Involvement of muscarinic cholinergic and α2-adrenergic mechanisms in growth hormone secretion during exercise in humans

The purpose of this study was to examine the role of muscarinic cholinergic and α₂-adrenergic mechanisms in growth hormone (GH) secretion during exercise in humans. The GH responses induced during moderate-intensity exercise (using a cycle ergometer at 60% maximal oxygen uptake, V˙O_2max, for 30 min) without treatment (control) and after the administration of a muscarinic cholinergic antagonist (atropine 1 mg) or after an α₂-adrenergic antagonist (yohimbine 15 mg) were compared in seven healthy men. Although, serum GH concentration had increased significantly after exercise in the control experiment [mean peak GH concentration 52.64 (SEM 18.60) ng · ml⁻¹], the increase was suppressed by the administration of either atropine [mean peak GH concentration 8.64 (SEM 7.47)  ng · ml⁻¹] or yohimbine [mean peak GH concentration 17.50 (SEM 7.89) ng · ml⁻¹]. The area under the curve of serum GH concentration against time was significantly lower in the experiment using these drugs [with atropine, mean area 458 (SEM 409) ng · ml⁻¹ · min], with yohimbine mean area 946 (SEM 435) ng · ml⁻¹ · min] than in the control experiment [mean area 3135 (SEM 1098) ng · ml⁻¹ · min]. These results suggest that muscarinic cholinergic and α₂-adrenergic mechanisms are involved in GH secretion during exercise in humans. Accepted: 9 March 2000     

Influence of temperature on the distribution of blood in humans as assessed by electrical impedance

This study investigated whether ambient temperature influences the distribution of blood as indicated by electrical impedance. In ten supine humans, the room temperature was raised from 14 to 35°C. Skin temperature and blood flow on the thorax increased by 3.6 (SD 0.3)°C and 84 (SD 40)%, respectively, and by 9.8 (SD 1)°C and 115 (SD 45)%, respectively, on the extremities (P < 0.05). Cardiac output remained unchanged, ear temperature and heart rate became elevated, and the oesophageal temperature and mean arterial pressure decreased (P < 0.05). At five discrete frequencies (1.5, 5, 50, 100, 200 kHz) thoracic impedance was increased by 1.2 (SD 1) to 1.5 (SD 1) Ω (P < 0.05). In contrast, total body impedance was reduced by 16.4 (SD 5) Ω and leg impedance was reduced by 4.0 (SD 2) Ω, while an index of intracellular water within the thorax (the difference between the admittances at 100 kHz and 1.5 kHz) was decreased by 10 (SD 1) · 10⁻⁴ S (P < 0.05). The results would suggest that total body impedance is dominated by the impedance of the extremities. The increase in thoracic impedance and a decrease in leg impedance (as in total body impedance) could be explained by a redistribution of blood from the thorax to the extremities during heating. Such a translocation of blood was confirmed by a reduced impedance based index of intracellular water within the thorax. Accepted: 4 June 1999     

Cortisol and testosterone concentrations in wheelchair athletes during submaximal wheelchair ergometry

It is yet unknown how upper body exercise combined with high ambient temperatures affects plasma testosterone and cortisol concentrations and furthermore, how these hormones respond to exercise in people suffering spinal cord injuries. The purpose of this study was to characterize plasma testosterone and cortisol responses to upper body exercise in wheelchair athletes (WA) compared to able-bodied individuals (AB) at two ambient temperatures. Four WA [mean age 36 (SEM 13) years, mean body mass 66.9 (SEM 11.8) kg, injury level T₇–T₁₁], matched with five AB [mean age 33.4 (SEM 8.9) years, mean body mass 72.5 (SEM 13.1) kg] exercised (cross-over design) for 20 min on a wheelchair ergometer (0.03 kg resistance · kg⁻¹ body mass) at 25 °C and 32 °C. Blood samples were obtained before (PRE), at min 10 (MID), and min 20 (END) of exercise. No differences were found between results obtained at 25 °C and 32 °C for any physiological variable studied and therefore these data were combined. Pre-exercise testosterone concentration was lower (P < 0.05) in WA [18.3 (SEM 0.9) nmol · l⁻¹] compared to AB [21.9 (SEM 3.6) nmol · l⁻¹], and increased PRE to END only in WA. Cortisol concentrations were similar between groups before and during exercise, despite higher rectal temperatures in WA compared to AB, at MID [37.21 (SEM  0.14) and 37.02 (SEM  0.08)°C, respectively] and END [37.36 (SEM 0.16) and 37.19 (SEM 0.10)°C, respectively]. Plasma norepinephrine responses were similar between groups. In conclusion, there were no differences in plasma cortisol concentrations, which may have been due to the low relative exercise intensities employed. The greater exercise response in WA for plasma testosterone should be confirmed on a larger population. It could have been the result of the lower plasma testosterone concentrations at rest in our group. Accepted: 4 September 2000     

Effect of strenuous strength training on the Na-K pump concentration in skeletal muscle of well-trained men

This study examined how strenuous strength training affected the Na-K pump concentration in the knee extensor muscle of well-trained men and whether leg muscle strength and endurance was related to the pump concentration. First, the pump concentration, taken as ³H-ouabain binding, was measured in top alpine skiers since strength training is important to them. Second, well-trained subjects carried out strenuous eccentric resistance training either 1, 2, or 3 times · week⁻¹ for 3 months. The Na-K pump concentration, the maximal muscle strength in a full squat lift (one repetition maximum, 1 RM), and the muscle endurance, taken as the number of full squat lifts of a mass of 70% of the 1 RM load, were measured before and after the training period. The mean pump concentration of the alpine skiers was 425 (SEM 11) nmol · kg⁻¹ wet muscle mass. The subjects in part two increased their maximal strength in a dose-dependent manner. The muscle endurance increased for all subjects but independently of the training programme. From a mean starting value of 356 (SEM 6) nmol · kg⁻¹ the mean Na-K pump concentration increased by 54 (SEM 15) nmol · kg⁻¹ (+15%, P < 0.001) when the results for all subjects were pooled. The effect was larger for those who had trained twice a week than for those who had trained only once a week (P=0.025), suggesting that the effect of strength training depended on the amount of training carried out. The muscle strength and endurance were not related to the pump concentration, suggesting that the pumping power of this enzyme did not limit the performance during heavy lifting. However, the individual improvements in the endurance test during the training period correlated with the individual changes in the pump concentration (r _Spearman=0.5; P=0.01) which could mean that a common factor both increases the pump concentration and makes the muscles more adapted to repeated heavy lifting. Accepted: 8 August 2000     

Physiological and metabolic responses of female games and endurance athletes to prolonged, intermittent, high-intensity running at 30° and 16°C ambient temperatures

Eight female games players (GP) and eight female endurance athletes (EA) ran intermittently at high-intensity and for prolonged periods in hot (30°C) and moderate (16°C) ambient temperatures. The subjects performed a two-part (A, B) test based on repeated 20-m shuttle runs. Part A comprised 60 m of walking, a maximal 15-m sprint, 60 m of cruising (90% maximal oxygen uptake, V˙O_2max) and 60 m of jogging (45% V˙O_2max) repeated for 75 min with a 3-min rest every 15 min. Part B involved an exercise and rest pattern of 60-s running at 100% V˙O_2max and 60-s rest which was continued until fatigue. Although the GP and EA did not respond differently in terms of distances completed, performance was 25 (SEM 4)% less (main effect trial, P < 0.01) in the hot (HT) compared with the moderate trial (MT). Sprints of 15 m took longer to complete in the heat (main effect, trial, P < 0.01), and sprint performance declined during HT but not MT (interaction, trial × time, P < 0.01). A very high correlation was found between the rate of rise in rectal temperature in HT and the distance completed [GP, r =−0.94, P < 0.01; EA (n = 7), r = −0.93, P < 0.01]. Blood lactate [La⁻ ]_b and plasma ammonia [NH₃]_p1 concentrations were higher for GP than EA, but were similar in HT and MT [La⁻ ]_b, HT: GP vs EA, 8.0 (SEM 0.9) vs 4.9 (SEM 1.1) mmol · l⁻¹; MT: GP vs EA, 8.0 (SEM 1.3) vs 4.4 (SEM 1.2) mmol · l⁻¹; interaction, group × time, P < 0.01; [NH₃]_p1, HT: GP vs EA, 70.1 (SEM 12.7) vs 43.2 (SEM 6.1) mmol · l⁻¹; MT: GP vs EA, 76.8 (SEM 8.8) vs 32.5 (SEM 3.8) μmol · l⁻¹; interaction, group × time, P < 0.01. Ad libitum water consumption was higher in HT [HT: GP vs EA, 18.9 (SEM 2.9) vs 13.5 (SEM 1.7) ml · kg⁻¹ · h⁻¹; MT: GP vs EA, 12.7 (SEM 3.7) vs 8.5 (SEM 1.5) ml · kg⁻¹ · h⁻¹; main effect, group, n.s.; main effect, trial, P < 0.01]. These results would suggest that elevated body temperature is probably the key factor limiting performance of prolonged, intermittent, high-intensity running when the ambient temperature is high, but not because of its effect on the metabolic responses to exercise. Accepted: 19 July 1999     

Influence of ultra-long-term fatigue on the oxygen cost of two types of locomotion

The aim of this study was to examine the effects of fatigue induced by a 65-km ultramarathon on the oxygen cost of running (C_r) and cycling (C_cycl). The day before and immediately after the race, a group of nine well-trained male subjects performed two sub-maximal 4-min exercise bouts: one cycling at a power corresponding to 1.5 W · kg⁻¹ body mass on an electromagnetically braked ergometer, and one running at 11 km · h⁻¹ on a flat asphalt roadway. Before oxygen cost determinations, the subjects performed 12 “ankle” jumps at a given frequency that was fixed by an electronic metronome (2.5 Hz). From the non-fatigued to the fatigued condition, there was a significant increase in minute ventilation for both running (P < 0.01) and cycling (P < 0.0001). Significant changes were also found in respiratory exchange ratio both for running (P=0.01) and cycling (P < 0.0001). However, running and cycling differed in that C_cycl increased significantly by [mean (SD)] 24.2 (11.5)% (P < 0.001), suggesting an alteration of muscle efficiency, while C_r did not change with fatigue [186.8 (14.1) mlO₂ · kg⁻¹ · km⁻¹ vs 186.8 (18.7) mlO₂ · kg⁻¹ · km⁻¹]. In addition, contact times during hopping increased significantly from 0.173 (0.019) ms to 0.194 (0.027) ms (P < 0.01). Analysis of the factors that determine C_r indicate that the subjects modified their movement pattern in order to decrease the mechanical cost of running in such long-term fatigue conditions. Accepted: 7 August 2000     

Age related blood flow around the Achilles tendon during exercise in humans

Injuries due to the overuse of tendons increase with age, and it has been suggested that this correlates with hypovascularity of the tendon. In the present study, the peritendinous blood flow was determined using xenon-133 washout at rest and during standardised intermittent exercise of the calf-muscle (1.5 s contraction, 1.5 s rest, 40 min) in young (n=6; 26 years), middle-aged (n=6; 48 years), and older (n=6; 74 years) individuals. At rest, the older individuals had a lower peritendinous blood flow compared with the two other age groups. During exercise, blood flow in all three groups rose 2.5–3.5-fold to reveal similar blood flows [2.7 (SEM 0.5) to 7.8 (SEM 1.0) ml · 100 g tissue⁻¹ min⁻¹ (young group); 3.0 (SEM 0.4) to 7.3 (SEM 1.6) ml · 100 g tissue⁻¹ min⁻¹ (middle-aged group); 1.6 (SEM 0.2) to 5.5 (SEM 1.1) ml 100 g tissue⁻¹ · min⁻¹ (older group)]. The findings demonstrated that the peritendinous blood flow to the zone of the tendon with the highest incidence of injury from overuse is unaltered by age during exercise, and indicates that factors other than blood flow are important for the increased incidence with age of injuries from overuse. Accepted: 23 October 2000     

Plasma catecholamine responses and neural adaptation during short-term resistance training

Low exercise-induced plasma adrenaline (A) responses have been reported in resistance-trained individuals. In the study reported here, we investigated the interaction between strength gain and neural adaptation of the muscles, and the plasma A response in eight healthy men during a short-term resistance-training period. The subjects performed 5 resistance exercises (E1–E5), consisting of 6 sets of 12 bilateral leg extensions performed at a 50% load, and with 2 days rest in between. Average electromyographic (EMG) signal amplitude was recorded before and after the exercises, from the knee extensor muscles in isometric maximal voluntary contraction (MVC) as well as during the exercises (aEMG_max and aEMG_exerc, respectively). Total oxygen consumed during the exercises (V˙O_2tot) was also measured. All of the exercises were exhaustive and caused significant decreases in MVC (34–36%, P < 0.001). As expected, the concentric one-repetition maximum (1-RM), MVC and aEMG_max were all higher before the last exercise (E5) than before the first exercise (E1; 7, 9 and 19%, respectively, P < 0.05). In addition, in E5 the aEMG_exerc:load and V˙O_2tot:load ratios were lower than in E1 (−5 and −14%, P < 0.05), indicating enhanced efficiency of the muscle contractions, However, the post-exercise plasma noradrenaline (NA) and A were not different in these two exercises [mean (SD) 10.2 (3.8) nmol · l⁻¹ vs 11.3 (6.0) nmol · l⁻¹, ns, and 1.2 (1.0) nmol · l⁻¹ vs 1.9 (1.1) nmol · l⁻¹, ns, respectively]. However, although NA increased similarly in every exercise (P < 0.01), the increase in A reached the level of statistical significance only in E1 (P < 0.05). The post-exercise A was also already lower in E2 [0.7 (0.7) nmol · l⁻¹, P < 0.05) than in E1, despite the higher post-exercise blood lactate concentration than in the other exercises [9.4 (1.1) mmol · l⁻¹, P < 0.05]. Thus, the results suggest that the observed attenuation in the A response can not be explained by reduced exercise-induced strain due to the strength gain and neural adaptation of the muscles. Correlation analysis actually revealed that those individuals who had the highest strength gain during the training period even tended to have an increased post-exercise A concentration in the last exercise as compared to first one (r=0.76, P < 0.05). Accepted: 10 February 2000     

Substrate utilisation during exercise and shivering

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (V˙O₂) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the V˙O₂ recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The V˙O₂ measured during the different levels of shivering averaged 0.49 l · min⁻¹ (level 1: low), 0.6 l · min⁻¹ (level 2: low-moderate), and 0.9 l · min⁻¹ (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same V˙O₂ (9.5% and 14.7%, respectively). The average (SD) HGO during level 3 exercise was 3.0 (0.91) mg · kg⁻¹ . min⁻¹ compared to 2.76 (1.0) mg · kg⁻¹ . min⁻¹ during shivering. The values for Rd were 3.06 (0.98) mg · kg⁻¹ · min⁻¹ during level 3 exercise and 2.68 (0.82) mg · kg⁻¹ · min⁻¹ during shivering. Blood glucose levels did not differ between conditions, averaging 5.4 (0.3) mmol . l⁻¹ over all levels of shivering and 5.2 (0.3) mmol · l⁻¹ during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol · l⁻¹ over all levels of shivering and 0.47 (0.16) mmol · l⁻¹ during exercise. The figures for B-HBA were 0.44 (0.13) mmol · l⁻¹ during all levels of shivering and 0.32 (0.1) mmol · l⁻¹ during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol · l⁻¹ during shivering and 80.6 (16.1) pmol · l⁻¹ during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes. Accepted: 12 February 1997     

Are the blood pressure and endocrine responses of healthy subjects exposed to cold stress altered by an acutely increased sodium intake?

In the study reported here, we examined blood pressure and endocrine responses in cold conditions during salt load in young healthy subjects who had previously shown increased resting blood pressure during acutely increased sodium intake. Subjects (n=53) added 121 mmol sodium into their normal diet for 1 week. If their mean arterial pressure had increased by a minimum of 5 mmHg compared to the previous measure they were selected for subsequent experiments. The subjects (n=8) were given 121 mmol supplemental sodium · day⁻¹ for 14 days. They were then put into a wind tunnel for 15 min (temperature −15 °C, wind speed 3.5 · ms⁻¹). Their blood pressure increased (P < 0.05) during the cold exposure, independent of the sodium intake. Their mean (SEM) plasma noradrenaline increased from 3.58 (0.62) nmol · l⁻¹ to 5.61 (0.79) nmol · l⁻¹ (P < 0.05) when the subjects were given a normal diet, and from 2.45 (0.57) nmol · l⁻¹ to 5.06 (0.56) nmol · l⁻¹ (P < 0.05) when the subjects were given an elevated sodium diet. The starting concentrations and the endpoint concentrations were statistically similar. The plasma levels of the N-terminal fragment of pro-atrial natriuretic peptide decreased during the whole-body cold exposure: with the sodium load the change was from 256.6 (25.5) nmol · l⁻¹ to 208.0 (25.3) nmol · l⁻¹, and with the normal diet, from 205.8 (16.4) nmol · l⁻¹ to 175.1 (16.1) nmol · l⁻¹. The haematocrit and red blood cell count increased (P < 0.05) with normal and elevated sodium diet in cold conditions, but haemoglobin increased (P < 0.05) only with high salt in cold conditions. To conclude, acutely increased sodium intake does not change the blood pressure response or hormonal responses to exposure to acute cold stress in healthy subjects. Accepted: 28 September 2000     

Muscle blood flow and flow heterogeneity during exercise studied with positron emission tomography in humans

Blood flow is the main regulator of skeletal muscle's oxygen supply, and several studies have shown heterogeneous blood flow among and within muscles. However, it remains unclear whether exercise changes the heterogeneity of flow in exercising human skeletal muscle. Muscle blood flow and spatial flow heterogeneity were measured simultaneously in exercising and in the contralateral resting quadriceps femoris (QF) muscle in eight healthy men using H¹⁵ ₂O and positron emission tomography. The relative dispersion (standard deviation/mean) of blood flow was calculated as an index of spatial flow heterogeneity. Average muscle blood flow in QF was 29 (10) ml · (kg muscle)⁻¹ · min⁻¹ at rest and 146 (54) ml · (kg muscle)⁻¹ · min⁻¹ during exercise (P=0.008 for the difference). Blood flow was significantly (P < 0.001) higher in the vastus medialis and the vastus intermedius than in the vastus lateralis and the rectus femoris, both in the resting and the exercising legs. Flow was more homogeneous in the exercising vastus medialis and more heterogeneous (P < 0.001) in the exercising vastus lateralis (P=0.01) than in the resting contralateral muscle. Flow was more homogeneous (P < 0.001) in those exercising muscles in which flow was highest (vastus intermedius and vastus medialis) as compared to muscles with the lowest flow (vastus lateralis and the rectus femoris). These data demonstrate that muscle blood flow varies among different muscles in humans both at rest and during exercise. Muscle perfusion is spatially heterogeneous at rest and during exercise, but responses to exercise are different depending on the muscle. Accepted: 16 June 2000     

Substrate utilization in boys during exercise with [13C]-glucose ingestion

The influence of glucose ingestion on substrate utilization during prolonged exercise in children and adolescents is currently unknown. In the present study we determined the effect of intermittent exogenous glucose (GLU_exo) ingestion on substrate utilization during prolonged exercise, in adolescent boys ages 13–17 years. Healthy untrained volunteers performed four 30-min exercise bouts on a cycle ergometer, separated by 5-min rest periods (≅60% maximum O₂ consumption), on two occasions spaced 1–4 weeks apart. Two trials were performed, a control trial (CT), in which subjects ingested water intermittently during the exercise, and a glucose trial (GT), in which subjects ingested a ¹³C-enriched GLU_exo drink (≅3 g glucose · kg body mass⁻¹), also intermittently during the exercise. Total free fatty acids (FAT_total), glucose (GLU_total) and carbohydrate (CHO_total) oxidation was determined from indirect calorimetry, while GLU_exo oxidation was calculated from the ¹³C/¹²C ratio in expired air after 5–10 min and 25–30 min of exercise in each bout. Heart rate and rating of perceived exertion (RPE) were determined at the same time intervals. The oxidation of CHO_total was 169.1 (12.9) g · 120 min⁻¹ and 203.1 (15.9) g · 120 min⁻¹ (P < 0.01) and that of FAT_total was 31.0 (4.2) g · 120 min⁻¹ and 17.1 (2.5) g · 120 min⁻¹ (P < 0.01) in CT and GT, respectively. GLU_exo oxidation in GT was 57.8 (4.3) g · 120 min⁻¹, or 34.2 (2.2)% of that ingested. Endogenous glucose oxidation was 169.1 (12.9) g · 120 min⁻¹ and 145.3 (11.9) g · 120 min⁻¹ (P < 0.01) in CT and GT, respectively. Insulin and glucose concentrations were higher in GT than in CT by 226% and 37%, respectively (both P < 0.05). Free fatty acids and glycerol concentrations were lower in GT than in CT, by 27% and 79%, respectively (both P < 0.05). Heart rate was similar between trials, but RPE was lower in GT vs CT at both 115 and 135 min. Thus, under these experimental conditions, GLU_exo intake spares endogenous carbohydrate and fat by 16% and 45%, respectively, contributes to approximately 25% of the total energy demand of exercise, and lowers the RPE. Accepted: 21 May 2000     

Gas exchange responses to continuous incremental cycle ergometry exercise in primary pulmonary hypertension in humans

In patients suffering from primary pulmonary hypertension (PPH), a raised pulmonary vascular resistance may limit the ability to increase pulmonary blood flow as work rate increases. We hypothesised that oxygen uptake (V˙O₂) may not rise appropriately with increasing work rate during incremental cardiopulmonary exercise tests. Nine PPH patients and nine normal subjects performed symptom-limited maximal continuous incremental cycle ergometry exercise. Mean peak V˙O₂ [1.00 (SD 0.22) compared to 2.58 (SD 0.64) l · min⁻¹] and mean V˙O₂ at lactic acidosis threshold [LAT, 0.73 (SD 0.17) compared to 1.46 (SD 0.21 · l) ml · min⁻¹] were much lower in patients than in normal subjects (both P < 0.01, two-way ANOVA with Tukey test). The mean rate of change of V˙O₂ with increasing work rate above the LAT [5.9 (SD 2.1) compared to 9.4 (SD 1.3) ml · min⁻¹ · W⁻¹, P < 0.01)] was also much lower in patients than in normal subjects [apparent δ efficiency 60.3 (SD 38.8)% in patients compared to 31.0 (SD 4.9)% in normal subjects]. The patients displayed lower mean values of end-tidal partial pressure of carbon dioxide than the normal subjects at peak exercise [29.7 (SD 6.8) compared to 42.4 (SD 5.8) mmHg, P < 0.01] and mean oxyhaemoglobin saturation [89.1 (SD 4.1) compared to 93.6 (SD 1.8)%, P < 0.05]. Mean ventilatory equivalents for CO₂ [49.3 (SD 11.4) compared to 35.0 (SD 7.3), P < 0.05] and O₂ [44.2 (SD 10.7) compared to 29.9 (SD 5.1), P < 0.05] were greater in patients than normal subjects. The sub-normal slopes for the V˙O₂-work-rate relationship above the LAT indicated severe impairment of the circulatory response to exercise in patients with PPH. The ventilatory abnormalities in PPH suggested that the lung had become an inefficient gas exchange organ because of impaired perfusion of the ventilated lung. Accepted: 17 April 2000     

The effects of drafting on stroking variations during swimming in elite male triathletes

The aim of this study was to determine the effects of drafting behind another swimmer on the metabolic response and stroke characteristics. Six highly trained male triathletes performed two maximal 400-m swims, one in a drafting (D) and one in a non-drafting condition (ND). Their metabolic response was assessed by measuring the oxygen uptake (V˙O₂) and the blood lactate concentration at the end of each 400 m. Swimming velocity, stroke frequency, stroke length, and stroke index (velocity multiplied by stroke length) were recorded every 50 m. In the D and ND conditions, there was no difference in V˙O₂ [66.7 (1.7) ml · kg⁻¹ · min⁻¹ vs 65.6 (1.2) ml · kg⁻¹ · min⁻¹, respectively], however, the lactate concentrations were lower in D than in ND [9.6 (0.9) mM vs 10.8 (0.9) mM, respectively, P < 0.01]. In D, the performance [1.39 (0.02) m · s⁻¹ vs 1.34 (0.02) m · s⁻¹, respectively, P < 0.01] and the stroking parameters (i.e., stroke length and stroke index) increased significantly, while the stroke frequency remain unchanged. In D, a stable pace was maintained, while in ND, velocity decreased significantly throughout the 400 m. In D, the performance gains were related to the 400-m D velocity (r=0.78, P < 0.05), and to the body fat mass (BFM, r=0.99, P < 0.01). The stroke index in D was also related to BFM (r=0.78, P < 0.05). Faster and leaner swimmers achieved greater performance gains and stroke index when drafting. Thus, drafting during swimming increases the performance and contributes to the maintenance of stable stroking parameters such as stroke frequency and stroke length during a 400-m swim. Accepted: 10 April 2000     

Cardiovascular responses to upright and supine exercise in humans after 6 weeks of head-down tilt (−6°)

Seven healthy men performed steady-state dynamic leg exercise at 50 W in supine and upright postures, before (control) and repeatedly after 42 days of strict head-down tilt (HDT) (−6°) bedrest. Steady-state heart rate (f _c), mean arterial blood pressure, cardiac output (Q˙ _c), and stroke volume (SV) were recorded. The following data changed significantly from control values. The f _c was elevated in both postures at least until 12 days, but not at 32 days after bedrest. Immediately after HDT, SV and Q˙ _c were decreased by 25 (SEM 3)% and 19 (SEM 3)% in supine, and by 33 (SEM 5)% and 20 (SEM 3)% in upright postures, respectively. Within 2 days there was a partial recovery of SV in the upright but not in the supine posture. The SV and Q˙ _c during supine exercise remained significantly decreased for at least a month. Submaximal oxygen uptake did not change after HDT. We concluded that the cardiovascular response to exercise after prolonged bedrest was impaired for so long that it suggested that structural cardiac changes had developed during the HDT period. Accepted: 6 June 2000     

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios −Δ[La] · ΔpH⁻¹ (where Δ[La] is change in lactic acid concentration and ΔpH is change in pH) and Δ[HCO₃ ⁻] · ΔpH⁻¹ (where Δ[HCO₃ ⁻] is change in bicarbonate concentration) in blood plasma. The difference between −Δ[La] · ΔpH⁻¹ and Δ[HCO₃ ⁻] · ΔpH⁻¹ yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, Δ[HCO₃ ⁻] · ΔpH⁻¹ can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7–8 days (group 1) or 11–12 days (group 2) after their return from a Himalayan expedition (2800–7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia −Δ[La] · ΔpH⁻¹ amounted to [mean (SEM)] 92 (6) mmol · l⁻¹ before altitude, of which 19 (4), 48 (1) and 25 (3) mmol · l⁻¹ were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude −Δ[La] · ΔpH⁻¹ was increased to 128 (12) mmol · l⁻¹ (P < 0.01) in group 1 and decreased to 72 (5) mmol · l⁻¹ in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol · l⁻¹ in group 1 and to 10 (2) mmol · l⁻¹ in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol · l⁻¹]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La⁻ and H⁺ across cell membranes is differently influenced by high-altitude acclimatization. Accepted: 14 September 2000     

Measurement and prediction of peak shivering intensity in humans

Prediction equations of shivering metabolism are critical to the development of models of thermoregulation during cold exposure. Although the intensity of maximal shivering has not yet been predicted, a peak shivering metabolic rate (Shiv_peak) of five times the resting metabolic rate has been reported. A group of 15 subjects (including 4 women) [mean age 24.7 (SD 6) years, mean body mass 72.1 (SD 12) kg, mean height 1.76 (SD 0.1) m, mean body fat 22.3 (SD 7)% and mean maximal oxygen uptake (V˙O_2max) 53.2 (SD 9) ml O₂ · kg⁻¹ · min⁻¹] participated in the present study to measure and predict Shiv_peak. The subjects were initially immersed in water at 8°C for up to 70 min. Water temperature was then gradually increased at 0.8 °C · min⁻¹ to a value of 20 °C, which it was expected would increase shivering heat production based on the knowledge that peripheral cold receptors fire maximally at approximately this temperature. This, in combination with the relatively low core temperature at the time this water temperature was reached, was hypothesized would stimulate Shiv_peak. Prior to warming the water from 8 to 20 °C, the oxygen consumption was 15.1 (SD 5.5) ml · kg⁻¹ · min⁻¹ at core temperatures of approximately 35 °C. After the water temperature had risen to 20 °C, the observed Shiv_peak was 22.1 (SD 4.2) ml O₂ · kg⁻¹ · min⁻¹ at core and mean skin temperatures of 35.2 (SD 0.9) and 22.1 (SD 2.2) °C, respectively. The Shiv_peak corresponded to 4.9 (SD 0.8) times the resting metabolism and 41.7 (SD 5.1)% of V˙O_2max. The best fit equation predicting Shiv_peak was Shiv_peak (ml O₂ · kg⁻¹ · min⁻¹)=30.5 + 0.348 ×V˙O_2max (ml O₂ · kg⁻¹ · min⁻¹) − 0.909 × body mass index (kg · m⁻²) − 0.233 × age (years); (P=0.0001; r ²=0.872). Accepted: 7 September 2000     

Blood metabolite and catecholamine responses to prolonged exercise following either acute plasma volume expansion or short-term training

 To determine the effect of acute plasma volume (PV) expansion on substrate utilization, blood metabolites and catecholamines to prolonged, moderate intensity cycle exercise, eight untrained men mean maximal oxygen uptake,O_2max 4.10 (SEM 0.32) l · min⁻¹ were infused (10 ml·kg⁻¹) with a 6% dextran (DEX) solution. These responses were also compared to those elicited using a short-term training (TR) protocol involving cycling for 90 to 120 min · day⁻¹ at 60% O_2max for 3 consecutive days. In general DEX, which resulted in a calculated expansion of PV by 23.9%, was without effect in modifying exercise oxygen uptake or the reduction in the respiratory exchange ratio (R) observed during prolonged exercise. In addition, the concentrations of blood glucose, glycerol, alanine and serum free fatty acids, although altered (P < 0.05) by exercise, were not altered by DEX. Blood lactate concentration was only higher (P < 0.05) at 30 min of exercise during DEX compared to the control. With the exception of blood lactate concentration, which was reduced (P < 0.05), TR did not change R or the concentrations of other blood metabolites. The concentrations of nonadrenaline and adrenaline, were depressed (P < 0.05) by DEX and TR at 60 and 90 min of exercise. These results would suggest that mechanisms as yet undefined can compensate for the estimated 10% reduction in arterial oxygen content mediated by acute PV expansion and enable prolonged exercise to be performed without adjustments in substrate selection and substrate mobilization. Accepted: 23 August 1996     

Creatine supplementation alters the response to a graded cycle ergometer test

To determine the effects of creatine supplementation on cardiorespiratory responses during a graded exercise test (GXT) 36 trained adults (20 male, 16 female; 21–27 years old) performed two maximal GXTs on a cycle ergometer. The first GXT was done in a non-supplemented condition, and the second GXT was done following 7 days of ingesting either 5 g creatine monohydrate, encased in gelatin capsules, four times daily (CS, 13 male, 6 female), or the same number of glucose capsules (PL, 7 male, 10 female). CS significantly (P < 0.05) improved total test time [pre-CS=1217 (240) s, mean (std. dev.) versus post-CS=1289 (215) s], while PL administration had no effect (P > 0.05) on total test time [pre-PL=1037 (181) s versus post-PL=1047 (172) s]. In addition, both oxygen consumption (V˙ _O2) and heart rate at the end of each of the first five GXT stages were significantly lower after CS, but were unchanged after PL. Moreover, the ventilatory threshold occurred at a significantly greater V˙ _O2 for CS [pre-CS=2.2 (0.4) l · min⁻¹ or 66% of peak V˙ _O2 versus post-CS=2.6 (0.5) l · min⁻¹ or 78% of peak V˙ _O2; pre-PL=2.6 (0.9) l · min⁻¹ or 70% peak V˙ _O2 versus post-PL=2.6 (1.1) l · min⁻¹ or 68% of peak V˙ _O2]. Neither CS nor PL had an effect on peak V˙ _O2 [pre-CS=3.4 (0.7) l · min⁻¹ versus post-CS=3.3 (0.7) l · min⁻¹; pre-PL=3.7 (1.1) l · min⁻¹ versus post-PL=3.7 (1.1) l · min⁻¹]. Apparently, CS can alter the contributions of the different metabolic systems during the initial stages of a GXT. Thus, the body is able to perform the sub-maximal workloads at a lower oxygen cost with a concomitant reduction in the work performed by the cardiovascular system. Accepted: 20 April 2000     

In vivo 4-androstene-3,17-dione and 4-androstene-3β,17β-diol supplementation in young men

To determine if known androgenic hormone precursors for testosterone in the androgen pathway would be readily transformed to testosterone, eight male subjects [mean age 23.8 (SEM 3) years, bodymass 83.1 (SEM 8.7) kg, height 175.6 (SEM 8.5) cm] underwent a randomized, double-blind, cross-over, placebo-controlled oral treatment with 200 mg of 4-androstene-3,17-dione (Δ4), 4-androstene-3β,17β-diol (Δ4Diol), and placebo (PL). The periods of study were separated by 7 days of washout. Blood was drawn at baseline and subsequently every 30 min for 90 min after treatment. Analysis revealed mean area-under-the-curve (AUC) serum Δ4 concentrations to be higher during Δ4 treatment [2177 (SEM 100) nmol · l⁻¹] than Δ4Diol [900 (SEM 96) nmol · l⁻¹] or PL [484 (SEM 82) nmol · l⁻¹; P < 0.0001]. The Δ4 treatment also revealed a significant effect on total testosterone with a mean AUC [1632.5 (SEM 121) nmol · l⁻¹] that was greater than PL [1418.5 (SEM 131) nmol · l⁻¹; P < 0.05] but not significantly different from those observed after Δ4Diol treatment [1602.9 (SEM 119) nmol · l⁻¹; P = 0.77]. Free testosterone concentrations followed a similar pattern where mean AUC for the Δ4 treatment [6114.0 (SEM 600) pmol · l⁻¹] was greater than after PL [4974.6 (SEM 565) pmol · l⁻¹; P < 0.06] but not significantly different from those observed after Δ4Diol [5632.0 (SEM 389) pmol · l⁻¹; P = 0.48]. The appearance and apparent conversion to total and free testosterone over 90 min was stronger for the Δ4 treatment (r = 0.91, P < 0.045) than for Δ4Diol treatment (r = 0.69, NS) and negatively correlated for PL (r = −0.90, P < 0.02). These results would suggest that Δ4, and perhaps Δ4Diol, taken by month are capable of producing in vivo increases in testosterone concentrations in apparently healthy young men as has already been observed in women after treatment with Δ4. Accepted: 26 August 1999