Blood lactate changes during isocapnic buffering in sprinters and long distance runners

This study was carried out to compare blood lactate changes in isocapnic buffering phase in an incremental exercise test between sprinters and long distance runners, and to seek the possibility for predicting aerobic or anaerobic potential from blood lactate changes in isocapnic buffering phase. Gas exchange variables and blood lactate concentration ([lactate]) in six sprinters (SPR) and nine long distance runners (LDR) were measured during an incremental exercise test (30 W.min-1) up to subject's voluntary exhaustion on a cycle ergometer. Using a difference between [lactate] at lactate threshold (LT) and [lactate] at the onset of respiratory compensation phase (RCP) and the peak value of [lactate] obtained during a recovery period from the end of the exercise test, the relative increase in [lactate] during the isocapnic buffering phase ([lactate]ICBP) was assessed. The [lactate] at LT (mean +/- SD) was similar in both groups (1.36 +/- 0.27 for SPR vs. 1.24 +/- 0.24 mmol.l-1 for LDR), while the [lactate] at RCP and the peak value of [lactate] were found to be significantly higher in SPR than in LDR (3.61 +/- 0.33 vs. 2.36 +/- 0.45 mmol.l-1 for RCP, P < 0.001, 10.18 +/- 1.53 vs. 8.10 +/- 1.61 mmol.l-1 for peak, P < 0.05). The [lactate]ICBP showed a significantly higher value in SPR (22.5 +/- 5.9%, P < 0.05) compared to that in LDR (14.2 +/- 5.0%) as a result of a twofold greater increase of [lactate] from LT to RCP (2.25 +/- 0.49 for SPR vs. 1.12 +/- 0.39 mmol.l-1 for LDR). In addition, the [lactate]ICBP inversely correlated with oxygen uptake at LT (VO2LT, r = -0.582, P < 0.05) and maximal oxygen uptake (VO2max, r = -0.644, P < 0.01). The results indicate that the [lactate]ICBP is likely to give an index for the integrated metabolic, respiratory and buffering responses at the initial stage of metabolic acidosis derived from lactate accumulation.     

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

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

Continuous intramuscular pH measurement during the recovery from brief, maximal exercise in man

Muscle pH and temperature were measured before, and continuously for 30 min after, a 30-s maximal sprint exercise in ten subjects. These measurements were made with a needle-tipped pH electrode and a thermocouple placed in vastus lateralis. Venous blood samples were collected for pH, lactate and catecholamine estimations and measurements were also made of the arterial blood pressure and heart rate. The muscle and venous pH decreased from 7.17 +/- 0.01 (mean +/- SEM) and 7.39 +/- 0.01 to 6.57 +/- 0.04 and 7.04 +/- 0.03, respectively, in response to the exercise. No significant recovery occurred in either pH measurement for 10 min, after which muscle pH increased to 7.03 +/- 0.03 and venous pH to 7.29 +/- 0.01 by 30 min. Muscle temperature increased by 2.1 degrees C with exercise and also failed to return to pre-exercise values by 30 min. Blood lactate concentration increased from 0.75 +/- 0.04 mmol l-1 before exercise to a peak value of 15.76 +/- 0.35 mmol l-1 5 min after completion of the exercise, and then declined slowly to 10.30 +/- 0.61 mmol l-1 by 30 min. Arterial blood pressure increased transiently with exercise but recovered rapidly, whereas the exercise-induced tachycardia was sustained throughout the recovery period. The recovery from the metabolic and cardiovascular responses to maximal sprint exercise in man is incomplete 30 min after cessation of the exercise.     

Gastric emptying and serum insulin levels after intake of glucose-polymer solutions

To examine the gastric emptying characteristics of four drinks varying in carbohydrate composition and concentration, five men ingested 600 ml of one of the different drinks on four separate occasions. All drinks contained Na+ 71 mmol.l-1, Cl- 60 mmol.l-1, Mg+2 5 mmol.l-1 and citrate 7 mmol.l-1; the carbohydrate component was either 3% glucose, 3% glucose-polymer (GP), 5% GP or 10% GP. With 99mTc-diethylene-triaminepenta-acetic acid (DTPA) as a marker, a scintillation camera and computer were used to measure the rate of gastric emptying. The half-emptying times (T 1/2) were inversely related to the glucose content of the solutions. The T 1/2 for 3% PG was 22.4 +/- 4.4 min (mean +/- SE) and for 10% GP 50 +/- 3.3 min (p less than 0.005). There was no significant difference in T 1/2 between the 3% glucose and 3% GP solutions. The increments in blood glucose (highest blood levels from 7.4 +/- 0.3 mmol.l-1 to 8.9 +/- 0.8 mmol.l-1), serum insulin (from 28 +/- 6 mU.l-1 to 77 +/- 13 mU.l-1) and C-peptide (from 3.6 +/- 0.4 micrograms.l-1 to 5.8 +/- 0.9 micrograms.l-1) were related to the amount of carbohydrate ingested. In all cases the serum insulin levels were high enough to inhibit the liberation of free fatty acids from the adipose tissue. It is concluded that the amount of carbohydrate in glucosyl units in the solution is a major determinant of gastric emptying.(ABSTRACT TRUNCATED AT 250 WORDS)     

Properties of uracil transport by vegetative mycelium of Trichoderma viride

The transport of radioactively labelled uracil into submerged mycelium of T. viride was measured by means of a membrane filtration technique. It was found to be time-dependent (up to 90 min) and concentration-dependent (up to 8 mmol l-1). Its concentration dependence was biphasic and consisted from the saturatable part (at the uracil concentration below 0.2 mmol l-1) with KM = 0.08 +/- 0.02 mmol l-1 and Vmax = 1.74 +/- 0.3 nmol (mg dry wt.)-1 h-1, and from the region at higher uracil concentration which showed only a weak saturatability with the substrate. The transport measured in the saturatable part of the curve was also pH- and temperature-dependent. The optimal pH was between 5.4 and 6.4 and the optimal temperature was at 37 degrees C. The activation energy of 54 kJ mol-1 and the temperature quotient of Q10 = 2.1 could be calculated from the temperature dependence. The entry of uracil was in part inhibited by nucleobases and their analogues, nucleosides, nucleotides and amino acids. The inhibitors had similar inhibitory efficiency about 50% at 0.2 mmol l-1. 3,3',4',5-tetrachlorosalicylanilide (TCS), the uncoupling agent, significantly inhibited the uracil transport, but its inhibitory efficiency decreased upon increasing the uracil concentration. Ionophore antibiotics valinomycin and monensin also inhibited the uracil transport. Inhibitors of RNA-polymerase, rifamycin and rifampicin were without effect. The results suggest that at low uracil concentrations (below 0.2 mmol l-1), its transport is mediated by a carrier and is driven by the electrochemical potential of protons. At higher uracil concentrations, the transport may be driven by the concentration difference of uracil with the contribution of the protonmotive force. It is feasible that inhibitors of uracil transport tested exert their inhibition by the dissipation of the driving force rather than by the direct competition with the substrate-binding site.     

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

The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners (VO2max = 68.2 +/- 3.4 ml X kg-1 X min-1). On three separate occasions, the runners performed a 30 min treadmill run at 70% VO2max. Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P less than 0.05) reaching peak levels at 30 min post-feeding (7.90 +/- 0.24 mmol X l-1). With the onset of exercise, glucose levels dropped to a low of 5.89 +/- 0.85 mmol X l-1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21 +/- 0.31 mmol X l-1 and 5.95 +/- 0.23 mmol X l-1 respectively, and were not significantly different (P less than 0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise.     

The responses of the catecholamines and beta-endorphin to brief maximal exercise in man

The responses to brief maximal exercise of 10 male subjects have been studied. During 30 s of exercise on a non-motorized treadmill, the mean power output (mean +/- SD) was 424.8 +/- 41.9 W, peak power 653.3 +/- 103.0 W and the distance covered was 167.3 +/- 9.7 m. In response to the exercise blood lactate concentrations increased from 0.60 +/- 0.26 to 13.46 +/- 1.71 mmol.l-1 (p less than 0.001) and blood glucose concentrations from 4.25 +/- 0.45 to 5.59 +/- 0.67 mmol.l-1 (p less than 0.001). The severe nature of the exercise is indicated by the fall in blood pH from 7.38 +/- 0.02 to 7.16 +/- 0.07 (p less than 0.001) and the estimated decrease in plasma volume of 11.5 +/- 3.4% (p less than 0.001). The plasma catecholamine concentrations increased from 2.2 +/- 0.6 to 13.4 +/- 6.4 nmol.l-1 (p less than 0.001) and 0.2 +/- 0.2 to 1.4 +/- 0.6 nmol.l-1 (p less than 0.001) for noradrenaline (NA) and adrenaline (AD) respectively. The plasma concentration of the opioid beta-endorphin increased in response to the exercise from less than 5.0 to 10.2 +/- 3.9 p mol.l-1. The post-exercise AD concentrations correlated with those for lactate as well as with changes in pH and the decrease in plasma volume. Post-exercise beta-endorphin levels correlated with the peak speed attained during the sprint and the subjects peak power to weight ratio. These results suggest that the increases in plasma adrenaline are related to those factors that reflect the stress of the exercise and the contribution of anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute upregulation of blood-brain barrier glucose transporter activity in seizures

Brain extraction of (18)F-labeled 2-fluoro-2-deoxy-D-glucose (FDG) was significantly higher in pentylene tetrazole (PTZ)-treated rats (32 +/- 4%) than controls (25 +/- 4%). The FDG permeability-surface area product (PS) was also significantly higher with PTZ treatment (0.36 +/- 0.05 ml. min(-1). g(-1)) than in controls (0.20 +/- 0.06 ml. min(-1). g(-1)). Cerebral blood flow rates were also elevated by 50% in seizures. The internal carotid artery perfusion technique indicated mean [(14)C]glucose clearance (and extraction) was increased with PTZ treatment, and seizures increased the PS by 37 +/- 16% (P < 0.05) in cortical regions. Because kinetic analyses suggested the glucose transporter half-saturation constant (K(m)) was unchanged by PTZ, we derived estimates of 1) treated and 2) control maximal transporter velocities (V(max)) and 3) a single K(m). In cortex, the glucose transporter V(max) was 42 +/- 11% higher (P < 0.05) in PTZ-treated animals (2.46 +/- 0.34 micromol. min(-1). g(-1)) than in control animals (1.74 +/- 0.26 micromol. min(-1). g(-1)), and the K(m) = 9.5 +/- 1.6 mM. Blood-brain barrier (BBB) V(max) was 31 +/- 10% greater (P < 0.05) in PTZ-treated (2.36 +/- 0. 30 micromol. min(-1). g(-1)) than control subcortex (1.80 +/- 0.25 micromol. min(-1). g(-1)). We conclude acute upregulation of BBB glucose transport occurs within 3 min of an initial seizure. Transporter V(max) and BBB glucose permeability increase by 30-40%.     

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

Beta-adrenoceptor stimulation in vivo shifts potassium into the cells. To examine whether human erythrocytes participate in this process, we measured, along with serum or plasma potassium, the concentrations of potassium and sodium in erythrocytes. Beta-adrenoceptor stimulation was obtained by infusion of either fenoterol or hexoprenaline into 6 volunteers at rest or by endogenous amines provoked in 14 volunteers during ergometric exercise. Metabolic effects were followed at rest on serum insulin, C-peptide, and growth hormone levels, and during exercise on pH on lactate concentration in blood. The potassium concentration (mean +/- S.E.M.) dropped (p less than 0.01) in serum from 4.64 +/- 0.37 to 3.19 +/- 0.43 mmol x l-1 in the first hour at rest and in plasma from 5.70 +/- 0.93 to 4.63 +/- 0.45 in 90 sec directly after exercise. The concentration of erythrocyte sodium dropped (p less than 0.001) from 9.68 +/- 0.73 to 8.81 +/- 0.62 mmol x l-1 in cells and from 9.62 +/- 1.16 to 8.55 +/- 1.24 during exercise for 90 s, respectively. Changes in the concentration ratio of cellular sodium to potassium confirmed this sodium shift. An increased sodium transport in erythrocytes due to beta-adrenoceptor stimulation in vivo appears to complement a shift of serum potassium into the cells and may be mediated by the membrane-bound sodium, potassium ATPase.     

The hormonal responses to repetitive brief maximal exercise in humans

The responses of nine men and nine women to brief repetitive maximal exercise have been studied. The exercise involved a 6-s sprint on a non-motorised treadmill repeated 10 times with 30 s recovery between each sprint. The total work done during the ten sprints was 37,693 +/- 3,956 J by the men and 26,555 +/- 4,589 J by the women (M greater than F, P less than 0.01). This difference in performance was not associated with higher blood lactate concentrations in the men (13.96 +/- 1.70 mmol.l-1) than the women (13.09 +/- 3.04 mmol.l-1). An 18-fold increase in plasma adrenaline (AD) occurred with the peak concentration observed after five sprints. The peak AD concentration in the men was larger than that seen in the women (9.2 +/- 7.3 and 3.7 +/- 2.4 nmol.l-1 respectively, P less than 0.05). The maximum noradrenaline (NA) concentration occurred after ten sprints in the men (31.6 +/- 10.9 nmol.l-1) and after five sprints in the women (27.4 +/- 20.8 nmol.l-1). Plasma cardiodilatin (CDN) and atrial natriuretic peptide (ANP) concentrations were elevated in response to the exercise. The peak ANP concentration occurred immediately post-exercise and the response of the women (10.8 +/- 4.5 pmol.l-1) was greater than that of the men (5.1 +/- 2.6 pmol.l-1, P less than 0.05). The peak CDN concentrations were 163 +/- 61 pmol.l-1 for the women and 135 +/- 61 pmol.l-1 for the men. No increases in calcitonin gene related peptide (CGRP) were detected in response to the exercise. These results indicate differences between men and women in performance and hormonal responses. There was no evidence for a role of CGRP in the control of the cardiovascular system after brief intermittent maximal exercise.     

Imaging of human brain creatine kinase activity in vivo

Creatine kinase activity and high-energy phosphate concentration have been investigated using localized 31P spectroscopy in the human brain in vivo. The phase-modulated rotating frame imaging technique, incorporating magnetization transfer and inversion recovery, has been used to produce a 1-dimensional rate profile map of steady-state enzyme activity. Large differences in the flux from phosphocreatine (PCr) to ATP have been discovered between volumes of human brain consisting of predominantly gray (2.0 cm) and white (4.5 cm) matter. The concentration of PCr changes slightly (2.0 cm = 5.20 +/- 0.45 mmol.l-1, 4.5 cm = 4.63 +/- 0.31 mmol.l-1), while the ATP concentration remains within limits (3.30 +/- 0.4 mmol.l-1). No change in pHi was detected between the two regions in normal volunteers (n = 6). The forward rate constant of the PCr----ATP reaction in regions of predominantly gray matter (0.30 +/- 0.04 s-1) was twice that of white matter (0.16 +/- 0.02 s-1) in vivo.     

Kinetics of lactate and pyruvate transport in cultured rat myotubes

Skeletal muscle transport of lactate and pyruvate was studied in primary cultures of rat myotubes, applying the pH-sensitive fluorescent indicator 2', 7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. The initial rate of decrease in intracellular pH (pHi) upon lactate or pyruvate incubation was used to determine total transport (carrier mediated and diffusion). Both lactate and pyruvate transport could be inhibited by a combination of 0.5 mM 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid, 5 mM mersalyl and 10 mM alpha-cyano-4-hydroxycinnamate. The kinetic parameters, Km and Vmax, for carrier-mediated transport of lactate were 9.9+/-1.1 mM and 0. 69+/-0.02 mmol l-1 s-1, respectively. For pyruvate, Km and Vmax were 4.4+/-1.3 mM and 0.30+/-0.05 mmol l-1 s-1, respectively. The diffusion component of the total transport was 0.0040+/-0.0005[S] (n=4) and 0.0048+/-0.0003[S] (n=4) for lactate and pyruvate, respectively. Furthermore, it was observed that the two monocarboxylate transporter isoforms present in mature skeletal muscles, MCT1 and MCT4 (formerly called MCT3 (M.C. Wilson, V.N. Jackson, C. Heddle, N.T. Price, H. Pilegaard, C. Juel, A. Bonen, I. Montgomery, O.F. Hutter, A.P. Halestrap, Lactic acid efflux from white skeletal muscle is catalyzed by the monocarboxylate transporter isoform MCT3, J. Biol. Chem. 273 (1998) 15920-15926)), were also expressed in primary culture of myotubes.     

Branchial and renal handling of urea in the gulf toadfish,Opsanus beta: the effect of exogenous urea loading

The objective of this study was to determine whether the pulsatile facilitated diffusion transport mechanism (tUT) found in the gills of the gulf toadfish (Opsanus beta) and the active secretion transporter thought to be present in its kidney could be saturated when faced with elevated plasma urea concentrations. Toadfish were infused with four consecutive exogenous urea loads at a rate of 0, 150, 300 and 600 micromol kg(-1) h(-1). Initial plasma and urine urea concentrations were 8.1+/-0.9 and 12.4+/-1.5 mmol l(-1), respectively, and steadily increased with increasing infused loads of urea to a maximum of 36.8+/-2.8 mmol l(-1) in the plasma and 39.8+/-6.5 mmol l(-1) in the urine. There was only a very weak relationship (r=0.17) between pulse size (measured as branchial excretion during pulsatile excretion of urea) and plasma urea concentration (slope=9.79 micromol-N kg(-1) per mmol-N l(-1); P<0.05) suggesting that the branchial excretion mechanism was already saturated at normal plasma urea concentrations. Urine flow rate (0.15+/-0.03 ml kg(-1) h(-1)) and glomerular filtration rate (0.025+/-0.004 ml kg(-1) h(-1)) remained constant throughout the experiment despite the increased volume load. Renal urea secretion rate maintained a strong linear relationship (r=0.84) to plasma urea levels (slope=0.391 micromol-N kg(-1) h(-1) per mmol-N l(-1); P<0.001) with no observable transport maximum, suggesting that the renal secretory transport mechanism was not saturated even at plasma urea levels well above normal, in contrast to the branchial excretion mechanism.     

The acute effect of 30 min of moderate exercise on high density lipoprotein cholesterol in untrained middle-aged men

Fifteen middle-aged, untrained (defined as no regular exercise) men (mean age 49.9 years, range 42-67) cycled on a cycle ergometer at 50 rpm for 30 min at an intensity producing 60% predicted maximum heart rate [(fc,max), where fc,max = 220 - age]. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (Tg) concentrations were measured from fasting fingertip capillary blood samples collected at rest, after 15 and 30 min of exercise, and at 15 min post-exercise. The mean HDL-C level increased significantly from the resting level of 0.85 mmol.l-1 to 0.97 mmol.l-1 (P < 0.05) after 15 min of exercise, increased further to 1.08 mmol.l-1 (P < 0.01) after 30 min of exercise and remained elevated at 1.07 mmol.l-1 (P < 0.01) at 15 min post-exercise. These increases represented changes above the mean resting level of 14.1%, 27.1% and 25.9% respectively. The HDL-C/LDL-C ratio increased significantly from a resting ratio of 0.20 to 0.26 after 30 min of exercise (P < 0.01) and to 0.24 at 15 min post-exercise (P < 0.05). The mean Tg level increased significantly from a resting level of 0.88 mmol.l-1 to 1.05 mmol.l-1 after 15 min, and to 1.06 mmol.l-1 after 30 min of exercise (P < 0.05 at each time). The TC/HDL-C ratio decreased significantly (P = 0.05) after 30 min of exercise and at 15 min post-exercise by 18.8% and 14%, respectively. No significant changes were observed in the levels of TC or LDL-C over time.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between lactate and ventilatory thresholds: coincidental or cause and effect?

To determine if blood lactate (LA) is the stimulus responsible for 'breakaway' ventilation (VE), the lactate (LT) and ventilation (VT) thresholds were monitored during one-legged cycling exercise. Ten healthy volunteer male subjects (Mean 2-legged VO2max = 4.27 l X min-1) performed prior exercise (PE) to reduce muscle glycogen stores by cycling at 75-85% of maximal heart rate (HR max) for 60-75 min, followed by a 30 h low carbohydrate diet. Pre- and post- LT and VT tests were performed on a cycle ergometer employing a continuous protocol with increments of 16 W every 3 min. Muscle biopsies were taken from the vastus lateralis muscle before the PE ride, prior to the threshold test 24 h later, and before testing the non-exercised (NE) leg. An I.V. catheter placed in the antecubital vein was used for serial blood samples taken at rest, and during the final 30 s of each progressive load. Gas analysis was calculated every 30 s (Beckman Metabolic Measurement Cart). Biopsies (N = 3) showed that the exercise and diet regimen elicited glycogen reduction which significantly (p less than 0.05) reduced R and the blood LA concentration in both the PE (2.62 to 1.99 mmol X l-1) and NE (2.87 to 2.26 mmol X l-1) legs at LT. At VT, LA concentrations were also significantly reduced in the PE (3.35 to 2.56 mmol X l-1) and NE (3.59 to 2.74 mmol X l-1) legs. VO2 and VE, however, were similar between pre- and post- tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluating in vitro and in vivo the interference of ascorbate and acetaminophen on glucose detection by a needle-type glucose sensor.

The aim of this work was to assess, in vitro and in vivo, the interference of ascorbate and acetaminophen on glucose measurements by a needle-type glucose sensor detecting hydrogen peroxide generated during the enzymatic oxidation of glucose, and to ascertain whether the protection against interference by the membranes used in the construction of the electrode is feasible. The oxidation of ascorbate and acetaminophen on a platinum electrode set at a 650 mV potential yielded a current representing 75 +/- 5% and 25 +/- 6% of that generated by the oxidation of an equimolar concentration of hydrogen peroxide, respectively. The bias introduced by the presence of 100 mumol l-1 ascorbate on the reading of 5 mmol l-1 glucose by the complete sensor (electrode + membranes) would be minimal (approximately 0.4 mmol l-1). By contrast, the bias introduced by 200 mumol l-1 of acetaminophen (a plasma concentration easily reached in clinical practice) was about 7 mmol l-1. The sensor was implanted subcutaneously in anaesthetized rats (n = 3). Using the current generated in the presence of a plasma acetaminophen concentration of about 200 mumol l-1 for glucose monitoring would lead to a major underestimation (approx. 6 mmol l-1) of subcutaneous glucose concentrations.     

Blood pressure and endocrine responses of healthy subjects in cold pressor test after acutely increased dietary sodium intake

The objective of the study was to compare blood pressure and endocrine responses in a cold pressure test in young healthy subjects who had shown increased blood pressure during an acutely increased sodium intake. Subjects (n = 53) added 121 mmol sodium into their normal diet for one week. If the mean arterial pressure had increased by a minimum of 5 mmHg compared to the control measure, they were selected for the experiments. The selected subjects (n = 8) were given 121 mmol supplemental sodium d-1 for 14 days after which they immersed the right hand into a cold (+10 degrees C) water bath for 5 min. The blood pressure increased (P < 0.05) during the test and was independent of the sodium intake. The plasma noradrenaline increased from 2.41 +/- 0.38 nmol l-1 to 2.82 +/- 0.42 nmol l-1 (P < 0.05) with normal diet and from 1.85 +/- 0.29 nmol l-1 to 2.40 +/- 0.37 nmol l-1 (P < 0.05) with high sodium diet. The starting concentrations and the endpoint concentrations were statistically similar. The plasma levels of natriuretic peptides (NT-proANP, ANP and BNP) did not change during the test, and the concentrations were independent of the sodium diet. To conclude, acutely increased sodium intake does not change blood pressure or hormonal responses in a cold pressor test in young healthy subjects.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O2 consumption (% VO2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol.l-1 (Than = 83.6% VO2max, SD 8.9). Time-dependent changes in blood lactate concentration [( lab]) during exercise occurred in two phases: the oxygen uptake (VO2) transient phase (from 0 to 4 min) and the VO2 steady-state phase (4-30 min). During the transient phase, [lab] increased markedly (1.30 mmol.l-1.min-1, SD (0.13). During the steady-state phase, [lab] increased slightly (0.02 mmol.l-1.min-1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [lab] in half of the subjects. Following hyperlacticaemia (8.8 mmol.l-1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% VO2max), [lab] decreased during the VO2 transient (-0.118 mmol.l-1.min-1, SD 0.209) and steady-state (-0.088 mmol.l-1.min-1, SD 0.103) phases of 30 min exercise (91.4% VO2max, SD 4.8). In conclusion, it was not possible from the Than to determine the maximal [lab] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the VO2 transient phase of exercise performed at an intensity above the Than. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [lab] during the VO2 steady state was also affected.     

Post-exercise ketosis and the glycogen content of liver and muscle in rats on a high carbohydrate diet

Post-exercise ketosis is known to be suppressed by physical training and by a high carbohydrate diet. As a result it has often been presumed, but not proven, that the development of post-exercise ketosis is closely related to the glycogen content of the liver. We therefore studied the effect of 1 h of treadmill running on the blood 3-hydroxybutyrate and liver and muscle glycogen concentrations of carbohydrate-loaded trained (n = 72) and untrained rats (n = 72). Resting liver and muscle glycogen levels were 25%-30% higher in the trained than in the untrained animals. The resting 3-hydroxybutyrate concentrations of both groups of rats were very low: less than 0.08 mmol.l-1. Exercise did not significantly influence the blood 3-hydroxybutyrate concentrations of trained rats, but caused a marked post-exercise ketosis (1.40 +/- 0.40 mmol.l-1 h after exercise) in the untrained animals, the time-course of which was the approximate inverse of the changes in liver glycogen concentration. Interpreting the results in the light of similar data obtained after a normal and low carbohydrate diet it has been concluded that trained animals probably owe their relative resistance to post-exercise ketosis to their higher liver glycogen concentrations as well as to greater peripheral stores of mobilizable carbohydrate.     

Smoking impairs muscle recovery from exercise

Cigarette smoking is a leading cause of many adverse health consequences. Chronic nicotine exposure leads to insulin resistance and may increase the risk of developing non-insulin-dependent diabetes mellitus in young otherwise healthy smokers. To evaluate smoking-induced effects on carbohydrate metabolism, we studied muscle glycogen recovery from exercise in a young healthy population of smokers. The study used 31P-13C NMR spectroscopy to compare muscle glycogen and glucose 6-phosphate levels during recovery in exercised gastrocnemius muscles of randomized cohorts of healthy male smokers (S) and controls (C). Data for the two groups were as follows: S, > or =20 cigarettes/day (n = 8), 24 +/- 2 yr, 173 +/- 3 cm, 70 +/- 4 kg and age- and weight-matched nonsmoking C (n = 10), 23 +/- 1 yr, 175 +/- 3 cm, 67 +/- 3 kg. Subjects performed single-leg toe raises to deplete glycogen to approximately 20 mmol/l, and glycogen resynthesis was measured during the first 4 h of recovery. Plasma samples were assayed for glucose and insulin at rest and during recovery. Test subjects were recruited from the general community surrounding Yale University. Glycogen was depleted to similar levels in the two groups [23.5 +/- 1.2 (S) and 19.1 +/- 1.3 (C) mmol/l]. During the 1st h of recovery, glycogen synthesis rates were similar [13.8 +/- 1.1 (S) and 15.3 +/- 1.3 (C) mmol x l-1 x h-1]. Between hours 1 and 4, glycogen synthesis was impaired in smokers [0.8 +/- 0.2 (S) and 4.5 +/- 0.5 (C) mmol x l-1 x h-1, P = 0.0002] compared with controls. Glucose 6-phosphate was reduced in smokers during hours 1-4 [0.105 +/- 0.006 (S) and 0.217 +/- 0.019 (C) mmol/l, P = 0.0212]. We conclude that cigarette smoking impairs the insulin-dependent portion of muscle recovery from glycogen-depleting exercise. This impairment likely results from a reduction in glucose uptake.