Splanchnic and renal vasoconstrictor and metabolic responses to neuropeptide Y in resting and exercising man.

The local clearance of neuropeptide Y (NPY) and whether NPY influences splanchnic and renal metabolism in man have not been investigated previously. The influence of NPY on splanchnic and renal blood flows at physiologically elevated levels has also not been investigated. The effects of a 40-min constant NPY infusion (3 pmol kg-1 min-1) at rest and during 130 min of exercise (50% of VO2max) were studied in six healthy subjects and compared with resting and exercising subjects receiving no NPY. Blood samples were drawn from arterial, hepatic and renal vein catheters for the determination of blood flows (indicators: cardiogreen and para-aminohippuric acid [PAH]), NPY, catecholamines, glucose, lactate and glycerol. NPY infusion was accompanied by: (1) significant fractional extraction of NPY-like immunoreactivity (NPY-Li) by splanchnic tissues at rest (58 +/- 5%) and during exercise (53 +/- 6%), while no arterial-venous differences could be detected across the kidney; (2) a reduction in splanchnic and renal blood flows of up to 18 and 13% respectively (P less than 0.01-0.001) at rest without any additional changes during exercise; and (3) metabolic changes as reflected in: (a) a more marked fall in arterial glucose during exercise compared to the reference group (P less than 0.05); (b) a 35% lower splanchnic glucose release (P less than 0.01) during exercise due to diminished glycogenolysis (P less than 0.01); and (c) a lower arterial lactate level (18% P less than 0.05) together with unchanged splanchnic lactate uptake during exercise, suggesting reduced lactate production by extrahepatic tissues. The disappearance of plasma NPY-Li after the infusions was biphasic with two similar half-lives at rest (4 and 39 min) and during exercise (3 and 43 min).     

Splanchnic and renal vasoconstriction during neuropeptide Y infusion in healthy humans.

To assess whether neuropeptide Y (NPY) causes vasoconstriction in human splanchnic and renal tissues, six healthy subjects were given NPY intravenously in the basal resting state for 15 min. The NPY dose of 10, 25, and 50 pmol kg-1 min-1 was increased every 5 min. The infusion was accompanied by elevated arterial plasma levels of NPY-like immunoreactivity (Li) which were 15, 40, and 85 times higher than the basal value. After the infusion plasma NPY-Li fell with two half-lives of 5 +/- 0.4 and 29 +/- 1.7 min but was still 4 times the basal values 60 min after the infusion (P less than 0.01). A vasoconstrictor effect was seen at about 500 pM plasma NPY-Li. During the NPY infusion splanchnic and renal blood flows decreased by 26% and 29% respectively. The blood flows in these regions were still below the basal value 40 to 60 min after the NPY infusion. Plasma noradrenaline fell by 20% (P less than 0.02) and arterial glucose by 3% (P less than 0.005) during the NPY infusion. It is concluded that NPY causes a dose-dependent long-lasting vasoconstriction in human renal and splanchnic tissues. The results also suggest that elevated plasma NPY-levels may be associated with changes in the turnover of noradrenaline and glucose.     

Effect of anaesthetizing the region of the paraventricular hypothalamic nuclei on energy metabolism during exercise in the rat

The ventromedial and posterior hypothalamic nuclei are known to influence glucoregulation during exercise. The extensive projections of the paraventricular hypothalamic nucleus (PVN) to the sympathetic nervous system suggest that the PVN also may be involved in glucoregulation during exercise. The region of the PVN was anaesthetized with bupivacaine before running (26 m min^-1) or continued rest, via previously implanted bilateral brain cannulas aimed at the dorsal aspect of the PVN. Control rats were treated identically to PVN-anaesthetized rats, but were not infused. Blood, for determination of plasma concentrations of metabolites and hormones, was drawn from a tail artery, and ³H-glucose was infused in a tail vein for glucose turnover determinations. At rest, no significant changes in plasma concentrations of metabolites or hormones were induced by anaesthesia of the region of the PVN. During exercise, glucose production and utilization and plasma concentrations of glucose, lactate, glycerol, noradrenaline, adrenaline, corticosterone, and glucagon increased (P < 0.02) and plasma insulin decreased (P < 0.02) in all rats. However, initially in exercise, adrenaline (4.3 ±0.8 vs. 7.9 ± 1.0 nmol 1^-1 in controls, P < 0.05, t= 6 min) and later corticosterone levels (1.37 ± 0.06 vs. 1.69 ± 0.10 nmol 1^-1 in controls, P < 0.05, t = 20 min) were attenuated by PVN anaesthesia. Initially during exercise, glucose utilization was higher and plasma glucose lower in PVN-anaesthetized rats compared to controls (16.6 ± 0.8 vs. 12.7 ± 0.6 μmol min^-1 100 g^-1 and 7.1 ± 0.2 vs. 8.1 ± 0.2 mmol 1^-1, respectively. P < 0.05, t= 6 min) and exercise-induced liver glycogen breakdown was only significant in the controls. In conclusion, the region of the PVN does not influence glucoregulation at rest, but affects glucoregulation during exercise, by stimulating adrenaline and corticosterone secretion during exercise.     

Role of adenosine in exercise‐induced human skeletal muscle vasodilatation

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ～48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (F_aBF) by ～20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min^?1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min^?1 mmHg^?1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) F_aBF from 0.3 ± 0.03 L min^?1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min^?1. Continuous infusion of adenosine at rest and during one‐legged exercise at ～62% of peak power output increased (P < 0.05) F_aBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min^?1, respectively. One‐legged exercise alone increased (P < 0.05) F_aBF to 4.7 ± 1.7 L min^?1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ～20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

Long-lasting coronary vasoconstrictor effects and myocardial uptake of endothelin-1 in humans

The effect of intravenous administration of the endothelium-derived vasoconstrictor peptide endothelin-1 (ET-1 0.2, 1 and 8 pmol kg^?1 min^?1) on coronary blood flow in relation to plasma ET-1 as well as blood lactate and glucose levels were investigated in six healthy volunteers. Coronary sinus blood flow was measured by thermodilution. Administration of ET-1 elevated arterial plasma ET 35-fold, dose-dependently increased mean arterial blood pressure from 95±5 mmHg to 110±6 mmHg (P<0.01) and reduced heart rate from 64±4 beats min^?1 to 58±4 beats min^?1 (P<0.05) at 8 pmol kg^?1 min^?1. Coronary sinus blood flow was reduced maximally by 23±4% (P<0.01) and coronary vascular resistance increased by 48±11% (P<0.01). Coronary sinus oxygen saturation decreased from 35±1% to 22±2% at 2 min after the infusion (P<0.01). A coronary constrictor response was observed at a 4-fold elevation in plasma ET. The reduction in coronary sinus blood flow lasted 20 min and coronary sinus oxygen saturation was still reduced 60 min after the infusion. Myocardial oxygen uptake or arterial oxygen saturation were not affected by ET-1. Myocardial lactate net uptake decreased by 40% whereas glucose uptake was unaffected. At the highest infusion rate there was a net removal of plasma ET by 24±3% over the myocardium (P<0.05). The results show that ET-1 induces long-lasting reduction in coronary sinus blood flow via a direct coronary vasoconstrictor effect in healthy humans observable at a 4-fold elevation in plasma ET-1. Furthermore, there is a net removal of circulating ET-1 by the myocardium.     

Skeletal muscle glycolysis during submaximal exercise following acute β-adrenergic blockade in man

The present study describes the influence of β-adrenergic blockade on glycogen utilization and lactate accumulation in skeletal muscle of exercising man. Twelve physically active men were examined during 25 min of continuous cycle exercise equivalent to 65% of their maximal oxygen uptake both with and without oral administration of 80 mg of propranolol (Inderal®). Heart rate, oxygen uptake, rate of perceived exertion (RPE) and blood lactate concentration were measured during exercise. Muscle biopsies were obtained from m. vastus lateralis after 5 and 25 min of exercise, β-adrenergic blockade decreased steady state exercise heart rate by (mean + SD) 35 ± 10 beats min^-1 (P < 0.001) and oxygen uptake from 2.47 to 2.39 1-min^-1 (P < 0.01). Muscle glycogen decreased from the 5th to the 25th min of exercise, and β-blockade had no significant effect on this decrease. In contrast to without drug, β-blockade resulted in a decrease (P < 0.05) in muscle lactate concentration from the 5th (6.9 mmolkg^-1 w./w.) to the 25th min (4.8 mmolkg^-1 w./w.). Similarly blood lactate levels were lower (P < 0.05) with than without β-blockade in the last but not the first 10 min of exercise. The alteration in muscle lactate concentration pattern following β-blockade, may imply that adrenergic effects per se contribute to the stimulation of glycolysis during submaximal exercise, except in its earliest phase. Nevertheless, the effect is not great enough to produce substantial differences in glycogen utilization.     

An acute oral dose of caffeine does not alter glucose kinetics during prolonged dynamic exercise in trained endurance athletes

This study investigated the possible influence of oral caffeine administration on endogenous glucose production and energy substrate metabolism during prolonged endurance exercise. Twelve trained endurance athletes [seven male, five female; peak oxygen consumption ( ) = 65.5 ml·kg^–1·min^–1] performed 60 min of cycle ergometry at 65% twice, once after oral caffeine administration (6 mg·kg^–1) (CAF) and once following consumption of a placebo (PLA). CAF and PLA were administered in a randomized double-blind manner 75 min prior to exercise. Plasma glucose kinetics were determined with a primed-continuous infusion of [6,6-²H]glucose. No differences in oxygen consumption ( ), and carbon dioxide production ( ) were observed between CAF and PLA, at rest or during exercise. Blood glucose concentrations were similar between the two conditions at rest and also during exercise. Exercise did lead to an increase in serum free fatty acid (FFA) concentrations for both conditions; however, no differences were observed between CAF and PLA. Both the plasma glucose rate of appearance ( ) and disappearance ( ) increased at the onset of exercise (P<0.05), but were not affected by CAF, as compared to PLA. CAF did lead to a higher plasma lactate concentration during exercise (P<0.05). It was concluded that an acute oral dose of caffeine does not influence plasma glucose kinetics or energy substrate oxidation during prolonged exercise in trained endurance athletes. However, CAF did lead to elevated plasma lactate concentrations. The exact mechanism of the increase in plasma lactate concentrations remains to be determined. Electronic Publication     

Splanchnic release of neuropeptide Y during prolonged exercise with and without beta-adrenoceptor blockade in healthy man.

Plasma levels of neuropeptide Y- (NPY-) like immunoreactivity (Li) and catecholamines in the brachial artery, femoral vein and hepatic vein were monitored during physical exercise in a total of 19 healthy men to detect any local release from the leg and splanchnic region. In addition, propranolol (0.15 mg kg-1 i.v.) was given during exercise to determine whether beta-adrenoceptor blockade influenced the increase in plasma NPY-Li and catecholamines. Leg and splanchnic blood flows were measured using indicator dilution techniques and indocyanine green dye. Graded arm exercise was associated with elevations of arterial plasma NPY-Li (two-fold) and noradrenaline (12-fold) comparable to those previously found during leg exercise. During prolonged leg exercise a significant vasoconstriction and release of NPY-Li and noradrenaline was observed in the splanchnic region while no net exchange was found in the exercising leg where marked vasodilatation occurred. Administration of propranolol during exercise produced a clear-cut additional increase in plasma NPY-Li as well as in noradrenaline and adrenaline. It is concluded that splanchnic vasoconstriction during exercise is associated with a local release of both NPY-Li and noradrenaline. The additional elevation in plasma NPY-Li and catecholamines after propranolol during exercise is probably due to increased nerve activity and/or decreased disposal.     

A comparison of blood gases and acid-base measurements in arterial,arterialized venous,and venous blood during short-term maximal exercise

Summary The purpose of this study was to determine the relationship between blood gases and acid-base measurements in arterial, arterialized venous, and venous blood measured simultaneously during short-term maximal exercise. Ten well-trained male cyclists performed a graded maximal exercise test on a cycle ergometer to determine the power output corresponding to their peak oxygen consumption (test I), and a short-term maximal test on a cycle ergometer at peak power output (test 11). During test 11 arterial, arterialized venous and venous blood were sampled simultaneously for determination of partial pressures of oxygen and carbon dioxide, pH, bicarbonate (HCO₃ ^–), base excess (BE), and lactate (La). Samples were taken at rest, the end of 1 min of exercise (1 ME), at the end of exercise (EE), and at 2 min of recovery (REC). During test II, subjects maintained a peak power output of 370.6 (62.1) W [mean (SD)] for 4.5, SD 1.6 min. Except at rest venous and arterialized venous measurements tended to be the same at all sampling intervals, but differed significantly from measurements in arterial blood (P<0.05). BE was the only variable that rendered consistently significant correlations between arterial and arterialized venous blood at each sampling interval. The pooled correlation coefficient between arterial and arterialized venous BE was r=0.83 [regression equation: BE_a=(0.84 BE_av)–0.51]. Arterial La was significantly higher than venous La at 1 ME (2.8, 0.7 vs 0.8, 0.3mmol · 1^–1) and higher than both venous and arterialized venous La at EE. At EE La concentration was 9.2, SD 2.0, 4.6, SD 0.4, and 5.1, SD 0.1 mmol · 1^–1 in arterial, venous, and arterialized venous blood respectively. It is concluded that except for base excess, blood gases and acid base measurements in venous and arterialized venous blood do not accurately reflect values found in arterial blood during short-term maximal exercise. We suggest that these differences may be due in part to clearance by inactive muscle near the sampling site or vasoconstriction at the inactive sampling site.     

Cardiovascular reflexes during sustained handgrip exercise: role of muscle fibre composition,potassium and lactate

Summary Six healthy men performed sustained static handgrip exercise for 2 min at 40% maximal voluntary contraction followed by a 6-min recovery period. Heart rate (f _c), arterial blood pressures, and forearm blood flow were measured during rest, exercise, and recovery. Potassium ([K⁺]) and lactate concentrations in blood from a deep forearm vein were analysed at rest and during recovery. Mean arterial pressure (MAP) andf _c declined immediately after exercise and had returned to control levels about 2 min into recovery. The time course of the changes in MAP observed during recovery closely paralleled the changes in [K⁺] (r=0.800,P<0.01), whereas the lactate concentration remained elevated throughout the recovery period. The close relationship between MAP and [K⁺] was also confirmed by experiments in which a 3-min arterial occlusion period was applied during recovery to the exercised arm by an upper arm cuff. The arterial occlusion affected MAP whilef _c recovered at almost the same rate as in the control experiment. Muscle biopsies were taken from the brachioradialis muscle and analysed for fibre composition and capillary supply. The MAP at the end of static contraction and the [K⁺] appearing in the effluent blood immediately after contraction were positively correlated to the relative content of fast twitch (% FT) fibres (r=0.886 for MAP vs %FT fibres,P<0.05 andr=0.878 for [K⁺] vs %FT fibres,P<0.05). Capillary to fibre ratio showed an inverse correlation to % FT fibres (r=–0.979,P<0.01). These results indicated that activation of FT rather than slow twitch fibres during static contraction induced a more marked arterial pressure reflex. It was concluded that the arterial pressure reflex would seem to be mediated through stimulation of unmyelinized free nerve endings in the contracted muscle. The [K⁺] would appear to be a more likely candidate than lactate as a mediator for this pressure reflex.     

Exercise‐induced changes in brain glucose and serotonin revealed by microdialysis in rat hippocampus: effect of glucose supplementation

The aim of this study was to assess extracellular glucose changes in hippocampus in response to physical exercise and to determine the influence of glucose supplementation. In the same time, we have observed the changes in serotonin, in order to study the relationship between glucose and serotonin during exercise. Both glucose and serotonin were assessed using microdialysis. Exercise induced an increase in extracellular glucose levels over baseline during exercise to 121.1 ± 3.0% (P < 0.001), then a decrease to baseline during recovery. The serotonin followed glucose changes during the first 90 min of exercise, but followed a different pattern during recovery, increasing to a maximum of 129.9 ± 7.0% after 30 min of recovery (P < 0.001). When a 15% glucose solution was infused (10 μL min^–1) during exercise and recovery, blood glucose concentration was increased, but extracellular brain glucose decreased to reach a minimum of 73.3 ± 4.6% after 90 min of recovery (P < 0.001). Serotonin was always the mirror‐reflect of cerebral glucose, with a maximum increase of 142.0 ± 6.9% after 90 min of recovery (P < 0.001). These results show that exercise induces changes in brain glucose and 5‐hydroxytryptamine (5‐HT) levels, which were dramatically modified by glucose infusion. Taking into account the implication of brain 5‐HT in central fatigue, they suggest that if glucose supplementation, before and during exercise, undoubtedly increase performance because of its peripheral positive action, it would have a negative impact on the quality of recovery after the end of the exercise.     

The influence of blood sampling site on lactate concentration during submaximal exercise at 4 mmol · 1−1 lactate level

This study examined lactate concentration during incremental and submaximal treadmill exercise at work rates corresponding to 4 mmol· 1^–1 lactate concentration, determined by fingertip (OBLAI) and venous blood (OBLA2). Initially, eight subjects performed a 4-min incremental exercise test until exhaustion. On two other occasions, seven of the subjects undertook submaximal exercise tests (30 min) at work rates corresponding to OBLA1 and OBLA2. Blood was simultaneously obtained from both sites at rest and at the end of each exercise stage during the incremental exercise, and at 5, 10, 20 and 30 min during the submaximal exercise and 5 min into recovery. Fingertip blood lactate concentrations were significantly higher (P<0.05) than venous blood at rest, throughout the incremental exercise, consistently during exercise at OBLA1 and OBLA2, and into recovery. Data also revealed an exercise intensity-dependent lactate difference between the two sampling sites during both exercise protocols. Exercise at OBLA1 did not result in a progressive increase in lactate level nor exhaustion, and the lactate value at the end of 30 min corresponded to the predetermined value. However, exercise at OBLA2 resulted in a significantly higher (P<0.05) lactate level than OBLA1, the lactate concentration at the end of 30 min was substantially higher than the predetermined value (P<0.05) and exhaustion was evident. It is concluded that the lactate concentration value during incremental and submaximal exercise (at 4 mmol·l^–1 OBLA) is dependent on the blood sampling site. This finding should be considered in studies concerned with the determination of OBLA.     

Influence of α-adrenergic receptor stimulation on splanchnic intravascular volume in conscious humans

The influence of selective α-adrenergic receptor stimulation on total splanchnic intravascular volume and blood volume in individual splanchnic organs in humans has not been previously examined. The present study employed a previously validated quantitative radionuclide imaging technique, involving a gamma camera and Tc-99m labeled erythrocytes, to measure changes in total splanchnic, hepatic, splenic, and extrahepatosplenic volume during a 20-minute phenylephrine infusion (30–120 μ min^-1 iv). Changes in total splanchnic volume were estimated from changes in total splanchnic radioactivity, blood radioactivity, and estimated in vivo tissue attenuation. Radionuclide-estimated total splanchnic volume increased 477±96 ml (P < 0.0003) at the end of phenylephrine infusion. Hepatic volume increased 25±5% (P < 0.0003), splenic volume decreased 46±7% (P < 0.0003), and extrahepatosplenic volume decreased 15±2% (P < 0.0003). Systolic and diastolic arterial pressures increased from 119±4 to 138 ± 5 mmHg (P < 0.0003) and from 83+1 to 96 ± 2 mmHg (P < 0.0003), respectively. Heart rate decreased from 62±2 to 51±3 bpm (P < 0.0003). Thus, in man, selective α-adrenergic receptor stimulation is associated with an increase in splanchnic intravascular volume that is due to an increase in hepatic volume and occurs despite decreases in splenic and extrahepatosplenic volumes. This increase in total splanchnic volume would be associated with a decrease in venous return from the splanchnic vasculature to the right heart which would act to decrease cardiac output.     

Enhanced cerebral CO2 reactivity during strenuous exercise in man

Light and moderate exercise elevates the regional cerebral blood flow by ~20% as determined by ultrasound Doppler sonography (middle cerebral artery mean flow velocity; MCA V _mean). However, strenuous exercise, especially in the heat, appears to reduce MCA V _mean more than can be accounted for by the reduction in the arterial CO₂ tension (P _aCO₂). This study evaluated whether the apparently large reduction in MCA V _mean at the end of exhaustive exercise relates to an enhanced cerebrovascular CO₂ reactivity. The CO₂ reactivity was evaluated in six young healthy male subjects by the administration of CO₂ as well as by voluntary hypo- and hyperventilation at rest and during exercise with and without hyperthermia. At rest, P _aCO₂ was 5.1±0.2 kPa (mean ± SEM) and MCA V _mean 50.7±3.8 cm s⁻¹ and the relationship between MCA V _mean and P _aCO₂ was linear (double-log slope 1.1±0.1). However, the relationship became curvilinear during exercise (slope 1.8±0.1; P<0.01 vs. rest) and during exercise with hyperthermia (slope 2.3±0.3; P<0.05 vs. control exercise). Accordingly, the cerebral CO₂ reactivity increased from 30.5±2.7% kPa⁻¹ at rest to 61.4±10.1% kPa⁻¹ during exercise with hyperthermia (P<0.05). At exhaustion P _aCO₂ decreased 1.1±0.2 kPa during exercise with hyperthermia, which, with the determined cerebral CO₂ reactivity, accounted for the 28±10% decrease in MCA V _mean. The results suggest that during exercise changes in cerebral blood flow are dominated by the arterial carbon dioxide tension.     

Plasma glucose,insulin and catecholamine responses to a Wingate test in physically active women and men

The influence of gender on the glucose response to exercise remains contradictory. Moreover, to our knowledge, the glucoregulatory responses to anaerobic sprint exercise have only been studied in male subjects. Hence, the aim of the present study was to compare glucoregulatory metabolic (glucose and lactate) and hormonal (insulin, catecholamines and estradiol only in women) responses to a 30-s Wingate test, in physically active students. Eight women [19.8 (0.7) years] and eight men [22.0 (0.6) years] participated in a 30-s Wingate test on a bicycle ergometer. Plasma glucose, insulin, and catecholamine concentrations were determined at rest, at the end of both the warm-up and the exercise period and during the recovery (5, 10, 20, and 30 min). Results showed that the plasma glucose increase in response to a 30-s Wingate test was significantly higher in women than in men [0.99 (0.15) versus 0.33 (0.20) mmol l^–1 respectively, P<0.05]. Plasma insulin concentrations peaked at 10 min post-exercise and the increase between this time of recovery and the end of the warm-up was also significantly higher in women than in men [14.7 (2.9) versus 2.3 (1.9) pmol l^–1 respectively, P<0.05]. However, there was no gender difference concerning the catecholamine response. The study indicates a gender-related difference in post-exercise plasma glucose and insulin responses after a supramaximal exercise.     

Carbohydrate feeding and exercise: effect of beverage carbohydrate content

Summary The purpose of this study was to determine the effect of ingesting fluids of varying carbohydrate content upon sensory response, physiologic function, and exercise performance during 1.25 h of intermittent cycling in a warm environment (T _db=33.4°C). Twelve subjects (7 male, 5 female) completed four separate exercise sessions; each session consisted of three 20 min bouts of cycling at 65% , with each bout followed by 5 min rest. A timed cycling task (1200 pedal revolutions) completed each exercise session. Immediately prior to the first 20 min cycling bout and during each rest period, subjects consumed 2.5 ml·kg BW⁻¹ of water placebo (WP), or solutions of 6%, 8%, or 10% sucrose with electrolytes (20 mmol·l⁻¹ Na⁺, 3.2 mmol·l⁻¹ K⁺). Beverages were administered in double blind, counterbalanced order. Mean (±SE) times for the 1200 cycling task differed significantly: WP=13.62±0.33 min, *6%=13.03±0.24 min, 8%=13.30±0.25 min, 10%=13.57±0.22 min (*=different from WP and 10%,P<0.05). Compared to WP, ingestion of the CHO beverages resulted in higher plasma glucose and insulin concentrations, and higher RER values during the final 20 min of exercise (P<0.05). Markers of physiologic function and sensory perception changed similarly throughout exercise; no differences were observed among subjects in response to beverage treatments for changes in plasma concentrations of lactate, sodium, potassium, for changes in plasma volume, plasma osmolality, rectal temperature, heart rate, oxygen uptake, rating of perceived exertion, or for indices of gastrointestinal distress, perceived thirst, and overall beverage acceptance. Compared to ingestion of a water placebo, consumption of beverages containing 6% to 10% sucrose resulted in similar physiologic and sensory response, while ingestion of the 6% sucrose beverage resulted in significantly improved end-exercise performance following only 60 min of intermittent cycling exercise.     

Reduced arterial O2 saturation during supine exercise in highly trained cyclists

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O₂ (SaO ₂) and lower arterial PO ₂ (PaO ₂). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO ₂ because of a lower maximal O₂ uptake (VPO _2max) and/or a more even ventilation–perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VPO _2max averaged 75±1.6 mL O₂ min^-1 kg^-1 (±SEM) and it was 10.6±1.7% lower during supine cycling (P<0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15±2% and 21±3%, respectively; P< 0.001) which related to a 0.8±0.1 L lower tidal volume (P<0.001). In all subjects and independent of work posture PaO ₂ and SaO ₂ decreased from rest to exhaustion (from 99±3 to 82±2 Torr and 98.1±0.2 to 95.2±0.4%, respectively; P<0.001); alveolar–arterial PO ₂ difference increased from 6±2 to 37±3 Torr in both body positions. At exhaustion arterial PCO ₂ was lower in upright than in supine (33.4±0.6 vs. 35.9±0.9 Torr; P<0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41±0.01) and at exhaustion (7.31±0.01 vs. 7.32±0.01, respectively). We conclude that despite a lower VPO _2max and supposedly an improved ventilation–perfusion distribution, altering body position from upright to supine does not influence arterial O₂ desaturation during intense exercise.     

Effects of a 24-h carbohydrate-poor diet on metabolic and hormonal responses during prolonged glucose-infused leg exercise

Summary Extant literature dealing with metabolic and hormonal adaptations to exercise following carbohydrate (CHO) reduced diets is not sufficiently precise to allow researchers to partial out the effects of reduced blood glucose levels from other general effects produced by low CHO diets. In order to shed light on this issue, a study was conducted to examine the effects of a 24-h CHO-poor diet on substrate and endocrine responses during prolonged (75 min; 60% ) glucose-infused leg exercise. Eight subjects exercised on a cycle ergometer in the two following conditions: 1) after a normal diet (CHO_N), and 2) after a 24-h low CHO diet (CHO_L). In both conditions, glucose was constantly infused intravenously (2.2 mg · kg⁻¹ · min⁻¹) from the 10th to the 75th min of exercise in relatively small amounts (10.4±0.8 g). No significant differences in blood glucose concentrations were found between the two conditions at rest and during exercise although a significant increase (p<0.01) in glucose level was observed in both conditions after 40 min of exercise. The CHO_L as compared to the CHO_N condition, was associated with significantly (p<0.05) lower resting concentrations of insulin, muscle glycogen (8.7 vs 10.6 g · kg⁻¹), and triacylglycerol, and greater concentrations of Β-hydroxybutyrate (0.5 vs 0.2 mmol · L⁻¹), and free fatty acids. During exercise, the CHO_L condition as compared to the CHO_N condition, was associated with significantly (p<0.05) lower insulin and R values, as well as greater free fatty acid (from min 20 to 60) and epinephrine (min 60 to 75) concentrations. Norepinephrine and glucagon concentrations also showed a net tendency (p<0.06) to be higher in the CHO_L condition. There were no significant differences at rest and during exercise in blood lactate and cortisol concentrations between the two conditions. These results demonstrate that blood glucose is not the sole determinant of the metabolic and hormonal responses during prolonged exercise following a low CHO intake and indicate that other factors may be involved in the regulatory mechanism.     

Exogenous endothelin-1 causes peripheral insulin resistance in healthy humans

In states of insulin resistance, increased plasma levels of endothelin-1 and a disturbed vascular reactivity have been reported. In order to investigate the effects of endothelin-1 on peripheral insulin sensitivity and the vasoactive interactions between insulin and endothelin-1, six healthy subjects were studied on two different occasions with the euglycaemic hyperinsulinaemic clamp technique combined with an intravenous infusion of either endothelin-1 (4 pmol kg^?1 min^?1) or 0.9% sodium chloride. During the endothelin-1 infusion, arterial plasma endothelin-1 levels rose 10-fold. The endothelin-1 infusion reduced insulin sensitivity as demonstrated by a 31 ± 7% decrease in whole-body glucose uptake (P < 0.05) and a 26 ± 11% fall in leg glucose uptake (P < 0.05) compared with the control protocol. During the state of hyperinsulinaemia, exogenous endothelin-1 increased mean arterial blood pressure by 8 ± 1% (P < 0.05) and decreased splanchnic and renal blood flow by 30 ± 6% (P < 0.001) and 20 ± 4% (P < 0.001), respectively. However, the endothelin-1 infusion did not lower skeletal muscle blood flow measured as leg and forearm blood flow. In summary, exogenous endothelin-1 induced insulin resistance in healthy humans by reducing insulin-dependent glucose uptake in skeletal muscle without decreasing skeletal muscle blood flow. Furthermore, endothelin-1 also preserved its vasoactive potency in the presence of hyperinsulinaemia.     

Effect of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exercise

The present study examined the effects of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exhaustive exercise. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) breathing air = MAX (maximal exercise), or (2) under hypercapnia (HC: 21% O₂, 6% CO₂) that had been maintained from 60 min before to 30 min after exercise = HC; and (3) exercise of the same intensity as HC in air = SUB (submaximal exercise). Arterialized blood was drawn from a superficial vein. Blood pH in HC was significantly lower than in MAX or SUB at rest, at the end of exercise and throughout recovery (P<0.05). Plasma lactate and ammonia concentration in HC was significantly lower than in MAX (P<0.05), and similar to that in SUB at the end of exercise and throughout recovery. Respiratory acidosis resulting from hypercapnia shifted the linear lactate to blood pH relationship during exhaustive exercise below that at normocapnia (P<0.001). The reduced slope of linear blood pH to ammonia relationship under hypercapnia (P<0.001) is attributed to lactic acidosis that is less, due to the lesser work intensity at the end of exhaustion, than that of normocapnia. From these results we conclude that (1) hypercapnia-induced respiratory acidosis promoted the decrease in blood pH due to lactate production throughout recovery; (2) plasma lactate concentration at maximal exercise was lowered under hypercapnia; (3) plasma ammonia concentration at maximal exercise was reduced, probably due to a less intense lactic acidosis.