Does the threshold of transcutaneous partial pressure of carbon dioxide represent the respiratory compensation point or anaerobic threshold?

On reaching the respiratory compensation point (RCP) during rapidly increasing incremental exercise, the ratio of minute ventilation (V_E) to CO₂ output (VCO₂) rises, which coincides with changes of arterial partial pressure of carbon dioxide (P _aCO₂). Since P _aCO₂ changes can be monitored by transcutaneous partial pressure of carbon dioxide (PCO_2,tc) RCP may be estimated by PCO_2,tc measurement. Few available studies, however, have dealt with comparisons between PCO_2,tc threshold (T _AT) and lactic, ventilatory or gas exchange threshold (V _AT), and the results have been conflicting. This study was designed to examine whether this threshold represents RCP rather than V _AT. A group of 11 male athletes performed incremental excercise (25 W · min^–1) on a cycle ergometer. The PCO_2,tc at (44°C) was continuously measured. Gas exchange was computed breath-by-breath, and hyperaemized capillary blood for lactate concentration ([la^–]_b) and P _aCO₂ measurements was sampled each 2 min. The T _AT was determined at the deflection point of PCO_2,tc curve where PCO_2,tc began to decrease continuously. The V _AT and RCP were evaluated with VCO₂ compared with oxygen uptake (VO₂) and V_E compared with the VCO₂ method, respectively. The PCO_2,tc correlated with P _aCO₂ and end-tidal PCO₂. At T _AT, power output [P, 294 (SD 40) W], VO₂ [4.18 (SD 0.57)l · min^–1] and [la^–] [4.40 (SD 0.64) mmol · l^–1] were significantly higher than those at V _AT[P 242 (SD 26) W, VO₂ 3.56 (SD 0.53) l · min^–1 and [la^–]_b 3.52 (SD 0.75), mmol · l^–1 respectively], but close to those at RCP [P 289 (SD 37) W; VO₂ 3.97 (SD 0.43) l · min^– and [la^–]_b 4.19 (SD 0.62) mmol · l^–1, respectively]. Accordingly, linear correlation and regression analyses showed that P, VO₂ and [la^–]_b at T _AT were closer to those at RCP than at V _AT. In conclusion, the T _AT reflected the RCP rather than V _AT during rapidly increasing incremental exercise.     

APCO2 surface electrode working on the principle of electrical conductivity

APCO₂ electrode working on the principle of electrical conductivity is described. The calibration curve can be linearized according to the formula . This linearity has been tested in thePCO₂ range of 0.93–9.33 kPa (7–70 Torr). For the experiments electrodes are used which have conductivity values of about 50 nS and drifts of maximally 5%/h at aPCO₂ of 5.33 kPa (40 Torr). The response time (T ₉₀) is about 20 s. The temperature sensitivity is 2.4 nS/1 K between 298K–310K. The standard error of the measurements is =0.33 nS. With these electrodes tissuePCO₂ can be measured on the surface of various organs.     

Absence of long-term modulation of ventilation by dead-space loading during moderate exercise in humans

The stability of arterial PCO₂ (P_aCO₂) during moderate exercise in humans suggests a CO₂-linked control that matches ventilation (_E) to pulmonary CO₂ clearance (CO₂). An alternative view is that _E is subject to long-term modulation (LTM) induced by hyperpnoeic history. LTM has been reported with associative conditioning via dead-space (V_D) loading in exercising goats (Martin and Mitchell 1993). Whether this prevails in humans is less clear, which may reflect differences in study design (e.g. subject familiarisation; V_D load; whether or not _E is expressed relative to CO₂; choice of P_aCO₂ estimator). After familiarisation, nine healthy males performed moderate constant-load cycle-ergometry (20 W-80 W-20 W; <lactate threshold, _L): day 1, pre-conditioning, n=3; day 2, conditioning (V_D=1.59 l, doubling _E at 20 W and 80 W), n=8 with 10 min rest between tests; and, after 1 h rest, post-conditioning, n=3. Gas exchange was determined breath-by-breath. Post-conditioning, neither the transient [phase 1, phase 2 (1, 2)] nor steady-state _E exercise responses, nor their proportionality to CO₂, differed from pre-conditioning. For post-conditioning trial 1, steady-state _E was 28.1 (4.7) l min^–1 versus 29.1 (3.8) l min^–1 pre-conditioning, and mean-alveolar PCO₂ (a validated P_aCO₂ estimator) was 5.53 (0.48) kPa [41.5 (3.6) mmHg] versus 5.59 (0.49) kPa [41.9 (3.7) mmHg]; the 1 _E increment was 4.2 (2.9) l min^–1 versus 5.2 (1.9) l min^–1; the 2 _E time-constant () was 64.4 (24.1) s versus 64.1 (25.3) s; _E/CO₂ was 1.12 (0.04) versus 1.10 (0.04); and the _E-CO₂ slope was 21.7 (3.4) versus 21.2 (3.2). In conclusion, we could find no evidence to support ventilatory control during moderate exercise being influenced by hyperpnoeic history associated with dead-space loading in humans.     

Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

Summary These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (P _a0₂) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO_2max) range = 65-77 ml·kg^–1·min^–1] performed a normoxic graded exercise test on a cycle ergometer toVO_2max at sea level. During incremental exercise atVO_2max 5 of the 12 subjects had ideal alveolar to arterial P02 gradients (P _A-aO₂) of above 5 kPa (range 5-5.7) and a decline from restingP _aO₂ (P _aO₂) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (P _A-aO₂) of 4.0-4.3 kPa with P _aO₂ of 0.4-1.3 kPa while the remaining 3 subjects hadP _A-aO₂ of 4.3-5 kPa with P _aO₂ between 1.7 and 2.0 kPa. The correlation between P_AO₂ andP _aO₂ atVO_2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSP _aO₂ and arterial partial pressure of carbon dioxide VSP _aO₂ atVO_2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

Transmural gradient of tissue gas tensions in the canine left ventricular myocardium during coronary clamping and reactive hyperemia

Mass spectrometry was used for the continuous, simultaneous and quantitative measurement of oxygen (PO₂) and carbon dioxide (PCO₂) partial pressures in the subendocardial and subepicardial layers of the left ventricle in 11 anaesthetized ventilated dogs. Under control conditions,PO₂ was significantly lower in the subendocardium (13.5±4.5 mm Hg) than in the subepicardium (20.7±2.3 mm Hg), whereasPCO₂ did not differ significantly (43±8.8 and 51±9.2 mm Hg respectively). These variables were not correlated with blood pressure or coronary blood flow. Subendocardial and subepicardialPO₂ decreased less than 5 s after coronary occlusion. These changes were more rapid and severe in the subendocardium. After occlusion for 90 s: subendocardialPO₂ was 4.1±6.3 mm Hg while subepicardialPO₂ was 6.7±15.0 mm Hg (P<0.05).PCO₂ reached peak values of 56±25 mm Hg subendocardial and 82±22 mm Hg subepicardial at 2.67±0.71 min and 3.43±0.93 min after coronary clamping. A reactive hyperemia occurred after coronary unclamping with different time courses and amplitudes for systolic and diastolic stroke flows whilePO₂ recovered with different kinetics. SubendocardialPO₂ increased with a lower initial slope, probably in relation with the delay in the diastolic hyperemia. The observed delayed subendocardial hyperoxia, unrelated to the hyperemia, may indicate a delay in the recovery of normal work and metabolism in the inner layers of the myocardium.     

Analysis of alveolar PCO 2 control during the menstrual cycle

We attempted to analyze how is regulated during progesterone-induced hyperventilation in the luteal phase. A model for the CO₂ control loop was constructed, in which the function of the CO₂ exchange system was described as and that of the CO₂ sensing system as . Using this model, we estimated (1) the primary increase in produced by progesterone stimulation and (2) the effectiveness (E) of the loop to regulateP _{A CO 2}, defined as P _{A CO 2} (op)/P _{A CO 2} (cl) in which op signifies open-loop and cl, closed-loop. These respiratory variables were investigated throughout the menstrual cycle in 8 healthy women. During the luteal phase, on average, increased by 9.4% andP _{A CO 2},B andH decreased by 0.33 kPa (2.5 mm Hg), 0.47 kPa (3.5 mm Hg) and 13.6%, respectively, whileS and did not change significantly. (op) increased progressively on successive days of the luteal phase whileE remained unchanged at a value of 7.9, thus there was a progressive decrease inP _{A CO 2}. The decrease inH was considered to lessen P _{A CO 2} (op) and so reduce the final deviation ofP _{A CO 2} (P _{A CO 2} (cl)) during the luteal phase. The decrease inB was found to be dependent on (op).     

Physiological responses to intermittent and continuous exercise at the same relative intensity in older men

We investigated the physiological responses in older men to continuous (CEx) and intermittent (IEx) exercise. Nine men [70.4 (1.2) years, O_2peak: 2.21 (0.20) l min^–1; mean (SE)] completed eight exercise tests (two CEx and six IEx) on an electronically braked cycle ergometer in random order. CEx and IEx were performed at 50% and 70% O_2peak. IEx was performed using 60sE:60sR, 30sE:30sR and 15sE:15sR exercise to rest ratios. The duration of exercise was adjusted so that the total amount of work completed was the same for each exercise test. Oxygen uptake (O₂), minute ventilation (_E) and heart rate (HR) were measured at the mid-point of each exercise test. Arterialised blood samples were obtained at rest and during exercise and analysed for pH and PCO₂. At the same relative intensity (50% or 70% O_2peak), IEx resulted in a significantly lower (P<0.01) O₂, _E and HR than CEx. There were no significant differences (P>0.05) in O₂, _E and HR measured at the mid point of the three exercise to rest ratios at 50% and 70% O_2peak. pH and PCO₂ during CEx and IEx at 50% O_2peak were not significantly different from rest. CEx performed at 70% O_2peak resulted in significant decreases (P<0.05) in pH and PCO₂. There was a significant decrease (P<0.05) in pH only during the 60sE:60sR IEx at 70% O_2peak. Changes in arterialised PCO₂ during the 60sE:60sR, 30sE:30sR and 15sE:15sR at both 50% and 70% O_2peak exercise tests were not significant. When exercising at the same percentage of O_2peak and with the total amount of work fixed, IEx results in significantly lower physiological responses than CEx in older men. All results are given as mean (SE).     

Transcutaneous,noninvasiveP O 2 monitoring in adults during exercise and hypoxemia

A new, commercially available, transcutaneous (tc)P _{O 2} monitor was tested in adult females and in laboratory animals to assess its applicability in measuring arterial oxygen tension during physiological stress. Observed values on dogs correlated well with direct measurements of arterialP _{O 2} and with previous data obtained from measurements of arterial blood during exercise and hypoxemia. In our female subjects the unit responded rapidly to changes in inspired ambient oxygen and electrical stability was excellent during maximal exercise tests. TranscutaneousP _{O 2} decreased to an average of 87.8 Torr during maximum exercise breathing 20.9% O₂, and to 32 Torr while breathing 12.6% O₂ at maximum work. Two distinct patterns of response in tcP _{O 2} were observed during hypoxic and normoxic exercise. The technique appears to have substantial future application both in clinical and physiological investigation involving adult subjects.     

In vivo measurement of carbon dioxide tension with a miniature electrode

A commercially available catheter type electrode with whichP _CO2 can be continuously measured in vivo and in vitro gave progressively less accurate results the longer the measuring period was extended. This proved to be due to temperature effects and a change in sensitivity with time. A correction procedure for these effects was developed which was based on two observations. 1. The relationship between temperature and the logarithm of the sensitivity of the electrodeamplifier combination was linear and virtually identical for 9 electrodes: 8% change in sensitivity for a deviation of 1° C from the temperature during calibration. 2. The change in sensitivity due to drift of the electrode output is approximately a logarithmic function of time: 1 h after calibration all electrodes exhibited a decreased sensitivity, varying between 0.3 and 16.7%. The drift effect can be dealt with by repeated calibrations, preferably at 1^1/2 h intervals.The adequacy of the correction procedure was assessed in in vivo measurements in cats and dogs. The meanP _CO2 difference between the in vivo measurement, corrected for temperature and drift, and samples analyzed with a conventional electrode, was 0.005 kPa (0.04 mm Hg) with a standard deviation of 0.187 kPa (1.39 mm Hg).     

Effect of H+ and elevated PCO 2on membrane electrical properties of rat cerebral arteries

Some membrane electrical properties of muscle cells from the middle cerebral artery of the rat were recorded with intracellular microelectrodes. The resting membrane potential (E _m) of this preparation was –63 mV. Reduction of extracellular pH to 7.0 in the face of a constantP _{CO 2}of 40 mm Hg had no significant effect onE _m. Similarly the slope of the steady-state voltage/current curves was not different at pH 7.0 compared to control at pH 7.4. In marked contrast, whenP _{CO 2}was elevated to around 60 to 70 mm Hg there was a rapid hyperpolarization and reduction in the slope of the voltage current curve suggesting an increased conductance for one or more ionic species. In addition elevation ofP _{CO 2}increased the slope of theE _m vs. log[K]₀ curve from 46 mV/decade to 59 m V/decade which is in good agreement with a Nernstian potential for a K⁺ selective membrane. These data suggest that while the smooth muscle cells of rat cerebral arteries are relatively insensitive to a small reduction in extracellular pH; reduction of intracellular pH by elevatingP _{CO 2}induces hyperpolarization by increasing K⁺ conductance (g _k). However, it is not clear from these experiments if theP _{CO 2}effects are mediated entirely by changes in pH or if there is a direct membrane action of CO₂.This work is supported by Grant no. HL27862     

The involvement of expiratory termination in the vagally mediated facilitation of ventilatory CO2 responsiveness during hyperoxia

In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO₂ during hyperoxia was investigated.Following total inactivation, the relationship between ventilation ( ) and arterialPCO₂ (P _aCO₂) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO₂ responsiveness, was studied further.Differential vagal cold blockade to a temperature (5–11°C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration,T _E) had no effect on either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0°C did the ventilatory depression during hypercapnia emerge, largely becauseT _E failed to shorten in response to the hypercapnic stimulus.It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of and its CO₂ responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.Supported by the Deutsche Forschungsgemeinschaft, SFB 114Preliminary reports of this work have been presented in Pflügers Arch 355: (Suppl) R47 (1975); 377: (Suppl) R54 (1978) and in Proc. XXVIII. Int. Congr. of Physiol. Sciences, Budapest, Vol VIV, 515 (1980)     

Interpretation of gas-blood ratio inP O 2polarography

Summary The differences inP _{O 2}readings between gas and blood were studied with a Clark-type electrode in the range of 38.5 to 713 mm HgP _{O 2}.The tonometered blood samples were taken in two different ways. The results showed that the gas-blood ratior _b(equilibrating gasP _{O 2}reading/equilibrated bloodP _{O 2}reading) depended not only on the sampling method but also on theP _{O 2}range: it varied from 1.005 to 1.032 for aP _{O 2}of 96.5 mm Hg, and from 1.040 to 1.081 for aP _{O 2}of 713 mm Hg according to the sampling procedure.A theoretical analysis demonstrated that the variation ofr _bwith the bloodP _{O 2}can be attributed to the influence of the degree of oxygen saturation of the hemoglobin on theP _{O 2}gradient existing in the blood diffusion boundary layer adhering to the electrode membrane.This work was supported by grants from the High Authority of the European Coal and Steel Community and from the Fonds de la Recherche Scientifique Médicale, Belgium.     

Interstitial PCO2 and pH in rat hippocampal slices measured by means of a novel fast CO2/H+-sensitive microelectrode based on a PVC-gelled membrane

We describe here the construction and properties of a double-barrelled microelectrode (tip diameter 4–10 m) which permits simultaneous measurements of PCO₂ and pH, and which has a 90% response time of only one or a few seconds for a step change in PCO₂. The fast response of the CO₂-sensitive barrel is due to (i) the use of a PVC-gelled (tridodecylamine-containing) membrane solution which enables the construction of extremely short ( 4 m), yet mechanically stable, membrane columns, and (ii) the presence of carbonic anhydrase in the filling solution. Recordings made in the pyramidal layer of area CA1 in rat hippocampal slices showed that the deviation in the acid direction of the basal interstitial pH (pH₀) from that of the perfusion solution was attributable to a higher PCO₂ level within the tissue. Most of the late acid shift evoked by stimulation of the Schaffer collaterals (5- to 20-s trains at 10 Hz) could also be explained on the basis of an accumulation of interstitial CO₂ at a constant HCO ₃ ^– concentration. This conclusion was supported by the finding that inhibition of extracellular carbonic anhydrase activity by 10 M benzolamide completely abolished the activity-induced fall in pH₀, but not the increase in PCO₂. The initial stimulus-induced alkalosis was accompanied by a slight decrease in PCO₂ only, implying a parallel increase in the interstitial HCO ₃ ^– concentration. Benzolamide produced a dramatic enhancement of the early alkaline shift as well as of the simultaneous fall in PCO₂. The latter effect of the drug unmasks a cellular CO₂ sink that is induced by neuronal activity.     

Cellular mechanism of force development in cat middle cerebral artery by reducedPCO2

These studies were undertaken to determine the effect of reducing aPCO₂ below physiological levels on cat middle cerebral artery. Upon reduction ofPCO₂ from 37 to 14 torr (pH 7.4) we observed membrane depolarization and force development. ReducingPCO₂ decreased the slope of theE _m vs. log [K]_o curve and increased the slope of the steady-state I/V relationship suggesting that the change inE _m was due to reduction of outward K⁺ conductance (g _k). Elevation of pH from 7.37 to 7.6 had a very similar effect on these cerebral arterial muscle cells, depolarizing the muscle membrane (reducing theE _m vs. log [K]_o curve) and increasing the slope of the I/V relationship to statistically equivalent values as reduction ofPCO₂. ReturningPCO₂ from 14 to 37 torr rapidly relaxed these preparations, but only transiently. This relaxation was followed by a rebound contraction within 3 min, demonstrating a transient nature for the action of elevatingPCO₂ in cerebral arteries. The response to changing pH_o followed a slower time course but did not change with time. These studies demonstrate that both elevated pH_o and reducedPCO₂ activate cerebral arterial muscle by a mechanism which includes reduction ing _k. However, it can not be determined if these similar responses and reduction, ofg _k are mediated by changing pH_i or mediated through different mechanisms. It is possible that pH_o andPCO₂ can modify cerebral arterial tone by direct mechanisms and not necesarily by their effect on pH_i. It is clear, however, that reduction ofPCO₂ and elevation of pH_o both activate cerebral arterial muscle by a mechanism which includes reduction ofg _k.This study was supported by NIH grant no. HL-32871. Dr. Harder is an established investigator of the American Heart Association     

Ventilatory response of prepubertal boys and adults to carbon dioxide at rest and during exercise

Summary The aim of this study was to determine whether the greater ventilation in children at rest and during exercise is related to a greater CO₂ ventilatory response. The CO₂ ventilatory response was measured in nine prepubertal boys [10.3 years (SD 0.1)] and in 10 adults [24.9 years (SD 0.8)] at rest and during moderate exercise ( CO₂ = 20 ml·kg^–1·min^–1) using the CO₂-rebreathing method. Three criteria were measured in all subjects to assess the ventilatory response to CO₂: the CO₂ sensitivity threshold (Th), which was defined as the value of end titalPCO₂ (P _ETCO₂) where the ventilation increased above its steady-state level; the reactivity slope expressed per unit of body mass (SBM), which was the slope of the linear relation between minute ventilation ( _E) andP _ETCO₂ above Th; and the slope of the relationship between the quotient of tidal volume (V _T) and inspiration time (t _I) andP _ETCO₂ (V _T ·t _I ^–1 ·P _ETCO₂ ^–1) values above Th. The _E,V _T, breathing frequency (f _R), oxygen uptake ( O₂), and CO₂ production ( CO₂) were also measured before the CO₂-rebreathing test. The following results were obtained. First, children had greater ventilation per unit body weight than adults at rest (P<0.001) and during exercise (P<0.01). Second, at rest, onlyV _T ·t _I ^–1 ·P _ETCO₂ ^–1 was greater in children than in adults (P<0.001). Third, during exercise, children had a higher S_BM (P < 0.02) andV _T ·t _I ^–1 ·P _ETCO₂ ^–1 (P<0.001) while Th was lower (P<0.02). Finally, no correlation was found between _E/ CO₂ and Th while a significant correlation existed between _E/ CO₂ and S_BM (adults,r=0.79,P<0.01; children,r=0.73,P<0.05). We conclude that children have, mainly during exercise, a greater sensitivity of the respiratory centres than adult. This greater CO₂ sensitivity could partly explain their higher ventilation during exercise, though greater CO₂ production probably plays a role at rest.     

A method for estimating bicarbonate buffering of lactic acid during constant work rate exercise

A method to estimate the CO₂ derived from buffering lactic acid by HCO₃ ^– during constant work rate exercise is described. It utilizes the simultaneous continuous measurement of O₂ uptake ( O₂) and CO₂ output ( CO₂), and the muscle respiratory quotient (RQ_m). The CO₂ generated from aerobic metabolism of the contracting skeletal muscles was estimated from the product of the exercise-induced increase in O₂ and RQ_m calculated from gas exchange. By starting exercise from unloaded cycling, the increase in CO₂ stores, not accompanied by a simultaneous decrease in O₂ stores, was minimized. The total CO₂ and aerobic CO₂ outputs and, by difference, the millimoles (mmol) of lactate buffered by HCO₃ ^– (corrected for hyperventilation) were estimated. To test this method, ten normal subjects performed cycling exercise at each of two work rates for 6 min, one below the lactic acidosis threshold (LAT) (50 W for all subjects), and the other above the LAT, midway between LAT and peak O₂ [mean (SD), 144 (48) W]. Hyperventilation had a small effect on the calculation of mmol lactate buffered by HCO₃ ^– [6.5 (2.3)% at 6 min in four subjects who hyperventilated]. The mmol of buffer CO₂ at 6 min of exercise was highly correlated (r = 0.925, P < 0.001) with the increase in venous blood lactate sampled 2 min into recovery (coefficient of variation = ±0.9 mmol·l^–1). The reproducibility between tests done on different days was good. We conclude that the rate of release of CO₂2 from HCO₃ ^– can be estimated from the continuous analysis of simultaneously measured CO₂, O₂, and an estimate of muscle substrate.     

Breath-by-breath determinations of airway occlusion pressure in the developing lamb

The ventilatory effects of breath-by-breath measurements of airway occlusion pressure, i.e., airway pressure determined 100 ms after initiation of inspiration (P _{0. 1}) were evaluated in seven lambs studied sequentially between 7 and 28 days after birth. P _0.1 was determined by computer-aided, on-line regression analysis of the inspiratory pressure versus time (dP/dt) by means of a pneumatic occlusion valve that allowed occlusion times to vary in proportion to respiratory rate. No significant changes were found in minute ventilation, tidal volume, respiratory rate or end-tidal CO₂ concentration when the valve was operating as a one-way valve (opening pressure 0.02 kPa or 0.2 cm H₂0) compared to when in occlusion mode [opening pressure 0.18–0.2 kPa or 1.8–2.0 cmH₂0, mean occlusion time 44 (25) ms]. The calculated P _0.1 values correlated well with those obtained from manual occlusions (r = 0.87, P < 0.0001). This new technique, which detects and discards irregular or non-linear (r < 0.95) inspiratory pressure profiles, enables breath-by-breath determinations of inspiratory drive in rapidly breathing lambs with minimal impact on respiratory pattern and ventilation.These results were presented in part at the annual meetings of the American Pediatric Society and the Society for Pediatric Research 1992     

Hyperpnoea and CO2 sensitivity of the respiratory centres during exercise

Summary The aim of this study was to specify whether exercise hyperpnoea was related to the CO₂ sensitivity of the respiratory centres measured during steady-state exercise of mild intensity. Thus, ventilation , breathing pattern [tidal volume (V _T), respiratory frequency (f), inspiratory time (T _I), total time of the respiratory cycle (T _TOT),V _T/T _I,T _I/T _TOT] and CO₂ sensitivity of the respiratory centres determined by the rebreathing method were measured at rest (SCO_{2 re}) and during steady-state exercise (SCO_{2 ex}) of mild intensity [CO₂ output =20 ml·kg⁻¹·min⁻¹] in 11 sedentary male subjects (aged 20–34 years). The results showed that SCO_{2 re} and SCO_{2 ex} were not significantly different. During exercise, there was no correlation between and SCO_{2 ex} and, for the same , all subjects had very close values normalized for body mass (bm), regardless of their SCO_{2 ex} ( =1.44 l·min⁻¹·kg⁻¹ SD 0.10). A highly significant positive correlation between SCO_{2 ex} andV _T (normalised for bm) (r=0.80,P<0.01),T _I (r=0.77,P<0.01) andT _TOT (r=0.77,P<0.01) existed, as well as a highly significant negative correlation between SCO_{2 ex} and (normalised for bm^−0.25) (r=−0.73,P<0.01). We conclude that the hyperpnoea during steady-state exercise of mild intensity is not related to the SCO_{2 ex}. The relationship between breathing pattern and SCO_{2 ex} suggests that the breathing pattern could influence the determination of the SCO_{2 ex}. This finding needs further investigation.     

Secretin and VIP-stimulated adenylate cyclase from rat heart

The exact positions of microelectrodes used to measure thePO₂ in the cerebral cortex of the rat were determined by staining the tissue with Alcian Blue. The measurement sites were subsequently located under a light microscope and correlated with the capillary and cellular arrangement of the cortex. The microelectrodes used for thePO₂ measurements were made of gold glass fibers; the Alcian Blue was injected hydrostatically through a micropipette attached to thePO₂ microelectrode. The sites where dye had been deposited were seen under a light microscope as green blue spots about 100 m in diameter. The capillaries were visualized by silver nitrate perfusion. Differences between the localPO₂ values in the neo- and the archeocortex were found. In the neocortex the meanPO₂ was 31 mm Hg, capillary volume 1.6%, capillary surface area 980/mm², capillary length 13.5/mm; whereas in the archeocortex these values where 21 mm Hg, 0.9%, 820/mm² and 9.4/mm respectively. These data indicate a relationship between the microcirculatory transport system and the local oxygen tension and provide further evidence that the meanPO₂ level tends to decrease when moving from the surface into the archeocortex.Supported by the Deutsche ForschungsgemeinschaftReported in part at the 3rd Symposium of ISOTT, Cambridge, GB, 1977; and at the 27th International Congress of Physiological Sciences, Paris, France, 1977     

Effects of two successive maximal exercise tests on pulmonary gas exchange in athletes

Pulmonary extravascular water accumulation may be involved in exercise-induced hypoxaemia in highly aerobically trained athletes. We hypothesized that if such an alteration were present in elite athletes performing a maximal exercise test, the impairment of gas exchange would be worse during a second exercise test following the first one. Eight male athletes performed two incremental exercise tests separated by a 30-min recovery period. Pulmonary gas exchange and ventilatory data were measured during exercise tests performed in normoxia. Arterial blood samples were drawn each minute during rest, exercise, and recovery. Pulmonary diffusing capacity for CO (D _LCO) was measured at rest, after the first (T1) and the second (T2) test. All the subjects underwent a spirometric test at rest and after T2. Maximal and recovery data for 0₂ uptake and minute ventilation were not statistically different between T1 and T2. Partial pressure of arterial 0₂ (P _aO₂) decreased during both tests but was lower during T2 for rest, 60 W, and 120 W (P < 0.02). Alveolar-arterial difference in partial pressure of 0₂ (P _A-a0₂) increased during both the tests but was significantly larger during T2 for rest, 60 W, and 120 W (P < 0.01). The P _aO₂ and P _A-aO₂ data at maximal exercise were not significantly different between T1 and T2. Compared to rest, P _A-aO₂ remained significantly larger during recovery for both T1 and T2 (P < 0.0001). The P _A-aO₂ during T2 recovery was larger than T1 recovery (P < 0.008). Spirometric data did not change. The D _LCO measurements after T1 and T2 were not significantly different from rest. These results showed an alteration of P _aO₂ and P _A-aO₂ during T1, which tended to be worse during and after T2; however, these data do not allow us to make a definitive statement as to the cause of the hypoxaemia. Our study confirmed that exhausting exercise caused hypoxaemia. It also demonstrated that the disturbance in pulmonary gas exchange persisted for at least 30 min following the end of the exercise period and became worse during submaximal intensities of the following incremental exercise test.