sulphoconjugated catecholamines

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml · min^–1 · kg^–1 body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P < 0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol · 1^–1, respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol · 1^–1, respectively P < 0.01]. The higher plasma [NA-S] after HYP (P < 0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.     

Effects of prolonged cycle ergometer exercise on maximal muscle power and oxygen uptake in humans

Summary The mechanical power (W_tot, W·kg^–1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO_2max)] of 20–40 min duration. The oxygen uptake [VO₂ (W·kg^–1, 1 ml O₂ = 20.9 J)] and venous blood lactate concentration ([la]_b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, W_tot decreased linearly with the intensity of the priming exercise (W_tot = 11.9–0.25·VO₂). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO_2max, W_tot, VO₂ and [la]_b remained constant until the end of the exercise. For exercise intensities greater than 60% VO_2max, VO₂ and [la]_b showed continuous upward drifts and W_tot continued decreasing. Under these conditions, the rate of decrease of W_tot was linearly related to the rate of increase of V [(d W_tot/dt) (W·kg^–1·s^–1) = 5.0·10^–5 –0.20·(d VO₂/dt) (W·kg^–1·s^–1)] and this was linearly related to the rate of increase of [la]_b [(d VO₂/dt) (W·kg^–1·s^–1) = 2.310^–4 + 5.910^–5·(d [la]_b/dt) (mM·s^–1)]. These findings would suggest that the decrease of W_tot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO₂ (upwards) and of W_tot (downwards) during intense exercise at constant W_tot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles).     

Hormonal regulation of potassium shifts during graded exhausting exercise

Summary Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3:5-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol·1^–1, SEM 0.12 at the end of exercise vs 3.80 mmol·1^–1, SEM 0.05 basal,P<0.001), plasma adrenaline (2.14 nmol·1^–1, SEM 0.05 at the end of exercise vs 0.30 nmol·1^–1, SEM 0.02 basal,P<0.001), plasma noradrenaline (1.10 nmol·1^–1, SEM 0.64 at the end of exercise vs 1.50 nmol·1^–1, SEM 0.05 basal,P< 0.001), serum aldosterone (0.92 nmol·1^–1, SEM 0.14 at the end of exercise vs 0.36 nmol·1^–1, SEM 0.05 basal,P<0.01), and plasma cAMP (35.4 nmol·1^–1, SEM 2.3 at the end of exercise vs 21.4 nmol·1^–1, SEM 4.5 basal,P<0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol·1^–1, SEM 0.01,P<0.01; and 0.85 nmol·1^–1, SEM 0.12,P<0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU·1^–1, SEM 0.58 at the end of exercise vs 5.47 mlU·1^–1, SEM 0.41 basal, NS) but increased significantly (P<0.02) at the end of the recovery period (7.12 mlU·1^–1, SEM 0.65). Serum potassium increases with exhausting exercise appeared to be caused not only by its release from contracting muscles but also by an -adrenergic stimulation produced by adrenaline and noradrenaline. On the other hand, the increased levels of plasma noradrenaline maintained during the recovery period may have served to avoid excessive hypokalaemia through the stimulation of muscle -receptors. Thus, catecholamines may play an important role in the regulation of serum potassium concentrations during and after exercise. Any disturbance of these adrenergic effects may lead either to an excessive increase or to a decrease of kalaemia, with the consequent risk of arrhythmias linked to exercise.     

Adjustment of metabolism,catecholamines and β-adrenoceptors to 90 min of cycle ergometry

Adrenaline infusion of 0.1 g · kg^–1 · min^–1 in healthy volunteers results in an increase of hepatic glucose production, an increase of the absolute number of occupied -adrenoceptors and specific changes in metabolism. To compare these effects with the changes induced by an endogenous catecholamine release, we investigated healthy volunteers during cycle ergometry. After fasting at least 14 h seven healthy subjects exercised for 90 min at an intensity of 20% below their individual anaerobic threshold. The rate of glucose production as well as the turnover rates of alanine and leucine were calculated using stable isotope tracers. High and low affinity -adrenergic binding sites on lymphocytes were determined by an equilibrium binding assay with (–)¹²⁵ Iodocyanopindolol. After 90 min of cycling the rate of appearance of glucose increased significantly from means of 2.0 (SD 0.2) to 2.65 (SD 0.50) mg · kg^–1 · min^–1 with unchanged blood concentrations of glucose and lactate. The flux of the amino acids alanine and leucine decreased significantly from means of 0.91 (SD 0.21) to 0.62 (SD 0.14) mg · kg^–1 · min^–1 and from 0.40 (SD 0.05) to 0.32(SD 0.04) mg · kg^–1 · min^–1, respectively. The mean free fatty acid concentration increased significantly from 0.65 (SD 0.33) to 1.27 (SD 0.45) mmol · l^–1 during the endurance trial. The increase of glucose turnover and the decrease of amino acid flux point to a metabolic shift towards enhanced utilization of free fatty acids. Adrenaline and noradrenaline concentrations showed a moderate but significant increase from means of 0.61 (SD 0.20) to 0.99 (SD 0.36) nmol · l^–1 and from 2.27 (SD 0.75) to 3.46 (SD 0.38) nmol · 1^–1, respectively. The number of high affinity -adrenergic binding sites per cell (-adrenoceptors) nearly doubled from 770 (SD 130) to 1490 (SD 150) during 90 min of cycling. The observed endogenous plasma catecholamine concentrations were not sufficient to change significantly the relative receptor occupancy. This would seem to indicate that the aerobic exercise induced effects depended more on the absolute number of occupied -adrenoceptors than on their relative receptor occupancy. When compared to the results of the adrenaline infusion experiment the increases of the hepatic glucose production and the increase of -adrenoceptors were very similar in both groups despite ten times higher adrenaline plasma concentrations in the infusion group. This would seem to indicate that -adrenoceptors mediated effects do not correlate with catecholamine plasma concentrations.     

Capillary-venous differences of free plasma catecholamines at rest and during graded exercise

Summary Levels of free plasma catecholamines were simultaneously determined in 10 cyclists using capillary blood from one ear lobe and venous blood from one cubital vein. Catecholamine concentrations were higher in the ear lobe blood than in the venous blood at rest and during graded exercise. Average differences amounted to 1.7 nmol · l^–1 (dopamine), 2.1 nmol · l^–1 (noradrenaline) and 1.9 nmol · l^–1 (adrenaline) at rest and increased only to 8.8 nmol · l^–1 for noradrenaline during exercise. We assume that higher concentrations of dopamine and adrenaline in the capillary blood point to a significant neuronal release of these catecholamines, similar to noradrenaline. Catecholamine concentrations in capillary blood may better reflect sympathetic drive and delivery of catecholamines to the circulation than the concentrations in venous blood.Supported by Bundesinstitut für Sportwissenschaften, Köln-Lövenich, FRG     

Threshold increases in plasma growth hormone in relation to plasma catecholamine and blood lactate concentrations during progressive exercise in endurance-trained athletes

Plasma human growth hormone ([HGH]), adrenaline ([A]), noradrenaline ([NA]) and blood lactate ([La^–]_b) concentrations were measured during progressive, multistage exercise on a cycle ergometer in 12 endurance-trained athletes [aged 32.0 (SEM 2.0) years]. Exercise intensities (3 min each) were increased by 50 W until the subjects felt exhausted. Venous blood samples were taken after each intensity. The [HGH] and catecholamine concentrations increased negligibly during exercise of low to moderate intensities revealing an abrupt rise at the load corresponding to the lactate threshold ([La^–]-T). Close correlations (P < 0.001) were found between [La^–]_b and plasma [HGH] (r = 0.64), [A] (r = 0.71) and [NA] (r = 0.81). The mean threshold exercise intensities for [HGH], [A] and [NA], detected by log-log transformation, [154 (SEM 19) W, 162 (SEM 15) W and 160 (SEM 17) W, respectively] were not significantly different from the [La^–]-T [161 (SEM 12) W]. The results indicated that the threshold rise in plasma [HGH] followed the patterns of plasma catecholamine and blood lactate accumulation during progressive exercise in the endurancetrained athletes.     

Glucoregulation and hormonal changes during prolonged exercise in boys and girls

A group of 17 children, 8.5–11 years old, performed a 60-min cycle exercise at 60% of maximal oxygen uptake (VO_2max) 2 h after a standardized breakfast. They were 10 young boys (pubertal stage =1) and 7 young girls (pubertal stage 2) of similarVO_2max (respective values were 48.5 ml min^–1 kg^–1, SEM 1.8; 42.1 ml min^–1 kg^–1, SEM 2.4). Blood samples of 5 ml were withdrawn by heparinized catheter, the subjects being in a supine position, 30 min before the test, then after 0, 15, 30 and 60 min of exercise and following 30 min recovery. Haematocrit was immediately measured. Thereafter plasma was analysed for glucose, non-esterified fatty acid, glycerol, catecholamine (noradrenaline, adrenaline), insulin and glucagon concentrations. This study showed two main results. First, the onset of exercise induced a significant glucose decrease (of about 11,4%) in all the children. Secondly, both the glycaemic and the hormonal responses were obviously different according to the sex. In boys only, the initial glucose drop was significantly correlated to the pre-exercise insulin values. Whatever the time, the glycaemic levels and the catecholamine responses were lower in girls than in boys, whereas the insulin values remained higher. However, none of these two hormonal parameters seemed to be really responsible for the lower glucose values in girls. On the one hand, the great individual variability of noradrenaline and adrenaline and differences in their relative intensity at the end of the exercise between boys and girls might contribute to the lower catecholamine levels in girls. On the other hand, the lack of a significant relationship in girls between the glucose decrease after exercise and the pre-exercise insulin values might be explained by a relative insulin insensitivity concomitant with the earlier growth spurt in girls, as demonstrated in subjects at rest by other authors. Finally the mechanisms of all these gender differences remain to be clarified and might be accounted for by a different maturation level in boys and girls.     

Catecholamines,lymphocyte subsets,and cyclic adenosine monophosphate production in mononuclear cells and CD4+ cells in response to submaximal resistance exercise

We examined the effect of 30 min of submaximal resistance exercise on free and sulphoconjugated plasma catecholamine concentrations determined by high performance (-pressure) liquid chromatography separation, the distribution of circulating lymphocytes quantified by flow cytometry, and isoproterenol induced cyclic adenosine monophosphate (cAMP) production in mononuclear cells (MNL) and CD4⁺ cells. Venous blood samples were taken before, immediately after and 45 min after exercise. Resistance exercise increased free plasma adrenaline (A) and noradrenaline (NA) concentrations, whereas sulphoconjugated catecholamine concentrations remained unchanged. Exercise induced leucocytosis and lymphocytosis was predominantly manifested by an increase in the number of total lymphocytes, monocytes, CD3⁺, CD8⁺ cells and CD3^– CD16/CD56^– cells. Redistribution resulted in a decrease in the CD4^–: CD8⁺ ratio. The total number and distribution of lymphocytes returned to baseline after 45-min rest. An exercise-induced increase in the number of CD3^– CD16/CD56⁺ cells was significantly correlated with the increase in plasma NA (r = 0.66;P = 0.035), indicating a NA dependent process of redistribution. The cAMP-production in MNL was significantly elevated after resistance exercise, when cells were stimulated with 1 mol·1^–1 isoproterenol [pre-exercise 16.5 (SD 3.3); postexercise 21.6 (SD 9.8); 45 min postexercise 10.7 (SD 2.8)]. The cAMP production in CD4⁺ cells was not affected by exercise. Therefore, it is discussed whether redistribution is responsible for the exercise induced increase in cAMP production in MNL.     

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.     

Plasma renin activity,aldosterone and catecholamine levels when swimming and running

Summary The purpose of this study was to determine the response of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and catecholamines to two graded exercises differing by posture. Seven male subjects (19–25 years) performed successively a running rest on a treadmill and a swimming test in a 50-m swimming pool. Each exercise was increased in severity in 5-min steps with intervals of 1 min. Oxygen consumption, heart rate and blood lactate, measured every 5 min, showed a similar progression in energy expenditure until exhaustion, but there was a shorter time to exhaustion in the last step of the running test. PRA, PAC and catecholamines were increased after both types of exercise. The PRA increase was higher after the running test (20.9 ng AngI · ml^–1 · h^–1) than after swimming (8.66 ng AngI · ml^–1 · h^–1). The PAC increase was slightly greater after running (123 pg · ml^–1) than swimming (102 pg · ml^–1), buth the difference was not significant. Plasma catecholamine was higher after the swimming test. These results suggest that the volume shift induced by the supine position and water pressure during swimming decreased the PRA response. The association after swimming compared to running of a decreased PRA and an enhanced catecholamine response rule out a strict dependence of renin release under the effect of plasma catecholamines and is evidence of the major role of neural pathways for renin secretion during physical exercise.     

The hormonal responses to repetitive brief maximal exercise in humans

Summary The responses of nine men and nine women to brief repetitive maximal exercise have been studied. The exercise involved a 6-s sprint on a non-motorised treadmill repeated 10 times with 30 s recovery between each sprint. The total work done during the ten sprints was 37,693±3,956 J by the men and 26,555±4,589 J by the women (M > F,P<0.01). This difference in performance was not associated with higher blood lactate concentrations in the men (13.96± 1.70 mmol·^–1) than the women (13.09±3.04 mmol·l^–1). An 18-fold increase in plasma adrenaline (AD) occurred with the peak concentration observed after five sprints. The peak AD concentration in the men was larger than that seen in the women (9.2 +- 7.3 and 3.7 ± 2.4 nmol · l^–1 respectively,P<0.05). The maximum noradrenaline (NA) concentration occurred after ten sprints in the men (31.6±10.9 nmol·l^–1) and after five sprints in the women (27.4 ± 20.8 nmol · l^–1). Plasma cardiodilatin (CDN) and atrial natriuretic peptide (ANP) concentrations were elevated in response to the exercise. The peak ANP concentration occurred immediately postexercise and the response of the women (10.8 ± 4.5 pmol · l^–1 was greater than that of the men (5.1 ± 2.6 pmol · l^–1,P<0.05). The peak CDN concentrations were 163 ± 61 pmol · l^–1 for the women and 135 ± 61 pmol · l^–1 for the men. No increases in calcitonin gene related peptide (CGRP) were detected in response to the exercise. These results indicate differences between men and women in performance and hormonal responses. There was no evidence for a role of CGRP in the control of the cardiovascular system after brief intermittent maximal exercise.     

The responses of the catecholamines and β-endorphin to brief maximal exercise in man

Summary The responses to brief maximal exercise of 10 male subjects have been studied. During 30 s of exercise on a non-motorised treadmill, the mean power output (mean±SD) was 424.8±41.9 W, peak power 653.3±103.0 W and the distance covered was 167.3±9.7 m. In response to the exercise blood lactate concentrations increased from 0.60±0.26 to 13.46±1.71 mmol·l^–1 (p<0.001) and blood glucose concentrations from 4.25±0.45 to 5.59±0.67 mmol·l^–1 (p<0.001). The severe nature of the exercise is indicated by the fall in blood pH from 7.38±0.02 to 7.16±0.07 (p<0.001) and the estimated decrease in plasma volume of 11.5±3.4% (p<0.001). The plasma catecholamine concentrations increased from 2.2±0.6 to 13.4±6.4 nmol·l^–1 (p<0.001) and 0.2±0.2 to 1.4±0.6 nmol·l^–1 (p<0.001) for noradrenaline (NA) and adrenaline (AD) respectively. The plasma concentration of the opioid-endorphin increased in response to the exercise from <5.0 to 10.2±3.9 p mol·l^–1. The post-exercise AD concentrations correlated with those for lactate as well as with changes in pH and the decrease in plasma volume. Post-exercise-endorphin levels correlated with the peak speed attained during the sprint and the subjects peak power to weight ratio. These results suggest that the increases in plasma adrenaline are related to those factors that reflect the stress of the exercise and the contribution of anaerobic metabolism. In common with other situations that impose stress,-endorphin concentrations are also increased in response to brief maximal exercise.     

Effect of muscle mass on lactate formation during exercise in humans

To elucidate the mechanisms of lactate formation during submaximal exercise, eight men were studied during one- (1-LE) and two-leg (2-LE) exercise (approximately 11-min cycling) using the catheterization technique and muscle biopsies (quadriceps femoris muscle). The absolute exercise intensity and thus the energy demand for the exercising limb was the same [mean 114 (SEM 7) W] during both 1-LE and 2-LE. At the end of exercise partial pressure of O₂ and O₂ saturation in femoral venous blood were lower and arterial adrenaline and noradrenaline were higher during 2-LE than during 1-LE. Mean arterial blood lactate concentration increased to 10.8 (SEM 0.8) (2-LE) and 5.2 (SEM 0.4) mmol · 1^–1 (1-LE) after 10 min of exercise. The intramuscular metabolic response to exercise was attenuated during 1-LE [mean, lactate = 49 (SEM 9); glucose 6-P = 3.3 (SEM 0.3); nicotinamide adenine dinucleotide, reduced = 0.17 (SEM 0.02); adenosine 5-diphosphate 2.7 (SEM 0.1) mmol · kg dry mass^–1] compared to 2-LE [76 (SEM 6); 6.1 (SEM 0.7); 0.21 (SEM 0.02); 3.0 (SEM 0.1) mmol · kg dry mass^–1, respectively]. To elucidate whether the lower plasma adrenaline concentration could contribute to the attenuated metabolic response, additional experiments were performed on four of the eight subjects with infusion of adrenaline during 1-LE (1-LEE). Average plasma adrenaline concentration was increased during 1-LEE and reached 2–4 times higher levels than during 2-LE. Post-exercise muscle lactate and glucose 6-P contents were higher during 1-LEE than during 1-LE and were similar to those during 2-LE. Also, leg lactate release was elevated during 1-LEE versus 1-LE. It was concluded that during submaximal dynamic exercise the intramuscular metabolic response not only depended on the muscle power output, but also on the total muscle mass engaged. Plasma adrenaline concentrations and muscle oxygenation were found to be dependent upon the working muscle mass and both may have affected the metabolic response during exercise.     

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.     

Kinetics of heart rate and catecholamines during exercise in humans

Summary To elucidate the role of factors other than the nervous system in heart rate (f _c) control during exercise, the kinetics off _c and plasma catecholamine concentrations were studied in ten heart transplant recipients during and after 10-min cycle ergometer exercise at 50 W. Thef _c did not increase at the beginning of the exercise for about 60 s. Then in the eight subjects who completed the exercise it increased following an exponential kinetic with a mean time constant of 210 (SEM 22) s. The two other subjects were exhausted after 5 and 8 min of exercise during whichf _c increased linearly. At the cessation of the exercise,f _c remained unchanged for about 50 s and then decreased exponentially with a time constant which was unchanged from that at the beginning of exercise. In the group of eight subjects plasma noradrenaline concentration ([NA]) increased after 30 s to a mean value above resting of 547 (SEM 124) pg · ml^–1, showing a tendency to a plateau, while adrenaline concentration ([A]) did not increase significantly. In the two subjects who became exhausted an almost linear increase in [NA] occurred up to about 1,300 pg · ml^–1 coupled with a significant increase in [A]. During recovery an immediate decrease in [NA] was observed towards resting values. The values of thef _c increase above resting levels determined at the time of blood collection were linearly related with [NA] increments both at the beginning and end of exercise with a similar slope, i.e. about 2.5 beats · min^–1 per 100 pg · ml^–1 of [NA] change. These findings would seem to suggest that in the absence of heart innervation the increase inf _c depends on plasma [NA].     

Effects of hydration state on plasma testosterone,cortisol and catecholamine concentrations before and during mild exercise at elevated temperature

This investigation examined the influence of pre-exercise hydration status, and water intake during low intensity exercise (5.6 km · h^–1 at 5% gradient) in the heat (33° C), on plasma testosterone (TEST), cortisol (CORT), adrenaline (A), and noradrenaline (NA) concentrations at baseline (BL), pre-exercise (PRE), and immediately (IP), 24 h (24 P), and 48 h postexercise (48 P). Ten active men participated in four experimental treatments. These treatments differed in preexercise hydration status [euhydrated or hypohydrated (HY, –3.8 (SD 0.7)% body mass)] and water intake during exercise (water ad libitum or no water intake during exercise, NW). There were no significant changes in TEST, CORT, or A concentrations with time (BL, PRE, IP, 24 P, and 48 P), or among treatments. However, significant increases from BL and PRE plasma NA concentrations were observed at IP during all four treatment conditions. In addition, HY + NW resulted in significantly higher plasma NA concentrations at IP compared to all other treatments. These results suggest that moderate levels of hypohydration during prolonged, low intensity exercise in the heat do not influence plasma TEST, CORT, or A concentrations. However, plasma NA appears to respond in a sensitive manner to these hydration and exercise stresses.     

Atrial natriuretic peptide in plasma after prolonged physical strain,energy deficiency and sleep deprivation

Summary Plasma concentrations of atrial natriuretic peptide (ANP) were investigated daily in 16 male cadets during a 6-day military training course with continuous heavy physical activities, sleep and energy deficiency (course 1). At the end of another similar course (course 11) 15 cadets were studied during 30-min cycle exercise at 50% maximal oxygen uptake with and without glucose infusion. A small, but not significant increase was found in the plasma concentrations of ANP during course I from 9.6 (SEM 1.1) pmol·l^–1 in the control experiment to 11.1 (SEM 0.5) pmol·l^–1 on day 5. During course II a small but significant increase was found from 7.8 (SEM 0.5) pmol·l^–1 in the control experiment to 9.1 (SEM 0.5) pmol·l^–1 at the end of the course. Plasma osmolality and chloride concentration decreased during the course. During the exercise test a significant increase was seen in ANP concentration from 8.2 (SEM 0.8) to 13.1 (SEM 2.0) pmol·l^–1 in the control experiment and from 9.4 (SEM 0.7) to 13.5 (SEM 1.2) pmol·l^–1 during the course. This response was attenuated by glucose infusion, an effect which may have been due to an exercise induced increase in plasma chloride concentration being abolished. In contrast, the potassium concentration response to exercise was increased during the course but unaffected by glucose infusion. In conclusion, the large increases in endogenous plasma catecholamine concentration shown to take place during previous courses were not reflected in the plasma concentrations of ANP, indicating only a moderate cardiac stress or no cardiac work overload during such courses.     

The effect of glycogen availability on power output and the metabolic response to repeated bouts of maximal,isokinetic exercise in man

The relationship of glycogen availability to performance and blood metabolite accumulation during repeated bouts of maximal exercise was examined in 11 healthy males. Subjects performed four bouts of 30 s maximal, isokinetic cycling exercise at 100 rev · min^–1, each bout being separated by 4 min of recovery. Four days later, all subjects cycled intermittently to exhaustion [mean (SEM) 106 (6) min] at 75% maximum oxygen uptake Subjects were then randomly assigned to an isoenergetic low-carbohydrate (CHO) diet [7.8 (0.6)% total energy intake,n = 6] or an isoenergetic high-CHO diet [81.5 (0.4)%,n = 5], for 3 days. On the following day, all subjects performed 30 min cycling at 75% and, after an interval of 2 h, repeated the four bouts of 30 s maximal exercise. No difference was seen when comparing total work production during each bout of exercise before and after a high-CHO diet. After a low-CHO diet, total work decreased from 449 (20) to 408 (31) J · kg^–1 body mass in bout 1 (P < 0.05), from 372 (15) to 340 (18) J · kg^–1 body mass in bout 2 (P < 0.05), and from 319 (12) to 306 (16) J · kg^t-1 body mass in bout 3 (P < 0.05), but was unchanged in bout 4. Blood lactate and plasma ammonia accumulation during maximal exercise was lower after a low-CHO diet (P < 0.001), but unchanged after a high-CHO diet. In conclusion, muscle glycogen depletion impaired performance during the initial three, but not a fourth bout of maximal, isokinetic cycling exercise. Irrespective of glycogen availability, prolonged submaximal exercise appeared to have no direct effect on subsequent maximal exercise performance.     

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.