Naloxone-provoked vaso-vagal response to head-up tilt in men

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg· kg^–1) on cardiovascular responses to 50° head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8–40) to 5 (3–10) min (median and range; (P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) ; P < 0.01 of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats · min^–1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg min 1^–1,P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1 · mint, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats · min^–1 (P < 0.02 compared to control) and MAP remained stable. The episode of hypotensive-bradycardia appeared as mean control HR decreased to 77 (SEM 7)beats · min^–1, TPR to 31.4(SEM 7.7)mmHg · min · 1^–1 and MAP to 60 (SEM 5)mmHg (P < 0.01), and the volunteers were tilted supine. Cardiovascular effects of naloxone on central hypovolaemia included a reduced elevation of HR and blood pressures and provocation of the episode of hypotensive-bradycardia.     

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.     

Exercise training mode affects the hemodynamic responses to lower body negative pressure in women

To determine if different exercise modes used to improve cardiovascular fitness result in differing cardiovascular responses to lower body negative pressure (LBNP) in exercise-trained women, seven chronically exercising female runners (RUN) and 11 swimmers (SWIM) of similar fitness levels maximal oxygen uptake, [ , mean (SEM) = 50 (2) and 45 (2) ml·kg^–1·min^–1, respectively; P > 0.05] underwent serial exposures to LBNP at pressures of 0, –1.3, –2.7 and –5.3 kPa (referenced to ambient barometric pressure). Forearm vascular resistance (venous occlusion plethysmography) increased with LBNP but did not differ between groups at any level of LBNP. At 0 and –1.3 kPa, the total peripheral resistance index (TPRI; impedance cardiography) was significantly (P < 0.05) higher in RUN than SWIM [1.118 (0.028) vs 0.787 (0.040) at 0 kPa and 1.245 (0.100) vs 0.840 (0.040) kPa·1·min^–1 m^–2 at –1.3 kPa]. At an LBNP of –2.7 kPa, stroke index (SI) was significantly higher in SWIM than RUN [57.8 (4.6) vs 41.9 (4.0) ml·beat^–1 · m^–2] while TPRI remained greater in RUN than SWIM. At –5.3 kPa, SWIM exhibited a higher cardiac index [3.232 (0.209) vs 2.447 (0.189) 1·min^–1·m^–2] and SI [49.4 (4.4) vs 31.0 (4.5) ml·beat^–1·m^–2] but reduced heart rate [71 (3) vs 83 (5)beats·min^–1] and TPRI [0.968 (0.043) vs 1.655 (0.128) kPa·1·min^–1 · m^–2]. Mean arterial pressure declined significantly at an LBNP of –5.3 kPa in both groups; pulse pressure was lower (P < 0.05) in RUN than SWIM at LBNP values of –2.7 and –5.3 kPa. These data suggest that: (1) female runners experience a greater increase in systemic vasoconstriction even though female swimmers can better maintain their cardiac index at high levels of LBNP, and (2) training mode appears to affect the pulse pressure responses to LBNP in exercise-trained women.     

Sustained noradrenaline sulphate response in long-distance runners and untrained subjects up to 2 h after exhausting exercise

Summary We investigated the response of plasma and platelet free catecholamine ([CA]) and sulphated catecholamine ([CA-S]) concentrations after an incremental treadmill test to exhaustion and during recovery. In triathletes (n = 9) plasma and platelet [CA] and [CA-S] were measured before, immediately after and 0.5 and 24 h after exercise. In long-distance runners (n = 9) and in controls (n = 10) plasma [CA] and [CA-S] were determined 2 h instead of 24 h after exercise. Platelet [CA] and [CA-S] remained unchanged throughout the study. Plasma [CA] increased after exercise in all groups (P<0.05) and returned to pre-exercise values within 0.5 h of recovery. Plasma sulphoconjugated noradrenaline concentration ([NA-S]) was elevated after exercise in the triathletes, long-distance runners and in controls [9.96 (SEM 0.84) nmol·1^–1, 11.8 (SEM 1.19) nmol·1^–1, 9.53 (SEM 1.10) nmol·l^–1, respectively;P<0.05] compared with resting values [7.13 (SEM 1.04) nmol·l^–1, 6.19 (SEM 0.56) nmol·l^–1, 6.76 (SEM 0.67) nmol·1^–1, respectively] and remained elevated after 0.5 h of recovery [9.94 (SEM1.14) nmol·l^–1, 10.96 (SEM 0.80) nmol·l^–1, 8.95 (SEM 0.99) nmol·l^–1, respectively;P<0.05]. In the long-distance runners and controls plasma [NA-S] remained elevated during 2 h of recovery [9.96 (SEM 0.76) nmol·l^–1, 9.03 (SEM 0.88) nmol·l^–1, respectively]. These results would indicate that plasma [NA-S] increases after sympathetic nervous system activation by an exhausting incremental exercise test and remain elevated up to 2 h after exercise.     

The effect of pedaling frequency on glycogen depletion rates in type I and type II quadriceps muscle fibers during submaximal cycling exercise

Summary This study was conducted to determine whether the pedaling frequency of cycling at a constant metabolic cost contributes to the pattern of fiber-type glycogen depletion. On 2 separate days, eight men cycled for 30 min at approximately 85% of individual aerobic capacity at pedaling frequencies of either 50 or 100 rev·min^–1. Muscle biopsy samples (vastus lateralis) were taken immediately prior to and after exercise. Individual fibers were classified as type I (slow twitch), or type II (fast twitch), using a myosin adenosine triphosphatase stain, and their glycogen content immediately prior to and after exercise quantified via microphotometry of periodic acid-Schiff stain. The 30-min exercise bout resulted in a 46% decrease in the mean optical density (D) of type I fibers during the 50 rev·min^–1 condition [0.52 (0.07) to 0.28 (0.04)D units; mean (SEM)] which was not different (P>0.05) from the 35% decrease during the 100 rev · min^–1 condition [0.48 (0.04) to 0.31 (0.05)D units]. In contrast, the meanD in type II fibers decreased 49% during the 50 rev·min^–1 condition [0.53 (0.06) to 0.27 (0.04) units]. This decrease was greater (P<0.05) than the 33% decrease observed in the 100 rev·min –1 condition [0.48 (0.04) to 0.32 (0.06) units). In conclusion, cycling at the same metabolic cost at 50 rather than 100 rev·min^–1 results in greater type II fiber glycogen depletion. This is attributed to the increased muscle force required to meet the higher resistance per cycle at the lower pedal frequency. These data are consistent with the view that force development as opposed to velocity of contraction determines the degree of type II fiber recruitment when the metabolic cost of exercise is held constant.     

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min^–1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO_{2 peak}). During exercise the subjects ingested either a 15 g · 100 ml^–1 U-¹⁴C labelled glucose solution or H₂O labelled with a U-¹⁴C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma¹⁴C glucose and¹⁴CO₂ specific activities, and respiratory gas exchange. Simultaneously, 2-³H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l^–1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l^–1; infusion 5.0 (0.09) mmol · l^–1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l^–1;P<0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min^–1 kg fat free mass^–1 (FFM);P<0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min^–1 kg FFM^–1;P<0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P<0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) mol · min^–1 kg FFM^–1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.     

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     

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 mechanical effects of contractions on blood flow to the muscle

To determine whether muscle contractions can increase muscle blood flow independently from metabolic factors, we isolated the vasculature of the left diaphragm or gastrocnemius muscle of anesthetized and mechanically ventilated dogs. Arterial blood flow was controlled with a constant pressure source and the arterial pressure (P _a) was decreased in steps to obtain pressure-flow relationships (P- ) . The local vasculatures were maximally dilated with nitroprusside [mean (SD)114.0 (32.0) g·min^–1], adenosine [1.43(0.41) mmol·l^–1·min^–1], and acetylcholine [l.43(0.41) mmol·l^–1·min^–1] and theP- with and without spontaneous contractions (n = 6) , stimulated twitches (n = 12, 2–4 Hz), or tetanic trains (n = 7, 25 Hz) in the diaphragm and stimulated twitches (n = 6, 2–4 Hz), or tetanic contractions (n = 6, 12–16 trains) in the gastrocnemius were compared. The pressure axis intercept decreased (P < 0.5) with spontaneous contractions in the diaphragm and the slope did not change. AtP _a of 13.3 kPa, flow increased from 36.2 (34.9) to 43.9 (38.2) ml·min^–1·100 g^–1 (P < 0.05). During twitch contractions, the slope and intercept of theP- were not significantly different from vasodilatation alone, but the flow at a pressure of 13.3 kPa increased slightly. In the gastrocnemius (n = 6), continuous and intermittent tetanic contractions did not affectP- or flow atP _a of 100 mmHg (n = 6). Furthermore, increasing venous pressure to 6.7 kPa did not affect flow in this muscle. We conclude that the muscle pump has only a small direct effect on muscle blood flow and its main effect is to reduce venous pressures.     

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.     

Increase in energy cost of running at the end of a triathlon

The purpose of the present study was to verify the increase in energy cost of running at the end of a triathlon. A group 11 trained male subjects performed a triathlon (15-km swimming, 40-km cycling, 10-km running). At least 1 week later the subjects ran 10-km as a control at the same pace as the triathlon. Oxygen uptake ( O₂), ventilation ( _E) and heart rate (HR) were measured during both 10-km runs with a portable telemetry system. Blood samples were taken prior to the start of the triathlon and control run, after swimming, cycling, triathlon run and control run. Compared to the control values the results demonstrated that triathlon running elicited a significantly higher (P < 0.005) mean O₂ [51.2 (SEM 0.4) vs 47.8 (SEM 0.4) ml·min^–1·kg^–] _E [86 (SEM 4.2) vs 74 (SEM 5.3) l·min^–1], and HR [162 (SEM 2) vs 156 (SEM 1.9) beats·min^–1)]. The triathlon run induced a greater loss in body mass than the control run [2 (SEM 0.2) vs 0.6 (SEM 0.2) kg], and a greater decrease in plasma volume [14.4% (SEM 1.5) vs 6.7% (SEM 0.9)]. The lactate concentrations observed at the end of both 10-km runs did not differ [2.9 (SEM 0.2) vs 2.5 (SEM 0.2) m·mol·l^–1]. Plasma free fatty acids concentrations were higher (P < 0.01) after the triathlon than after the control run [1.53 (SEM 0.2) to 0.51 (SEM 0.07) mmol·l^–1]. Plasma creatine kinase concentrations rose under both conditions from 58 (SEM 12) to 112 (SEM 14) UI·l^–1 after the triathlon, and from 61 (SEM 7) to 80 (SEM 6) UI·l^–1 after the control run. This outdoor study of running economy at the end of an Olympic distance triathlon demonstrated a decrease in running efficiency.     

Comparison of haemodynamic effects during venous air infusion and after decompression in pigs

We have compared haemodynamic effects of venous gas emboli during continuous air infusion into the right atrium and after rapid decompression in pigs. Eight anaesthetized and spontaneously breathing pigs received continuous air infusion at a rate of either 0.05 ml·kg^–1 · min^–1 (six pigs, air infusion group) or 0.10 ml·kg^–1 · min^–1 (two pigs). Another eight pigs (decompression group) underwent a 30-min compression to 5 bar (500 kPa, absolute pressure), followed by a rapid decompression (2 bar·min^–1). Haemodynamic variables were measured or calculated, and bubbles in the pulmonary artery were monitored using transoesophageal echocardiography. The results showed less variation in the maximal increase in mean pulmonary arterial pressure ( _{a, pulm}) during air infusion (0.05 ml·kg^–1 · min^–1) than after decompression, although the mean maximal increase did not differ between the two groups [28.0 mmHg (3.73 kPa), 95% confidence interval (CI) 23.5–32.5, vs 32.0 mmHg (4.27 kPa), 95% CI 25.3-38.7, P=0.3]. The _a,pulm stabilized or decreased very slowly after peak values were reached in the air infusion group, whereas the _a,pulm decreased rapidly during the same period in the decompression group. No significant changes in mean arterial pressure were observed during air infusion (0.05 ml· kg^–1 · min^–1), in contrast to the rapid increase and the subsequent decrease, that appeared after decompression. Finally, the maximal bubble count was much lower in the air infusion group than in most of the pigs in the decompression group. The two pigs that received 0.10 ml·kg^–1 · min^–1 stopped breathing after 5-min infusion, developed arterial hypotension and died.     

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.     

The influence of a respiratory acidosis on the exercise blood lactate response

Summary The purpose of the present study was to examine the influence of a respiratory acidosis on the blood lactate (La) threshold and specific blood La concentrations measured during a progressive incremental exercise test. Seven males performed three step-incremental exercise tests (20 W · min^–1) breathing the following gas mixtures; 21% O₂ balance-nitrogen, and 21% O₂, 4% CO₂ balance-nitrogen or balance-helium. The log-log transformation of La oxygen consumption (VO₂) relationship and a 1 mmol ·1^–1 increase above resting values were used to determine a La threshold. Also, theVO₂ corresponding to a La value of 2 (La2) and 4 (La4) mmol · 1^–1 was determined. Breathing the hypercapnic gas mixtures significantly increased the resting partial pressure of carbon dioxide (PCO₂) from 5.6 kPa (42 mm Hg) to 6.1 kPa (46 mm Hg) and decreased pH from 7.395 to 7.366. During the incremental exercise test,PCO₂ increased significantly to 7.2 kPa (54 mm Hg) and 6.8 kPa (51 mm Hg) for the hypercapnic gas mixtures with nitrogen and helium, respectively, and pH decreased to 7.194 and 7.208. In contrast, bloodPCO₂ decreased to 4.9 kPa (37 mm Hg) at the end of the normocapnic exercise test and pH decreased to 7.291. A blood La threshold determined from a log-log transformation [1.20 (0.28) 1·min^–1] or as an increase of 1 mmol·1^–1[1.84 (0.46) 1·min^–1] was unaffected by the acid-base alterations. Similarly, theVO₂ corresponding to La2 and La4 was not affected by breathing the hypercapnic gas mixtures [2.12 (0.46) 1·min^–1 and 2.81 (0.52) 1·min^–1, respectively]. Blood La values were reduced significantly at maximal exercise while breathing the hypercapnic gas mixtures (5.72±1.34 mmol ·1^–1) compared with the normocapnic test (6.96±1.14 mmol·1^–1). It is concluded that respiratory-induced acid-base manipulations due to the inspiration of 4% CO₂ have a negligible influence on the blood La response during a progressive exercise test at low and moderate power outputs. Lower blood La values are observed at maximal exercise with an induced respiratory acidosis but this negative influence is less than what has been reported for an induced metabolic acidosis.     

Atrial natriuretic peptide response to endurance physical training in the rat

Summary The effect of an endurance physical training programme on the plasma and atrial natriuretic peptides (ANP) and on renal glomerular ANP receptors was evaluated in male normotensive Wistar rats. Maximal O₂ uptake was significantly greater in the endurance trained (117.1 Ml O₂ · kg^–1 · min^–1, SEM 6.18 versus the control rats 84.2 ml O₂ · kg^–1 · min^–1, SEM 4.88, P<0.01. In addition, various muscle oxidative enzymes were also significantly higher in endurance trained animals. An increase in resting plasma [ANP] was observed after 11 weeks of physical training (40.02 pg · ml^–1, SEM 7.07 vs 22.8 pg.ml^–1, SEM 3.83, P<0.05). Glomerular ANP receptor density was lower in trained rats (272 fmol · mg^–1 protein, SEM 3.1 vs 380 fmol · mg^–1 protein, SEM 6.1, P < 0.05), whereas atrial tissue [ANP] was not significantly different between controls and trained animals. However, in trained rats, circulating [ANP] was closely correlated with left atrial [ANP] (r = –0.92, P<0.05). Resting systolic blood pressure had not changed at the end of this physical training programme. It is considered that under physiological conditions ANP may be involved in long-term extracellular fluid volume homeostasis through the regulation of renal glomerular ANP receptors, and that the left atrium might play a significant role in this long term fluid volume control.     

Limb vasodilatory capacity and venous capacitance of trained runners and untrained males

Aerobically trained athletes possess enhanced vasodilatory capacity and venous capacitance in their exercising muscles. However, whether they also possess these characteristics in their non-specific exercising muscles is undetermined. This study examined vasodilatory capacity and venous capacitance of specific (legs) and non-specific exercising muscles (arms) of ten trained runners and ten active but untrained males aged 18–35 years. Venous occlusion plethysmography determined baseline and peak blood flow after 5 min of reactive hyperaemia. Forearm and leg venous capacitance were determined as the difference between baseline and 2 min of venous occlusion at 50 mmHg. During reactive hyperaemia, trained runners had higher leg (48.4±5.3 ml·100 ml tissue^–1·min^–1) and arm (40.8±2.1 ml·100 ml tissue^–1·min^–1) vasodilatory capacity compared to the untrained (leg: 37.3±2.5 ml·100 ml tissue^–1·min^–1; arm: 34.2±2.2 ml·100 ml tissue^–1·min^–1; P<0.05), and higher calf vascular conductance (0.51±0.06 ml·100 ml tissue^–1·min^–1·mmHg^–1 versus 0.35±0.03 ml·100 ml tissue^–1·min^–1·mmHg^–1; P<0.05). The trained also had higher venous capacitance in both arms (3.5±0.2 ml 100·ml^–1) and legs (4.8±0.1 ml·100 ml^–1) compared to the untrained (3.0±0.2 ml 100·ml^–1; 4.2±0.2 ml·100 ml^–1; P<0.05). These findings show that vasculature adaptations to running occur in both specific and non-specific exercising muscles.     

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.     

Thermal tolerance following artificially induced polycythaemia

Polycythaemia has been shown to improve physical performance, possibly due to increased arterial oxygen transport. Enhanced thermoregulatory function may also accompany this manipulation, since a greater proportion of the cardiac output becomes available for heat dissipation. We further examined this possibility in five trained men, who participated in three-phase heat stress trials (20 min rest, 20 min cycling at 30% peak power W_peak and 20 min at 45% W_peak at 38.3 (SEM 0.7)°C [relative humidity 41.4 (SEM 2.9)%]. Trials were performed during normocythaemia (control) and polycythaemia, obtained by reinfusion of autologous red blood cells and resulting in significant elevation of arterial oxygen transport. During the polycythaemic trials, the subjects demonstrated diminished thermal strain, as evidenced by a significant reduction in cardiac frequency (f _c: 12 beats · min^–1 lower throughout the test;P < 0.05), and reduced auditory canal temperatures (T _ae) during the latter 20-min phase (P < 0.05). Forearm sweat onset was more rapid (363.0 compared to 1083.0 s;P < 0.05), and forearm sweat rate (. _msw) sensitivity was elevated from 1.80 to 2.91 · mg · cm^–2 · min^–1 · °C^–1 (P < 0.05). Foreheadm _sw was depressed during the final 20 min, while forearmm _sw was greater during all test phases, averaging 0.94 and 1.20 mg · cm^–2 · min^–1, respectively, over the 60 min. Skin blood flows for the upper back, upper arm and forearm were reduced (P < 0.05). Polycythaemia enhanced thermoregulation, through an elevation in forearm sweat sensitivity and.m _sw, but not via increased cutaneous blood flow. These modifications occurred simultaneously with decreases inf _c andT _ae, resulting in greater thermal tolerance.     

Effect of heat stress on muscle blood flow during dynamic handgrip exercise

Summary During exercise in a hot environment, blood flow in the exercising muscles may be reduced in favour of the cutaneous circulation. The aim of our study was to examine whether an acute heat exposure (65–70°C) in sauna conditions reduces the blood flow in forearm muscles during handgrip exercise in comparison to tests at thermoneutrality (25° C). Nine healthy men performed dynamic handgrip exercise of the right hand by rhythmically squeezing a water-filled rubber tube at 13% (light), and at 34% (moderate) of maximal voluntary contraction. The left arm served as a control. The muscle blood flow was estimated as the difference in plethysmographic blood flow between the exercising and the control forearm. Skin blood flow was estimated by laser Doppler flowmetry in both forearms. Oesophageal temperature averaged 36.92 (SEM 0.08) ° C at thermo-neutrality, and 37.74 (SEM 0.07) ° C (P<0.01) at the end of the heat stress. The corresponding values for heart rate were 58 (SEM 2) and 99 (SEM 5) beats -min^–1 (P<0.01), respectively. At 25° C, handgrip exercise increased blood flow in the exercising forearm above the control forarm by 6.0 (SEM 0.8) ml · 100 ml^–1 · min^–1 during light exercise, and by 17.9 (SEM 2.5) ml · 100 ml^–1 · min^–1 during moderate exercise. In the heat, the increases were significantly higher: 12.5 (SEM 2:2) ml · 100 ml^–1 · min^–1 at the light exercise level (P<0.01), and 32.2 (SEM 5.9) ml · 100 ml^–1·min^–1 (P<0.05) at the moderate exercise level. Skin blood flow was not significantly different in any of the test conditions between the two forearms. These results suggested that hyperthermia of the observed magnitude did not reduce blood flow in active muscles during light or moderate levels of dynamic handgrip exercise.