Venous Lactate Concentration Research Articles

Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise

The aim of this study was to elucidate the mechanism by which the disappearance of blood lactate following severe exercise is enhanced during active recovery in comparison with recovery at rest. Rates of decline of arterialised venous blood lactate concentrations in man after maximal one-leg exercise were compared during four different modes of recovery: passive (PR), exercise of the muscles involved in the initial exercise (SL), exercise of the corresponding muscles in the hitherto-inactive leg (OL), or exercise of one arm (RA). Recovery exercise workloads were each 40% of the onset of blood lactate accumulation (OBLA) for the limb used. In comparison with PR, SL and OL accelerated the fall in blood lactate to similar extents whereas RA was without effect. The first-order rate constant (min-1) for decline of arterialised venous blood lactate concentration after the intense exercise was 0.027 (0.003) in PR, 0.058 (0.025) in SL, 0.034 (0.002) in OL, and in RA was 0.028 (0.002) [mean (SEM), n = 6 subjects]. Preliminary studies had shown that RA in isolation elevated blood lactate whereas SL and OL did not. Thus, with appropriate workloads, exercise of either hitherto active or passive muscles enhanced blood lactate decline during recovery from intense exercise. This suggests that the effect resulted principally from the uptake and utilisation of lactate in the circulation by those exercising muscles rather than from increased transport of lactate to other sites of clearance by sustained high blood flow through the previously active muscles.

Lactate Metabolism in Normal and Growth-Retarded Human Fetuses

Lactate concentration and oxygen content were measured in 21 normal (AGA) and 34 intrauterine growth-retarded (IUGR) infants at the time of elective cesarean section. Maternal lactate and umbilical arterial and venous lactate concentrations were significantly higher in IUGR infants compared with AGA infants. However, when IUGR patients were subdivided according to pulsatility index (PI) measurements of the umbilical artery, no differences were detected between AGA and IUGR patients with PI less than 4 SD, whereas IUGR patients with PI greater than 4 SD had higher lactate concentrations in maternal arterial blood and umbilical arterial and venous blood from both other groups. There was a significant inverse linear relationship between umbilical arterial lactate concentration and umbilical venoarterial differences for both lactate concentrations and for lactate/oxygen quotients. These relationships were significantly different in IUGR fetuses with PI greater than 4 SD compared with AGA and IUGR fetuses with PI less than 4 SD. AGA and IUGR fetuses with PI less than 4 SD have arterial lactate concentrations less than 2 mM even at low oxygen concentrations (O2 content less than 2 mM, O2 saturations less than 20%). At comparable levels of oxygenation, IUGR fetuses with PI greater than 4 SD have a marked lactacidemia. The data suggest that coupling Doppler assessment of flow velocimetry with biochemical analyses of fetal blood can be useful in identifying a subset of IUGR human fetuses at risk of intrauterine hypoxia.

Effects of dietary yeast culture supplementation during the conditioning period on equine exercise physiology

Two groups of previously unconditioned young adult horses participated in 6 weeks of gradually increasing exercise on an inclined plane treadmill while receiving a cornoats-hay diet with or without a commercially available dietary yeast culture preparation. Forced treadmill exercise at a workload of 11.98 j/kg/m, equivalent to a workrate of 18.34 j/sec/kg and an estimated ground speed of 5.36 m/sec, began at 5 minutes per day (2.75 Mjoules/500 kg body-weight) and was increased by 5 minutes per week to a maximum of 35 minutes per day (19.25 Mjoules/500 kg) after 6 weeks. Treadmill exercise increased venous plasma lactate concentrations in direct proportion to the duration of an exercise bout, but the increases tended to be smaller after a given amount of work as the horses became conditioned. At the end of 35 minutes of exercise, plasma lactate concentrations averaged 30.08 mg/dl in the supplemented horses and 41.29 mg/dl in the unsupplemented horses (p<.01). Plasma glucose concentrations decreased significantly and triglyceride concentrations increased significantly in both groups as exercise duration exceed 10 minutes. Changes in plasma glucose concentrations were not significantly affected by yeast culture supplementation, while the supplemented horses exhibited somewhat slower rates of increased plasma triglyceride concentrations. During the 35-minute exercise bouts, significantly lower heart rates were recorded in the supplemented horses during the first 5 and the final 10 minutes of the workouts (p<.01), suggesting an enhanced state of athletic fitness. The digestible energy required for work (Mcal/500 kg bodyweight) was calculated to be 0.454 (Mcal/Mjoule) (Mjoules of work/500 kg bodyweight) + 0.024 Mcal/500 kg bodyweight (r2=0.95), with an efficiency of converting dietary DE to work of 53% for both groups of horses. Although the exercise challenges to these horses were not severe, these results suggest that dietary yeast culture supplementation of horses entering into conditioning programs may well enhance athletic training.

Metabolic consequences of reduced frequency breathing during submaximal exercise at moderate altitude

The intention of this study was to determine the metabolic consequences of reduced frequency breathing (RFB) at total lung capacity (TLC) in competitive cyclists during submaximal exercise at moderate altitude (1520 m; barometric pressure, PB = 84.6 kPa; 635 mm Hg). Nine trained males performed an RFB exercise test (10 breaths.min-1) and a normal breathing exercise test at 75-85% of the ventilatory threshold intensity for 6 min on separate days. RFB exercise induced significant (P less than 0.05) decreases in ventilation (VE), carbon dioxide production (VCO2), respiratory exchange ratio (RER), ventilatory equivalent for O2 consumption (VE/VO2), arterial O2 saturation and increases in heart rate and venous lactate concentration, while maintaining a similar O2 consumption (VO2). During recovery from RFB exercise (spontaneous breathing) a significant (P less than 0.05) decreases in blood pH was detected along with increases in VE, VO2, VCO2, RER, and venous partial pressure of carbon dioxide. The results indicate that voluntary hypoventilation at TLC, during submaximal cycling exercise at moderate altitude, elicits systemic hypercapnia, arterial hypoxemia, tissue hypoxia and acidosis. These data suggest that RFB exercise at moderate altitude causes an increase in energy production from glycolytic pathways above that which occurs with normal breathing.

Lactate concentration differences in plasma, whole blood, capillary finger blood and erythrocytes during submaximal graded exercise in humans

The aim of the study was to investigate the distribution of lactate in plasma, whole blood, erythrocytes, and capillary finger blood, before and during submaximal exercise. Ten healthy male subjects performed submaximal graded cycle ergometer exercise for 20-25 min. Venous blood samples and capillary finger blood samples were taken before exercise and every 5th min during exercise for lactate determination. The plasma lactate concentration was significantly higher (P less than 0.001, approximately 50%) than in the erythrocytes. This difference was not altered by the venous blood lactate concentration or exercise intensity. A significant difference (P less than 0.01) in lactate concentration was also found between capillary whole blood and venous whole blood. It was concluded that direct comparisons between lactate in capillary finger blood, venous whole blood and plasma could not be made.

Occlusion time dependency of regional noradrenaline release and cardiac arrhythmias during reperfusion of acutely ischaemic heart in the dog in vivo

The aim was to study the occlusion time dependency of reperfusion induced increases in regional cardiac noradrenaline release from the ischaemic area in relation to the incidence of ventricular arrhythmias. The left anterior descending coronary artery was ligated for 15, 30 and 60 min in three separate groups of dogs (n = 10 per group). Each occlusion period was followed by a 30 min reperfusion period. The coronary sinus and the epicardial vein running in parallel with the left anterior descending coronary artery were cannulated for measurement of noradrenaline and lactate. 30 adult mongrel dogs, 22.5(SEM 1.1) kg, were used for the study. The animals were anaesthetised with sodium pentobarbitone. During occlusion, epicardial venous blood noradrenaline concentrations remained unchanged up to 30 min, but increased from 0.133(0.027) ng.ml-1 to 0.289(0.069) ng.ml-1 after 60 min of occlusion (p less than 0.05). However, epicardial venous blood lactate concentrations increased immediately upon occlusion, and remained elevated (p less than 0.05) during the whole period of occlusion in all groups. Neither noradrenaline nor lactate concentrations in coronary sinus blood increased during occlusion. During reperfusion, nine dogs showed early ventricular fibrillation. The highest incidence of fibrillation (n = 5/10) was found in the 15 min occlusion group, but the difference was not significant between groups. Epicardial venous blood noradrenaline concentrations increased to 0.371(0.076) ng.ml-1, 0.470(0.178) ng.ml-1, and 1.824(0.713) ng.ml-1 upon reperfusion following 15, 30 and 60 min occlusion, respectively (each p less than 0.05). Maximum increases in epicardial venous blood noradrenaline concentrations during reperfusion were correlated with duration of preceding occlusion (r = 0.60, n = 21, p less than 0.01). Maximum increases in mean arrhythmic ratios observed during the first 10 min of reperfusion were proportionally related to mean epicardial venous blood noradrenaline concentrations. The increases in epicardial venous blood noradrenaline concentrations and the incidence of ventricular arrhythmias in the 60 min occlusion group were greater (p less than 0.05) than in the other two groups. This study shows that noradrenaline is released progressively from the ischaemic area during occlusion for 60 min. The amount of noradrenaline washed out upon reperfusion and the incidence of reperfusion ventricular arrhythmias both appear to be dependent upon duration of preceding occlusion. The results suggest that cardiac noradrenaline released locally from the ischaemic region may contribute to the genesis of reperfusion ventricular arrhythmias, but not to that of reperfusion ventricular fibrillation.

Intestinal Hemodynamics During Laparotomy

The effects of thoracic epidural anesthesia (TEA) and dopamine infusion (4 micrograms.kg-1.min-1) on superior mesenteric artery blood flow (SMABF), the mesenteric arteriovenous oxygen difference (AVDO2), and the mesenteric venous lactate concentration were studied in nine patients before abdominal aortic reconstruction. Thoracic epidural anesthesia reduced SMABF, as measured by electromagnetic flowmetry, to 77% +/- 8% (mean +/- SEM) of control (P less than 0.05), and mean arterial pressure to 46% +/- 4% of control (P less than 0.01). The mesenteric AVDO2 increased from 27 +/- 3 to 39 +/- 6 mL/L (P less than 0.05) and superior mesenteric venous lactate from 1.03 +/- 0.11 to 1.60 +/- 0.38 mmol/kg (P less than 0.05); systemic AVDO2 and lactate did not change. Dopamine had no significant effect on SMABF and mean arterial pressure before TEA. However, dopamine increased SMABF during TEA (from 77% +/- 8% to 137% +/- 21% of control; P less than 0.01), returned mesenteric AVDO2 to 27 +/- 3 mL/L (P less than 0.05), and elevated mean arterial pressure to 62% +/- 4% of control (P less than 0.05). It is concluded that the decrease in perfusion pressure during TEA reduces SMABF with resultant evidence of intestinal reductive metabolism. The intestinal blood flow during TEA was improved by dopamine.

Application of a standardised treadmill exercise test for clinical evaluation of fitness in 10 thoroughbred racehorses.

Clinical exercise stress testing is an important diagnostic tool for evaluating exercise intolerance and degree of fitness in human athletes. The purpose of this paper was to describe the methodology necessary to perform a clinical exercise test and report the results of performance evaluations on 10 Thoroughbred racehorses using this test. The test utilised an open flow gas analysis system for ease of use with untrained horses and a fast time response lactate analyser for rapid data analysis. Exercise test measurements used to evaluate fitness included peak oxygen consumption (mean VO2peak = 161.9 +/- 12.9 ml/kg/min), peak heart rate (mean HRpeak = 232 +/- 10 b/m), peak venous blood lactate concentration (mean LAC peak = 15.2 +/- 5.8 mmol/l), peak packed cell volume (mean PCV peak = 0.64 +/- 0.3 l/l) and the maximum number of steps completed (mean STEPmax = 8.7 +/- 0.5 steps). The relationship between these exercise test measurements with velocity and time post exercise was also evaluated. Change in serum creatine kinase levels resulting from exercise test were minimal (mean delta SCK = 72 +/- 53 u/l).

Methodology and repeatability of a standardised treadmill exercise test for clinical evaluation of fitness in horses.

This paper describes the methodology necessary to perform a clinical exercise test and the expected variability in an individual horse's exercise test measurements based on comparing the results of two repetitions of the test with six horses. The exercise test measurements were obtained with an open flow respiratory gas analysis system, fast time response lactate analyser and an on-board heart rate monitor during an incremental inclined treadmill exercise test. With the exception of peak venous lactate concentration (LACpeak), the results indicate that the mean variability in peak oxygen consumption (VO2peak) peak carbon dioxide production (VCO2peak), peak respiratory exchange ratio (Rpeak), peak heart rate (HRpeak), peak packed cell volume (PCVpeak), peak total plasma protein (TPPpeak) and the maximum number of steps completed during the exercise test (STEPmax) was less than 5 per cent. Variation in the regression analysis of VO2, VCO2 and HR versus velocity was also less than 5 per cent. Slightly higher variation was recorded for LAC and R. Mean variation in the regression analysis of PCV and TPP versus velocity was more than 16 per cent. Mean variation for all of the post exercise test measurements was less than 10 per cent at 1, 5 and 15 mins post exercise. Therefore, the results obtained during a single exercise test are a reliable assessment of a horse's metabolic capability.

Evaluation of the effects of a regular training program in two thoroughbred yearlings using an exercise stress test

Summary The purpose of this study was to evaluate the effects of a regular training program in two Thoroughbred yearlings (one filly, one colt) using an exercise stress test. The training program consisted of treadmill exercise incorporating long/slow distance work, speed work and work on inclines with gradually increasing bouts of intensity at the trot and gallop. The parameters measured during the exercise stress test were: peak aerobic power (VO 2 max) (mg/kg/min); peak CO 2 production (VCO 2 max) (mg/kg/min); peak respiratory quotient (RQ) (VCO 2 /VO 2 ) peak heart rate (b/min); peak lactate (mmol/l); peak hematocrit (%RBC); peak total serum protein (mg/dl); CPK (pre-post test) (iu). Post-test recovery rates were recorded for oxygen consumption (% total increase); venous lactate concentration (% total increase); heart rate (% total increase). The exercise tests were performed at the beginning and end of the training period. Musculoskeletal strength was evaluated based on the number of steps completed (of the exercise test). Routine physical and lameness evaluations were performed at the start of the program. With the exception of a mild bout of pneumonia and the formation of a hoof abscess in the filly, both yearlings handled the training program well. The individual peak results of the exercise stress tests of each of the yearlings is compared to mean values calculated from exercise stress tests performed by other yearlings admitted to TUSVM Large Animal Hospital for performance evaluations. Comparison of the parameters measured between the first and second exercise test demonstrates an increase in peak aerobic power, and a shift from anaerobic to predominantly aerobic energy metabolism following a regular exercise program.

Lactate removal ability and graded exercise in humans

Venous lactate concentrations of nine athletes were recorded every 5 s before, during, and after graded exercise beginning at a work rate of 0 W with an increase of 50 W every 4th min. The continuous model proposed by Hughson et al. (J. Appl. Physiol. 62: 1975-1981, 1987) was well fitted with the individual blood lactate concentration vs. work rate curves obtained during exercise. Time courses of lactate concentrations during recovery were accurately described by a sum of two exponential functions. Significant direct linear relationships were found between the velocity constant (gamma 2 nu) of the slowly decreasing exponential term of the recovery curves and the times into the exercise when a lactate concentration of 2.5 mmol/l was reached. There was a significant inverse correlation between gamma 2 nu and the rate of lactate increase during the last step of the exercise. In terms of the functional meaning given to gamma 2 nu, these relationships indicate that the shift to higher work rates of the increase of the blood lactate concentration during graded exercise in fit or trained athletes, when compared with less fit or untrained ones, is associated with a higher ability to remove lactate during the recovery. The results suggest that the lactate removal ability plays an important role in the evolution pattern of blood lactate concentrations during graded exercise.

Differences in cardiorespiratory responses during and after arm crank and cycle exercise

The differences in cardiorespiratory responses were examined during and after intermittent progressive maximal arm-crank and cycle exercise. Arm-crank exercise was performed in a standing position using no torso restraints to maximize the amount of active skeletal muscle mass. Recovery was followed for 16 min. In the tests a variety of ventilatory gas exchange variables, heart rate, the blood pressure, and the arm venous blood lactate concentration were measured in 21 untrained healthy men aged 24-45 years. At equal submaximal external workloads for arm cranking and cycling (50 and 100 W) the respiratory frequency, tidal volume, pulmonary ventilation, oxygen uptake, carbon dioxide output, the respiratory exchange ratio, heart rate, the arm venous blood lactate concentration, and the ventilatory equivalent for oxygen were higher (P less than 0.001) during arm cranking than cycling. The maximal workload for arm cranking was 44% lower than that for cycling (155 +/- 37 vs 277 +/- 39 W, P less than 0.001) associated with significantly (P less than 0.001) lower maximal tidal volume (-20%), oxygen uptake (-22%), carbon dioxide output (-28%), systolic blood pressure (-17%) and oxygen pulse (-22%) but a higher ventilatory equivalent for carbon dioxide (+22%) and arm venous blood lactate concentration (+37%). However, these responses after arm-crank and cycle exercises behaved almost similarly during recovery. The high cardiorespiratory stress induced by arm work should be taken into account when the work stress and work-rest regimens in actual manual tasks are assessed, and when arm work is used for clinical testing, and in physiotherapy particularly for patients with heart or pulmonary diseases.

Blood lactate during constant-load exercise at aerobic and anaerobic thresholds

Venous blood lactate concentrations [1ab] were measured every 30 s in five athletes performing prolonged exercise at three constant intensities: the aerobic threshold (Thaer), the anaerobic threshold (Than) and at a work rate (IWR) intermediate between Thaer and Than. Measurements of oxygen consumption (VO2) and heart rate (HR) were made every min. Most of the subjects maintained constant intensity exercise for 45 min at Thaer and IWR, but at Than none could exercise for more than 30 min. Relationships between variations in [1ab] and concomitant changes in VO2 or HR were not statistically significant. Depending on the exercise intensity (Thaer, IWR, or Than) several different patterns of change in [1ab] have been identified. Subjects did not necessarily show the same pattern at comparable exercise intensities. Averaging [1ab] as a function of relative exercise intensity masked spatial and temporal characteristics of individual curves so that a common pattern could not be discerned at any of the three exercise levels studied. The differences among the subjects are better described on individual [1ab] curves when sampling has been made at time intervals sufficiently small to resolve individual characteristics.

Decreased exercise muscle lactate release after high altitude acclimatization.

Blood lactate concentration during exercise decreases after acclimatization to high altitude, but it is not clear whether there is decreased lactate release from the exercising muscle or if other mechanisms are involved. We measured iliac venous and femoral arterial lactate concentrations and iliac venous blood flow during cycle exercise before and after acclimatization to 4,300 m. During hypoxia, at a given O2 consumption the venous and arterial lactate concentrations, the venous and arterial concentration differences, and the net lactate release were lower after acclimatization than during acute altitude exposure. While breathing O2-enriched air after acclimatization at a given O2 consumption the venous and arterial lactate concentrations and the venous and arterial concentration differences were significantly lower, and the net lactate release tended to be lower than while breathing ambient air at sea level before acclimatization. We conclude that the lower lactate concentration in venous and arterial blood during exercise after altitude acclimatization reflected less net release of lactate by the exercising muscles, and that this likely resulted from the acclimatization process itself rather than the hypoxia per se.

Hypothalamic influences on cardiovascular response of beagles to dynamic exercise.

We studied nine young adult beagles at rest and during four levels of dynamic exercise before and after electrolytic lesions were made in the hypothalamus in the region of the fields of Forel. The beagles were habituated to run freely on a motor-driven treadmill and were instrumented chronically to allow repeated measurement of cardiovascular variables. Variables measured or calculated included O2 consumption, cardiac output, arteriovenous O2 difference, systemic arterial pressure, systemic vascular resistance, heart rate, and mixed venous blood lactate concentration. In addition, regional blood flow was measured with radioactive microspheres in two beagles at rest and during peak exercise (6.4 km/h, 20% grade). After prelesion treadmill studies, the beagles were anesthetized and the tips of stainless steel electrodes were placed bilaterally in the hypothalamus in locations that when stimulated (100-300 microA) evoked increases in cardiovascular and muscle motor function. Lesioning (5 mA; 15 s) abolished the responses evoked by stimulation. By contrast, the cardiovascular variables measured in the beagles at rest and during dynamic exercise were similar pre- and postlesion. Therefore, loss of hypothalamic sites that produce increases in cardiovascular and muscle motor function when stimulated electrically does not appear to comprise the cardiovascular response of awake beagles to dynamic exercise.

A Field Test for Determining the Speed Obtained Through Anaerobic Glycolysis in Runners*

A field test for the evaluation of the speed generated by the anaerobic lactacid mechanism has been developed in runners. The test consists of 1200 m of continuous running: in the first 1000 m the speed corresponding to the anaerobic threshold is progressively reached; in the last 200 m an all-out sprint is performed. The speed at the anaerobic threshold is subtracted from the speed reached in the final 200-m all-out sprint. In 39 runners examined (marathon runners, n = 13; 5000-10000-m runners, n = 10; 400-800-m runners, n = 7; sprinters, n = 9), the additional speed generated above the anaerobic threshold was correlated with the venous blood lactate concentration reached 5 min after the all-out effort (r = 0.93). The anaerobic speeds measured by the test were in keeping with the characteristics of the runners under study, i.e., anaerobic speeds were highest for the sprinters, intermediate for the middle-distance runners, and lowest for the marathon runners. Since the speed generated above the anaerobic threshold by the aerobic fuel breakdown can be subtracted, the contribution of creatine phosphate is minimal, and the speed exceeding the anaerobic threshold is highly correlated with lactate accumulation, the present test should measure the speed generated by anaerobic glycolysis.

Temporal relationship between blood flow changes and release of ions and metabolites from muscles upon single weak contractions.

The temporal changes in muscular blood flow and in the release of ions and metabolites have been studied during and after short-lasting isometric contractions. Blood velocities in the human femoral artery were measured using pulsed bidirectional Doppler ultrasound equipment during single contractions of the quadriceps muscle group. Contractions of 5 s and 30 s duration and at a tension of 10% MVC (maximal voluntary contraction) were investigated. Even the contractions of 5 s duration caused conspicuous post-contraction increases in femoral arterial flow. The following substances were analysed in the femoral vein during and following the contractions: potassium, lactate, inorganic phosphate, calcium, sodium, oxygen and haemoglobin. Following contractions of 5 s duration, an increase in the venous potassium concentration (by 0.9 mM) was found, but there was no change in concentration of any of the other substances analysed. Following contractions of 30 s duration a more marked increase in the venous potassium concentration (by 1.5 mM) was found, and in addition substantial changes in venous lactate concentration and oxygen saturation. There were small but statistically significant changes in the concentrations of inorganic phosphate and calcium, but no change in the sodium concentration. The time-course and magnitude of the changes in venous potassium concentration fit well with the idea that potassium is important in the initiation and regulation of the functional hyperaemia in contracting muscles.

Skeletal muscle O2 consumption and energy metabolism during hypoxemia.

We determined the relationship of O2 transport (TO2) to O2 consumption (VO2) and to changes in cellular bioenergetics in an isolated blood-perfused rabbit hindlimb preparation (n = 8) during hypoxemia. The preparations were subjected to reductions in TO2 by progressively decreasing partial pressure of arterial O2 (PaO2). At each level of PaO2 we obtained simultaneous measures of arterial and venous blood gases, venous lactate concentration, and changes in the relative concentrations of inorganic phosphate, phosphocreatine, and ATP measured with 31P magnetic resonance spectroscopy. The ratio of the change in vascular resistance (R) to the corresponding decrease in TO2 was taken as an index of vascular autoregulation with hypoxemia. Linear and logarithmic functions were fitted by least squares to the TO2-VO2 data from each experiment. TO2-VO2 relationships were characterized as O2 conforming (linear function, n = 4) or O2 regulating (logarithmic function, n = 4), depending on the goodness of fit. Those preparations showing an O2-conforming pattern had higher control VO2 (2.42 +/- 0.14 vs. 1.66 +/- 0.19 ml.min-1.kg-1; P less than 0.05) and a lesser degree of vascular autoregulation (0.07 +/- 0.03 vs. 0.21 +/- 0.02; P less than 0.01) than the O2-regulating group. Decreases in VO2 were always accompanied by increases in inorganic phosphate and lactate and decreases in phosphocreatine, indicating O2 supply limitation and anaerobic ATP production. There was no evidence of cellular adaptation to hypoxia by decreasing energy needs or of VO2 limitation by the depletion of adenine nucleotides.

O2 metabolism of the sheep diaphragm during flow resistive loaded breathing.

To determine whether O2 availability limited diaphragmatic performance, we subjected unanesthetized sheep to severe (n = 11) and moderate (n = 3) inspiratory flow resistive loads and studied the phrenic venous effluent. We measured transdiaphragmatic pressure (Pdi), systemic arterial and phrenic venous blood gas tensions, and lactate and pyruvate concentrations. In four sheep with severe loads, we measured O2 saturation (SO2), O2 content, and hemoglobin. We found that with severe loads Pdi increased to 74.7 +/- 6.0 cmH2O by 40 min of loading, remained stable for 20-30 more min, then slowly decreased. In every sheep, arterial PCO2 increased when Pdi decreased. With moderate loads Pdi increased to and maintained levels of 40-55 cmH2O. With both loads, venous PO2, SO2, and O2 content decreased initially and then increased, so that the arteriovenous difference in O2 content decreased as loading continued. Hemoglobin increased slowly in three of four sheep. There were no appreciable changes in arterial or venous lactate and pyruvate during loading or recovery. We conclude that the changes in venous PO2, SO2, and O2 content may be the result of changes in hemoglobin, blood flow to the diaphragm, or limitation of O2 diffusion. Our data do not support the hypothesis that in sheep subjected to inspiratory flow resistive loads O2 availability limits diaphragmatic performance.

Effects of nisoldipine on systemic and leg blood flow, oxygen transport and metabolism, and hemodynamics during exercise in effort angina pectoris

The acute effects of 10 mg of oral nisoldipine on hemodynamics, oxygen transport and metabolism, and distribution of cardiac output, at rest and during semiupright bicycle exercise, were evaluated in 10 men with effort angina receiving long-term β 1 blockade. Cardiac output and leg blood flow were measured using the thermodilution technique. At rest, nisoldipine decreased systemic resistance from 18.9 ± 1.0 to 15.9 ± 1.2 dynes · s · cm −5 · 10 2 (p < 0.05) and cardiac output increased from 4.8 ± 0.2 to 5.3 ± 0.3 liters/min (p < 0.05) without changing leg blood flow. During maximal exercise with nisoldipine, systemic resistance was reduced (10.6 ± 0.9 to 8.6 ± 0.5 dynes · s · cm −5 · 10 2, p < 0.05) and cardiac output increased 18% (10.3 ± 0.7 to 12.2 ± 0.6 liters/min, p < 0.05) when compared with control values. Exercise heart rate was higher with nisoldipine (113 ± 4 vs 106 ± 4 beats/ min, p < 0.01), but the mean arterial pressure was not significantly changed, giving a higher rate-pressure product. The increase in mean pulmonary artery wedge pressure was attenuated (26 ± 3 vs 30 ± 3 mm Hg during control exercise, p < 0.05), but ST depression was unaltered. Exercise leg flow was reduced by nisoldipine from 4.3 ± 0.4 to 3.9 ± 0.3 liters/min (p = 0.07) and the proportion of cardiac output distributed to the legs was reduced from 42 ± 3 to 33 ± 3% (p < 0.01). Despite this, leg oxygen saturation and extraction, femoral venous and arterial lactate concentration, femoral venoarterial lactate difference, leg lactate production and femoral venous pH did not change, indicating no significant alteration in leg oxygen transport or oxidative metabolism. In keeping with its vasodilator action, nisoldipine altered rest and exercise hemodynamics. Although exercise cardiac output increased, flow was redistributed away from exercising muscle without changing oxygen transport or metabolism.