Pulmonary O2 diffusing capacity at exercise by a modified rebreathing method

The rebreathing technique for the measurement of the pulmonary O₂ diffusing capacity, \(D_{{\text{O}}_{\text{2}} }\) , previously developed for resting conditions [Cerretelli et al., J. appl. Physiol. 37, 526–532 (1974)] has been modified for application to exercise and simplified to one rebreathing maneuver only. The changes consist:

1. in administering in the course of a normoxic exercise a priming breath of an O₂ free mixture just before the onset of rebreathing in order to achieve rapidly the appropriate starting \(P_{{\text{O}}_{\text{2}} }\) values on the linear part of the O₂ dissociation curve as required by the method;
2. in calculating mixed venous blood O₂ tension by extrapolation of the alveolar to mixed venous blood \(P_{{\text{O}}_{\text{2}} }\) equilibration curve, instead of determining it separately.

While the mean \(D_{{\text{O}}_{\text{2}} }\) value of 21 measurements on 5 subjects at rest was 30 ml·min^?1·Torr^?1±3 (S.E.), in 2 subjects exercising on a bicycle ergometer, \(D_{{\text{O}}_{\text{2}} }\) was found to increase from a resting value of about 32 ml·min^?1·Torr^?1 to 107 ml·min^?1·Torr^?1 for an eightfold increase of O₂ uptake. The validity and the applicability of the method are critically discussed.     

Exercise-induced oxyhemoglobin desaturation and pulmonary diffusing capacity during high-intensity exercise

The purpose of this investigation was to examine if exercise-induced arterial oxyhemoglobin desaturation selectively observed in highly trained endurance athletes could be related to differences in the pulmonary diffusing capacity (D _L) measured during exercise. The D _L of 24 male endurance athletes was measured using a 3-s breath-hold carbon monoxide procedure (to give D _LCO) at rest as well as during cycling at 60% and 90% of these previously determined ${\dot V}$ O_2max. Oxyhemoglobin saturation (S _aO₂%) was monitored throughout both exercise protocols using an Ohmeda Biox II oximeter. Exercise-induced oxyhemoglobin desaturation (DS) (S _aO₂%? ${\dot V}$ O_2max) was observed in 13 subjects [88.2 (0.6)%] but not in the other 11 nondesaturation subjects [NDS: 92.9 (0.4)%] (P?≤?0.05), although ${\dot V}$ O_2max was not significantly different between the groups [DS: 4.34 (0.65) l?/?min vs NDS: 4.1 (0.49) l?/?min]. At rest, no differences in either D _LCO [m1 CO?·?mmHg^?1?·?min^?1: 41.7 (1.7) (DS) vs 41.1 (1.8) (NDS)], D _LCO?/ ${\dot V}$ _A [8.2 (0.4) (DS) vs 7.3 (0.9) (NDS)], MVV [l?/?min: 196.0 (10.4) (DS) vs 182.0 (9.9) (NDS)] or FEV₁/FVC [86.3 (2.2) (DS) vs 82.9 (4.7) (NDS)] were found between groups (P?≥?0.05). However, ${\dot V}$ _E?/ ${\dot V}$ O₂ at ${\dot V}$ O_2max was lower in the DS group [33.0 (1.1)] compared to the NDS group [36.8 (1.5)] (P?≤?0.05). Exercise D _LCO (m1 CO?·?mmHg^?1?·?min^?1?) was not different between groups at either 60% ${\dot V}$ O_2max [DS: 55.1 (1.4) vs NDS: 57.2 (2.1)] or at 90% ${\dot V}$ O_2max [DS: 61.0 (1.8) vs NDS: 61.4 (2.9)]. A significant relationship (r?=?0.698) was calculated to occur between S _aO₂% and ${\dot V}$ _E?/ ${\dot V}$ O₂ during maximal exercise. The present findings indicate that the exercise-induced oxyhemoglobin desaturation seen during submaximal and near-maximal exercise is not related to differences in D _L, although during maximal exercise S _aO₂ may be limited by a relatively lower exercise ventilation.     

Physical training and exercise diffusing capacity

Summary The diffusing capacity (D _L,CO) has been measured repeatedly by an improved brief steady-state technique in a total of 13 experimental and 4 control subjects. Both resting and exercise (D _L,CO) were initially somewhat higher in the more athletic subjects. However, physical training sufficient to increase the predicted maximum oxygen intake by an average of 12% over a 6–15 week period was without significant influence upon (i) the restingD _L,CO (whether standardized for respiratory rate, tidal volume, or respiratory minute volume) and (ii) exerciseD _L,CO at the mean oxygen consumption of the individual. When account was taken of the increase in maximum oxygen intake, there was some increase in the predictedD _L,CO max (< 5%); however, this was too small to be of great practical significance. Existing evidence for an increase of restingD _L,CO with training is shown to be insubstantial. The underlying hypothesis thatD _L,CO limits oxygen transfer is also weak; if a small increase ofD _L,CO does occur during training, this is by virtue of the close association betweenD _L,CO and pulmonary blood flow.     

Operating lung volumes are affected by exercise mode but not trunk and hip angle during maximal exercise

Introduction

Despite VO_2peak being, generally, greater while running compared to cycling, ventilation (V _E) during maximal exercise is less while running compared to cycling. Differences in operating lung volumes (OLV) between maximal running and cycling could be one explanation for previously observed differences in V _E and this could be due to differences in body position e.g., trunk/hip angle during exercise.

Purpose

We asked whether OLV differed between maximal running and cycling and if this difference was due to trunk/hip angle during exercise.

Methods

Eighteen men performed three graded maximal exercise tests; one while running, one while cycling in the drop position (i.e., extreme hip flexion), and one while cycling upright (i.e., seated with thorax upright). Resting flow-volume characteristics were measured in each body position to be used during exercise. Tidal flow-volume loops were measured throughout the exercise.

Results

V _E during maximal running (148.8 ± 18.9 L min^?1) tended to be lower than during cycling in the drop position (158.5 ± 24.7 L min^?1; p = 0.07) and in the upright position (158.5 ± 23.7 L min^?1; p = 0.06). End-inspiratory and end-expiratory lung volumes (EILV, EELV) were significantly larger during drop cycling compared to running (87.1 ± 4.1 and 35.8 ± 6.2 vs. 83.9 ± 6.0 and 33.0 ± 5.7 % FVC), but only EILV was larger during upright cycling compared to running (88.2 ± 3.5 % FVC). OLV and V _E did not differ between cycling positions.

Conclusion

Since OLV are altered by exercise mode, but cycling position did not have a significant impact on OLV, we conclude that trunk/hip angle is likely not the primary factor determining OLV during maximal exercise.     

Central and peripheral hemodynamics during maximal leg extension exercise

Summary The purpose of this study was to examine the central and peripheral hemodynamic adaptations to maximal leg extension exercise. Seventeen men (¯X=25 years, 84 kg) performed leg extension exercise (Universal equipment) for 12 repetitions (90s) to fatigue. Each repetition consisted of a 3s lifting motion, 1s pause, and 3s lowering motion. Impedance cardiography was used to measure stroke volume (SV), cardiac output ( ), systolic time intervals, and impedance contractility indices on a beat-by-beat basis. There were significant increases in systolic, diastolic, mean arterial pressure, total peripheral resistance, and HR during exercise. The mean remained similar throughout the protocol. SV decreased even though indices of myocardial performance indicated an enhancement of contractility. The magnitude of and SV were dependent upon the phase of leg extension. SV and during the lifting portions of the exercise were smaller than the lowering portions. The differences in SV and during the concentric and eccentric phases of the exercise most likely reflect the large static forces in exercising muscle which impeded venous return and increased afterload.     

Rebreathing and single breath pulmonary CO diffusing capacity in man at rest and exercise studied by C18O isotope.

The pulmonary diffusing capacity for carbon monoxide, Dco, was estimated in normal subjects, using both a single breath technique (DcoSB) and a rebreathing technique (DcoRB). In order to measure CO by mass spectrometry, the stable isotope C(18)O was used. In three normal subjects Dco was measured at different lung volumes at rest, and at different levels of bicycle exercise. DcoRB was found on the average 30% higher than DcoSB when compared at the same mean lung volume, and both increased slightly during exercise. The advantages and drawbacks of the rebreathing method are critically discussed.     

CO and NO pulmonary diffusing capacity during pregnancy: Safety and diagnostic potential

This paper reviews the scientific evidence for the safety of carbon monoxide (CO) and nitric oxide (NO) inhalation to measure pulmonary diffusing capacity (DL_CO and DL_NO) in pregnant women and their fetuses. In eight earlier studies, 650 pregnant women had DL_CO measurements performed at various times during pregnancy, with a minimum of two to four tests per session. Both pregnant subjects that were healthy and those with medical complications were tested. No study reported adverse maternal, fetal, or neonatal outcomes from the CO inhalation in association with measuring DL_CO. Eleven pregnant women, chiefly with pulmonary hypertension, and 1105 pre-term neonates, mostly with respiratory failure, were administered various dosages of NO (5–80 ppm for 4 weeks continuously in pregnant women, and 1–20 ppm for 15 min to 3 weeks for the neonates). NO treatment was found to be an effective therapy for pregnant women with pulmonary hypertension. In neonates with respiratory failure and pulmonary hypertension, NO therapy improved oxygenation and survival and has been associated with only minor, transient adverse effects. In conclusion, maternal carboxyhemoglobin ([Hb_CO]) levels can safely increase to 5% per testing session when the dose-exposure limit is 0.3% CO inhalation for ≤3 min, and for NO, 80 ppm for ≤3 min. The risk of late fetal or neonatal death from increased Hb_CO from diffusion testing is considerably less than the risk of death from all causes reported by the Centers for Disease Control, and is therefore considered “minimal risk”.     

Limitations to oxygen transport and utilization during sprint exercise in humans: evidence for a functional reserve in muscle O2 diffusing capacity

Key points

• Severe acute hypoxia reduces sprint performance.
• Muscle V˙O2 during sprint exercise in normoxia is not limited by O₂ delivery, O₂ offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle of young healthy men.
• A large functional reserve in muscle O₂ diffusing capacity exists and remains available at exhaustion during exercise in normoxia; this functional reserve is recruited during exercise in hypoxia.
• During whole‐body incremental exercise to exhaustion in severe hypoxia, leg V˙O2 is primarily dependent on convective O₂ delivery and less limited by diffusion constraints than previously thought.
• The kinetics of O₂ offloading from haemoglobin does not limit V˙O2 peak in hypoxia.
• Our results indicate that the limitation to V˙O2 during short sprints resides in mechanisms regulating mitochondrial respiration.

Abstract

To determine the contribution of convective and diffusive limitations to V˙O2 peak during exercise in humans, oxygen transport and haemodynamics were measured in 11 men (22 ± 2 years) during incremental (IE) and 30 s all‐out cycling sprints (Wingate test, WgT), in normoxia (Nx, P_IO2: 143 mmHg) and hypoxia (Hyp, P_IO2: 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6–7% before both WgTs to left‐shift the oxyhaemoglobin dissociation curve. Leg V˙O2 was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O₂ diffusing capacity (D_MO2) was calculated. In the WgT mean power output, leg BF, leg O₂ delivery and leg V˙O2 were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05); however, peak WgT D_MO2 was higher in Hyp (51.5 ± 9.7) than Nx (20.5 ± 3.0 ml min⁻¹ mmHg⁻¹, P < 0.05). Despite a similar P_aO2 (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary P_O2 (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, D_MO2 and leg V˙O2 were 12 and 14% higher, respectively, during WgT than IE in Hyp (both P < 0.05). D_MO2 was insensitive to COHb (COHb: 0.7 vs. 7%, in IE Hyp and WgT Hyp). At exhaustion, the Y equilibration index was well above 1.0 in both conditions, reflecting greater convective than diffusive limitation to the O₂ transfer in both Nx and Hyp. In conclusion, muscle V˙O2 during sprint exercise is not limited by O₂ delivery, O₂ offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O₂ diffusing capacity.

Abbreviations

a‐vO₂diff

arteriovenous oxygen concentration difference

BF

blood flow

C_aO2

arterial content of oxygen

CO

carbon monoxide

COHb

carboxyhaemoglobin

D_LO2

lung O₂ diffusing capacity

D_MO2

muscle O₂ diffusing capacity

D_O2

O₂ diffusing capacity

ECG

electrocardiogram

F_IO2

inspired oxygen fraction

FV

femoral vein

HR_max

maximal heart rate

HR_peak

peak heart rate during Wingate

Hyp

hypoxia

LBF

leg blood flow

Nx

normoxia

S_O2

haemoglobin saturation with O₂

ODC

oxyhaemoglobin dissociation curve

P₅₀

partial oxygen pressure at 50% S_O2

P_aO2

arterial oxygen pressure

P_CO2

carbon dioxide pressure

P_O2

oxygen pressure

P_{O2 cap}

capillary O₂ pressure

P_{O2 mit}

mitochondrial O₂ pressure

P _{FV O2}

femoral vein P_O2

P_IO2

inspiratory O₂ pressure

V˙CO2

carbon dioxide production

V˙CO2 peak

peak carbon dioxide production

V˙ Epeak

peak pulmonary ventilation

V˙O2

oxygen consumption

V˙O2 max

maximal oxygen consumption

V˙O2 peak

peak oxygen uptake

W_peak‐i

instantaneous peak power output

W_mean‐10

mean power output during the first 10 s of the sprint exercise

W_mean‐30

mean power output during the whole sprint exercise

WgT

isokinetic 30 s Wingate test

     

The effect of O2 breathing on maximal aerobic power

Summary Time of performance, blood lactic acid concentration (L.A.), heart rate (H.R.) and maximal oxygen consumption ( ) were measured during air and oxygen breathin in 11 subjects performing a supramaximal exercise with an O₂ requirement of 70 to 80 ml/kg·min to exhaustion. In addition the subjects were tested for maximal aerobic power with an indirect method. In one subject the rate of lactic acid increase in blood was also measured.The measured with both the direct and the indirect method appears to be about 8% higher when breathing pure oxygen; lactic acid production rate decreases correspondingly. Maximal H.R. and maximal L.A. concentration were found to be the same.In submaximal exercise steady state H.R. is lower by about 8–9 beats/min when breathing oxygen. Also when breathing oxygen H.R. is a linear function of the work load.From experimental data obtained in subjects of different , breathing both air or O₂, the energy equivalent of L.A. could be calculated as amounting to about 47 ml of O₂ or 235 cal per g of L.A. produced.This work was supported by a grant from the National Research Council of Italy (C.N.R.)     

Total blood volume in endurance-trained postmenopausal females: relation to exercise mode and maximal aerobic capacity

We have recently shown that postmenopausal female distance runners demonstrate elevated levels of blood volume compared with sedentary healthy peers. We also found a strong positive relation between blood volume and maximal oxygen consumption. In young adult males, endurance exercise training increases blood volume when performed in the upright, but not in the supine body position. Based on these observations, we hypothesized that among postmenopausal females, the elevation in blood volume would be absent or attenuated in women who train in the horizontal vs. upright body position, and that the lower blood volume in the former would be associated with lower maximal aerobic capacity. Thus, we measured supine resting plasma and total blood volumes (Evans blue dye) and maximal oxygen consumption in postmenopausal women: 10 sedentary controls, 10 swimmers and 10 runners matched for age (60 ± 2; 59 ± 2; 58 ± 2 years, mean ± SE) and hormone replacement use (5 per group). The swimmers and runners were further matched for training volume (4.5 ± 0.2 vs. 4.8 ± 0.6 h week^–1), relative performance (78 ± 5 vs. 75 ± 3% of age-group world record) and fat-free mass (45.5 ± 0.8 vs. 44.9 ± 1.5 kg). Total blood volume and maximal oxygen consumption were highest in the runners (81.2 ± 4; 52.4 ± 3 mL kg^–1, respectively) and progressively lower in the swimmers (68.8 ± 3; 44.2 ± 2) and controls (59.2 ± 2; 37.9 ± 2; all P < 0.05). In the pooled population, blood volume was positively related to maximal oxygen consumption (r= 0.72, P < 0.0001). We conclude that in endurance-trained postmenopausal females matched for training volume and competitive performance: (1) blood volume is lower in those who train in the horizontal (swimmers) compared with the upright position (runners); (2) the lower blood volume is associated with a lower maximal aerobic capacity. Nevertheless, blood volume and maximal oxygen consumption are higher in postmenopausal women who train in the horizontal position than in sedentary controls.     

Active and passive recovery from maximal aerobic capacity work

Summary Thirteen subjects performed two identical maximal aerobic capacity tasks on the bicycle ergometer, at one time recovering while sitting absolutely quiet and once while continuing to pedal at the same RPM against minimal resistance. The heart rate, oxygen-debt pay-off, and carbon-dioxide expulsion curves during recovery were established. Comparison of the Active and Passive recovery data showed no difference above their respective levels of return (Zero load pedaling or resting), except for substantially slower pay-off of the lactic part of the oxygen debt.This work (project Hokulani) was supported in part by a grant from the University Research Fund.     

Increased steady-state VO2 and larger O2 deficit with CO2 inhalation during exercise

Aim: To examine whether inhalation of CO₂‐enriched gas would increase steady‐state during exercise and enlarge O₂ deficit. Methods: Ten physically active men ( 53.7 ± 3.6 mL min^?1 kg^?1; ± SD) performed transitions from low‐load cycling (baseline; 40 W) to work rates representing light (≈ 45%; 122 ± 15 W) and heavy (≈ 80%; 253 ± 29 W) exercise while inhaling normal air (air) or a CO₂ mixture (4.2% CO₂, 21% O₂, balance N₂). Gas exchange was measured with Douglas bag technique at baseline and at min 0–2, 2–3 and 5–6. Results: Inhalation of CO₂‐enriched air consistently induced respiratory acidosis with increases in PCO₂ and decreases in capillary blood pH (P < 0.01). Hypercapnic steady‐state was on average about 6% greater (P < 0.01) than with air in both light and heavy exercise, presumably because of increased cost of breathing (ΔVE 40–50 L min^?1; P < 0.01), and a substrate shift towards increased lipid oxidation (decline in R 0.12; P < 0.01). during the first 2 min of exercise were not significantly different whereas the increase in from min 2–3 to min 5–6 in heavy exercise was larger with CO₂ than with air suggesting a greater slow component. As a result, O₂ deficit was greater with hypercapnia in heavy exercise (2.24 ± 0.51 L vs. 1.91 ± 0.45 L; P < 0.05) but not in light (0.64 ± 0.21 L vs. 0.54 ± 0.20 L; ns). Conclusion: Inhalation of CO₂‐enriched air and the ensuing respiratory acidosis increase steady‐state in both light and heavy exercise and enlarges O₂ deficit in heavy exercise.     

P300, N400, aerobic fitness, and maximal aerobic exercise

Electrophysiological effects of aerobic fitness and maximal aerobic exercise were investigated by comparing P300 and N400 before and after a maximal cycling test. Event-related potentials (ERPs) were obtained from 20 students divided into two matched groups defined by their aerobic fitness level (cyclists vs. sedentary subjects). The session of postexercise ERPs was performed immediately after body temperature and heart rate returned to preexercise values. At rest, no significant differences were observed in ERP parameters between cyclists and sedentary subjects. This finding argued against the hypothesis that ERP modifications may be directly assumed by aerobic fitness level. The postexercise session of ERPs showed a significant P300 amplitude increase and a significant P300 latency decrease in all subjects. Similarly, N400 effect increased significantly after the maximal exercise in all subjects. ERP changes were of the same magnitude in the two groups. The present study argues for a general arousing effect of maximal aerobic exercise, independently of the aerobic fitness level.     

Effect of hyperoxia on aerobic and anaerobic performances and muscle metabolism during maximal cycling exercise

The hyperoxia-improved tolerance to maximal aerobic performance was studied in relation to exercising muscle metabolic state. Five students were submitted to four different tests on a cycle ergometer, each being conducted under normoxia and hyperoxia (60% FiO2) on separate days: Test 1, a progressive exercise until exhaustion to determine the maximal work load (Wmax) which was unchanged by hyperoxia; Test 2, an exercise at Wmax (287 +/- 12 W) until exhaustion to determine the performance time (texh) which was elevated by 38% under hyperoxia but exhaustion occurred at the same arterial proton and lactate concentrations; Test 3 (S-Exercise test) consisted of cycling at Wmax for 90% normoxic-texh (4.8 +/- 0.5 min under both O2 conditions) then followed by a 10-s sprint bout during which the total work output (Wtot) was determined; Wtot was elevated by 15% when exercising under hyperoxia; Test 4 (M-Exercise test) consisted also of cycling at Wmax for 4.8 +/- 0.5 min with blood and muscle samples taken at rest and at the end of the exercise to compare the level of different metabolites. During hyperoxic M-Exercise test, glycogen was twice more depleted whereas glucose-6-phosphate and lactate were less accumulated when compared with normoxia. No significant differences were observed for pyruvate, phosphocreatine and muscle/blood lactate ratio between the two conditions. Conversely to normoxia, levels of ATP, ADP and total NADH were maintained at their resting level under 60% FiO2. These data lead us to suppose a higher oxidation rate for pyruvate and NADH in mitochondria, thereby lowering the metabolic acidosis and allowing a better functioning of the glycolytic and contractile processes to delay the time to exhaustion.     

Total blood volume in endurance-trained postmenopausal females: relation to exercise mode and maximal aerobic capacity.

We have recently shown that postmenopausal female distance runners demonstrate elevated levels of blood volume compared with sedentary healthy peers. We also found a strong positive relation between blood volume and maximal oxygen consumption. In young adult males, endurance exercise training increases blood volume when performed in the upright, but not in the supine body position. Based on these observations, we hypothesized that among postmenopausal females, the elevation in blood volume would be absent or attenuated in women who train in the horizontal vs. upright body position, and that the lower blood volume in the former would be associated with lower maximal aerobic capacity. Thus, we measured supine resting plasma and total blood volumes (Evans blue dye) and maximal oxygen consumption in postmenopausal women: 10 sedentary controls, 10 swimmers and 10 runners matched for age (60 +/- 2; 59 +/- 2; 58 +/- 2 years, mean +/- SE) and hormone replacement use (5 per group). The swimmers and runners were further matched for training volume (4.5 +/- 0.2 vs. 4.8 +/- 0.6 h week-1), relative performance (78 +/- 5 vs. 75 +/- 3% of age-group world record) and fat-free mass (45.5 +/- 0. 8 vs. 44.9 +/- 1.5 kg). Total blood volume and maximal oxygen consumption were highest in the runners (81.2 +/- 4; 52.4 +/- 3 mL kg-1, respectively) and progressively lower in the swimmers (68.8 +/- 3; 44.2 +/- 2) and controls (59.2 +/- 2; 37.9 +/- 2; all P < 0. 05). In the pooled population, blood volume was positively related to maximal oxygen consumption (r = 0.72, P < 0.0001). We conclude that in endurance-trained postmenopausal females matched for training volume and competitive performance: (1) blood volume is lower in those who train in the horizontal (swimmers) compared with the upright position (runners); (2) the lower blood volume is associated with a lower maximal aerobic capacity. Nevertheless, blood volume and maximal oxygen consumption are higher in postmenopausal women who train in the horizontal position than in sedentary controls.     

Measurement of single-breath carbon monoxide transfer factor (diffusing capacity) during progressive exercise

The transfer factor (diffusing capacity) for carbon monoxide (TLCO) is known to rise with increasing levels of work, but uncertainty remains as to the exact relationship of TLCO and the transfer coefficient (KCO) to oxygen uptake (VO2). We have studied the effects of increasing levels of work on TLCO and KCO in 22 normal male subjects using the single-breath technique and a standardized protocol. Additionally, we have investigated whether young people were different from a middle-age group, the need for carboxyhaemoglobin corrections in current smokers and non-smokers, and the variations of cardiac frequency during breath-holding. Our results show that TLCO and KCO increase in a curvilinear manner up to maximal VO2, a quadratic equation describing the relationship. There was no effect of age up to 50 years. There was no significant increase in the carboxyhaemoglobin levels, and therefore this correction is unnecessary. Cardiac frequency showed no significant variation during the breath-holding manoeuvre, except at rest and at low levels of exercise.     

Physiological mechanisms dissociating pulmonary CO2 and O2 exchange dynamics during exercise in humans

During moderate exercise (below the lactate threshold, (thetaL)), muscle CO(2) production ( Q(CO2)) kinetics are monoexponential, with a time constant (tau) similar to that of O(2) consumption. Following a delay incorporating the muscle-lung vascular transit time, Q(CO2) is expressed at the lungs (V(CO2)) with an appreciably longer tau, reflecting the influence of intervening high-capacitance CO(2) stores. Above (thetaL), kinetics become complex, resulting from the conflation of the differing rates of HCO(3)(-) breakdown and degrees of compensatory hyperventilation with that of the underlying aerobic component. During incremental exercise, the increased rate of relative to pulmonary O(2) uptake (V(CO2)) can be used to quantify (thetaL) validly if aerobic and hyperventilatory sources can be ruled out, i.e. (thetaL) is then attributable to the decrease in muscle and blood [HCO(3)(-)]. In many cases, however, very rapid incrementation of work rate and/or prior depletion of CO(2) stores (by volitional or anticipatory hyperventilation) can yield a 'false positive' non-invasive estimation of (thetaL) ('pseudo-threshold') resulting from a slowing of the rate of wash-in of transient CO(2) stores.     

Relationship between isocapnic buffering and maximal aerobic capacity in athletes

This study was performed to clarify the relationship between isocapnic buffering and maximal aerobic capacity (V˙O_{2 max} ) in athletes. A group of 15 trained athletes aged 21.1 (SD 2.6) years was studied. Incremental treadmill exercise was performed using a modified version of Bruce's protocol for determination of the anaerobic threshold (AT) and the respiratory compensation point (RC). Ventilatory and gas exchange responses were measured with an aeromonitor and expressed per unit of body mass. Heart rate and ratings of perceived exertion were recorded continuously during exercise. The mean V˙O_{2 max} , oxygen uptake (V˙O₂) at AT and RC were 58.2 (SD 5.8)?ml?·?kg^?1?·?min^?1, 28.0 (SD 3.3)?ml?·?kg^?1?·?min^?1 and 52.4 (SD 6.7)?ml?· kg^?1?·?min^?1, respectively. The mean values of AT and RC, expressed as percentages of V˙O_{2 max} , were 48.3 (SD 4.2)% and 90.0 (SD 5.2)%, respectively. The mean range of isocapnic buffering defined as V˙O₂ between AT and RC was 24.4 (SD 4.5) ml?·?kg^?1?·?min^?1, and the mean range of hypocapnic hyperventilation (HHV) defined as V˙O₂ between RC and the end of exercise was 5.8 (SD 3.0)?ml?·?kg^?1?·?min^?1. The V˙O_{2 max} per unit mass was significantly correlated with AT (r?=?0.683, P?V˙O_{2 max} /mass was closely correlated with both the range of isocapnic buffering (r?=?0.803, P?r?=?0.878, P?V˙O_{2 max} per unit mass and the range of HHV (r?=?0.011, NS.). These findings would suggest that the prominence of isocapnic buffering, in addition to the anaerobic threshold, may have been related to V˙O_{2 max} of the athletes. The precise mechanisms underlying this proposed relationship remain to be elucidated.