Oral [13C]bicarbonate measurement of CO2 stores and dynamics in children and adults

During exercise, less additional CO2 is stored per kilogram body weight in children than in adults, suggesting that children have a smaller capacity to store metabolically produced CO2. To examine this, tracer doses of [13C]bicarbonate were administered orally to 10 children (8-12 yr) and 12 adults (25-40 yr) at rest. Washout of 13CO2 in breath was analyzed to estimate recovery of tracer, mean residence time (MRT), and size of CO2 stores. CO2 production (VCO2) was also measured breath by breath using gas exchange techniques. Recovery did not differ significantly between children [73 +/- 13% (SD)] and adults (71 +/- 9%). MRT was shorter in children (42 +/- 7 min) compared with adults (66 +/- 15 min, P less than 0.001). VCO2 per kilogram was higher in the children (5.4 +/- 0.9 ml.min-1.kg-1) compared with adults (3.1 +/- 0.5, P less than 0.0001). Tracer estimate of CO2 production was correlated to VCO2 (r = 0.86, P less than 0.0001) and when corrected for mean recovery accurately predicted the VCO2 to within 3 +/- 14%. There was no difference in the estimate of resting CO2 stores between children (222 +/- 52 ml CO2/kg) and adults (203 +/- 42 ml CO2/kg). We conclude that orally administered [13C]bicarbonate can be used to assess CO2 transport dynamics. The data do not support the hypothesis of lower CO2 stores under resting conditions in children.     

Response of respiratory exchange ratio (R) to sinusoidal work load in humans

An examination was made of the response of respiratory exchange ratio (R), carbon dioxide output (VCO2) and oxygen uptake (VO2) to sinusoidal work load with periods (T) of 1-16 min in six healthy men to determine whether R response is sinusoidal. The influence of the ratio of the amplitude of VCO2 to that of VO2 and the phase lag between them on R response was also studied by computer simulation. The results and conclusions obtained are as follows: 1) With decrease in the period, the amplitudes of VO2 and VCO2 dropped exponentially, becoming least at T of 1 min (T = 1 min). In contrast, the amplitude of R was largest at T = 4 min and subsequently decreased progressively. 2) The peak amplitude of R at T = 4 min can be explained by the larger phase lag and relatively low of amplitude of VCO2 to VO2. 3) The smallest amplitude of R at T = 1 min was due not to the ratio of amplitude or phase lag, but to remarkably smaller amplitudes of VO2 and VCO2. 4) The phase lag of VO2 to sinusoidal work load was smaller than that of VCO2. Phase lag of R was considerably larger than that of VO2 or VCO2. 5) The response curve of VO2 and VCO2 is a sinusoidal curve with the same period as exercise. However, the response of R is not a real sinusoidal but a deformed biphasic curve with a high crest and low trough. The deformity is determined by the phase lag between VO2 and VCO2 response and also the ratio of amplitude of VCO2 to that of VO2.     

Recovery of (13)CO2 during rest and exercise after [1-(13)C]acetate, [2-(13)C]acetate, and NaH(13)CO3 infusions

For estimating the oxidation rates (Rox) of glucose and other substrates by use of (13)C-labeled tracers, we obtained correction factors to account for label dilution in endogenous bicarbonate pools and TCA cycle exchange reactions. Fractional recoveries of (13)C label in respiratory gases were determined during 225 min of rest and 90 min of leg cycle ergometry at 45 and 65% peak oxygen uptake (VO(2 peak)) after continuous infusions of [1-(13)C]acetate, [2-(13)C]acetate, or NaH(13)CO(3). In parallel trials, [6,6-(2)H]glucose and [1-(13)C]glucose were given. Experiments were conducted after an overnight fast with exercise commencing 12 h after the last meal. During the transition from rest to exercise, CO(2) production increased (P < 0.05) in an intensity-dependent manner. Significant differences were observed in the fractional recoveries of (13)C label as (13)CO(2) at rest (NaH(13)CO(3), 77.5 +/- 2.8%; [1-(13)C]acetate, 49.8 +/- 2.4%; [2-(13)C]acetate, 26.1 +/- 1.4%). During exercise, fractional recoveries of (13)C label from [1-(13)C]acetate, [2-(13)C]acetate, and NaH(13)CO(3) were increased compared with rest. Magnitudes of label recoveries during both exercise intensities were tracer specific (NaH(13)CO(3), 93%; [1-(13)C]acetate, 80%; [2-(13)C]acetate, 65%). Use of an acetate-derived correction factor for estimating glucose oxidation resulted in Rox values in excess (P < 0.05) of glucose rate of disappearance during hard exercise. We conclude that, after an overnight fast: 1) recovery of (13)C label as (13)CO(2) from [(13)C]acetate is decreased compared with bicarbonate; 2) the position of (13)C acetate label affects carbon dilution estimations; 3) recovery of (13)C label increases in the transition from rest to exercise in an isotope-dependent manner; and 4) application of an acetate correction factor in glucose oxidation measurements results in oxidation rates in excess of glucose disappearance during exercise at 65% of VO(2 peak). Therefore, bicarbonate, not acetate, correction factors are advocated for estimating glucose oxidation from carbon tracers in exercising men.     

Effects of maintained weight loss on sleep dynamics and neck morphology in severely obese adults

The goals of the study were to determine if moderate weight loss in severely obese adults resulted in (i) reduction in apnea/hypopnea index (AHI), (ii) improved pharyngeal patency, (iii) reduced total body oxygen consumption (VO(2)) and carbon dioxide production (VCO(2)) during sleep, and (iv) improved sleep quality. The main outcome was the change in AHI from before to after weight loss. Fourteen severely obese (BMI > 40 kg/m(2)) patients (3 males, 11 females) completed a highly controlled weight reduction program which included 3 months of weight loss and 3 months of weight maintenance. At baseline and postweight loss, patients underwent pulmonary function testing, polysomnography, and magnetic resonance imaging (MRI) to assess neck morphology. Weight decreased from 134 +/-6.6 kg to 118 +/- 6.1 kg (mean +/- s.e.m.; F = 113.763, P < 0.0001). There was a significant reduction in the AHI between baseline and postweight loss (subject, F = 11.11, P = 0.007). Moreover, patients with worse sleep-disordered breathing (SDB) at baseline had the greatest improvements in AHI (group, F = 9.00, P = 0.005). Reductions in VO(2) (285 +/- 12 to 234 +/-16 ml/min; F = 24.85, P < 0.0001) and VCO(2) (231 +/- 9 to 186 +/- 12 ml/min; F = 27.74, P < 0.0001) were also observed, and pulmonary function testing showed improvements in spirometry parameters. Sleep studies revealed improved minimum oxygen saturation (minSaO(2)) (83.4 +/- 61.9% to 89.1 +/- 1.2%; F = 7.59, P = 0.016), and mean SaO(2) (90.4 +/- 1.1% to 93.8 +/- 1.0%; F = 6.89, P = 0.022), and a significant increase in the number of arousals (8.1 +/- 1.4 at baseline, to 17.1 +/- 3.0 after weight loss; F = 18.13, P = 0.001). In severely obese patients, even moderate weight loss (approximately 10%) boasts substantial benefit in terms of the severity of SDB and sleep dynamics.     

Ambient oxygen regulates epithelial metabolism and nitric oxide production in the human nose.

The effects of ambient O(2) tension on epithelial metabolism and nitric oxide (NO) production (VNO) in the nasal airway were examined in nine healthy volunteers. Nasal VNO, O(2) consumption (VO(2)), and CO(2) production (VCO(2)) were measured during normoxia followed by gradual hypoxia from 21 to 0% O(2) concentration. Nasal VO(2), VCO(2), and respiratory quotient during normoxia were determined to be 1.19 +/- 0.04 ml/min, 1.60 +/- 0.04 ml/min, and 1.35 +/- 0.04, respectively. Hypoxia exposure to the nasal cavity significantly decreased both VCO(2) and VNO [VCO(2): 1.60 +/- 0.04 to 0.96 +/- 0.03 ml/min (P < 0.01), VNO: 530 +/- 15 to 336 +/- 9 nl/min (P < 0.01)]. VNO was reduced commensurately with gradual decline in O(2) tension, and the apparent K(m) value for O(2) was determined to be 23.0 microM. These results indicate that the nasal epithelial cells exchange O(2) and CO(2) with ambient air in the course of their metabolism and that nasal epithelial cells can synthesize NO by using ambient O(2) as a substrate. We conclude that air-borne O(2) diffuses into the epithelium where it may be utilized for either cell metabolism or NO synthesis.     

Increasing P(50) does not improve DO(2CRIT) or systemic VO(2) in severe anemia

Reducing the hemolobin (Hb)-O(2) binding affinity facilitates O(2) unloading from Hb, potentially increasing tissue mitochondrial O(2) availability. We hypothesized that a reduction of Hb-O(2) affinity would increase O(2) extraction when tissues are O(2) supply dependent, reducing the threshold of critical O(2) delivery (DO(2 CRIT)). We investigated the effects of increased O(2) tension at which Hb is 50% saturated (P(50)) on systemic O(2) uptake (VO(2) (SYS)), DO(2 CRIT), lactate production, and acid-base balance during isovolemic hemodilution in conscious rats. After infusion of RSR13, an allosteric modifier of Hb, P(50) increased from 36.6 +/- 0.3 to 48.3 +/- 0.6 but remained unchanged at 35.4 +/- 0.8 mmHg after saline (control, CON). Arterial O(2) saturations were equivalent between RSR13 and saline groups, but venous PO(2) was higher and venous O(2) saturation was lower after RSR13. Convective O(2) delivery progressively declined during hemodilution reaching the DO(2 CRIT) at 3.4 +/- 0.8 ml x min(-1) x 100 g(-1) (CON) and 3.6 +/- 0.6 ml x min(-1) x 100 g(-1) (RSR13). At Hb of 8.1 g/l VO(2) (SYS) started to decrease (CON: 1.9 +/- 0.1; RSR13: 1.8 +/- 0.2 ml x min(-1) x 100 g(-1)) and fell to 0.8 +/- 0.2 (CON) and 0.7 +/- 0.2 ml x min(-1). 100 g(-1) (RSR13). Arterial lactate was lower in RSR13-treated than in control animals when animals were O(2) supply dependent. The decrease in base excess, arterial pH, and bicarbonate during O(2) supply dependence was significantly less after RSR13 than after saline. These findings demonstrate that during O(2) supply dependence caused by severe anemia, reducing Hb-O(2) binding affinity does not affect VO(2) (SYS) or DO(2 CRIT) but appears to have beneficial effects on oxidative metabolism and acid base balance.     

A prototype gas exchange monitor for exercise stress testing aboard NASA Space Station

A monitor was developed to track weightlessness deconditioning aboard the National Aeronautics and Space Administration (NASA) Space Station by measuring the O2 uptake (VO2) and CO2 production (VCO2) and calculating maximum VO2 and anaerobic threshold during an exercise stress test. The system uses two flowmeters in series to achieve a completely automatic flow calibration, and it uses breath-by-breath compensation for sample line transport delay. The accuracy of the system was measured over the range of VO2 and VCO2 from 100 to 800 ml/min by means of simulation. Accuracy was 0.54% for VO2 and 2.9% for VCO2. The system was further evaluated using two laboratory methods, the first method being comparison with a breath-by-breath system. As volunteers performed a maximum effort on a cycle ergometer, the mean difference in readings between the two systems was 17 ml/min for VO2 and 8.0 ml/min for VCO2. The correlation coefficient squared was greater than 0.96 for both. The second laboratory test was to use the system for 2 mo in a Human Performance Laboratory. Readings of maximum VO2 (VO2max) and anaerobic threshold were repeatable and consistent with the individual's activity level. The accuracy and convenience of operation will make this a valuable instrument aboard the Space Station.     

Instrumentation simultaneously measuring VCO2 and VO2 in humans using titration methods

An instrument has been developed for the simultaneous measurement of carbon dioxide excretion (VCO2) and oxygen uptake (VO2). This instrument, the Nutrimeter, gives these breath-averaged measurements continuously without having to determine respiratory flow rate, perform timed spirometric gas collections, or determine absolute CO2 or O2 concentrations. It can be used on ventilated or nonventilated patients in long- and short-term studies. VO2 is determined via the replenishment technique. VCO2 is determined via a new technique, absorption-titration, described here. Bench test results of VCO2 measurements show a standard error of the estimate (SEE) +/- 0.591% of full scale (500 ml/min) and maximum single point error (MSPE) of +/- 3.54% over a 100--350 ml/min range. VO2 measurements show SEE +/- 0.518% of full scale (1,000 ml/min) and MSPE +/- 2.42% over a 100--450 ml/min range. In 31 human clinical trials the Nutrimeter was compared with the open-circuit spirometric collection and micro-Scholander analysis technique. VCO2 measurements show SEE +/- 2.208% and MSPE +/- 10.57% over 135--315 ml/min. VO2 measurements show SEE +/- 1.134% of full scale and MSPE +/- 9.54% over 170--360 ml/min. Response time is 60 s optimally for step changes in VO2 (0--90% of steady-state value), 90 s for VCO2.     

The energetics of barnacle geese (Branta leucopsis) flying in captive and wild conditions

Experimental data on the relationship between mean heart rate (f(H)) and mean rate of oxygen consumption (VO(2)) of captive barnacle geese during flights in a wind tunnel are assessed in terms of their capacity to predict the typical VO(2) of wild barnacle geese, based on the recordings of their f(H), while undertaking autumn migratory flights between Spitsbergen (78 degrees N) and Caerlaverock, Scotland (55 degrees N). A significant linear relationship has been demonstrated between the f(H) and simultaneously recorded VO(2) of a single barnacle goose (B-B) flying in the wind tunnel (VO(2)=1.42 f(H)-304, r(2)=0.82, P<0.001, N=12 flights). Data recorded from three additional geese (N=4 flights), lay within the 95% prediction intervals of the relationship for goose B-B. When these geese (mean body mass=2.06 kg, n=4) were flown in the wind tunnel (WT) without the mask, they had a mean f(H) of 451+/-23 beats min(-1), yielding an estimate for VO(2) of 336+/-33 ml min(-1). However, f(H) has also been recorded from wild barnacle geese (mean migratory f(H) of 253 beats min(-1)), and substitution of this value into the above calibration equation results in an unrealistically low value for mean migratory VO(2) of only 55 ml min(-1). Various factors, such as differences in heart mass, selective tissue perfusion, environmental temperature and flock formation, which might account for some of the difference in f(H) between the captive and wild geese are discussed. Comparison with other WT studies shows that inter-species minimum mass-specific VO(2) declines with increasing body mass (M(b); range 0.035-2.8 kg) as 173 M(b)(-0.224), r(2)=0.848.     

Kinetics of CO uptake and diffusing capacity in transition from rest to steady-state exercise.

In the transition from rest to steady-state exercise, O2 uptake from the lungs (VO2) depends on the product of pulmonary blood flow and pulmonary arteriovenous O2 content difference. The kinetics of pulmonary blood flow are believed to be somewhat faster than changes in pulmonary arteriovenous O2 content difference. We hypothesized that during CO breathing, the kinetics of CO uptake (VCO) and diffusing capacity for CO (DLCO) should be faster than VO2 because changes in pulmonary arteriovenous CO content difference should be relatively small. Six subjects went abruptly from rest to constant exercise (inspired CO fraction = 0.0005) at 40, 60, and 80% of their peak VO2, measured with an incremental test (VO2peak). At all exercise levels, DLCO and VCO rose faster than VO2 (P less than 0.001), and DLCO rose faster than VCO (P less than 0.001). For example, at 40% VO2peak, the time constant (tau) for DLCO in phase 2 was 19 +/- 5 (SD), 24 +/- 5 s for VCO, and 33 +/- 5 s for VO2. Both VCO and DLCO increased with exercise intensity but to a lesser degree than VO2 at all exercise intensities (P less than 0.001). In addition, no significant rise in DLCO was observed between 60 and 80% VO2peak. We conclude that the kinetics of VCO and DLCO are faster than VO2, suggesting that VCO and DLCO kinetics reflect, to a greater extent, changes in pulmonary blood flow and thus recruitment of alveolar-capillary surface area. However, other factors, such as the time course of ventilation, may also be involved.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanistic basis for the gas exchange threshold in Thoroughbred horses.

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.     

Effect of centrally administered gamma-aminobutyric acid on metabolic function

gamma-Aminobutyric acid (GABA) content of the brain increases during hypoxia and hypercapnia and GABA by itself is a central ventilatory depressant and may depress metabolism as well. Therefore the effect of centrally administered GABA by ventriculocisternal perfusion on O2 consumption (VO2) and CO2 production (VCO2) was studied in pentobarbital-anesthetized dogs. GABA (30 mM) in mock cerebrospinal fluid (CSF) was perfused for 15 min at the rate of 1.0 ml/min followed by perfusion with mock CSF alone. Body temperature, perfusion pressure, and CSF pH were kept constant. Minute ventilation (VE) was kept constant mechanically. Under these conditions, VO2, VCO2, alveolar ventilation (VA), and relative pulmonary dead space volume (VD/VT) were measured. During perfusion with 30 mM GABA, mean VO2 (+/- SE) decreased from 96.5 +/- 3.3 to 81.9 +/- 5.1 ml/min, VCO2 from 72.1 +/- 3.8 to 60.7 +/- 3.0 ml/min, and VA from 1.7 +/- 0.1 to 1.3 +/- 0.1 l/min. VD/VT increased from 0.55 +/- 0.02 to 0.65 +/- 0.01. Perfusion with mock CSF alone restored these parameters to initial levels within 15 min. We conclude that centrally administered GABA depresses VO2 and VCO2. This reduction in metabolic function is independent of the central modulatory effects of GABA on respiration.     

Validity of inspiratory and expiratory methods of measuring gas exchange with a computerized system.

The accuracy of a computerized metabolic system, using inspiratory and expiratory methods of measuring ventilation, was assessed in eight male subjects. Gas exchange was measured at rest and during five stages on a cycle ergometer. Pneumotachometers were placed on the inspired and expired side to measure inspired (VI) and expired ventilation (VE). The devices were connected to two systems sampling expired O(2) and CO(2) from a single mixing chamber. Simultaneously, the criterion (Douglas bag, or DB) method assessed VE and fractions of O(2) and CO(2) in expired gas (FE(O(2)) and FE(CO(2))) for subsequent calculation of O(2) uptake (VO(2)), CO(2) production (VCO(2)), and respiratory exchange ratio. Both systems accurately measured metabolic variables over a wide range of intensities. Though differences were found between the DB and computerized systems for FE(O(2)) (both inspired and expired systems), FE(CO(2)) (expired system only), and VO(2) (inspired system only), the differences were extremely small (FE(O(2)) = 0.0004, FE(CO(2)) = -0.0003, VO(2) = -0.018 l/min). Thus a computerized system, using inspiratory or expiratory configurations, permits extremely precise measurements to be made in a less time-consuming manner than the DB technique.     

Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms

Exertional dyspnea limits exercise in some mitochondrial myopathy (MM) patients, but the clinical features of this syndrome are poorly defined, and its underlying mechanism is unknown. We evaluated ventilation and arterial blood gases during cycle exercise and recovery in five MM patients with exertional dyspnea and genetically defined mitochondrial defects, and in four control subjects (C). Patient ventilation was normal at rest. During exercise, MM patients had low Vo(2peak) (28 ± 9% of predicted) and exaggerated systemic O(2) delivery relative to O(2) utilization (i.e., a hyperkinetic circulation). High perceived breathing effort in patients was associated with exaggerated ventilation relative to metabolic rate with high VE/VO(2peak), (MM = 104 ± 18; C = 42 ± 8, P ≤ 0.001), and Ve/VCO(2peak)(,) (MM = 54 ± 9; C = 34 ± 7, P ≤ 0.01); a steeper slope of increase in ΔVE/ΔVCO(2) (MM = 50.0 ± 6.9; C = 32.2 ± 6.6, P ≤ 0.01); and elevated peak respiratory exchange ratio (RER), (MM = 1.95 ± 0.31, C = 1.25 ± 0.03, P ≤ 0.01). Arterial lactate was higher in MM patients, and evidence for ventilatory compensation to metabolic acidosis included lower Pa(CO(2)) and standard bicarbonate. However, during 5 min of recovery, despite a further fall in arterial pH and lactate elevation, ventilation in MM rapidly normalized. These data indicate that exertional dyspnea in MM is attributable to mitochondrial defects that severely impair muscle oxidative phosphorylation and result in a hyperkinetic circulation in exercise. Exaggerated exercise ventilation is indicated by markedly elevated VE/VO(2), VE/VCO(2), and RER. While lactic acidosis likely contributes to exercise hyperventilation, the fact that ventilation normalizes during recovery from exercise despite increasing metabolic acidosis strongly indicates that additional, exercise-specific mechanisms are responsible for this distinctive pattern of exercise ventilation.     

Respiratory sinus arrhythmia is associated with efficiency of pulmonary gas exchange in healthy humans

Respiratory sinus arrhythmia (RSA) may be associated with improved efficiency of pulmonary gas exchange by matching ventilation to perfusion within each respiratory cycle. Respiration rate, tidal volume, minute ventilation (.VE), exhaled carbon dioxide (.VCO(2)), oxygen consumption (.VO(2)), and heart rate were measured in 10 healthy human volunteers during paced breathing to test the hypothesis that RSA contributes to pulmonary gas exchange efficiency. Cross-spectral analysis of heart rate and respiration was computed to calculate RSA and the coherence and phase between these variables. Pulmonary gas exchange efficiency was measured as the average ventilatory equivalent of CO(2) (.VE/.VCO(2)) and O(2) (.VE/.VO(2)). Across subjects and paced breathing periods, RSA was significantly associated with CO(2) (partial r = -0.53, P = 0.002) and O(2) (partial r = -0.49, P = 0.005) exchange efficiency after controlling for the effects of age, respiration rate, tidal volume, and average heart rate. Phase between heart rate and respiration was significantly associated with CO(2) exchange efficiency (partial r = 0.40, P = 0.03). These results are consistent with previous studies and further support the theory that RSA may improve the efficiency of pulmonary gas exchange.     

Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

System of automated gas-exchange analysis for the investigation of metabolic processes.

Conventional gas-exchange instruments are confined to the measurement of O(2) consumption (VO(2)) and CO(2) production (VCO(2)) and are subject to a variety of errors. This handicaps the performance of these devices at inspired O(2) fraction (FI(O(2))) > 0.40 and limits their applicability to indirect calorimetry only. We describe a device based on the automation of the Douglas bag technique that is capable of making continuous gas-exchange measurements of multiple species over a broad range of experimental conditions. This system is validated by using a quantitative methanol-burning lung model modified to provide reproducible (13)CO(2) production. The average error for VO(2) and VCO(2) over the FI(O(2)) range of 0.21-0.8. is 2.4 and 0.8%, respectively. The instrument is capable of determining the differential atom% volume of known references of (13)CO(2) to within 3.4%. This device reduces the sources of error that thwart other instruments at FI(O(2)) > 0. 40 and demonstrates the capacity to explore other expressions of metabolic activity in exhaled gases related to the excretion of (13)CO(2).     

Study on the limitation for detecting anaerobic threshold by respiratory frequency]

It has been reported that respiratory frequency (F) serves to determine anaerobic threshold (AT). The purpose of this study was to investigate whether the method detecting AT by using F is influenced by the subject's condition such as the existence of sport experiences. Ten healthy adults volunteered to perform progressive cycle ergometer exercise with workloads increased by 30-W (female:20-W) every 2 min at 60 rpm. VO2 at AT were determined by four different methods, which detect the point of 1)nonlinear increase in VE, VCO2, and increase in VE/VO2 without increasing in VE/VCO2 (AT-v), 2) nonlinear increase in F (visual estimation: AT-VF), 3) inflection in F by multisegment linear regression (AT-CF), 4) inflection with omitting above RC point as with 3) (AT-CF2). The mean VO2 at AT-VF (40.8 +/- 9.2 ml/kg/min) and AT-CF (42.7 +/- 9.9 ml/kg/min) was significantly higher compared with AT-V (28.2 +/- 10.4 ml/kg/min) and not RC (42.3 +/- 10.0 ml/kg/min). It would be possible that AT-VF and AT-CF indicated RC, but not AT. There were no significant differences between AT-CF2 (28.2 +/- 10.9 ml/kg/min) and AT-V, and a highly positive correlation (r = 0.79, p less than 0.05) was observed between them. It was recognized that F reached a plateau at AT in four of the subjects. The error between AT-V and AT-CF2 was observed individual variations and the error between them within 5% was observed in only one subject. These results suggest that F is inadequate as an indicator of the AT, because F may be influenced by entrainment of breathing and pedalling frequency.     

Effect of hyperoxia on substrate utilization during intense submaximal exercise

Six trained males [mean maximal O2 uptake (VO2max) = 66 ml X kg-1 X min-1] performed 30 min of cycling (mean = 76.8% VO2max) during normoxia (21.35 +/- 0.16% O2) and hyperoxia (61.34 +/- 1.0% O2). Values for VO2, CO2 output (VCO2), minute ventilation (VE), respiratory exchange ratio (RER), venous lactate, glycerol, free fatty acids, glucose, and alanine were obtained before, during, and after the exercise bout to investigate the possibility that a substrate shift is responsible for the previously observed enhanced performance and decreased RER during exercise with hyperoxia. VO2, free fatty acids, glucose, and alanine values were not significantly different in hyperoxia compared with normoxia. VCO2, RER, VE, and glycerol and lactate levels were all lower during hyperoxia. These results are interpreted to support the possibility of a substrate shift during hyperoxia.     

Effects of acute hypoxia on the estimation of lactate threshold from ventilatory gas exchange indices during an incremental exercise test

The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.4+/-1.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.91+/-0.10 l/min (for the VE/VO2) vs. 1.89+/-0.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.67+/-0.1 l/min (for the lactate) vs. 1.37+/-0.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.