Arterial diameter during central volume depletion in humans

The luminal diameter of the radial artery was followed by high frequency ultrasound during 50° head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16–45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) l · min^–1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats · min^–1], mean arterial pressure {MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]} and total peripheral resistance {TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg · min · l^–] [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa · min^–1]} increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats · min^–1, 46 (SEM 4) mmHg [6.1(SEM 0.53) kPa] and 18 (SEM 3) mmHg · min · l^–1 [2.4 (SEM 0.4) kPa · min^–1 · l^–], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 ± 2%) and temporal artery diameters (10 ± 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.     

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.     

Intravenous instrumentation alters the autonomic state in humans

Intravascular instrumentation may induce syncope or presyncope. It is not known whether asymptomatic subjects also have autonomic reactions, albeit concealed. We addressed this issue by studying 44 healthy young male subjects of various levels of fitness, ranging from inactivity to athletic [mean maximal oxygen uptake was 49.1 (SD 10.7) ml·kg^–1·min^–1, range 28.7–71.9 ml·kg^–1·min^–1]. The autonomic response to venous cannulation was quantified by measuring heart rate before cannulation (HR1), after cannulation (HR₂), and after complete pharmacological autonomic blockade (HR₀ = the intrinsic heart rate). The sympathovagal balance before and after cannulation was computed as HR₁/HR₀ and HR₂/HR₀, respectively. The group means of heart rate and sympathovagal balance decreased significantly (paired Student's t-test P <0.01) from 62.5 to 59.9 beats·min^–, and from 0.71 to 0.68, respectively. The maximal decrease in heart rate was 8.8 beats·min^–1, and in the sympathovagal balance was 0.11. Our study demonstrated that the asymptomatic subjects responded to intravenous instrumentation with a concealed autonomic reaction. Thus, from our findings it would seem that intravenous instrumentation interferes with measurements relating to autonomic nervous system activity.     

Hormonal regulation of potassium shifts during graded exhausting exercise

Summary Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3:5-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol·1^–1, SEM 0.12 at the end of exercise vs 3.80 mmol·1^–1, SEM 0.05 basal,P<0.001), plasma adrenaline (2.14 nmol·1^–1, SEM 0.05 at the end of exercise vs 0.30 nmol·1^–1, SEM 0.02 basal,P<0.001), plasma noradrenaline (1.10 nmol·1^–1, SEM 0.64 at the end of exercise vs 1.50 nmol·1^–1, SEM 0.05 basal,P< 0.001), serum aldosterone (0.92 nmol·1^–1, SEM 0.14 at the end of exercise vs 0.36 nmol·1^–1, SEM 0.05 basal,P<0.01), and plasma cAMP (35.4 nmol·1^–1, SEM 2.3 at the end of exercise vs 21.4 nmol·1^–1, SEM 4.5 basal,P<0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol·1^–1, SEM 0.01,P<0.01; and 0.85 nmol·1^–1, SEM 0.12,P<0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU·1^–1, SEM 0.58 at the end of exercise vs 5.47 mlU·1^–1, SEM 0.41 basal, NS) but increased significantly (P<0.02) at the end of the recovery period (7.12 mlU·1^–1, SEM 0.65). Serum potassium increases with exhausting exercise appeared to be caused not only by its release from contracting muscles but also by an -adrenergic stimulation produced by adrenaline and noradrenaline. On the other hand, the increased levels of plasma noradrenaline maintained during the recovery period may have served to avoid excessive hypokalaemia through the stimulation of muscle -receptors. Thus, catecholamines may play an important role in the regulation of serum potassium concentrations during and after exercise. Any disturbance of these adrenergic effects may lead either to an excessive increase or to a decrease of kalaemia, with the consequent risk of arrhythmias linked to exercise.     

Effect of acute mild hypoxia during exercise on plasma free and sulphoconjugated catecholamines

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml · min^–1 · kg^–1 body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P < 0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol · 1^–1, respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol · 1^–1, respectively P < 0.01]. The higher plasma [NA-S] after HYP (P < 0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.     

Finger and forearm vasodilatatory changes after local cold acclimation

Summary To determine the vascular changes induced by local cold acclimation, post-ischaemia and exercise vasodilatation were studied in the finger and the forearm of five subjects cold-acclimated locally and five non-acclimated subjects. Peak blood flow was measured by venous occlusion plethysmography after 5 min of arterial occlusion (PBF_isc), after 5 min of sustained handgrip at 10% maximal voluntary contraction (PBF_exe), and after 5 min of both treatments simultaneously (PBF_isc+exe). Each test was performed at room temperature (25° C, SE 1 C) (non-cooled condition) and after 5 min of 5'C cold water immersion (cooled condition). After the cold acclimation period, the decrease in skin temperature was more limited in the cold-acclimated compared to the non-acclimated (P<0.01). The PBF_isc was significantly reduced in the cooled condition only in the cold-acclimated subjects (finger: 8.4 ml · 100 ml^–1 · min^–1, SE 1.1,P<0.01; forearm: 5.8 ml · 100 ml^–1 · min^–1, SE 1.5,P<0.01) compared to the non-cooled condition. Forearm PBF_exe was significantly decreased in the cooled condition only in the cold-acclimated subjects (non-cooled: 7.4 ml · 100 ml^–1 · min^–1, SE 1.2; cooled: 3.9 ml · 100 ml^–1 ·min^–1, SE 2.6,P<0.05) indicating that muscle blood flow was also reduced. The application of PBF_isc+exe elicited an increase in peak blood flow only in the forearm of the non-acclimated subjects (non-cooled: 10.4 ml· 100 ml^–1 · min^–1, SE 2.0; cooled: 14.3 ml · 100 ml^–1 · min^–1, SE 2.6,P<0.05) and conversely only in the finger of the cold-acclimated (non-cooled finger: 25.7 ml · 100 ml^–1 · min^–1, SE 4.4; cooled finger: 19.2 ml · 100 ml^–1 · min^–1, SE 3.3,P<0.01). Therefore, subjects cold-acclimated locally showed decreased vasodilatatory responses only when exposed to cold.     

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.     

Reduced exercise hyperaemia in calf muscles working at high contraction frequencies

Summary The effects of muscle contraction frequency on blood flow to the calf muscle (Q _calf) were studied in six female subjects, who performed dynamic plantar flexions at frequencies of 20, 40, 60, 80 and 100 contractions · min^–1, in a supine position. TheQ _calf measured by a mercury-in-rubber strain gauge plethysmograph, increased as contraction frequency increased and reached a peak at 60–80 contractions · min^–1. After 100 plantar flexions at 60 contractions · min^–1, the meanQ _calf was 30.95 (SEM 4.52) ml · 100 ml^–1 · min^–1. At 100 contractions · min^–1, however, it decreased significantly compared with that at 60 contractions · min^–1 at a specified time (2 min or exhaustion) or after a fixed amount of work (100 contractions). The contraction frequency at whichQ _calf reached a peak depended on the duration of exercise. The heart rate showed its highest mean value at 60 contractions · min^–1 and decreased significantly at 100 contractions · min^–1. The mean blood pressure was lower at 100 contractions · min^–1 than at 60 contractions · min^–1. The relaxation period between contractions, measured by recording the electromyogram from the gastrocnemius muscles, shortened markedly as the frequency increased; the mean value at 100 contractions · min^–1 was 0.14 (SEM 0.02) s, which corresponded to 35.7% of the contraction time. This shortened relaxation period between contractions should have led to the inhibition of exercise hyperaemia at the higher contraction frequencies.     

Exhausting handgrip exercise reduces the blood flow in the active calf muscle exercising at low intensity

The calf and forearm blood flows (Q _calf and Q _forearm respectively), blood pressure, heart rate and oxygen uptake of six men and women were studied during combined leg and handgrip exercise to determine whether a reduction of exercise-induced hyperaemia would occur in the active leg when exhausting rhythmic handgrip exercise at 50% maximal voluntary contraction (MVC) was superimposed upon rhythmic plantar flexion lasting for 10 min at 10% MVC (P₁₀) prior to this combined exercise. The Q _calf and Q _forearm were measured by venous occlusion plethysmography during 5-s rests interposed during every minute of P₁₀ exercise and immediately after combined exercise. The muscle sympathetic nerve activity (MSNA) changes were also recorded during leg exercise alone and combined exercise. During plantar flexion performed 60 times · min^–1 with a load equal to 10% MVC (P₁₀), Q _calf was maintained at a constant level, which was significantly higher than the resting value (P < 0.001). When rhythmic handgrip contraction at 50% MVC (H₅₀) and P₁₀ were performed simultaneously, the combined exercise was concluded due to forearm exhaustion after a mean of 51.2 (SEM 5.5) s. At exhaustion, Q _calf had decreased significantly from 20.6 (SEM 3.0) ml · 100 ml^–1 · min^–1 (10th min during P₁₀ exercise) to 15.3 (SEM) ml · 100 ml^–1 · min^–1 (P = 0.001), whereas Q _forearm had increased significantly (0.001 < P < 0.01) from 8.6 (SEM 1.9) ml · 100 ml^–1 · min^–1 (10th min of P₁₀ exercise) to 26.2 (SEM 3.2) ml · 100 ml^–1 · min^–1. The mean blood pressure remained at an almost constant level during the 3rd to 10th min of P₁₀ exercise and increased markedly when H₅₀ was added. The calf vascular conductance during combined exercise decreased significantly (0.001 < P < 0.01) compared with that at the 10th min of P₁₀ alone. Although the MSNA (expressed as burst rate) remained unchanged during P₁₀ exercise for 10 min, it increased markedly when exhausting H₅₀ and P₁₀ exercise were performed simultaneously. These findings indicated that superimposition of exhausting handgrip exercise at 50% MVC caused a vasoconstriction in the exercising calf due to increased MSNA, which counteracted the vasodilatation in this active muscle.     

Intra- and extracranial artery blood velocity during a sudden blood pressure decrease in humans

The intra- and extracerebral Doppler artery blood velocity responses to a 10-mmHg abrupt blood pressure (BP) decrease in ten healthy men were studied. This decrease was obtained using two cuffs placed over both thighs. First, cuffs were inflated to pressures greater than the arterial BP for 5 min. Next, they were deflated to 60 mmHg in order to prevent venous return from the legs. We obtained a decrease in mean arterial BP of from 101 (10) to 90 (10) mmHg [mean (SD), P < 0.01] without modifications in the heart rate [HR, 88 (14) beats min⁻¹]. Middle cerebral artery mean blood velocity (MCAmv) decreased immediately from 50 (10) to 42 (12) cm s⁻¹ (P < 0.05). Simultaneously, temporal superficial artery mean blood velocity (TSAmv) decreased from 11 (3) to 7 (2) cm s⁻¹ (P < 0.05) and common carotid artery blood flow (CCAbf ) decreased from 305 (23) to 233 (33) ml min⁻¹ (P < 0.05). After 5 s, MCAmv and CCAbf returned to baseline values, whereas TSAmv [8 (2) cm s⁻¹], mean arterial BP [86 (10) mmHg] remained low and HR increased [92 (12) beats min⁻¹]. TSAmv, BP and HR returned to baseline values in 1 min. These data confirm that cerebral blood flow (CBF) is very rapidly regulated but that blood flow in extracranial territories is not and that it follows the arterial BP changes. Accepted: 8 April 1997     

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.     

Physiological strains while pushing or hauling

An experiment has been designed to compare two ways of load moving: pushing with a bar or hauling with a pelvic belt, against the same resistances, at the same speeds. This study has been carried out in the laboratory on a treadmill, using two groups: 15 healthy sedentary men and 10 endurance trained male athletes. The task consisted of pushing or hauling against the same resistance (3, 5 and 7 kg for the first group and 6, 8, 9 and 10 kg for the second) at two walking speeds (3 and 4 km · h^–1 for the first group and 3.7 and 4.7 km · h^–1 for the second). The physiological strains were studied by measuring heart rate (HR) and oxygen consumption ( ) in both experiments. In addition, perceived exertion was estimated in the second group according to a rating scale of perceived exertion (RPE). Analysis of variance showed that pushing with the arms was more strenuous than hauling with a pelvic belt with regard to HR, and RPE (P < 0.01). When resistances and speeds were grouped, the differences between pushing and hauling were equal to 3 beats · min^–1, 0.85 ml · min^–1 · kg^–1 for HR and , respectively, for the first experiment (sedentary subjects), wheras the differences were equal to 11.4 beats · min^–1, 1.66 ml · min^–1 · kg^–1 and 2.15 for HR, and RPE, respectively, for the second experiment (trained endurance athletes). In the endurance athletes, there was a parallel upward shift of the -HR linear relationship for pushing (covariance analysis, P < 0.01), which suggested that an element of static work (pushing with the upper limbs) added to the dynamic work could explain the higher physiological cost during pushing.     

Anaerobic threshold in children: determination from saliva analysis in field tests

The purpose of this study was to determine the anaerobic threshold of children by the analysis of saliva collected during field tests. A group of 25 children (mean age, 10.5 years) performed an incremental exercise test on a track, consisting of 4-min stages at increasing running velocities. Before each test (at rest) and at the end of each stage, both blood (via finger pricks) and saliva samples (for measurement of salivary concentrations of Na⁺ and Cl^–) were collected to determine lactate threshold (Th_1a-) and saliva threshold (Th_sa), respectively. There were no significant differences between values of Th_1a- and Th_sa when expressed either as running velocity [mean Th_1a-, 10.73 (SD 1.96) km · h^–1; mean Th_sa, 10.89 (SD 1.69) km · h^–1] or heart rate [Th_1a-, 182(SD 14) beats · min^–1 Th_sa 183 (SD 11) beats · min^–1]. In addition, correlations between Th_sa and Th_1a were high, when both values were expressed as running velocity in kilometres per hour (r = 0.89;P < 0.001), or heart rate in beats per minute (r = 0.90;P < 0.001). In conclusion, these findings suggested that saliva analysis would be a valid method for anaerobic threshold determination in field tests.     

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.     

Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( O_2max), high-intensity exercise (HIE)] and 50% of peak power output [60% O_2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg ^–1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg ^–1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min^–1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.     

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.     

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.     

Effects of hypotension on cutaneous and subcutaneous blood flow in anaesthetized humans

Summary The aim of this study was to determine the effect of controlled hypotension on subcutaneous and cutaneous haemodynamics in humans. Moderate hypotension was achieved with nitroglycerin (NTG) and sodium nitroprusside (SNP) infusion during narconeuroleptanalgesia in seven patients. Subcutaneous and cutaneous blood flow were measured by a superficial and deep heat clearance (HC) technique. The mean arterial pressure ( ) decreased by 23%–30% and heart rate (f _c) increased but only during NTG infusion (+22%; P < 0.02). Subcutaneous and cutaneous blood flows remained unchanged despite a significant decrease in calculated cutaneous resistance (NTG: –26%, P < 0.01; SNP: –34%, P < 0.02)) and subcutaneous vascular resistance changed only with SNP (–31%, P < 0.02). After hypotension was discontinued the subcutaneous blood flow decreased (–13%, P = 0.05), whereas subcutaneous vascular resistance returned to its control values. An inverse relationship was found between f _c and (NTG: r = –0.525, P < 0.01; SNP: r = –0.622, P < 0.01) as well as with subcutaneous blood flow (NTG: r = –0.653, P < 0.001; SNP: r = –0.573, P < 0.01). In addition, we found oscillatory changes in deep HC values which differed in magnitudes (NTG 0.22 (SEM 0.09) W · m^–1 · °C^–1 vs SNP 0.42 (SEM 0.1) W · m^t–1 · °C^–1, P< 0.01) and frequencies (NTG 0.02 (SEM 0.006) Hz vs SNP 0.01 (SEM 0.002) Hz, P < 0.01). Despite unchanged blood flow, the effects of controlled hypotension on cutaneous and subcutaneous haemodynamics were different depending on the type of drug. These differences may have been related to counterregulatory responses and/or to direct vascular effects.     

Continuous measurement of blood pressure, heart rate and left ventricular performance during and after isometric exercise in head-out water immersion

Experiments were performed to determine the changes in blood pressure (BP), heart rate (HR) and left ventricular function during and after isometric knee extension during thermoneutral (35°C) head-out water immersion (HWI) or in air. Seven healthy male subjects mean age 24 (SD 3) years kept their knees extended (60% maximal voluntary extension) until they reached exhaustion. The mean BP at rest was 80 (SD 10) and 78 (SD 8) mmHg [10.7 (SD 1.33) and 10.4 (SD 1.07) kPa] in air and during HWI, respectively, (NS). They increased progressively (P < 0.01) during contraction and reached maximal values of 148 (SD 22) and 143 (SD 26) mmHg [19.7 (SD 2.93) and 19.1 (SD 3.47) kPa] in air and in HWI, respectively, (NS). The mean HR at rest was 74 (SD 8) and 70 (SD 11) beats·min^–1 in air and in HWI, respectively, (NS). They also increased progressively (P < 0.01) and reached 126 (SD 14) and 118 (SD 17) beats·min^–1 in air and in HWI, respectively, (NS). The changes in BP and HR during contraction in HWI tended to be smaller than those in air (NS). Left ventricular end diastolic diameters (dd) at rest in HWI were greater than those in air and were maintained at higher values during and after isometric contraction. In contrast, dd decreased during isometric contraction in air (P < 0.01). The change of left ventricular systolic diameters (d _s) in HWI was no different to those in air. From these findings, isometric exercise in thermoneutral HWI would seem to be characterized by a greater d _d than in air and this could be useful for patients with deconditioning effects such as orthostatic hypotension.