CO2 Stores Research Articles

CO2 rebreathing: an undergraduate laboratory to study the chemical control of breathing

The Read CO2 rebreathing method (Read DJ. A clinical method for assessing the ventilatory response to carbon dioxide. Australas Ann Med 16: 20-32, 1967) provides a simple and reproducible approach for studying the chemical control of breathing. It has been widely used since the modifications made by Duffin and coworkers. Our use of a rebreathing laboratory to challenge undergraduate science students to investigate the control of breathing provided 8 yr of student-generated data for comparison with the literature. Students (age: 19-22 yr, Research Ethics Board approval) rebreathed from a bag containing 5% CO2 and 95% O2 (to suppress the peripheral chemoreflex to hypoxia). Rebreathing was performed, and ventilation measured, after hyperventilation to deplete tissue CO2 stores and enable the detection of the central chemoreflex threshold. We analyzed 43 data sets, of which 10 were rejected for technical reasons. The mean threshold and ventilatory sensitivity to CO2 were 43.3 ± 3.8 mmHg and 4.60 ± 3.04 l·min(-1)·mmHg(-1) (means ± SD), respectively. Threshold values were normally distributed, whereas sensitivity was skewed to the left. Both mean values agreed well with those in the literature. We conclude that the modified rebreathing protocol is a robust method for undergraduate investigation of the chemical control of breathing.

Chemosensitive signaling of locus coeruleus neurons in the Bullfrog, Lithobates catesbeianus

Bullfrogs, Lithobates catesbeianus, experience broad changes in pH inversely proportional to temperature while retaining whole body CO2 stores. Ventilatory patterns to maintain constant CO2 are controlled through negative feedback with chemosensory neurons detecting CO2/pH. We hypothesize that neurons of the locus coeruleus (LC) will respond to hypercapnic acidosis (HA). Whole‐cell patch‐clamp electrophysiological techniques were used to measure firing rates in excitatory (chemosensitivity index (CI)=260±35%), inhibitory (CI=24±18%), and non‐chemosensitive (CI=105±3%) LC neurons in bullfrog brainstem slice preparations. LC neurons have resting membrane potentials of −42±0.6mV, and when stimulated by HA membrane potentials are depolarized to −39±0.7mV (p<0.001). 81% of neurons increased and 11% decreased firing rates when exposed to HA, though increasing ΔCO2 to acidify the superfusate by >2‐fold (0.13–0.33pH units) did not produce different firing rates (p> 0.5). Greater than 80% of LC neurons are excited by HA which corroborate percentages typically reported for neonatal rat LC neurons; however, bullfrog excitatory output is doubled and appears to be maximally activated with lower CO2/H+ changes compared with neonatal rats. Our data begin to provide insight into a neurological mechanism for α‐stat pH regulation in bullfrogs based on chemosensitivity to CO2/pH.

CO2 rebreathing: an undergraduate lab to study the chemical control of breathing

Duffin and McAvoy's (1988) modification of the Read (1967) CO2 rebreathing (CO2RB) method is widely used to study chemical control of breathing (ChemoCB). We used a CO2RB laboratory to challenge undergraduate science majors (to investigate the ChemoCB). We collated and analyzed 8 years of data to study the reproducibility of the laboratory and compared the results to the literature. Students (aged 19–21 yrs; IRB approval) performed the technique using a rebreathing bag containing 95% O2 to suppress peripheral chemoreceptor activity. Ventilation was measured following hyperventilation to deplete tissue CO2 stores, which also enhances detection of the central chemoreflex threshold (CCT). Data were analyzed by 3 investigators. Of 37 data sets, 7 were rejected due to technical issues. CO2 sensitivity and CCT were 4.69±3.12 L/min/mmHg (mean±SD) and 43.5±3.9 mmHg respectively. The CCT was normally distributed, whereas sensitivity was skewed to the left. Values agree well with those reported by Duffin & McAvoy (1988). We conclude CO2RB is a robust method for undergraduate investigation of the principles of chemical control of breathing. Funded by Queen's University, NSERC and CIHR.

How do changes in exhaled CO2 measure changes in cardiac output? A numerical analysis model

In a previous study in anesthetized animals, the slope of percent decreases in exhaled CO₂ versus percent decreases in cardiac output (Q(T) inflation of vena cava balloons) was 0.73. To examine the mechanisms underlying this exhaled CO₂-Q(T) relationship, an iterative numerical analysis computer model of non-steady state CO(2) kinetics was developed. The model consisted of a large peripheral tissue compartment connected by venous return and [Formula: see text] to a small central pulmonary compartment. Equations were developed to describe the movement of CO₂ in this system. Decreases in Q(T) were accompanied by experimentally measured increases in alveolar dead space fraction (VD: (alv)/VT: (alv)), generated by decreased pulmonary vascular pressure during the Q(T) decrease. When the model was perturbed by a 40% decrease in Q(T) and an increase in VD: (alv)/VT: (alv) from 5 to 20.6%, average alveolar expired P(CO₂) (PAE(CO₂)) decreased from 37.5 to 29.4 mm Hg, similar to the animal experiments. Due to the high peripheral tissue compliance for CO₂, the computer model demonstrated that, after a decrease in Q(T), at least 1 h was required for compartment CO₂ stores to approach a new equilibrium state. The numerical analysis computer model helps to delineate the mechanisms underlying how decreased Q(T) resulted in decreased exhaled CO₂. The model permitted deconvolution of the effects of simultaneous variables and the interrogation of parameters that would be difficult to measure in actual experiments.

Importance of water temperature and thermal stratification dynamics for temporal variation of surface water CO2 in a boreal lake

Variation of the surface water CO2 concentration is likely to be the result of biological activity and physical processes such as water mixing and gas exchange with the atmosphere. Here we have studied the variations in surface water CO2 during the ice‐free period in the humic Lake Merasjärvi in northern Sweden. Meteorological, hydrological, and limnological data were collected using data logging equipment permitting high time resolution. The surface water of the lake was supersaturated with respect to CO2 throughout the study period. There were, however, considerable diurnal and longer‐term temporal variations of the surface water CO2 concentrations. Partial least squares models were used to link the logged CO2 data to the multivariate data set. On the longer‐term timescale (analyzed with 24 h means of the logged data), high concentrations of surface water CO2 were best related to the depth and temperature of the upper warmer layer (epilimnion), and to erosion of the underlying colder layer (hypolimnion). The diurnal variation (analyzed with 30 min means of the logged data) was best related to the thermal dynamics within the epilimnion, which regulated the surface water access to CO2 stores within this layer. Variables related to CO2 emission and photosynthesis (wind and photosynthetically active radiation) showed only weak correlations to variations of the surface water CO2 concentration. Accordingly, the CO2 flux, measured with the eddy‐covariance technique, was not correlated to the surface water CO2 concentration.

Generation Mechanism and Movement of Hypoxia in Strongly Enclosed Waters of Ports and Harbors

We conducted field observations in relation to hypoxia which occurs in strongly enclosed waters, such as ports and harbors, and examined generation mechanism and movement of hypoxia. Diurnal variations in hypoxia were driven by tide and wind in the strongly enclosed waters in the head of Osaka Bay. It was found that processes of the organism decomposition, oxygen consumption and carbon dioxide generation were different in and out of the ports. In the spring and summer when the water column is stratified, surface water absorbs CO2 and bottom water stores CO2 in strongly enclosed waters. On the other hand, in the end of summer, the stored CO2 upwells to the surface and causes spontaneous emission because the north wind induces the upwelling.

CO2 status as a controller of blood flow redistribution and auto‐resuscitation during anoxia‐induced apnea in the sheep

Spontaneous recovery of eupnea following an anoxia‐induced apnea (i.e. auto‐resuscitation ‐ AR) is reliant upon the transition to a "gasping" breathing pattern. Blood flow redistribution is likely to be an important determinant of successful AR by optimizing the reoxygenation process. We investigated how the duration of anoxia‐induced apnea and transition to and from gasping are influenced by factors affecting blood flow redistribution; specifically, we altered CO2 stores and the capacity for hypoxia‐induced sympathetic vasoconstriction. In 5 urethane‐chloralose anesthetized spontaneously breathing sheep, apneas were induced by breathing nitrogen, with and without 5% CO2 before, and then following administration of phentolamine. Following hypocapnic anoxic apnea, AR occurred after 95±21s, typically after 2 gasps. The duration of apnea was reduced in the presence of hypercapnia (77±26s). Phentolamine delayed hypocapnic AR (149±75s), led to more gasping, and profoundly altered AR with hypercapnia. Indeed hypercapnic AR failed in 2 sheep, while in the remaining 3 sheep apnea was significantly prolonged (115±36s). Our results suggest hypercapnia facilitates effective blood flow redistribution and reduces the duration of apnea when vasomotor control is intact. However, when anoxia‐induced vasoconstriction is blocked, the presence of hypercapnia compromises and can even prevent successful AR.

Metabolic costs of foraging and the management of O2 and CO2 stores in Steller sea lions

The metabolic costs of foraging and the management of O2 and CO2 stores during breath-hold diving was investigated in three female Steller sea lions (Eumetopias jubatus) trained to dive between 10 and 50 m (N=1142 dives). Each trial consisted of two to eight dives separated by surface intervals that were determined by the sea lion (spontaneous trials) or by the researcher (conditioned trials). During conditioned trials, surface intervals were long enough for O2 to return to pre-dive levels between each dive. The metabolic cost of each dive event (dive+surface interval; DMR) was measured using flow-through respirometry. The respiratory exchange ratio (VO2/VCO2) was significantly lower during spontaneous trials compared with conditioned trials. DMR was significantly higher during spontaneous trials and decreased exponentially with dive duration. A similar decrease in DMR was not as evident during conditioned trials. DMR could not be accurately estimated from the surface interval (SI) following individual dives that had short SIs (<50 s), but could be estimated on a dive by dive basis for longer SIs (>50 s). DMR decreased by 15%, but did not differ significantly from surface metabolic rates (MRS) when dive duration increased from 1 to 7 min. Overall, these data suggest that DMR is almost the same as MRS, and that Steller sea lions incur an O2 debt during spontaneous diving that is not repaid until the end of the dive bout. This has important consequences in differentiating between the actual and 'apparent' metabolic rate during diving, and may explain some of the differences in metabolic rates reported in pinniped species.

Disappearance of isocapnic buffering period during increasing work rate exercise at high altitude

At sea level, ventilation kinetics are characterized during a ramp exercise by three progressively steeper slopes, the first from the beginning of exercise to anaerobic threshold, the second from anaerobic threshold to respiratory compensation point, and the third from respiratory compensation point to peak exercise. In the second ventilation phase, body CO2 stores are used to buffer acidosis owing to lactate production; it has been suggested that this extra CO2 production drives the ventilation increase. At high altitude, ventilation increases owing to hypoxia. We hypothesize that ventilation increase reduces body CO2 stores affecting ventilation kinetics during exercise. In eight healthy participants, we studied the ventilation kinetics during an exercise performed at sea level and at high altitude (4559 m). We used 30 W/2 min step incremental protocol both at sea level and high altitude. Tests were done on a cyclo-ergometer with breath-by-breath ventilation and inspiratory and expiratory gas measurements. We evaluated cardiopulmonary data at anaerobic threshold, respiratory compensation point, peak exercise and the VE/VCO2 slope. At high altitude: (a) peak VO2 decreased from 2595+/-705 to 1745+/-545 ml/min (P<0.001); (b) efficiency of ventilation decreased (VE/VCO2 slope from 25+/-2 to 38+/-4, P<0.0001); (c) at each exercise step end-tidal pressure change for CO2 was lower; and (d) the isocapnic buffering period disappeared in seven over eight participants and was significantly shortened in the remaining participant. Exercise performed at high altitude is characterized by two, instead of three, ventilation slopes.

Gaseous metabolism of the chicken embryo and hatchling during post-hypoxic recovery

In neonatal mammals, the drop in oxygen consumption (VO2) during moderate degrees of hypoxia is a manifestation of metabolic depression, and occurs without anaerobic energy compensation. We examined the possibility that embryos also respond to hypoxia with a similar hypometabolic response, by measuring the extent of the O2 debt during post-hypoxic recovery. In chicken embryos at incubation days 11 (E11) and 16 (E16), and hatchlings on the day of hatching (H1), VO2 and carbon dioxide production (VCO2) were measured with an open flow system. The protocol consisted of 1h in air, followed by 40 min in hypoxia (either 17% or 11% O2) and additional 45 min of post-hypoxic recovery. VO2 dropped in hypoxia, more with 11% than 17% O2, and more the younger the animal. During post-hypoxic recovery VO2 returned to, but did not exceed, the pre-hypoxic level, indicating that no O2 debt was contracted during hypoxia. In H1, the changes of VCO2 during hypoxia and post-hypoxia matched those of VO2. Differently, in the embryos, the changes in VCO2 during hypoxia and post-hypoxic recovery were minimal. This phenomenon is explained by changes in the large CO2 stores of the eggs, which buffer the changes in CO2 output of aerobic origin. We conclude that in the chicken embryo and hatchling the energetic shortfall during the hypoxic decrease in VO2 is not compensated by anaerobic energy supply, and represents a phenomenon of metabolic depression.

Cerebral blood flow during orthostasis: role of arterial CO2

Reductions in end-tidal Pco(2) (Pet(CO(2))) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in Pet(CO(2)) reflected decreases in arterial Pco(2) (Pa(CO(2))) and their relation to increases in alveolar ventilation (Va) and decreases in CBF. Fifteen healthy subjects (10 women and 5 men) were subjected to a 10-min head-up tilt (HUT) protocol. Pa(CO(2)), Va, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in Pet(CO(2)) and Pa(CO(2)) (-1.7 +/- 0.5 and -1.1 +/- 0.4 mmHg, P < 0.05) during minute 1 of HUT were associated with a significant increase in Va (+0.7 +/- 0.3 l/min, P < 0.05). However, further decreases in Pa(CO(2)) (-0.5 +/- 0.5 mmHg, P < 0.05), from minute 1 to the last minute of HUT, occurred even though Va did not change significantly (-0.2 +/- 0.3 l/min, P = not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (-7 +/- 2 and -8 +/- 2%, P < 0.05) from minute 1 to the last minute of HUT, despite minimal changes in Pa(CO(2)). These data suggest that decreases in Pet(CO(2)) and Pa(CO(2)) during upright posture are not solely due to increased Va but could be due to ventilation-perfusion mismatch or a redistribution of CO(2) stores. Furthermore, the reduction in Pa(CO(2)) did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in Pa(CO(2)) play a role in the CBF response to orthostatic stress.

Model for the behaviour of compartmental CO2 stores during incremental exercise

The respiratory exchange ratio (RER) is a valid method for determining fat and carbohydrate oxidation during exercise when the exchange of respiratory gas is in a state of steady flux between the tissue and fluid compartments and the alveoli. However, under incremental intensity or heavy exercise conditions, the movement of electrolytes, fluids, and CO(2) between body-fluid compartments is accentuated, leading to increased hydrogen-ion concentration ([H(+)]), decreased bicarbonate-ion concentration ([HCO(3) (-)]) and CO(2) stores, and the excretion of additional CO(2) at the alveoli (i.e. H(+)+HCO(3) (-) --> CO(2)+H(2)O) elevating the CO(2) minute volume. This non-respiratory CO(2) excretion can invalidate use of the RER for determination of fat and carbohydrate oxidation. Direct measurement of the labile CO(2) store and non-respiratory CO(2) excretion during exercise is difficult. Therefore, physicochemical models were derived to illustrate the likely behaviour of compartmental CO(2) stores during 8 W.min(-1) incremental cycling exercise to formulate correction factors to the RER for the non-respiratory CO(2) component. From these models, a polynomial regression equation was derived to describe the change in the total labile CO(2) store volume during incremental exercise from the relationship with blood HCO(3) (-) content: CO(2) volume (ml) = -17x(2)+464x+650, where x is the arterialised blood standard HCO(3) (-) concentration (mmol.l(-1)), relative to resting conditions. Non-respiratory CO(2) excretion (ml.min(-1)) was then determined from the rate of change in CO(2) volume. The modelling method could allow for straightforward calculation of the non-respiratory CO(2) excretion rate for future validation work.

Stimulation of Ventilation by Normobaric Hyperoxia in Exercising Dogs

In order to describe the factors which, during hyperoxic exercise, can counteract the chemoreceptor-mediated inhibition of ventilation by O2, minute ventilation (VE) and the pulmonary gas exchange were studied breath-by-breath in four dogs running on a treadmill (5 km x h(-1)) for 10 min during and following exposure to O2 of different durations. We found that a brief inhalation of O2 applied during the steady state of the VE response provoked a reduction in VE by 6.5 +/- 0.9 l x min(-1) whereas hyperoxia applied 2 min before the onset of exercise and maintained for 2.5 min during the running tests had a significantly weaker effect on VE (-1.8 +/- 0.2 l x min(-1), P < 0.05). The rise in pulmonary CO2 output (VCO2) during the prolonged O2 exposure was less than in normoxic exercise leading to a deficit of CO2 eliminated by the lungs of 181 ml. The return to air breathing provoked a rise in VE, which reached within 73 s a much higher level than the control tests (22.9 +/- 3.6 vs. 19.5 +/- 2.2 l x min(-1), P < 0.05); VE then subsided to control levels with a long exponential decline. The CO2 deficit during O2 breathing, was fully compensated after recovery in air within 6 min. No stimulatory effect on ventilation was observed at rest at the cessation of a similar exposure to O2 despite a higher end-tidal PCO2 (+4 +/- 1 mmHg) than in exercise. In conclusion, the stimulatory effect of O2 during exercise can be clearly revealed after recovery in air and seems to operate through a more complex mechanism than that thought to be involved at rest. We propose that the changes in CO2 stores in the exercising muscles could contribute to O2-induced stimulation during exercise, possibly through stimulation of muscle afferents responding to local circulatory changes. Finally, the observation that during continuous dopamine (DA) infusion (5 microg x kg(-1) x min(-1)) the VE response to recovery in air was only a slow decrease, suggests that the arterial chemoreceptors potentiate O2-induced hyperventilation, or that the vascular actions of DA counteract part of the effects provoked by CO2 accumulation in the exercising muscles.

Effect of altered body CO2 stores on pulmonary gas exchange dynamics during incremental exercise in humans.

The lactate threshold is a widely used and, at times, controversial construct in exercise physiology and pathophysiology. Its non-invasive estimation during incremental exercise depends upon CO2 output increasing as a function of O2 uptake, i.e. 'V-slope', as a result of bicarbonate buffering during the lactic acidosis. However, we hypothesised that the V-slope deflection could also occur as a consequence of metabolic CO2 being diverted proportionally more into the CO2 stores in the early phase of exercise. Eight healthy males performed two incremental exercise tests on a cycle ergometer, with and without controlled prior hyperventilation; the hyperventilation caused end-tidal PCO2 to decline by 10 mmHg, with the clearance of a CO2 volume averaging 2547 ml. This corresponded to an 'effective' CO2 capacitance of some 3.12 ml mmHg-1 kg-1. Gas exchange was determined breath-by-breath, and blood was sampled from the dorsum of the heated hand. Our results demonstrate that the early dynamics of CO2 wash-in to the previously depleted body stores can result in a 'pseudo-threshold', i.e. significantly before the onset of the actual lactic acidosis. Precautions should therefore be taken to avoid hyperventilation prior to non-invasive estimation of the lactate threshold.

EFFECT OF ALTERED BODY CO2 STORES ON PULMONARY GAS EXCHANGE DYNAMICS DURING INCREMENTAL EXERCISE IN HUMANS

The lactate threshold is a widely used and, at times, controversial construct in exercise physiology and pathophysiology. Its non-invasive estimation during incremental exercise depends upon CO2 output increasing as a function of O2 uptake, i.e. 'V-slope', as a result of bicarbonate buffering during the lactic acidosis. However, we hypothesised that the V-slope deflection could also occur as a consequence of metabolic CO2 being diverted proportionally more into the CO2 stores in the early phase of exercise. Eight healthy males performed two incremental exercise tests on a cycle ergometer, with and without controlled prior hyperventilation; the hyperventilation caused end-tidal PCO2 to decline by [sim]10 mmHg, with the clearance of a CO2 volume averaging 2547 ml. This corresponded to an 'effective' CO2 capacitance of some 3·12 ml mmHg-1 kg-1. Gas exchange was determined breath-by-breath, and blood was sampled from the dorsum of the heated hand. Our results demonstrate that the early dynamics of CO2 wash-in to the previously depleted body stores can result in a 'pseudo-threshold', i.e. significantly before the onset of the actual lactic acidosis. Precautions should therefore be taken to avoid hyperventilation prior to non-invasive estimation of the lactate threshold.

The Effects of Caffeine on the Kinetics of O2Uptake, CO2Production and Expiratory Ventilation in Humans During the On‐Transient of Moderate and Heavy Intensity Exercise

In order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n = 10) were assigned to either a MOD (50% VO2,max, n = 5) or HVY (80% VO2,max, n = 5) exercise condition. Constant-load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)-1). Alveolar gas exchange was measured breath-by-breath. A 2- or 3-component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63% of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 +/- 14 s (PLAC) and 41 +/- 10 s (CAFF); HVY: 99 +/- 30 s (PLAC) and 103 +/- 26 (CAFF) (mean +/- S.D.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 +/- 20 s (PLAC) and 59 +/- 21 s (CAFF); HVY: 168 +/- 35 s (PLAC) and 203 +/- 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 +/- 14 s (PLAC) and 53 +/- 17 s (CAFF); HVY: 65 +/- 13 s (PLAC) and 69 +/- 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on-transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre-exercise and exercise endtidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.

A protein titration hypothesis for the temperature-dependence of tissue CO2 content in reptiles and amphibians.

Whole-body CO2 stores are known to increase with cooling in reptiles and amphibians (-[CO2]/T ). The aim of this study was to determine the mechanism(s) producing this inverse relationship. The [CO2]/T coefficients were determined for eight reptilian and one amphibian species and were found to differ by a factor of approximately 10, from -0.21 mmol kg-1 &deg;C-1 in the Mediterranean spur-thighed tortoise Testudo graeca to -0.02 mmol kg-1 &deg;C-1 in the bullfrog Rana catesbeiana. The [CO2]/T coefficients were correlated with values in the literature for in vivo plasma pH/T coefficients ([CO2]/T=-0.18&shy;8.24pH/T; r2=0.87). Plasma electrolyte concentrations (Na+, K+, Ca2+, Mg2+, Cl-, inorganic phosphate, SO42- and lactate), [protein], [CO2], PCO2 and pH were measured in chronically cannulated resting black racer snakes Coluber constrictor. When the temperature was reduced from 30 to 10 &deg;C, pH increased slightly (by -0.0028 pH units &deg;C-1), PCO2 decreased by 7 mmHg, [CO2] increased by 3.2 mmol l-1 and [HPO42-+H2PO4-] increased by 0.7 mmol l-1. Concentrations of protein and of the remaining electrolytes were not significantly different (P>0.05) at 30 and 10 &deg;C. Net plasma protein charge, calculated from the principle of electroneutrality (the sum of the cations in mequiv = the sum of anions in mequiv), was -0.48 mequiv g-1 protein at 30 &deg;C and -0.38 mequiv g-1 protein at 10 &deg;C. This 21 % decrease was attributed to the increases in [CO2] (i.e. carbonic acid) and inorganic phosphate concentration. Between 30 and 10 &deg;C, skeletal muscle pH and [CO2] in C. constrictor increased (by -0.009 units &deg;C-1 and -0.125 mmol kg-1 &deg;C-1, respectively), [Na+] and [Cl-] each decreased by approximately 12 mequiv l-1, and [K+] and the percentage of water did not change significantly. It is concluded that the increase in whole-body CO2 stores with cooling in reptiles and amphibians results from the passive effects of temperature changes upon the ionization constants of proteins and the active adjustment of PCO2 (ventilatory regulation), so that -pK is greater than -pH. Active transmembrane ion-exchange processes do not appear to be involved.

OPTIMUM INTENSITY OF EXERCISE FOR FAT OXIDATION 1130

The purpose of this study was to determine the optimum intensity of exercise for fat oxidation. Eight women and 6 men (age: 25±1 yr; height: 173±3 cm; weight: 67.4±2.7 kg;% fat: 14.9±1.9; VO2max: 46.5±3.0) volunteered for this study. Subjects completed a graded exercise test on a cycle ergometer to measure VO2max. Work bouts equivalent to 30, 40, 50, 60, 70, and 80%VO2max were completed on a separate day. Each bout lasted 8 minutes, with approximately 5-min rest between bouts. Pulmonary gas exchange and end tidal CO2 (ET CO2) were measured continuously. A blood sample for lactate (LA) was obtained 2 minutes following each bout. The respiratory exchange ratio (RER), averaged over the last 3-4 minutes of each bout, was used with VO2 to calculate the rate of fat oxidation based on data from Zuntz. Data (Mean±SEM) follow: Table Fat oxidation increased until 60%VO2max, followed by decreases at both 70 and 80%VO2max. The RER values at 70 and 80%VO2max were influenced by the decrease in whole-body CO2 stores, making the calculated decrease in fat oxidation greater than it really was. The magnitude of the difference in fat oxidation between 40 and 70%VO2max was small, suggesting that the optimum intensity of exercise for fat oxidation can be represented by a broad range of values. This range of exercise intensities is consistent with recommendations for making improvements in VO2max as well as in maintaining fat balance.

Determinations of oxygen consumption in critically ill patients: practical aspects

The determination of oxygen consumption (VO2) in critically ill patients is useful to evaluate metabolic expenditure, to calculate cardiac output and to assess the adequacy of oxygen supply to the tissues by the relationship between oxygen delivery (DO2) and VO2. Only the last application requires a high degree of accuracy in measurement. Highly accurate devices have been developed over the last few years although there are still problems with their use during spontaneous ventilation, mechanical ventilation with high FiO2, and treatment with inhaled nitric oxide (NO). Due to Haldane's transformation and the body's large CO2 stores, VO2 should only be measured in steady-state conditions, avoiding changes in ventilatory conditions or cardiac output. Air leaks should be carefully avoided since measurements would be erroneous. There is generally good agreement between Fick-derived VO2 and VO2 obtained by indirect calorimetry; discrepancies between the two methods in the study of changes in VO2 in response to ...

Ventilatory and blood acid-base adjustments to a decrease in body temperature from 30 to 10YC in black racer snakes Coluber constrictor

There is increasing evidence that many amphibian and reptilian species use relatively slow ion-exchange mechanisms in addition to ventilation to adjust pH as body temperature changes. Large changes in blood bicarbonate concentration with changes in temperature have previously been reported for the snake Coluber constrictor. The purpose of the present study was to determine the ventilatory and pH adjustments associated with the increase in CO2 stores when the snakes are cooled. Body temperature was lowered from 30 to 10 &deg;C within 4 h, at which time measurements of inspired minute ventilation (V.air), O2 consumption (VO2) and CO2 production (V.CO2) were started and continued for 56 h. The decrease in temperature produced a transient fall in the respiratory exchange ratio (V.CO2/VO2) to 0.2-0.3 and a steady-state value of 0.65&plusmn;0.14 (mean &plusmn; s.d., N=7) was not achieved until about 35 h. There were concomitant transient reductions in V.air and V.air/V.O2. However, V.air/V.CO2 initially increased, with a corresponding reduction in arterial PCO2 (PaCO2) and increase in arterial pH. By 35 h, V.air/V.CO2 had decreased and PaCO2 had increased to steady-state levels, but pH decreased very little because of a gradual increase in bicarbonate concentration. We conclude that the drop in temperature imposed a metabolic acidosis for approximately 35 h because of the time required to increase bicarbonate concentration, and that the acidosis was compensated for by an elevated V.air/V.CO2. Steady-state breathing and acid-base status were not achieved until the relatively slow increase in CO2 stores had been completed.