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.     

Diurnal variations of serum erythropoietin in trained and untrained subjects

The diurnal variations of serum-erythropoietin concentration ([s-EPO]) were investigated in six physically trained (T) and eight untrained (UT) men. The T subjects had a higher mean maximal oxygen uptake than UT subjects [75.7 (SEM 1.6) ml · min^–1 · kg^–1 versus 48.3 (SEM 1.4) ml · min^–1 · kg^–1, P < 0.0001] and a lower mean body mass index [BMI, 21.7 (SEM 0.7) kg · m^–2 versus 24.4 (SEM 0.6) kg · m^–2, P=0.02]. Each subject was followed individually for 24 h as they performed their normal daily activities. Venous blood samples were collected from awakening (0 min) until the end of the 24-h period (1440 min). Both T and UT had a nadir of [s-EPO] 120 min after awakening [10.0 (SEM 0.3) U · 1^–1 versus 11.5 (SEM 2.1) U · 1^–1, P > 0.05]. The UT and T increased their [s-EPO] to peak values at 960 min and 960–1200 min, respectively (ANOVA P=0.03) after awakening [UT: 18.4 (SEM 2.8) U · l^–1; T: 16.2 (SEM 2.5) U · l^–1, P > 0.05]. The mean 24-h [s-EPO] were 14.5 (SEM 1.0) U · l^–1 and 14.9 (SEM 0.9) U · l^–1 in T and UT, respectively (P > 0.05). The individual mean 24-h [s-EPO] were not correlated to body mass, BMI or maximal oxygen uptaken. Significant diurnal variations in [s-EPO] occurred in these healthy subjects irrespective of their levels of physical activity.     

Caffeine increases maximal anaerobic power and blood lactate concentration

Summary The aim of this study was to specify the effects of caffeine on maximal anaerobic power (W _max). A group of 14 subjects ingested caffeine (250 mg) or placebo in random double-blind order. TheW _max was determined using a force-velocity exercise test. In addition, we measured blood lactate concentration for each load at the end of pedalling and after 5 min of recovery. We observed that caffeine increasedW _max [964 (SEM 65.77) W with caffeine vs 903.7 (SEM 52.62) W with placebo;P<0.02] and blood lactate concentration both at the end of pedalling [8.36 (SEM 0.95) mmol · l^–1 with caffeine vs 7.17 (SEM 0.53) mmol · l^–1 with placebo;P<0.011 and after 5 min of recovery [10.23 (SEM 0.97) mmol · l^–1 with caffeine vs 8.35 (SEM 0.66) mmol · l^–1 with placebo;P<0.04]. The quotient lactate concentration/power (mmol · l^–1 · W^–1) also increased with caffeine at the end of pedalling [7.6 · 10^–3 (SEM 3.82 · 10^–5) vs 6.85 · 10^–3 (SEM 3.01 · 10^–5);P<0.01] and after 5 min of recovery [9.82·10^–3 (SEM 4.28 · 10^–5) vs 8.84 · 10^–3 (SEM 3.58 · 10^–5);P<0.02]. We concluded that caffeine increased bothW _max and blood lactate concentration.     

The effect of short and long duration exercise on serum erythropoietin concentrations

Summary The effects of short and long duration exercise on serum erythropoietin concentrations [EPO]_s were studied in seven male cross-country skiers of national team standard and eight male marathon runners, respectively. The short duration exercise was performed as 60 min of cycling at an intensity of 80%–95% of maximal heart rate. Arterial blood oxygen saturations monitored by pulse-oximetry remained unchanged throughout exercise. The partial pressure of O₂ at which haemoglobin was half-saturated with O₂ calculated from forearm venous blood gas tension and blood O₂ saturation, and the erythrocyte 2,3-diphosphoglycerate did not change significantly during the exercise. Blood lactate concentrations were increased at the end of exercise [from 1.3 (SEM 0.1) to 3.6 (SEM 0.3) mmol · 1^–1]. The [EPO]_s determined (by enzyme-linked immunosorbent assay) pre-exercise, 5 min, 6 h, 19 h, and 30 h after the exercise were unchanged [from 16.1 (SEM 2.6) to 19.1 (SEM 3.2), 17.9 (SEM 3.0), 17.0 (SEM 2.5), and 18.6 (SEM 2.9) U·l^–1, respectively]. The [EPO]_s were not correlated to the earlier parameters. The long duration exercise consisted of habitual training, a 3 week break from training followed by 2 and 4 weeks of re-training. The [EPO]_s, body fat (BF), and serum free-testosterone concentrations determined at the end of each period remained unchanged. The maximal oxygen uptakes were decreased after the break from training and increased during retraining (P=0.04). Body mass (m _b) increased after the break in training (P=0.02). The [EPO]_s were correlated to BF,r=0.42,P=0.02;m _b,r=0.45,P=0.01; and free-testosterone concentrations,r=0.44,P=0.01. Thus, short and long-duration exercise had no direct influence on [EPO]_s; but relationships among [EPO]_s, free-testosterone concentrations and body composition were noted.     

Does functional alteration of the gonadotropic axis occur in endurance trained athletes during and after exercise?

In men, the hypothalamic-pituitary-testicular axis controls the secretion of testosterone which, in this sex, is a major anabolic hormone. Physical exercise modulates testosterone concentration, affecting the whole axis by poorly understood mechanisms. We have reported in this preliminary study the short and longterm effects of exercise on the function of the gonadotropic axis in trained compared to untrained subjects. Environmental factors known to interfere with pituitary function were minimized. Four marathon and four sedentary men, were studied during 5 days successively using different combinations of two factors: duration and intensity of running tests. Day 0 (DO) was a rest day, and the exercises were: D1 and D2 brief (20 min), light (50% maximal heart rate, HR_max, D1) or intense (80% HR_max, D2), D3 and D4 prolonged (120 min) and light (50% HR_max, D3) or intense (80% HR_max, D4). Testosterone (free and total) and luteinizing hormone (LH) concentrations were measured before, during and after exercise. The baseline concentrations of plasma testosterone were lower in the long distance runners than in the sedentary group [41.8 (SEM 5.5) vs 64.5 (SEM 7.9) pmol · 1^–1, respectively;P < 0.05]. This phenomenon was centrally mediated as LH concentration was apparentlyinappropriately low [3.4 (SEM 0.4) vs 4.3 (SEM 1.0) UI · 1^–1;P > 0.05]. Light to moderate exercise did not modify testosterone and LH concentrations. Conversely, intense and prolonged exercise increased testosterone concentration [73.2 (SEM 9.0) vs 92 (SEM 11.0) pmol · 1^–1 in the long distance runners and sedentary group, respectively;P < 0.05] and lowered LH concentrations [2.1 (SEM 0.3) vs 3.4 (SEM 0.3) UI · 1^–1 in the long distance runners and sedentary group, respectively;P <0.05 compared to DO, at the same time]. In our conditions of exercise, negative feedback of testosterone upon LH persisted, as positive feedback of low testosterone concentrations was apparently lacking (inappropriately low LH concentration with regard to low basal testosterone concentration).     

Effect of physical training on the responses of serum adrenocorticotropic hormone during prolonged exhausting exercise

Summary The purpose of this study was to investigate the effects of physical training on the responses of serum adrenocorticotropic hormone (ACTH) and cortisol concentration during low-intensity prolonged exercise. Five subjects who had fasted for 12 h cycled at the same absolute intensity that elicited 50% of pre-training maximal oxygen uptake ( O_2max), either until exhaustion or for up to 3 h, before and after 7 weeks of vigorous physical training [mean daily energy consumption during training exercise, 531 kcal (2230 kJ)]. In the pre-training test, serum ACTH and cortisol concentrations did not increase during the early part of the exercise. Increases in concentrations of both hormones occurred in all subjects when blood glucose concentration decreased during the later phase of the exercise. The mean values and SEM of serum ACTH and cortisol concentrations at the end of the exercise were 356 ng · l^–1, SEM 79 and 438 g · l^–1, SEM 36, respectively. After the physical training, O_2max of the subjects improved significantly from the mean value of 50.2 ml · kg^–1 · min^–1, SEM 2.5 to 57.3 ml · kg^–1 · min^–1, SEM 2.0 (P < 0.05). In the post-training test, exercise time to exhaustion was prolonged in three subjects. Comparing the pre- and post training values observed after the same length of time that the subjects had exercised in the pre-training test, the post-training values of serum ACTH (44 ng · l^–1, SEM 3) and cortisol (167 g · l^–1, SEM 30) concentration were less than the pre-training value (P < 0.05). However, after the subjects stopped exercising in the post-training test, the serum ACTH (214 ng · l^–1, SEM 49) and cortisol (275 g · l^–1, SEM 50) concentrations were not significantly different from those measured after the subjects stopped exercising in the pre-training test (P > 0.10). In conclusion, high-intensity physical training reduced the responses of both hormones during prolonged exercise, propbably because of a delayed decrease of blood glucose concentration after physical training, while the level of the blood glucose concentration which induces ACTH and cortisol secretion did not change.     

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.     

Physiological responses to maximal intensity intermittent exercise

Summary Physiological responses to repeated bouts of short duration maximal-intensity exercise were evaluated. Seven male subjects performed three exercise protocols, on separate days, with either 15 (S₁₅), 30 (S₃₀) or 40 (S₄₀) m sprints repeated every 30 s. Plasma hypoxanthine (HX) and uric acid (UA), and blood lactate concentrations were evaluated pre- and postexercise. Oxygen uptake was measured immediately after the last sprint in each protocol. Sprint times were recorded to analyse changes in performance over the trials. Mean plasma concentrations of HX and UA increased during S₃₀ and S₄₀ (P<0.05), HX increasing from 2.9 (SEM 1.0) and 4.1 (SEM 0.9), to 25.4 (SEM 7.8) and 42.7 (SEM 7.5) µmol · l^–1, and UA from 372.8 (SEM 19) and 382.8 (SEM 26), to 458.7 (SEM 40) and 534.6 (SEM 37) µmol · l^–1, respectively. Postexercise blood lactate concentrations were higher than pretest values in all three protocols (P<0.05), increasing to 6.8 (SEM 1.5), 13.9 (SEM 1.7) and 16.8 (SEM 1.1) mmol · l^–1 in S₁₅, S₃₀ and S₄₀, respectively. There was no significant difference between oxygen uptake immediately after S₃₀ [3.2 (SEM 0.1) l · min^–1] and S₄₀ [3.3 (SEM 0.4) l · min^–1], but a lower value [2.6 (SEM 0.1) l · min^–1] was found after S₁₅ (P<0.05). The time of the last sprint [2.63 (SEM 0.04) s] in S₁₅ was not significantly different from that of the first [2.62 (SEM 0.02) s]. However, in S₃₀ and S₄₀ sprint times increased from 4.46 (SEM 0.04) and 5.61 (SEM 0.07) s (first) to 4.66 (SEM 0.05) and 6.19 (SEM 0.09) s (last), respectively (P<0.05). These data showed that with a fixed 30-s intervening rest period, physiological and performance responses to repeated sprints were markedly influenced by sprint distance. While 15-m-sprints could be repeated every 30 s without decreases in performance, 40-m sprint times increased after the third sprint (P<0.05) and this exercise pattern was associated with a net loss to the adenine nucleotide pool.     

Post-exercise rehydration in man: effects of electrolyte addition to ingested fluids

This study examined the effects on water balance of adding electrolytes to fluids ingested after exercise-induced dehydration. Eight healthy male volunteers were dehydrated by approximately 2% of body mass by intermittent cycle exercise. Over a 30-min period after exercise, subjects ingested one of the four test drinks of a volume equivalent to their body mass loss. Drink A was a 90 mmol·l^–1 glucose solution; drink B contained 60 mmol·l^–1 sodium chloride; drink C contained 25 mmol·l^–1 potassium chloride; drink D contained 90 mmol·l^–1 glucose, 60 mmol·l^–1 sodium chloride and 25 mmol·l^–1 potassium chloride. Treatment order was randomised. Blood and urine samples were obtained at intervals throughout the study; subjects remained fasted throughout. Plasma volume increased to the same extent after the rehydration period on all treatments. Serum electrolyte (Na⁺, K⁺ and Cl^–) concentrations fell initially after rehydration before returning to their pre-exercise levels. Cumulative urine output was greater after ingestion of drink A than after ingestion of any of the other drinks. On the morning following the trial, subjects were in greater net negative fluid balance [mean (SEM);P<0.02] on trial A [745 (130) ml] than on trials B [405 (51) ml], C [467 (87) ml] or D [407 (34) ml]. There were no differences at any time between the three electrolyte-containing solutions in urine output or net fluid balance. One hour after the end of the rehydration period, urine osmolality had fallen, with a significant treatment effect (P=0.016); urine osmolality was lowest after ingestion of drink A. On the morning after the test, subjects were in greater net negative sodium balance (P<0.001) after trials A and C than after trials B and D. Negative potassium balance was greater (P<0.001) after trials A and B than after C and D. Chloride balance was positive after drink D and a smaller negative balance (P<0.001) was observed after drink B than after A and C. These results suggest that although the measured blood parameters were similar for all trials, better whole body water and electrolyte balance resulted from the ingestion of electrolyte-containing drinks. There appeared, however, to be no additive effect of including both sodium and potassium under the conditions of this experiment.     

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.     

Pathways of phosphate transport in chick jejunum

The effect of vitamin D₃ on intestinal phosphate (P_i) absorption was studied in everted sacs prepared from jejunum of either vitamin D-deficient (–D) or vitamin D-replete (+D) chicks. Vitamin D₃ stimulates the maximal velocity (V _max) of a mucosal active P_i transport mechanism from 125 to 314 nmol·min^–1·g^–1 tissue.K _m of this process remains virtually unchanged (–D: 0.15 mmol·l^–1; + D: 0.18 mmol·l^–1).Active P_i entry into the epithelium depends on extracellular Na⁺. Reduction of buffer Na⁺ reducesV _max in the + D group to 182 nmol·min^–1·g^–1 tissue but has no significant effect in the –D animals (V _max=105 nmol·min^–1·g^–1 tissue). In this group, the predominant effect of Na⁺ substitution is a shift ofK _m to 1.13 mmol·l^–1, whileK _m in the +D group is changed only to 0.53 mmol·l^–1.Transeptithelial P_i transport in the + D group involves the mucosal phosphate pump and hence an intracellular pathway, proceeding at a rate of 48 nmol·min^–1·g^–1 tissue. This is in contrast to –D P_i transfer (8 nmol·l^–1·g^–1 tissue) which is by a diffusional, Na⁺-insensitive, and presumably paracellular pathway.Transepithelial calcium transport (–D: 3.3 nmol·min^–1·g^–1; + D: 7.6 nmol·min^–1·g^–1 tissue) does not require the presence of extracellular Na⁺ and apparently involves pathways different from those of the P_i absorptive system.Presented in part at the Annual Meeting of the Austrian Biochemical Society, Salzburg, September 1978     

Plasma metabolites, volume and electrolytes following 30-s high-intensity exercise in boys and men

It has been shown that boys recover faster than men following brief, high-intensity exercise. Better to understand this difference, plasma metabolite concenration, volume, electrolyte concentration [electrolyte], and hydrogen ion concentration [H⁺] changes were compared in five prepubescent boys [mean age 9.6 (SD 0.9) years] and 5 men [mean age 24.9 (SD 4.3) years] following 30-s, all-out cycling. Blood was collected prior to, at the end, and at the 1st, 3rd and 10th min following exercise. At the 10th min of recovery, the men's lactate concentration was 14.2 (SD 1.8) mmol · l^–1 and [H⁺] was 66.1 (SD 5.9) nmol · l^–1, compared with 5.7 (SD 0.7) mmol · l^–1 and 47.5 (SD 1.2) nmol · l^–1 respectively, in the boys (P < 0.01 for both). The glycerol concentration was higher in the boys at the end of exercise and until the 3rd min of recovery. Plasma volume (PV) decreased more in the men [16.9 (SD 3.0)%] than in the boys [9.4 (SD 2.8)%]. In both groups, [electrolyte] increased after exercise, tending to be higher in the men. Recovery of plasma [electrolyte] and PV started earlier in the boys (1st min) than in the men (3rd min). These findings would support the notion of a lesser reliance on glycolytic energy pathways in children and may explain the faster recovery of muscle power in boys compared to men.     

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.     

Exercise induces pentane production and neutrophil activation in humans. Effect of propranolol

Summary The effect of -adrenergic receptor blockade on exercise-induced lipid peroxidation in man has been examined by measuring the production of pentane in expired air. For this purpose, five healthy male subjects were subjected to dynamic exercise of graded intensity on a cycle ergometer (10 min at 45%, 5 min at 60% and 75% maximal oxygen uptake 1 h after ingestion of either a placebo or 40-mg propranolol. At rest, mean pentane concentration ([pent]) with placebo was 4.13 pmol · l^–1, SD 2.14. After exercise, this value significantly increased by 310% (17.1 pmol · l^–1, SD 7.73, P < 0.01). Oral administration of 40-mg propranolol significantly lowered the mean resting [pent] to 1.75 pmol · l^–1, SD 0.77, P < 0.05. After exercise, the increase of [pent] was much smaller (240%) and was less significant (P < 0.2) than with the placebo. The mechanism of this inhibitory effect of propranolol remains to be elucidated. However, as indicated by the measurement of plasma myeloperoxidase concentration, it can be concluded that the antioxidant property of propranolol cannot be attributed to the inhibition of neutrophil activation, a possible source of free radicals during exercise.     

Exercise and the oxidation and storage of glucose,maize-syrup solids and sucrose determined from breath13CO2

In order to determine which of maize syrup solids, glucose and sucrose were more readily oxidised during exercise and least readily oxidised afterwards, the rates of oxidation of three almost identical isoenergetic solutions of carbohydrates (330 ml of 18.5% w/v solutions of glucose, maize syrup solids and sucrose, 989–1050 kJ total energy) naturally enriched with¹³C were examined at rest and during and after 1 h uphill walking at 75% maximum oxygen uptake ( ) in nine subjects [mean (SEM) , 45.4 (0.9) ml·kg^–1-min^–1]. Rates of production of expired¹³CO₂ were used to estimate rates of oxidation of each exogenous substrate. Energy expenditure and the contributions from total carbohydrate and fat oxidation were calculated from whole-body gas exchange. At rest, aize syrup solids were oxidised less than sucrose during the 1st h [glucose 2.7 (0.2) g · h^–1, maize syrup solids 1.9 (0.3) g · h^–1, sucrose 3.7 (0.2) g · h^–1; maize syrup solids vs sucroseP < 0.01], but this difference disappeared after a further 3 h at rest [glucose 8.3 (0.5) g · h^–1, maize syrup solids 7.7 (0.5) g · h^–1, sucrose 8.1 (0.4) g · h-1]. During exercise, all the carbohydrates were oxidised to the same extent [glucose 23.0 (2.8) g · h^–1, maize syrup solids 23.9 (3.4) g · h^–1, sucrose 27.5 (2.6) g · h^–1) but during 4 h of recovery after exercise, maize syrup solids were oxidised least [glucose 4.6 (0.1) g · h^–1, maize syrup solids 3.7 (0.1) g · h^–1, sucrose 6.4 (0.1) g · h^–1;P < 0.05] suggesting that it may be stored to a greater extent. The results suggest that 18.5% glucose, maize syrup solids and sucrose solutions were equally well oxidised during exercise. During recovery from exercise maize syrup solids were oxidised less than glucose, which in turn was oxidised less than sucrose.     

Diurnal variations of serum erythropoietin at sea level and altitude

This study tested the hypothesis that the diurnal variations of serum-erythropoietin concentration (serum-EPO) observed in normoxia also exist in hypoxia. The study also attempted to investigate the regulation of EPO production during sustained hypoxia. Nine subjects were investigated at sea level and during 4 days at an altitude of 4350 m. Median sea level serum-EPO concentration was 6 (range 6–13) U·l^–1. Serum-EPO concentration increased after 18 and 42 h at altitude, [58 (range 39–240) and 54 (range 36–340) U·l^–1, respectively], and then decreased after 64 and 88 h at altitude [34 (range 18–290) and 31 (range 17–104) U·l^–1, respectively]. These changes of serum-EPO concentration were correlated to the changes in arterial blood oxygen saturation (r = –0.60,P = 0.0009), pH (r = 0.67,P = 0.003), and in-vivo venous blood oxygen half saturation tension (r = –0.68,P = 0.004) but not to the changes in 2, 3 diphosphoglycerate. After 64 h at altitude, six of the nine subjects had down-regulated their serum-EPO concentrations so that median values were three times above those at sea level. These six subjects had significant diurnal variations of serum-EPO concentration at sea level; the nadir occurred between 0800–1600 hours [6 (range 4–13) U·l^–1], and peak concentrations occurred at 0400 hours [9 (range 8–14) U·l^–1,P = 0.02]. After 64 h at altitude, the subjects had significant diurnal variations of serum-EPO concentration; the nadir occurred at 1600 hours [20 (range 16–26) U·l^–1], and peak concentrations occurred at 0400 hours [31 (range 20–38) U·l^–1,P = 0.02]. This study demonstrated diurnal variations of serum-EPO concentration in normoxia and hypoxia, with comparable time courses of median values. The results also suggested that EPO production at altitude is influenced by changes in pH and haemoglobin oxygen affinity.     

Effects of muscarinic blockade on the thermic effect of oral or intravenous carbohydrate

Summary Muscarinic blockade by atropine has been shown to decrease the thermic effect of a mixed meal, but not of intravenous glucose. To further delineate the mechanisms involved in the atropine-induced inhibition of thermogenesis after a meal, plasma substrate and hormone concentrations, energy expenditure (EE) and substrate oxidation rates were measured before and during a continuous glucose infusion (44.4 mol·kg^–1·min^–1) with or without atropine. After 2 h of glucose infusion, a 20-g oral fructose load was administered while the glucose infusion was continued. Plasma insulin concentrations attained a plateau at 596 (SEM 100) pmol·l^–1 after 120 min of glucose infusion and were not affected by muscarinic blockade; plasma glucose concentrations peaked at 13.3 (SEM 0.5) mmol·l^–1 at 90 min and decreased progressively thereafter; no difference was observed with or without atropine. Plasma free fatty acid and glucagon concentrations, with or without atropine, were both decreased to 201 (SEM 18) mol·l^–1 and 74 (SEM 4) ng·l^–1, respectively, after 2 h of glucose infusion, and were not further suppressed after oral fructose. Carbohydrate oxidation rates (CHO_ox) increased to 20.8 (SEM 1.4) mol·kg^–1·min^–1 and lipid oxidation rates (L_ox) decreased to 1.5 (SEM 0.3) mol·kg^–1·min^–1 between 90 and 120 min after the beginning of glucose infusion and were not affected by atropine. Glucose-induced thermogenesis was similar with [6.5% (SEM 1.4%) of basal EE] or without [6.0% (SEM 1.0%), NS) muscarinic blockade during the 30 min preceding fructose ingestion. During the second half-hour after fructose ingestion, atropine infusion inhibited markedly the stimulation of CHO_ox [+2.8 (SEM 1.0) mol·kg^–1·min^–1 vs +6.9 (SEM 1.0) mol·kg^–1·min^–1, saline, P<0.02] and the suppression of L_ox [–0.8 (SEM 0.2) mol·kg^–1·min^–1 vs –1.4 (SEM 0.2) mol·kg^–1·min^–1, saline, P<0.05]. Carbohydrate-induced thermogenesis during the second half-hour after fructose ingestion, increased to 13.0% (SEM 2.0%) without atropine and was suppressed to 7.7% (SEM 1.9%) (P< 0.05, vs saline) with atropine. It was concluded that muscarinic blockade suppressed the increase of thermogenesis observed after oral fructose, but not during intravenous glucose infusion and that this suppression occurred independently of alterations of plasma insulin concentrations.     

Effect of repeated bouts of short-term exercise on plasma free and sulphoconjugated catecholamines in humans

We tested the hypothesis that measurement of plasma catecholamine sulphate concentration after exercise reflects the overall activation of the sympathoadrenergic system during the whole period of repeated bouts of short-term exercise. A group of 11 male athletes performed two exercise tests at similar average power outputs consisting of three sets each. The tests either started with one set of three very intense sprints (95% of maximal running speed) followed by two sets of three less intense sprints (85% of maximal running speed; HLX) or vice versa (LHX). Similar mean areas under the curve of free noradrenaline (NA) during HLX and LHX [622 (SEM 13) vs 611 (SEM 14) nmol?·?l^?1?·?min) as well as similar mean heart rates [143 (SEM 9) vs 143 (SEM 8) beats?·?min^?1] indicated comparable sympathetic activation during both exercise tests. Even so, plasma concentration of free NA was still significantly higher at the end of LHX than of HLX [35.7 (SEM 3.5) vs 22.5 (SEM 2.1) nmol?·?l^?1, respectively], i.e. when exercise ended with the more intense set of sprints. Plasma noradrenaline sulphate (NA-S) increased with exercise intensity showing higher mean increments after the first set of HLX compared to LHX [1.83 (SEM 0.42) vs 1.18 (SEM 0.29) nmol?·?l^?1; P?0.05]. However, after the end of HLX and LHX, increments in plasma NA-S were similar [4.52 (SEM 0.76) vs 4.06 (SEM 0.79) nmol?·?l^?1], suggesting that NA-S response changed in parallel with the overall activation of the sympathetic nervous system during repeated bouts of short-term exercise. The results supported the hypothesis that measurement of plasma NA-S immediately after repeated bouts of short-term exercise reflects overall activation of the sympathetic nervous system during prolonged periods of this type of exercise.     

Effects of exercise during normoxia and hypoxia on the growth hormone—insulin-like growth factor I axis

The response of plasma insulin-like growth factor I (IGF I) to exercise-induced increase of total human growth hormone concentration [hGH_tot] and of its molecular species [hGH_20kD] was investigated up to 48 h after an 1-h ergometer exercise at 60% of maximal capacity during normoxia (N) and hypoxia (H) (inspiratory partial pressure of oxygen = 92 mmHg (12.7 kPa);n = 8). Lactate and glucose concentrations were differently affected during both conditions showing higher levels under H. Despite similar maximal concentrations, the increase of human growth hormone (hGH) was faster during exercise during H than during N[hGH_tot after 30 min: 8.6 (SD 11.4) ng · ml^–1 (N); 16.2 (SD 11.6) ng · ml^–1 (H);P < 0.05]. The variations in plasma [hGH_20kD] were closely correlated to those of [hGH_tot], but its absolute concentration did not exceed 3% of the [hGH_tot]. Plasma IGF I concentration was significantly decreased 24 h after both experimental conditions [N from 319 (SD 71) ng · ml^-1 to 228 (SD 72) ng · ml^–1,P < 0.05; H from 253 (SD 47) to 200 (SD 47) ng · ml^–1,P < 0.01], and was still lower than basal levels 48 h after exercise during H [204 (SD 44) ng · ml^–1,P < 0.01]. Linear regression analysis yielded no significant correlation between increase in plasma [hGH_tot] or [hGH_20kD] during exercise and the plasma IGF I concentration after exercise. It was concluded that the exercise-associated elevated plasma [hGH] did not increase the hepatic IGF I production. From our study it would seem that the high energy demand during and after the long-lasting intensive exercise may have overridden an existing hGH stimulus on plasma IGH I, which was most obvious during hypoxia.