Pulmonary function of the green sea turtle, Chelonia mydas

Lung volumes, oxygen uptake (VO2), end-tidal PO2, and PCO2, diffusing capacity of the lungs for CO (DLCO), pulmonary blood flow (QL) and respiratory frequency were measured in the green sea turtle (Chelonia mydas) (49-127 kg body wt). Mean lung volume (VL) determined from helium dilution was 57 ml/kg and physiological dead space volume (VD) was about 3.6 ml/kg. QL, determined from acetylene uptake during rebreathing, increased in proportion to VO2 with temperature. Therefore, constant O2 content difference was maintained between pulmonary arterial and venous blood. DLCO, measured using a rebreathing technique, was 0.04 ml X kg-1 X min-1 X Torr-1 at 25 degrees C. Several cardiopulmonary characteristics in C. mydas are advantageous to diving: large tidal volume relative to functional residual capacity promotes fast exchange of the alveolar gas when the turtle surfaces for breathing: and the concomitant rise of pulmonary blood flow and O2 uptake with temperature assures efficient O2 transport regardless of wide temperature variations encountered during migrations.     

Muscle metabolism in track athletes, using 31P magnetic resonance spectroscopy.

We tested whether preferred running event in track athletes would correlate with the initial rate of phosphocreatine (PCr) resynthesis following submaximal exercise. PCr recovery was measured in the calf muscles of 16 male track athletes and 7 male control subjects following 5 min of repeated plantar flexion against resistance. Pi, PCr, and pH were measured using phosphorus magnetic resonance spectroscopy (31P MRS) with an 8-cm surface coil in a 1.8-T magnet. During exercise, work levels were gradually increased to deplete PCr to 50-60% of the initial value. No drop in pH was seen in any of the subjects during this exercise. The areas of the PCr peaks following exercise were fit to monoexponential curves. Two or three tests were performed on each subject and the results averaged. Athletes were divided into three groups based on their primary event: sprinters running 400 m or less, middle-distance athletes running 400-1500 m, and long-distance athletes running farther than 1500 m. The maximal rates of PCr resynthesis (mmol.min-1.kg-1 muscle weight) were 64.8 +/- 8.6, for long-distance runners; 41.4 +/- 11, for middle-distance runners; 32.0 +/- 7.0, for sprinters; and 38.6 +/- 10, for controls (mean +/- SE). The faster PCr recovery rates seen in long-distance runners compared with sprinters indicate greater oxidative capacity, which is consistent with the known differences between athletes in these events.     

The rate of phosphocreatine hydrolysis and resynthesis in exercising muscle in humans using 31P-MRS

Time-resolved 31-phosphorus nuclear magnetic resonance spectroscopy (31P-MRS) of the biceps femoris muscles was performed during exercise and recovery in six healthy sedentary male subjects (maximal oxygen uptake; 46.6 +/- 1.7 (SEM) ml.kg-1.min-1), 5 male sprinters (56.2 +/- 2.5), and 5 male long-distance runners (73.6 +/- 2.2). Each performed 4 min of knee flexion exercises at absolute values of 1.63 W and 4.90 W, followed by 5 min of recovery in a prone position in a 2.1 T superconducting magnet with a 67 cm bore. 31P-MRS spectra were recorded every 12.8 s during the rest-exercise-recovery sequence. Computer-aided contour analysis and pixel imaging of phosphocreatine peaks (PCr) and inorganic phosphate (Pi) were performed. The work loads in the present study were selected as mild exercise (1.63 W) and heavy exercise (4.90 W), corresponding to 18-23% and 54-70% of maximal exercise intensity. Long-distance runners showed a significantly smaller decrement in PCr and less acidification at a given exercise intensity compared to those shown by sedentary subjects. The transient responses of PCr and Pi during recovery were characterized by first-order kinetics. After exercise, the recovery rates of PCr and Pi were significantly faster in long-distance runners than in sedentary subjects (P < 0.05). Since it is postulated that PCr resynthesis is controlled by aerobic metabolism and mitochondrial creatine kinase, it is suggested that the faster PCr and Pi recovery rates and decreased acidification seen in long-distance runners during and after exercise might be attributed to their greater capacity for aerobic metabolism.     

Effect of endurance training on excessive CO2 expiration due to lactate production in exercise

We attempted to determine the change in total excess volume of CO2 output (CO2 excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO2 excess and distance-running performance. Six male endurance runners, aged 19-22 years, were subjects. Maximal oxygen uptake (VO2max), oxygen uptake (VO2) at anaerobic threshold (AT), CO2 excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for CO2 excess per unit of body mass per unit of blood lactate accumulation (delta la-) in exercise (CO2 excess.mass-1.delta la-), 12-min ERP, VO2 at AT (AT-VO2) and VO2max on average were 0.8 ml.kg-1.l-1.mmol-1, 97.8 m, 4.4 ml.kg-1. min-1 and 7.3 ml.kg-1.min-1, respectively. The percentage change in CO2 excess.mass-1.delta la- (15.7%) was almost same as those of VO2max (13.7%) and AT-VO2 (13.2%). It was found to be a high correlation between the absolute amount of change in CO2 excess.mass-1.delta la-, and the absolute amount of change in AT-VO2 (r = 0.94, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Peak blood ammonia and lactate after submaximal, maximal and supramaximal exercise in sprinters and long-distance runners

The purpose of this study was to elucidate the difference in peak blood ammonia concentration between sprinters and long-distance runners in submaximal, maximal and supramaximal exercise. Five sprinters and six long-distance runners performed cycle ergometer exercise at 50% maximal, 75% maximal, maximal and supramaximal heart rates. Blood ammonia and lactate were measured at 2.5, 5, 7.5, 10 and 12.5 min after each exercise. Peak blood ammonia concentration at an exercise intensity producing 50% maximal heart rate was found to be significantly higher compared to the basal level in sprinters (P less than 0.01) and in long-distance runners (P less than 0.01). The peak blood ammonia concentration of sprinters was greater in supra-maximal exercise than in maximal exercise (P less than 0.05), while there was no significant difference in long-distance runners. The peak blood ammonia content after supramaximal exercise was higher in sprinters compared with long-distance runners (P less than 0.01). There was a significant relationship between peak blood ammonia and lactate after exercise in sprinters and in long-distance runners. These results suggest that peak blood ammonia concentration after supramaximal exercise may be increased by the recruitment of fast-twitch muscle fibres and/or by anaerobic training, and that the processes of blood ammonia and lactate production during exercise may be strongly linked in sprinters and long-distance runners.     

Cardiopulmonary adaptations to pneumonectomy in dogs. I. Maximal exercise performance.

Maximal exercise performance was evaluated in four adult foxhounds after right pneumonectomy (removal of 58% of lung) and compared with that in seven sham-operated control dogs 6 mo after surgery. Maximal O2 uptake (ml O2.min-1.kg-1) was 142.9 +/- 1.9 in the sham group and 123.0 +/- 3.8 in the pneumonectomy group, a reduction of 14% (P less than 0.001). Maximal stroke volume (ml/kg) was 2.59 +/- 0.10 in the sham group and 1.99 +/- 0.05 in the pneumonectomy group, a reduction of 23% (P less than 0.005). Lung diffusing capacity (DL(CO)) (ml.min-1.Torr-1.kg-1) reached 2.27 +/- 0.08 in the combined lungs of the sham group and 1.67 +/- 0.07 in the remaining lung of the pneumonectomy group (P less than 0.001). In the pneumonectomy group, DL(CO) of the left lung was 76% greater than that in the left lung of controls. Blood lactate concentration and hematocrit were significantly higher at exercise in the pneumonectomy group. We conclude that, in dogs after resection of 58% of lung, O2 uptake, cardiac output, stroke volume, and DL(CO) at maximal exercise were restricted. However, the magnitude of overall impairment was surprisingly small, indicating a remarkable ability to compensate for the loss of one lung. This compensation was achieved through the recruitment of reserves in DL(CO) in the remaining lung, the development of exercise-induced polycythemia, and the maintenance of a relatively large stroke volume in the face of an increased pulmonary vascular resistance.     

Control of exercise hyperpnea during hypercapnia in humans

Previous studies have yielded conflicting results on the ventilatory response to CO2 during muscular exercise. To obviate possible experimental errors contributing to such variability, we have examined the CO2-exercise interaction in terms of the ventilatory response to exercise under conditions of controlled hypercapnia. Eight healthy male volunteers underwent a sequence of 5-min incremental treadmill exercise runs from rest up to a maximum CO2 output (VCO2) of approximately 1.5 l . min-1 in four successive steps. The arterial PCO2 (PaCO2) at rest was stabilized at the control level or up to 14 Torr above control by adding 0-6% CO2 to the inspired air. Arterial isocapnia (SD = 1.2 Torr) throughout each exercise run was maintained by continual adjustment of the inspired PCO2. At all PaCO2 levels the response in total ventilation (VE) was linearly related to exercise VCO2. Hypercapnia resulted in corresponding increases in both the slope (S) and zero intercept (V0) of the VE-VCO2 curve; these being directly proportional to the rise in PaCO2 (means +/- SE: delta S/ delta PaCO2, 2.73 +/- 0.28 Torr-1; delta V0/ delta PaCO2, 1.67 +/- 0.18 l . min-1 . Torr-1). Thus the ventilatory response to concomitant hypercapnia and exercise was characterized by a synergistic (additive plus multiplicative) effect, suggesting a positive interaction between these stimuli. The increased exercise sensitivity in hypercapnia is qualitatively consistent with the hypothesis that VE is controlled to minimize the conflicting challenges due to chemical drive and the mechanical work of breathing (Poon, C. S. In: Modelling and Control of Breathing, New York: Elsevier, 1983, p. 189-196).     

Pulmonary O2 diffusing capacity at exercise by a modified rebreathing method.

The rebreathing technique for the measurement of the pulmonary O2 diffusing capacity, DO2, previously developed for resting conditions [Cerretelli et al., J. appl. Physiol. 37, 526-532 (1974)] has been modified for application to exercise and simplified to one rebreathing maneuver only. The changes consist: 1) in administering in the course of a normoxic exercise a priming breath of an O2 free mixture just before the onset of rebreathing in order to achieve rapidly the appropriate starting PO2 values on the linear part of the O2 dissociation curve as required by the method; 2) in calculating mixed venous blood O2 tension by extrapolation of the alveolar to mixed venous blood PO2 equilibration curve, instead of determining it separately. While the mean DO2 value of 21 measurements on 5 subjects at rest was 30 ml-min-1 - Torr-1 +/- 3 (S.E.), in 2 subjects exercising on a bicycle ergometer, DO2 was found to increase from a resting value of about 32 ml- min-1 - Torr-1 to 107 ml - min-1 - Torr-1 for an eightfold increase of O2 uptake. The validity and the applicability of the method are critically discussed.     

Background ventilatory stimulus as a determinant of load compensation

Compensation for inspiratory flow-resistive loading was compared during progressive hypercapnia and incremental exercise to determine the effect of changing the background ventilatory stimulus and to assess the influence of the interindividual variability of the unloaded CO2 response on evaluation of load compensation in normal subjects. During progressive hypercapnia, ventilatory response was incompletely defended with loading (mean unloaded delta VE/delta PCO2 = 3.02 +/- 2.29, loaded = 1.60 +/- 0.67 1.min-1.Torr-1 CO2, where VE is minute ventilation and PCO2 is CO2 partial pressure; P less than 0.01). Furthermore the degree of defense of ventilation with loading was inversely correlated with the magnitude of the unloaded CO2 response. During exercise, loading produced no depression in ventilatory response (mean delta VE/delta VCO2 unloaded = 20.5 +/- 1.9, loaded = 19.2 +/- 2.5 l.min-1.l-1.min-1 CO2 where VCO is CO2 production; P = NS), and no relationship was demonstrated between degree of defense of the exercise ventilatory response and the unloaded CO2 response. Differences in load compensation during CO2 rebreathing and exercise suggest the presence of independent ventilatory control mechanisms in these states. The type of background ventilatory stimulus should therefore be considered in load compensation assessment.     

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.     

Sweating responses and the muscle metaboreflex under mildly hyperthermic conditions in sprinters and distance runners

To investigate the effects of different training methods on nonthermal sweating during activation of the muscle metaboreflex, we compared sweating responses during postexercise muscle occlusion in endurance runners, sprinters, and untrained men under mild hyperthermia (ambient temperature, 35°C; relative humidity, 50%). Ten endurance runners, nine sprinters, and ten untrained men (maximal oxygen uptakes: 57.5 ± 1.5, 49.3 ± 1.5, and 36.6 ± 1.6 ml·kg(-1)·min(-1), respectively; P < 0.05) performed an isometric handgrip exercise at 40% maximal voluntary contraction for 2 min, and then a pressure of 280 mmHg was applied to the forearm to occlude blood circulation for 2 min. The Δ change in mean arterial blood pressure between the resting level and the occlusion was significantly higher in sprinters than in untrained men (32.2 ± 4.4 vs. 17.3 ± 2.6 mmHg, respectively; P < 0.05); however, no difference was observed between distance runners and untrained men. The Δ mean sweating rate (averaged value of the forehead, chest, forearm, and thigh) during the occlusion was significantly higher in distance runners than in sprinters and untrained men (0.38 ± 0.07, 0.19 ± 0.03, and 0.11 ± 0.04 mg·cm(-2)·min(-1), respectively; P < 0.05) and did not differ between sprinters and untrained men. Our results suggest that the specificity of training modalities influences the sweating response during activation of the muscle metaboreflex. In addition, these results imply that a greater activation of the muscle metaboreflex does not cause a greater sweating response in sprinters.     

Plasma levels of renin, angiotensin II, and 6-ketoprostaglandin F1 alpha in endurance athletes

Twelve male runners and 12 matched nonathletes performed a prolonged uninterrupted graded exercise test on the bicycle ergometer up to exhaustion to study blood pressure and plasma levels of renin (PRA), vasoconstrictor angiotensin II (ANG II), and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), a metabolite of the vasodilator prostacyclin. In the athletes work load was increased by 30 W/4 min, and in the control subjects the increments of work load were adjusted to their lower exercise capacity to equalize total exercise duration. Blood was drawn, and blood pressure and O2 uptake (VO2) were measured at rest and at the fourth, eighth, and last steps of exercise. Peak VO2 averaged 60 +/- 1.6 ml . min-1 . kg-1 in the runners and 46.8 +/- 1.5 in the nonathletes. To evaluate differences between athletes and controls, PRA, ANG II, and 6-keto-PGF1 alpha were first adjusted for significant confounding factors, such as age, weight, hematocrit, 24-h urinary sodium excretion, and O2 uptake. PRA was significantly lower in the athletes (F = 11.2; P less than 0.01); ANG II was not different at rest, but its rise with exercise was less steep in the runners (F = 8.2; P less than 0.01), whereas 6-keto-PGF1 alpha was not different between the groups (F = 1.3; NS). Despite the differences in PRA and ANG II, however, blood pressure was similar in athletes and nonathletes (F = 0.0; NS).     

Carbon dioxide pressure-concentration relationship in arterial and mixed venous blood during exercise.

To calculate cardiac output by the indirect Fick principle, CO(2) concentrations (CCO(2)) of mixed venous (Cv(CO(2))) and arterial blood are commonly estimated from PCO(2), based on the assumption that the CO(2) pressure-concentration relationship (PCO(2)-CCO(2)) is influenced more by changes in Hb concentration and blood oxyhemoglobin saturation than by changes in pH. The purpose of the study was to measure and assess the relative importance of these variables, both in arterial and mixed venous blood, during rest and increasing levels of exercise to maximum (Max) in five healthy men. Although the mean mixed venous PCO(2) rose from 47 Torr at rest to 59 Torr at the lactic acidosis threshold (LAT) and further to 78 Torr at Max, the Cv(CO(2)) rose from 22.8 mM at rest to 25.5 mM at LAT but then fell to 23.9 mM at Max. Meanwhile, the mixed venous pH fell from 7.36 at rest to 7.30 at LAT and to 7.13 at Max. Thus, as work rate increases above the LAT, changes in pH, reflecting changes in buffer base, account for the major changes in the PCO(2)-CCO(2) relationship, causing Cv(CO(2)) to decrease, despite increasing mixed venous PCO(2). Furthermore, whereas the increase in the arteriovenous CCO(2) difference of 2.2 mM below LAT is mainly due to the increase in Cv(CO(2)), the further increase in the arteriovenous CCO(2) difference of 4.6 mM above LAT is due to a striking fall in arterial CCO(2) from 21.4 to 15.2 mM. We conclude that changes in buffer base and pH dominate the PCO(2)-CCO(2) relationship during exercise, with changes in Hb and blood oxyhemoglobin saturation exerting much less influence.     

Buffering capacity of deproteinized human vastus lateralis muscle

The in vitro deproteinized vastus lateralis muscle buffer capacity, carnosine, and histidine levels were examined in 20 men from 4 distinct populations (5 sprinters, 800-m runners; 5 rowers; 5 marathoners; 5 untrained). Needle biopsies were obtained at rest from the vastus lateralis muscle. The buffer capacity was determined in deproteinized homogenates by repeatedly titrating supernatant extracts over the pH range of 7.0-6.0 with 0.01 N HCl. Carnosine and histidine levels were determined on an amino acid AutoAnalyzer. Fast-twitch fiber percentage was determined by staining intensity of myosin adenosinetriphosphatase. High-intensity running performance was assessed on an inclined treadmill run to fatigue (20% incline; 3.5 m X s-1). Significantly (P less than 0.01) elevated buffer capacities, carnosine levels, and high-intensity running performances were demonstrated by the sprinters and rowers, but no significant differences existed between these variables for the marathoners vs. untrained subjects. Low but significant (P less than 0.05) interrelationships were demonstrated between buffer capacity, carnosine levels, and fast-twitch fiber composition. These findings indicate that the sprinters and rowers possess elevated buffering capabilities and carnosine levels compared with marathon runners and untrained subjects.     

The Role of Erythrocytic Acetylcholinesterase in Hormonal Regulation of Adaptation to Physical Exercise

Acetylcholinesterase (AchE) activity in erythrocytes and blood levels of cortisol and insulin were investigated in athletes training under different bioenergetic conditions (sprinters, middle-distance runners, and marathoners). The groups of sprinters and marathoners had a decreased enzyme activity compared to nonathletes (p < 0.05). In response to a standard exercise, load AchE activity increased in the groups of middle-distance runners and marathoners. A relationship was observed between the level of AchE activity and the cortisol-to-insulin ratio in the blood. This ratio is specific to the type of bioenergetic conditions and increases in the following order: controls, middle-distance runners, sprinters, and marathoners. In vitro experiments revealed an effect of insulin on AchE activity. This effect was significantly lower in sprinters than in the control group. A reduction in AchE activity and an increase in the cortisol-to-insulin ratio are considered as factors increasing metabolic turnover in athletes, mainly, lipid turnover. This mechanism ensures effective mobilization of substrates at the start of physical exercise and their recovery after. The observed relationship between the insulin level and the AchE activity may prove to be a mechanism of regulation of the insulin level. This relationship may change during adaptation to physical exercise, as in the case of sprinters, when the sensitivity of AchE to the inhibitory effect of insulin is decreased. A high blood level of cortisol and insulin is a distinctive feature of sprinters, which provides for a higher turnover of carbohydrates. In marathoners, low AchE activity leads to an increased effect of acetylcholine, which is manifested by an increased cortisol level and a decreased insulin level, thus providing for a higher lipid turnover.     

Physiological factors associated with the lower maximal oxygen consumption of master runners

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.     

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.     

The role of anaerobic ability in middle distance running performance

The purpose of this study was to assess the relationship between anaerobic ability and middle distance running performance. Ten runners of similar performance capacities (5 km times: 16.72, SE 0.2 min) were examined during 4 weeks of controlled training. The runners performed a battery of tests each week [maximum oxygen consumption (VO2max), vertical jump, and Margaria power run] and raced 5 km three times (weeks 1, 2, 4) on an indoor 200-m track (all subjects competing). Regression analysis revealed that the combination of time to exhaustion (TTE) during the VO2max test (r2 = 0.63) and measures from the Margaria power test (W.kg-1, r2 = 0.18; W, r2 = 0.05) accounted for 86% of the total variance in race times (P less than 0.05). Regression analysis demonstrated that TTE was influenced by both anaerobic ability [vertical jump, power (W.kg-1) and aerobic capacity (VO2max, ml.kg-1.min-1)]. These results indicate that the anaerobic systems influence middle distance performance in runners of similar abilities.     

In vivo regulation of plasma [H+] in ponies during acute changes in PCO2

The major objective of this study was to test the hypothesis that in ponies the change in plasma [H+] resulting from a change in PCO2 (delta H+/delta PCO2) is less under acute in vivo conditions than under in vitro conditions. Elevation of inspired CO2 and lowering of inspired O2 (causing hyperventilation) were used to respectively increase and decrease arterial PCO2 (Paco2) by 5-8 Torr from normal. Arterial and mixed venous blood were simultaneously sampled in 12 ponies during eucapnia and 5-60 min after Paco2 had changed. In vitro data were obtained by equilibrating blood in a tonometer at five different levels of PCO2. The in vitro slopes of the H+ vs. PCO2 relationships were 0.73 +/- 0.01 and 0.69 +/- 0.01 neq.1-1.Torr-1 for oxygenated and partially deoxygenated blood, respectively. These slopes were greater (P less than 0.001) than the in vivo H+ vs. PCO2 slopes of 0.61 +/- 0.03 and 0.57 +/- 0.03 for arterial and mixed venous blood, respectively. The delta HCO3-/delta pH (Slykes) was 15.4 +/- 1.1 and 17.0 +/- 1.1 for in vitro oxygenated and partially deoxygenated blood, respectively. These values were lower (P less than 0.001) than the in vivo values of 23.3 +/- 2.7 and 25.2 +/- 4.7 Slykes for arterial and mixed venous blood, respectively. In vitro, plasma strong ion difference (SID) increased 4.5 +/- 0.2 meq/l (P less than 0.001) when Pco2 was increased from 25 to 55 Torr. A 3.5-meq/l decrease in [Cl-] (P less than 0.001) and a 1.3 +/- 0.1 meq/l increase in [Na+] (P less than 0.001) accounted for the SID change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood osmolality in vitro: dependence on PCO2, lactic acid concentration, and O2 saturation

Changes of osmolality (Osm) were measured by freezing-point determination in true plasma of 10 healthy subjects. This was done after equilibration with CO2 (0.5-10.0%), after the addition of lactic acid (10 and 20 mmol/l), and after deoxygenation. The graph for the dependence of Osm on CO2 partial pressure (PCO2) in oxygenated blood resembles the classical CO2 absorption curve. The increase of Osm with PCO2 (approximately 0.2 mosmol . kg H2O-1 . Torr-1) is almost as great as the increase in dissolved CO2 plus bicarbonate (HCO-3). Addition of lactic acid shifts the curve upward by only 0.6 mosmol/mmol because of displacement of HCO-3. Deoxygenation has no significant effect at constant PCO2 despite an increase in [HCO-3]. This is probably due to the binding of 2,3-diphosphoglycerate to hemoglobin. It can be seen in the Osm-pH diagram that differences between CO2 and lactic acid titration largely disappear. For each lactic acid concentration there is a linear dependence corresponding to the linear [HCO-3]-pH relation in plasma. At constant pH, Osm increases after deoxygenation. The observed in vitro relation might explain part of the osmolality increase during physical exercise.