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.     

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.     

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.     

Plasma testosterone and catecholamine responses to physical exercise of different intensities in men

Summary Plasma testosterone, noradrenaline, and adrenaline concentrations during three bicycle ergometer tests of the same total work output (2160 J·kg^–1) but different intensity and duration were measured in healthy male subjects. Tests A and B consisted of three consecutive exercise bouts, lasting 6 min each, of either increasing (1.5, 2.0, 2.5 W·kg^–1) or constant (2.0, 2.0, 2.0 W·kg^–1) work loads, respectively. In test C the subjects performed two exercise bouts each lasting 4.5 min, with work loads of 4.0 W·kg^–1. All the exercise bouts were separated by 1-min periods of rest.Exercise B of constant low intensity resulted only in a small increase in plasma noradrenaline concentration. Exercise A of graded intensity caused an increase in both catecholamine levels, whereas, during the most intensive exercise C, significant elevations in plasma noradrenaline, adrenaline and testosterone concentrations occurred. A significant positive correlation was obtained between the mean value of plasma testosterone and that of adrenaline as well as noradrenaline during exercise.It is concluded that both plasma testosterone and catecholamine responses to physical effort depend more on work intensity than on work duration or total work output.This work was performed within the Scientific Exchange Programme between the Institute of Experimental Endocrinology, Slovak Academy of Sciences in Bratislava and Medical Research Centre, Polish Academy of Sciences, Warsaw/Project 10.4/     

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.     

Influence of moderate cold exposure on blood lactate during incremental exercise

Summary This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30°C or at 10°C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO₂) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la^–]_b. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, la} ^– Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°C [8.64 (SEM 2.37) nmol·l^–1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la^–]_b observed for submaximal high intensities during severe cold exposure.     

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.     

Endogenous opioids may modulate catecholamine secretion during high intensity exercise

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake ( O_2max)], nine fit men [mean (SE) ( O_2max, 63.9 (1.7) ml · kg^–1 · min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol · l^–1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol · l^–1 and 24 (2.2) versus 20 (1.7) nmol · · l^–1 respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol · l^–1 and 6.9 (1.1) versus 5.3 (0.9) mmol · l^–1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.     

Effect of the intensity of training on catecholamine responses to supramaximal exercise in endurance-trained men

In this study we investigated whether plasma catecholamine responses to the Wingate test are affected by the intensity of training in endurance-trained subjects. To do this we compared plasma adrenaline (A) and noradrenaline (NA) concentrations in response to a Wingate test in three different groups: specialist middle-distance runners (MDR) in 800-m and 1,500-m races, specialist long-distance runners (LDR) 5,000-m and 10,000-m races, and untrained subjects (UT). The maximal power (W _max) and the mean power (W) were determined from the Wingate test. Blood lactate (La), plasma A and NA concentrations were analysed at rest (La₀, A₀ and NA₀), immediately at the end of the exercise (A_max and NA_max) and after 5 min recovery (La_max, A₅ and NA₅). The ratio A_max/NA_max was considered as an index of the adrenal medulla responsiveness to the sympathetic nervous activity. At the end of the test, W _max and W were similar in the three groups but La_max was significantly greater in MDR compared to LDR and UT [15.2 (2.2) mmol l^–1, 11.7 (3.1) mmol l^–1, 11.6 (1.6) mmol l^–1, respectively, for MDR, LDR and UT; mean (SD)]. Concerning the plasma catecholamine concentrations in response to exercise, MDR and LDR A_max values [3.73 (1.53) nmol l^–1, 3.47 (0.74) nmol l^–1, respectively, for MDR and LDR] were significantly greater than those of UT [1.48 (0.32) nmol l^–1] who also exhibited the lowest NA_max values [11.09 (6.58) nmol l^–1] compared to MDR and LDR [20.43 (3.51) nmol l^–1; 15.85 (4.88) nmol l^–1, respectively, for MDR and LDR]. However, no significant differences were observed between the two trained groups either for A_max or NA_max. These results suggest that long-term endurance training can enhance plasma catecholamine concentrations in response to supramaximal exercise. However, as there were no significant differences between MDR and LDR A_max and NA_max values, the effect of the intensity of training remains to be clarified.     

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.     

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.     

Glucocorticoid response to exercise as measured by serum and salivary cortisol

Summary Serum and salivary cortisol concentrations were studied in 78 elite athletes engaged in different sports, by subjecting them to high-intensity laboratory exercise. The mean difference in the pre-exercise cortisol concentrations in the seven groups studied were more marked in serum (from 311 to 768 nmol · l^–1) than in saliva (from 17.9 to 22.7 nmol · 1^–1, only one group reaching 40 nmol ·^–1). Judging from the correlation coefficients based on total variances, the post-/pre-exercise differences in cortisol concentrations in serum depended chiefly on pre-exercise values, while those in saliva tended to depend more on the postexercise concentrations. The coefficients of correlation between that difference and either the pre- or postexercise values were –0.71 and 0.47, respectively, for serum, and –0.51 and 0.58, respectively, for saliva. This would suggest that salivary cortisol concentration might be a more suitable variable for assessing glucocorticoid activity in exercise than serum cortisol concentration, probably being less sensitive to pre-exercise emotional state.     

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.     

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.     

The acute effect of 30 min of moderate exercise on high density lipoprotein cholesterol in untrained middle-aged men

Summary Fifteen middle-aged, untrained (defined as no regular exercise) men (mean age 49.9 years, range 42–67) cycled on a cycle ergometer at 50 rpm for 30 min at an intensity producing 60% predicted maximum heart rate [(f _c,max), wheref _{c, max} = 220 - age]. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (Tg) concentrations were measured from fasting fingertip capillary blood samples collected at rest, after 15 and 30 min of exercise, and at 15 min post-exercise. The mean HDL-C level increased significantly from the resting level of 0.85 mmol · l^–1 to 0.97 mmol · 1^–1 (P<0.05) after 15 min of exercise, increased further to 1.08 mmol · 1^–1 (P<0.01) after 30 min of exercise and remained elevated at 1.07 mmol · 1^–1 (P<0.01) at 15 min post-exercise. These increases represented changes above the mean resting level of 14.1%, 27.1% and 25.9% respectively. The HDL-C/LDL-C ratio increased significantly from a resting ratio of 0.20 to 0.26 after 30 min of exercise (P < 0.01) and to 0.24 at 15 min post-exercise (P<0.05). The mean Tg level increased significantly from a resting level of 0.88 mmol · 1^–1 to 1.05 mmol · 1^–1 after 15 min, and to 1.06 mmol · I^–1 after 30 min of exercise (P<0.05 at each time). The TC/HDL-C ratio decreased significantly (P=0.05) after 30 min of exercise and at 15 min post-exercise by 18.8% and 14%, respectively. No significant changes were observed in the levels of TC or LDL-C over time. These results indicate that 30 min of moderate exercise elicits significant changes in HDL-C concentration during and up to 15 min after the exercise in untrained middle-aged men with low mean resting levels of HDL-C (0.85 mmol · 1^–1).     

The influence of blood sampling site on lactate concentration during submaximal exercise at 4 mmol · 1−1 lactate level

This study examined lactate concentration during incremental and submaximal treadmill exercise at work rates corresponding to 4 mmol· 1^–1 lactate concentration, determined by fingertip (OBLAI) and venous blood (OBLA2). Initially, eight subjects performed a 4-min incremental exercise test until exhaustion. On two other occasions, seven of the subjects undertook submaximal exercise tests (30 min) at work rates corresponding to OBLA1 and OBLA2. Blood was simultaneously obtained from both sites at rest and at the end of each exercise stage during the incremental exercise, and at 5, 10, 20 and 30 min during the submaximal exercise and 5 min into recovery. Fingertip blood lactate concentrations were significantly higher (P<0.05) than venous blood at rest, throughout the incremental exercise, consistently during exercise at OBLA1 and OBLA2, and into recovery. Data also revealed an exercise intensity-dependent lactate difference between the two sampling sites during both exercise protocols. Exercise at OBLA1 did not result in a progressive increase in lactate level nor exhaustion, and the lactate value at the end of 30 min corresponded to the predetermined value. However, exercise at OBLA2 resulted in a significantly higher (P<0.05) lactate level than OBLA1, the lactate concentration at the end of 30 min was substantially higher than the predetermined value (P<0.05) and exhaustion was evident. It is concluded that the lactate concentration value during incremental and submaximal exercise (at 4 mmol·l^–1 OBLA) is dependent on the blood sampling site. This finding should be considered in studies concerned with the determination of OBLA.     

Circulating leucocyte subpopulations in sedentary subjects following graded maximal exercise with hypoxia

Summary Ten healthy sedentary subjects [age, 27.5 (SD 3.5) years; height, 180 (SD 5) cm; mass, 69.3 (SD 6.3) kg] performed two periods of maximal incremental graded cycle ergometer exercise in a supine position. Randomly ordered and using an open spirometric system, one exercise was carried out during normoxia [maximal oxygen consumption ( O_2max)=38.6 (SD 3.5) ml·min^–1·kg^–1; maximal blood lactate concentration, 9.86 (SD 1.85) mmol·l^–1; test duration, 22.6 (SD 2.7) min], the other during hypoxia [ O_2max=33.2 (SD 3.2) ml·min^–1· kg^–1; maximal blood lactate concentration, 10.38 (SD 2.02) mmol·l^–1; test duration, 19.7 (SD 2.8) min]. At rest, immediately (0 p) and 60 min (60 p) after exercise, counts of leucocyte subpopulations (flow cytometry), cortisol and catecholamine concentrations were determined. At 0 p in contrast to normoxia, during hypoxia there was no significant increase of granulocytes. There were no significant differences between normoxia and hypoxia in the increases from rest to 0 p in counts of monocytes, total lymphocytes and lymphocyte subpopulations [clusters of differentiation (CD), CD3⁺, CD4⁺CD45RO^–, CD4⁺CD45RO⁺, CD8⁺CD45RO^–, CD8⁺CD45RO⁺, CD3⁺HLA-DR⁺, CD3^–CD16/CD56⁺, CD3⁺CD16/CD56⁺, CD 19⁺] as well as adrenaline, noradrenaline and cortisol concentrations. The counts of CD3 ^–CD16/CD56⁺-and CD8 ⁺CD45RO⁺-cells increased most. At 60 p, CD3^–CD16/CD56⁺ and CD3⁺CD16/CD56⁺-cell counts were below pre-exercise levels and under hypoxia slightly but significantly lower than under normoxia. We concluded that the exercise-induced mobilization and redistribution of most leucocyte and lymphocyte subpopulations were unimpaired under acute hypoxia at sea level. Reduced increases of granulocyte counts during the study and reduced cell numbers of natural killer cells and cytotoxic, not major histocompatibility complex-restricted T-cells, only indicated marginal effects on the immune system.     

Physiological changes and gastro-intestinal symptoms as a result of ultra-endurance running

Summary One hundred and seventy-two competitors of the Swiss Alpine Marathon, Davos, Switzerland, 1988, volunteered for this research project. of these volunteers 170 (158 men, 12 women) finished the race (99%). The race length was 67 km with an altitude difference of 1,900 m between the highest and lowest points. Mean age was 39 (SEM 0.8) years. Average finishing times were 8 h 18 min (men) and 8 h 56 min (women). Loss of body mass averaged 3.4% body mass [mean 3.3 (SEM 0.2)%; 4.0 (SEM 0.4)%; men and women, respectively]. Blood samples from a subgroup of 89 subjects (6 women and 83 men) were taken prior to and immediately after completion of the race. Changes in haemoglobin (9.3 mmol·l^–1 pre-race, 9.7 mmol·l^–1 post-race) and packed cell volume (0.44 pre, 0.48 post-race) were in line with the moderate level of dehydration displayed by changes in body mass. Mean plasma volume decreased by 8.3%. No significant changes in plasma osmolality, sodium, or chloride were observed but plasma potassium did increase by 5% (4.2 mmol·l^–1 pre-race, 4.4 mmol·l^–1 post-race). Mean fluid consumption was 3290 (SEM 103) ml. Forty-three percent of all subjects, and 33% of those who gave blood samples, complained of gastro-intestinal (GI) distress during the race. No direct relationship was found between the quantity or quality of beverage consumed and the prevalence of GI symptoms. The circulating concentration of several GI hormones was measured and several were found to be significantly elevated (P<0.05) after the race [mean values: gastrin 159.6 (SEM 17.8) ng·l^–1; vaso-active intestinal peptide 224.3 (SEM 20.1) ng·l^–1; peptide histidine isoleucine 311.1 (SEM 27.5) ng·l^–1 ; motilin 214.1 (SEM 15.1) ng·l^–1] but larger increases were not found to be significantly correlated with GI symptoms. Plasma cortisol, adrenaline, and noradrenaline concentrations were significantly higher after the race compared to resting values (P<0.05). There was a trend for post-race noradrenaline values to be lower in sufferers of GI disturbance. The post-race plasma noradrenaline concentration was significantly lower specifically in those runners with intestinal cramps. Also, the resting plasma cortisol concentration was significantly lower in those individuals who developed intestinal cramps during the race. Plasma creatine phosphokinase, alanine aminotransferase and aspartate aminotransferase activities were increased following the race, which may indicate that there was tissue damage. An increase in plasma potassium concentration was observed after the race in individuals with GI complaints [0.29 (SEM 0.07) mmol·l^–1 increase], whereas no increase was observed in individuals without GI symptoms. An inability of the Na⁺-K⁺ pump to keep pace with the needs of skeletal muscle (as well in the intestinal tract) may have accounted for the high plasma potassium values immediately following exercise and may have played a role in the development of GI disorders. However, many other sources of K⁺ release may have accounted for the elevated plasma K⁺ (skeletal muscle, liver and red blood cells) in such sufferers and the correlation between the increase in K⁺ and GI symptoms may be an indirect one.     

Immediate physiological responses of healthy volunteers to different types of music: cardiovascular,hormonal and mental changes

A group of 20 healthy volunteers [10 women, 10 men; median age 25 (20–33) years] were examined by means of pulsed wave Doppler echocardiography, blood sample analysis and psychological testing before and after listening to three different examples of music: a waltz by J. Strauss, a modern classic by H. W. Henze, and meditative music by R. Shankar. To assess small haemodynamic changes, mitral flow, which reflects left ventricular diastolic behaviour, was measured by Doppler ultrasound. Heart rate, arterial blood pressure and plasma concentrations of adrenocorticotropic hormone, cortisol, prolactin, adrenaline, noradrenaline, atrial natriuretic peptide (ANP) and tissue plasminogen activator (t-PA) were determined simultaneously. Transmitral flow profile is characterized by early E-wave and late atrial induced A-wave. Velocity-time integrals were measured and the atrial filling fraction was calculated. The mental state was measured by using a psychological score (Zerssen) with low values (minimum 0) for enthusiastic and high values (maximum 56) for depressive patterns. Music by J. Strauss resulted in an increase of atrial filling fraction (AFF; 29% vs 26%;P<0.05) and ANP (63 pg·ml^–1 vs 60 pg·ml^–1;P<0.05). The mental state was improved (Zerssen: 6.5 vs 11 points;P<0.05). After the music of H. W. Henze prolactin values were lowered (7.7 ng·ml^–1 vs 9.1 ng·ml^–1;P<0.01). The music of R. Shankar led to a decrease of cortisol concentrations (57 ng·ml^–1 vs 65 ng·ml^–1;P<0.001), noradrenaline concentrations (209 g·l^–1 vs 256 g·l^–1;P<0.01) andt-PAantigen concentrations (1.1 ng·ml^–1 vs 1.4 ng·ml^–1;P<0.05). Heart rate and blood pressure remained unchanged during the whole experiment. We concluded that different types of music induced changes of left ventricular diastolic function and plasma hormone concentrations. After rhythmic music (Strauss) AFF and ANP increased significantly, the mental state being improved. Meditative music (Shankar) lowered plasma cortisol, noradrenaline and t-PA concentrations; the observed increase of early left ventricular filling was not statistically significant. Prolactin concentrations decreased after modern music (Henze). Thus, it would seem to be possible to detect cardiovascular changes following different types of music by Doppler ultrasound and hormone analysis, meditative music having promising therapeutic implications in the treatment of conditions of stress.This paper contains data from J. Vollert's work for his doctoral degree.     

Modulation of low calcium induced field bursts in the hippocampus by monoamines and cholinomimetics

The influence of monoamine transmitter candidates, acetylcholine and related substances on rhythmic depolarization shifts (field bursts) in the CA1 area of hippocampal slices from rats in low calcium (0.2 mmol·l^–1) high magnesium (4 mmol·l^–1) was investigated. Acetylcholine (ACh), histamine (HA) and H₂-agonists, noradrenaline (NA) and beta-agonists at nano- to micromolar concentrations as well as dopamine (DA) and 8-bromo-cyclic AMP at 100 mol·l^–1 accelerated the field bursts. H₂-antagonists blocked HA actions, beta-antagonists blocked NA actions selectively; muscarinic antagonists blocked ACh, HA and NA actions. H₁-agonists, serotonin, dopamine and adenosine slowed the field bursts at micromolar concentrations. These effects parallel the action of the tested substances on afterhyperpolarizations in CA 1 pyramidal cells. High sensitivity and specificity make this response of the field bursts an excellent model to study postsynaptic transmitter actions in the central nervous system.