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.     

Effects of pre-exercise carbohydrate feedings on muscle glycogen use during exercise in well-trained runners

Summary The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners ( =68.2±3.4 ml·kg^–1·min^–1). On three separate occasions, the runners performed a 30 min treadmill run at 70% . Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P<0.05) reaching peak levels at 30 min post-feeding (7.90±0.24 mmol·l^–1). With the onset of exercise, glucose levels dropped to a low of 5.89±0.85 mmol·l^–1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21±0.31 mmol·l^–1 and 5.95±0.23 mmol·l^–1 respectively, and were not significantly different (P<0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise. Muscle glycogen utilization in the first 15 min of exercise was similar in trial C (18.8±8.3 mmol·kg^–1), trial F (16.3±3.8 mmol·kg^–1) and trial G (17.0±1.8 mmol·kg^–1), and total glycogen use was also similar in trial C (25.6±7.9 mmol·kg^–1), trial F (35.4±5.7 mmol·kg^–1) and trial G (24.6±3.2 mmol·kg^–1). In contrast to previous research, these results suggest that pre-exercise feedings of fructose or glucose do not affect the rate of muscle glycogen utilization during 30 min of treadmill running in trained runners.     

Plasma FFA responses to prolonged walking in untrained men and women

Summary Gender differences in plasma FFA responses to 90 min of treadmill walking at 35% were investigated in six men and six women following an overnight fast. The subjects represented average values for maximal oxygen uptake and body fat percentage for age and gender. Mean plasma FFA concentration at 45 and 90 min of exercise were significantly (P<0.05) higher for women (0.82 mmol·l^–01, 0.88 mmol·l^–01) than men (0.42 mmol·l^–01, 0.59 mmol·l^–1). Lower R values for women throughout the exercise period indicated a greater percentage fat in total metabolism than for men while the FFA/glycerol results supported greater lipolytic activity for women. The uniformity of percent fat in metabolism for women from rest to exercise showed that FFA release from adipose tissue increased rapidly with the onset of exercise which was not the case for men. Comparison of metabolic data as well as a statistical analysis (ANCOVA) controlling for the influence of and percentage body fat on FFA plasma concentration suggested that gender differences in FFA responses to prolonged submaximal exercise can be expected to occur in untrained subjects.     

Ammonia and lactate in the blood after short-term sprint exercise

Summary Nine well-trained subjects performed 15-, 30-and 45-s bouts of sprint exercise using a cycle ergometer. There was a significant difference in the mean power between a 15-s sprint (706.0 W, SD 32.5) and a 30-s sprint (627.0 W, SD 27.8;P<0.01). The mean power of the 30-s sprint was higher than that of the 45-s sprint (554.7 W, SD 29.8;P<0.01). Blood ammonia and lactate were measured at rest, immediately after warming-up, and 2.5, 5, 7.5, 10, 12.5 min after each sprint. The peak blood ammonia content was 133.8 mol·1^–1, SD 33.5,- for the 15-s sprint, 130.2 ol·1^–1, SD 44.9, for the 30-s sprint, and 120.8 mol ·1^–1, SD 24.6, for the 45-s sprint. Peak blood lactates after the 15-, 30- and 45-s sprints were 8.1 mmol · 1^–1, SD 1.7, 11.2 mmol · 1^–1, SD 2.4, and 14.7 mmol ·1^–1, SD 2.1, respectively. There was a significant linear relationship between peak blood ammonia and lactate in the 15-s (r, 0.709;P< 0.05), 30-s (r, 0.797;P<0.05) and 45-s (r, 0.696;P<0.05) sprints. Though the peak blood lactate content increased significantly with increasing duration of the sprints (P<0.01), no significant difference was found in peak blood ammonia content among the 15-, 30- and 45-s sprints. These results suggest that the peak value of ammonia in the blood appears in sprints within 15-s and that the blood ammonia level is linked to the lactate in the blood.     

Maximal heart rates and plasma lactate concentrations observed in middle-aged men and women during a maximal cycle ergometer test

Summary The purpose of this study was to investigate criteria for maximal effort in middle-aged men and women undertaking a maximal exercise test until they were exhausted if no measurements of oxygen uptake are made. A large group of 2164 men and 975 women, all active in sports and aged between 40 and 65 years, volunteered for a medical examination including a progressive exercise test to exhaustion on a cycle ergometer. In the 3rd min of recovery a venous blood sample was taken to determine the plasma lactate concentration ([la^–]_{p, 3min}). Lactate concentration and maximal heart rate (f _{c, max}) were lower in the women than in the men (P<0.001). Multiple regression analyses were performed to assess the contribution of sex to [la^–]_{p, 3 min}, independent of age and f _c max, It was found that [la^–]_{p,3 min} was about 2.5 mmol·l^–1 lower in women than in men of the same age and f _{c, max}. In our population 88% of the men and 85% of the women met a combination of the following f _{c, max} and [la^–]_{p, 3min} criteria: f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 8 mmol·l^–1 in the men and f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 5.5 mmol·1^–1 in the women.     

Blood lactate production and recovery from anaerobic exercise in trained and untrained boys

Summary Blood lactate production and recovery from anaerobic exercise were investigated in 19 trained (AG) and 6 untrained (CG) prepubescent boys. The exercises comprised 3 maximal test performances; 2 bicycle ergometer tests of different durations (15 s and 60 s), and running on a treadmill for 23.20±2.61 min to measure maximal oxygen uptake. Blood samples were taken from the fingertip to determine lactate concentrations and from the antecubital vein to determine serum testosterone. Muscle biopsies were obtained from vastus lateralis. Recovery was passive (seated) following the 60 s test but that following the treadmill run was initially active (10 min), and then passive. Peak blood lactate was highest following the 60 s test (AG, 13.1±2.6 mmol·l^–1 and CG, 12.8±2.3 mmol·l^–1). Following the 15 s test and the treadmill run, peak lactate values were 68.7 and 60.6% of the 60 s value respectively. Blood lactate production was greater (p<0.001) during the 15s test (0.470±0.128 mmol·l^–1·s^–1) than during the 60s test (0.184±0.042 mmol·l^–1·s^–1). Although blood lactate production was only nonsignificantly greater in AG, the amount of anaerobic work in the short tests was markedly greater (p<0.05-0.01) in AG than CG. Muscle fibre area (type II%) and serum testosterone were positively correlated (p<0.05) with blood lactate production in both short tests. Blood lactate elimination was greater (p<0.001) at the end of the active recovery phase than in the next (passive) phase. It is concluded that blood lactate production in prepubescent boys is related to serum testosterone level and muscle type II fibre area, indicating the role of maturation and training. Submaximal exercise is likely to increase blood lactate removal during recovery.     

Dehydration and serum biochemical changes in marathon runners

Summary The effects of a competitive marathon race on serum biochemical and haematological parameters have been evaluated. Blood samples were obtained shortly before and immediately after the race; urine samples were also obtained before and after the race. Body weight was recorded pre- and post-race. During the race subjects consumed a total of 1.41 of either water or a dilute glucose-electrolyte solution. The average weight loss of the runners was 2.09±0.77 kg (mean ± SD), corresponding to 2.9±0.8% of body weight. Small but significant increases in both haematocrit and haemoglobin concentration occurred; plasma volume was calculated to decrease by 4.7%. Serum potassium concentration showed no change, but the response was highly variable; serum sodium concentration increased in line with the decrease in plasma volume. In the group of subjects drinking water during the race, the pre-race plasma glucose concentration was 5.3±1.2 mmol·l^–1, this was unchanged after the race (5.0±1.2 mmol·l^–1). A significant increase (P<0.01) in the plasma glucose concentration, from 5.2±0.6 to 6.0±1.5 mmol·l^–1 occurred in the group of subjects drinking the glucose-electrolyte solution. Apart from this, there were no significant differences between the two groups.     

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.     

Effects of dichloroacetate on exercise performance in healthy volunteers

Dichloroacetate (DCA), a stimulator of the pyruvate dehydrogenase complex, decreases lactate levels and peripheral resistance and increases cardiac output. This study was performed to examine the effects of DCA on exercise performance in humans. Eight healthy male volunteers (age 20–28 years) were tested by bicycle spiro-ergometry using a microprocessor-controlled gas analysis system after infusion of DCA (50 mg/kg body weight) or saline. Prior infusion of DCA significantly reduced the increase of lactate levels during exercise when compared with infusion of saline (1.40±0.21 vs 2.10±0.09 mmol·l^–1 at 50% of the expected maximal working capacity, P<0.05; 8.53±0.45 vs 9.92±0.59 mmol·l^–1 at maximal working capacity, P<0.05). Oxygen uptake increased significantly after DCA when compared with saline from 7.5±0.4 vs 7.4±0.5 to 27.2±1.5 vs 23.7±1.7 (P<0.05) at anaerobic threshold and to 35.6±1.7 vs 30.5±1.0 ml · kg^–1 min^–1 (P<0.05) at maximal exercise capacity. Following DCA infusion the workload at which the anaerobic threshold was reached was significantly higher (160±7 vs 120±5 W, P<0.05) and the maximal working capacity was significantly increased (230±9 vs 209±8 W, P<0.05). In summary, DCA reduced the increase of lactate levels during exercise and increased oxygen uptake at the anaerobic threshold and at maximal working capacity, which was significantly increased. These results warrant further studies on a potential therapeutic application of DCA in patients with reduced exercise capacity.     

Transport ofl-cystine in isolated perfused proximal straight tubules

Unidirectional fluxes ofl-³⁵S-cystine and intracellular³⁵S activity were measured in isolated perfused segments of rabbit proximal straight tubule. The absorptive (lumen-to-both) flux ofl-³⁵S-cysteine showed a tendency toward saturation within the concentration limits imposed by the low solubility of cystine (0.3 mmol·l^–1). In contrast, for the bath-to-lumen fluxes, there was a linear relation between the bathing solution concentration ofl-³⁵S-cystine and the rate of³⁵S appearance in the lumen. Nonlinear fitting of both sets of unidirectional flux data gave a maximal cystine transport rate (J _max) of 1.45±0.27 (SEM) pmol min^–1 mm^–1, a Michaelis constant (K _m) of 0.20±0.07 mmol·l^–1, and an apparent permeability coefficient of 0.27±0.11 pmol min^–1 mm^–1 (mmol·l^–1)^–1 (approximately 0.06 m/s). The³⁵S concentration in the cell exceeded that in the lumen by almost 60-fold during the lumen-to-bath flux, and exceeded the bathing solution concentration by 4.7-fold during the bath-to-lumen flux. Thus cystine was accumulated by the cells across either membrane, but over 77% of the intracellular activity was in the form of cysteine. Although the presence of luminall-lysine or cycloleucine inhibited the absorptive flux of cystine, neither amino acid affected the bath-to-lumen flux.Some of the work described here was presented as an abstract at the 8th International Congress of Nephrology, Athens, Greece, 1981     

Perceived exertion and blood lactate concentration during graded treadmill running

The purpose of this study was to investigate the influences of treadmill gradients on the rating of perceived exertion (RPE) at two fixed blood lactate concentrations ( [La^–]_b). Ten subjects performed three different incremental treadmill protocols by running either uphill (concentrically-biased), downhill (eccentrically-biased), or on the flat (non-biased). Individual data of each protocol were interpolated to reflect [La^–]_b corresponding to 2.0 and 4.0 mmol·l^–1. At 2.0 mmol·l^–1 [La^– _b, RPE and treadmill speed during downhill running were greater than during level running which was greater than during uphill running (p < 0.05) . Also, the downhill heart rate (HR) was greater than the uphill HR, and downhill minute ventilation ( ) was greater than the level . Treadmill speed was the only measure at 4.0 mmol·l^–1 [La^–]_b to differ between gradients. There was a moderate correlation of RPE with HR at both [La^–]_b (r = 0.73 at 2.0 mmol·l^–1;r = 0.48 at 4.0 mmol·l^–1) while treadmill speed was moderately correlated with RPE only at 2.0 mmol·l^–1 [La^–]_b (r = 0.70). The results of this study demonstrated that the degree of eccentric-bias during running exercise is an influence of perceived exertion at a moderate but not at a high exercise intensity.     

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.     

The effects of extracellular potassium,ouabain, and prostaglandins on intracellular potassium activity in sheep cardiac Purkinje fibers

(1) Intracellular K activity (a _K ⁱ ) of sheep heart Purkinje fibers was measured using K-selective microelectrodes (liquid ion exchanger).a _K ⁱ in the resting state with an extracellular K of 4 mmol·l^–1 was 112.9±6.1 mmol·l^–1 (n=47) for a membrane potential (V _M) of –73.3±0.9 mV.V _M deviated from the calculated potassium equilibrium potential (E _K=–93 mV). (2) When extracellular K was decreased to 2 mmol·l^–1 or increased to 6 and 10 mmol·l^–1 E _K changed from –114 to –84 and –73 mV, with little change ina _K ⁱ . (3)a _K ⁱ andV _M significantly decreased after administration of 10^–6 mol·l^–1 ouabain. (4) Prostaglandins (PGI₂ 10–100 g·l^–1 and PGE₂ 0.01–1 g·l^–1) decreaseda _K ⁱ without greatly changingV _M. The differences betweenV _M andE _K became smaller. These effects indicate an increase in K permeability and may explain the antiarrhythmic action of prostaglandins.This study was supported by the Deutsche Forschungsgemeinschaft (grant Wi 328). In preliminary form part of the data has been presented (Pflügers Arch. 384: R 13, 1980, and Proc. XXVIII. Int Congr Physiol Sci, Vol XIV: 279, 1980)     

Electrophysiological effects of acetylcholine in sheep cardiac Purkinje fibers

The addition of acetylcholine (ACh) in concentrations of 10^–7 to 10^–5 mol·l^–1 to normal Tyrode solution results in the following changes of the electrical activity in sheep cardiac Purkinje fibers: prolongation of the action potential and shift of the plateau to more positive values, hyperpolarization of the maximum diastolic potential (E _max), and increase of the rate of diastolic depolarization.Prolongation of the action potential and shift of the plateau in the positive direction were more pronounced in distal Purkinje fibers, at low frequencies of stimulation, and in the presence of a reduced Ca (<3.6 mmol·l^–1) or K extracellular concentration (<5.4 mmol·l^–1); the effects persisted in Cl free media or after addition of Mn (2–10 mmol·l^–1) or verapamil (1–5 mg·l^–1).The effect of Ach on the maximum diastolic potential (stimulation frequency 60/min) was dependent on K₀. At 5.4 mmol·l^–1,E _max increased by 2 mV; at higher K₀ concentrations the change was less pronounced or absent; at low K₀ concentrations (membrane potential arrested at the plateau level) the addition of Ach invariably caused a depolarization. In unstimulated preparations the effect of Ach was unpredictable.The increase in rate of diastolic depolarization by Ach in 3.4 or 2.7 mmol·l^–1 K was large enough to result in spontaneous activity. When the membrane was depolarized to the plateau level (K₀<1.35 mmol·l^–1) Ach frequently reduced the frequency of oscillations.The effect of Ach was dose-dependent; desensitization was absent. Similar results were obtained with carbachol (10^–6 mol·l^–1) or choline (5·10^–3 mol·l^–1). The effect of Ach could selectively be abolished by atropine (10^–8 to 10^–6 mol·l^–1); it was not modified by succinylcholine (8·10^–5 mol·l^–1), phentolamine (10^–6 mol·l^–1) or propranolol (10^–6 mol·l^–1). The results indicate that the electrophysiological changes are due to stimulation of muscarinic receptors.Except for the hyperpolarization ofE _max the results in sheep Purkinje fibers are different and even opposite to those observed in the sino-atrial node and atrial muscle. Possible mechanisms and functional significance of the results are discussed.Supported by F.G.W.O. Belgium 3.0087.74     

Activation of sodium transport in human erythrocytes by β-adrenoceptor stimulation in vivo

Summary -adrenoceptor stimulation in vivo shifts potassium into the cells. To examine whether human erythrocytes participate in this process, we measured, along with serum or plasma potassium, the concentrations of potassium and sodium in erythrocytes. -adrenoceptor stimulation was obtained by infusion of either fenoterol or hexoprenaline into 6 volunteers at rest or by endogenous amines provoked in 14 volunteers during ergometric exercise. Metabolic effects were followed at rest on serum insulin, Cpeptide, and growth hormone levels, and during exercise on pH and on lactate concentration in blood. The potassium concentration (mean ±S.E.M.) dropped (p<0.001) in serum from 4.64±0.37 to 3.19±0.43 mmol·l^–1 in the first hour at rest and in plasma from 5.70±0.93 to 4.63±0.45 in 90 sec directly after exercise. The concentration of erythrocyte sodium dropped (p<0.001) from 9.68±0.73 to 8.81±0.62 mmol·l^–1 in cells and from 9.62±1.16 to 8.55±1.24 during exercise for 90 s, respectively. Changes in the concentration ratio of cellular sodium to potassium confirmed this sodium shift.An increased sodium transport in erythrocytes due to -adrenoceptor stimulation in vivo appears to complement a shift of serum potassium into the cells and may be mediated by the membranebound sodium, potassium ATPase.Supported by the Deutsche Forschungsgemeinschaft, grant Bo 425/8-5     

Metabolic and circulatory responses to the ingestion of glucose polymer and glucose/electrolyte solutions during exercise in man

Summary Six men exercised on a cycle ergometer for 60 min on two occasions one week apart, at 68±3% of . On one occasion, a dilute glucose/electrolyte solution (E: osmolality 310 mosmol · kg^–1, glucose content 200 mmol·l^–1) was given orally at a rate of 100 ml every 10 min, beginning immediately prior to exercise. On the other occasion, a glucose polymer solution (P: osmolality 630 mosmol · kg^–1, glucose content equivalent to 916 mmol · l^–1) was given at the same rate. Blood samples were obtained from a superficial forearm vein immediately prior to exercise and at 15-min intervals during exercise; further samples were obtained at 15-min intervals for 60 min at rest following exercise. Heart rate and rectal temperature were measured at 5-min intervals during exercise.Blood glucose concentration was not different between the two tests during exercise, but rose to a peak of 8.7±1.2 mmol · l^–1 (mean±SD) at 30 min post-exercise when P was drunk. Blood glucose remained unchanged during and after exercise when E was drunk. Plasma insulin levels were unchanged during exercise and were the same on both trials, but again a sharp rise in plasma insulin concentration was seen after exercise when P was drunk. The rate of carbohydrate oxidation during exercise, as calculated from and the respiratory exchange ratio, was not different between the two tests. A fall in plasma volume, calculated from changes in haematocrit and haemoglobin concentration, occurred after 15 mins of exercise: the fall was of the same magnitude (9%) at this point on both tests, but thereafter plasma volume was significantly lower with P than with E for the remainder of the exercise period and throughout recovery. Serum osmolality increased during exercise (p<0.05) on the P trial, but was unchanged on the E trial. Heart rate was higher (p<0.05) during the last 20 min of exercise on the P trial.These results suggest that the carbohydrate consumed during the P trial was not available to the working muscles during exercise, and was probably not emptied from the stomach and absorbed to any significant extent until exercise stopped. The differences in plasma volume and osmolality between the two trials are consistent with the net movement of water into the gut which is known to occur at rest when solutions of high osmolality are taken. In more prolonged exercise, this effective dehydration may impair performance.     

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.     

Effect of anaerobic and aerobic exercise of equal duration and work expenditure on plasma growth hormone levels

Summary Growth hormone (GH) and lactic acid levels were measured in five normal males before, during and after two different types of exercise of nearly equal total duration and work expenditure. Exercise I (aerobic) consisted of continuous cycling at 100 W for 20 min. Exercise II (anaerobic) was intermittent cycling for one minute at 285 W followed by two minutes of rest, this cycle being repeated seven times. Significant differences (P<0.01) were observed in lactic acid levels at the end of exercise protocols (20 min) between the aerobic (I) and anaerobic (II) exercises (1.96±0.33 mM·l^–1 vs 9.22±0.41 mM·l^–1, respectively). GH levels were higher in anaerobic exercise (II) than in aerobic (I) at the end of the exercise (20 min) (2.65±0.95 g·l^–1 vs 0.8±0.4 g·l^–1;P<0.10) and into the recovery period (30 min) (7.25±6.20 g·l^–1 vs 2.5±2.9 g·l^–1;P<0.05, respectively).     

Ca2+ influx induced by store release and cytosolic Ca2+ chelation in HT29 colonic carcinoma cells

Cl^– secretion in HT₂₉ cells is regulated by agonists such as carbachol, neurotensin and adenosine 5-triphosphate (ATP). These agonists induce Ca²⁺ store release as well as Ca²⁺ influx from the extracellular space. The increase in cytosolic Ca²⁺ enhances the Cl^– and K⁺ conductances of these cells. Removal of extracellular Ca²⁺ strongly attenuates the secretory response to the above-mentioned agonists. The present study utilises patch-clamp methods to characterise the Ca²⁺ influx pathway. Inhibitors which have been shown previously to inhibit non-selective cation channels, such as flufenamate (0.1 mmol·l^–1, n=6) and Gd³⁺ (10 mol·l^–1, n=6) inhibited ATP (0.1 mmol·l^–1) induced increases in whole-cell conductance (G _m). When Cl^– and K⁺ currents were inhibited by the presence of Cs₂SO₄ in the patch pipette and gluconate in the bath, ATP (0.1 mmol·l^–1) still induced a significant increase in G _m from 1.2±0.3 nS to 4.7±1 nS (n=24). This suggests that ATP induces a cation influx with a conductance of approximately 3–4 nS. This cation influx was inhibited by flufenamate (0.1 mmol·l^–1, n=6) and Gd³⁺ (10 mol·l^–1, n=9). When Ba²⁺ (5 mmol·l^–1) and 4,4-diisothiocyanatostilbene-2-2-disulphonic acid (DIDS, 0.1 mmol·l^–1) were added to the KCl/K-gluconate pipette solution to inhibit K⁺ and Cl^– currents and the cells were clamped to depolarised voltages, ATP (0.1 mmol·l^–1) reduced the membrane current (I _m) significantly from 86±14 pA to 54±11 pA (n=13), unmasking a cation inward current. In another series, the cation inward current was activated by dialysing the cell with a KCl/K-gluconate solution containing 5–10 mmol·l^–1 1,2-bis-(2-aminoethoxy)ethane-N,N,N,N-tetraacetic acid (EGTA) or 1,2-bis-(2-aminophenoxy) ethane-N,N,N,N-tetraacetic acid (BAPTA). The zero-current membrane voltage (V _m) and I _m (at a clamp voltage of +10 mV) were monitored as a function of time. A new steady-state was reached 30–120 s after membrane rupture. V _m depolarised significantly from –33±2 mV to –12±1 mV, and I _m fell significantly from 17±2 pA to 8.9±1.0 pA (n=71). This negative current, representing a cation inward current, was activated when Ca²⁺ stores were emptied and was reduced significantly (I _m) when Ca²⁺ and/or Na⁺ were removed from the bathing solution: removal of Ca²⁺ in the absence of Na⁺ caused a I _m of 5.0±1.2 pA (n=12); removal of Na⁺ in the absence of Ca²⁺ caused a I _m of 12.8±3.5 pA (n=4). The cation inward current was also reduced significantly by La³⁺, Gd³⁺, and flufenamate. We conclude that store depletion induces a Ca²⁺/Na⁺ influx current in these cells. With 145 mmol·l^–1 Na⁺ and 1 mmol·l^–1 Ca²⁺, both ions contribute to this cation inward current. This current is an important component in the agonist-regulated secretory response.     

Neuromuscular characteristics and fatigue in endurance and sprint athletes during a new anaerobic power test

The purpose of this study was to investigate neuromuscular and energy performance characteristics of anaerobic power and capacity and the development of fatigue. Ten endurance and ten sprint athletes performed a new maximal anaerobic running power test (MARP), which consisted ofn x 20-s runs on a treadmill with 100-s recovery between the runs. Blood lactate concentration [la^–]_b was measured after each run to determine submaximal and maximal indices of anaerobic power (P _3mmol·1 ^–1,P_5mmol·1 ^–1,P_10mmol·1 ^–1andP _max) which was expressed as the oxygen demand of the runs according to the American College of Sports Medicine equation: the oxygen uptake (ml·kg^–1·min^–1)=0.2·velocity (m·min^–1) +0.9·slope of treadmill (frac)·velocity (m·min^–1)+3.5. The height of rise of the centre of gravity of the counter movement jumps before (CMJ_rest) and during (CMJ) the MARP test, as well as the time of force production (t _F) and electromyographic (EMG) activity of the leg muscles of CMJ performed after each run were used to describe the neuromuscular performance characteristics. The maximal oxygen uptake ( _max), anaerobic and aerobic thresholds were determined in the _max test, which consisted ofn x 3-min runs on the treadmill. In the MARP-testP _max did not differ significantly between the endurance [116 (SD 6) ml·kg^–1·min^–1] and sprint [120 (SD 4) ml·kg^–1·min^–1] groups, even though CMJ_rest and peak [la^–]_b were significantly higher and _max was significantly lower in the sprint group than in the endurance group and CMJ_rest height correlated withP _max (r=0.50,P<0.05). The endurance athletes had significantly higher mean values ofP _3mmol·1 ^–1andP _5mmol·1 ^–1[89 (SD 7) vs 76 (SD 8) ml·kg^–1·min^–,P<0.001 and 101 (SD 5) vs 90 (SD 8) ml·kg^–1·min^–1,P<0.01. Significant positive correlations were observed between theP _3mmol·l ^–1and _max, anaerobic and aerobic thresholds. In the sprint group CMJ and the averaged integrated iEMG decreased andt _F increased significantly during the MARP test, while no significant changes occurred in the endurance group. The present findings would suggest thatP _max reflected in the main the lactacid power and capacity and to a smaller extent alactacid power and capacity. The duration of the MARP test and the large number of CMJ may have induced considerable energy and neuromuscular fatigue in the sprint athletes preventing them from producing their highest alactacidP _max at the end of the MARP test. Due to lower submaximal [la^–]_b (anaerobic sprinting economy) the endurance athletes were able to reach almost the sameP _max as the sprint athletes.