Algorithms,modelling and $$ \dot{V}{\text{O}}_{ 2} $$ kinetics

This article summarises the pros and cons of different algorithms developed for estimating breath-by-breath (B-by-B) alveolar O₂ transfer (\( \dot{V}{\text{O}}_{{ 2 {\text{A}}}} \)) in humans. \( \dot{V}{\text{O}}_{{ 2 {\text{A}}}} \) is the difference between O₂ uptake at the mouth and changes in alveolar O₂ stores (?VO_2s), which for any given breath, are equal to the alveolar volume change at constant \( F_{{{\text{AO}}_{ 2} }} [ (F_{{{\text{A}}i{\text{O}}_{ 2} }} \Updelta {\text{V}}_{{{\text{A}}i}} ) ] \) plus the O₂ alveolar fraction change at constant volume \( [V_{{{\text{A}}i - 1}} (F_{{{\text{A}}i}} -F_{{{\text{A}}i - 1}} )_{{{\text{O}}_{ 2} }} ] \), where V _Ai?1 is the alveolar volume at the beginning of a breath. Therefore, \( \dot{V}{\text{O}}_{{ 2 {\text{A}}}} \) can be determined B-by-B provided that V _Ai?1 is: (a) set equal to the subject’s functional residual capacity (algorithm of Auchincloss, A) or to zero; (b) measured (optoelectronic plethysmography, OEP); (c) selected according to a procedure that minimises B-by-B variability (algorithm of Busso and Robbins, BR). Alternatively, the respiratory cycle can be redefined as the time between equal FO₂ in two subsequent breaths (algorithm of Grønlund, G), making any assumption of V _Ai?1 unnecessary. All the above methods allow an unbiased estimate of \( \dot{V}{\text{O}}_{ 2} \) at steady state, albeit with different precision. Yet the algorithms “per se” affect the parameters describing the B-by-B kinetics during exercise transitions. Among these approaches, BR and G, by increasing the signal-to-noise ratio of the measurements, reduce the number of exercise repetitions necessary to study \( \dot{V}{\text{O}}_{ 2} \) kinetics, compared to A approach. OEP and G (though technically challenging and conceptually still debated), thanks to their ability to track ?VO_2s changes during the early phase of exercise transitions, appear rather promising for investigating B-by-B gas exchange.     

Exercise performance and \dot{V}{\text{O}}_{ 2} kinetics during upright and recumbent high-intensity cycling exercise

This study investigated cycling performance and oxygen uptake ( [(V)\dot]\textO ₂ )( \dot{V}{\text{O}}_{ 2} ) kinetics between upright and two commonly used recumbent (R) postures, 65°R and 30°R. On three occasions, ten young active males performed three bouts of high-intensity constant-load (85% peak-workload achieved during a graded test) cycling in one of the three randomly assigned postures (upright, 65°R or 30°R). The first bout was performed to fatigue and second and third bouts were limited to 7 min. A subset of seven subjects performed a final constant-load test to failure in the supine posture. Exercise time to failure was not altered when the body inclination was lowered from the upright (13.1 ± 4.5 min) to 65°R (10.5 ± 2.7 min) and 30°R (11.5 ± 4.6 min) postures; but it was significantly shorter in the supine posture (5.8 ± 2.1 min) when compared with the three inclined postures. Resulting kinetic parameters from a tri-exponential analysis of breath-by-breath [(V)\dot]\textO ₂ \dot{V}{\text{O}}_{ 2} data during the first 7 min of exercise were also not different between the three inclined postures. However, inert gas rebreathing analysis of cardiac output revealed a greater cardiac output and stroke volume in both recumbent postures compared with the upright posture at 30 s into the exercise. These data suggest that increased cardiac function may counteract the reduction of hydrostatic pressure from upright ~25 mmHg; to 65°R ~22 mmHg; and 30°R ~18 mmHg such that perfusion of active muscle presumably remains largely unchanged, and also therefore, [(V)\dot]\textO ₂ \dot{V}{\text{O}}_{ 2} kinetics and performance during high-intensity cycling.     

\dot{V}_{{{\text{O}}_{2} { \max }}} is not altered by self-pacing during incremental exercise

We tested the hypothesis that incremental cycling to exhaustion that is paced using clamps of the rating of perceived exertion (RPE) elicits higher $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ values compared to a conventional ramp incremental protocol when test duration is matched. Seven males completed three incremental tests to exhaustion to measure $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ . The incremental protocols were of similar duration and included: a ramp test at 30 W min^?1 with constant cadence (RAMP1); a ramp test at 30 W min^?1 with cadence free to fluctuate according to subject preference (RAMP2); and a self-paced incremental test in which the power output was selected by the subject according to prescribed increments in RPE (SPT). The subjects also completed a $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ ‘verification’ test at a fixed high-intensity power output and a 3-min all-out test. No difference was found for $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ between the incremental protocols (RAMP1 = 4.33 ± 0.60 L min^?1; RAMP2 = 4.31 ± 0.62 L min^?1; SPT = 4.36 ± 0.59 L min^?1; P > 0.05) nor between the incremental protocols and the peak $ \dot{V}_{{{\text{O}}_{2} }} $ measured during the 3-min all-out test (4.33 ± 0.68 L min^?1) or the $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ measured in the verification test (4.32 ± 0.69 L min^?1). The integrated electromyogram, blood lactate concentration, heart rate and minute ventilation at exhaustion were not different (P > 0.05) between the incremental protocols. In conclusion, when test duration is matched, SPT does not elicit a higher $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ compared to conventional incremental protocols. The striking similarity of $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ measured across an array of exercise protocols indicates that there are physiological limits to the attainment of $ \dot{V}_{{{\text{O}}_{2} { \max }}} $ that cannot be exceeded by self-pacing.     

$$\dot{V}{\text{O}}_{ 2}$$ kinetics and metabolic contributions during full and upper body extreme swimming intensity

Purpose

Our purpose was to characterize the oxygen uptake (\(\dot{V}{\text{O}}_{ 2}\)) kinetics, assess the energy systems contributions and determine the energy cost when swimming front crawl at extreme intensity. Complementarily, we compared swimming full body with upper body only.

Methods

Seventeen swimmers performed a 100 m maximal front crawl in two conditions: once swimming with full body and other using only the upper propulsive segments. The \(\dot{V}{\text{O}}_{ 2}\) was continuously measured using a telemetric portable gas analyser (connected to a respiratory snorkel), and the capillary blood samples for lactate concentration analysis were collected.

Results

A sudden increase in \(\dot{V}{\text{O}}_{ 2}\) in the beginning of exercise, which continuously rose until the end of the bout (time: 63.82 ± 3.38 s; \(\dot{V}{\text{O}}_{{ 2 {\text{peak}}}}\): 56.07 ± 5.19 ml min^?1 kg^?1; \(\dot{V}{\text{O}}_{ 2}\) amplitude: 41.88 ± 4.74 ml min^?1 kg^?1; time constant: 12.73 ± 3.09 s), was observed. Aerobic, anaerobic lactic and alactic pathways were estimated and accounted for 43.4, 33.1 and 23.5 % of energy contribution and 1.16 ± 0.10 kJ m^?1 was the energy cost. Complementarily, the absence of lower limbs lead to a longer time to cover 100 m (71.96 ± 5.13 s), slower \(\dot{V}{\text{O}}_{ 2}\) kinetics, lower aerobic and anaerobic (lactic and alactic) energy production and lower energy cost.

Conclusion

Despite the short duration of the event, the aerobic energy contribution covers about 50 % of total metabolic energy liberation, highlighting that both aerobic and anaerobic energy processes should be developed to improve the 100 m swimming performance. Lower limbs action provided an important contribution in the energy availability in working muscles being advised its full use in this short duration and very high-intensity event.

     

Effects of training on\dot V{\text{O}}_{\text{2}} max and\dot V{\text{O}}_{\text{2}} during two running intensities in rats

Endurance training increased \(\dot V{\text{O}}_{\text{2}} \) max significantly from 71.6±1.3 to 81.5±1.7 ml·kg^?1·min^?1 in female rats. Oxygen consumption and respiratory exchange ratios were observed in rats for 1 h at rest, running at 14.3 m·min^?1 on a 1% grade (easy exercise), and running at 28.7 m·min^?1 on a 15% grade (hard exercise). In hard exercise untrained rats had a higher respiratory exchange ratio (0.97 vs 0.90) and exercised at a higher percent \(\dot V{\text{O}}_{\text{2}} \) max (92 vs 74%) than trained animals. Blood lactate was higher during hard exercise than during rest or easy exercise, and higher in untrained than in trained animals during exercise. Blood glucose was significantly higher in trained than in untrained animals during hard exercise, but otherwise there were no differences between treatments or groups. These results suggest enhanced lipid oxidation and carbohydrate sparing in trained rats during prolonged exercise as the result of training. The improvement in whole-body \(\dot V{\text{O}}_{\text{2}} \) max due to training (13.9%) was less than the increase in tissue respiratory capacity (50–100%) reported to accompany endurance training of rats. The improvement in \(\dot V{\text{O}}_{\text{2}} \) max of rats as the result of training was of the same magnitude as the training response usually seen in humans.     

Slow $$ \dot{V}{\text{O}}_{2} $$ kinetics during moderate-intensity exercise as markers of lower metabolic stability and lower exercise tolerance

An analysis of previously published data obtained by our group on patients characterized by markedly slower pulmonary [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics (heart transplant recipients, patients with mitochondrial myopathies, patients with McArdle disease) was carried out in order to suggest that slow [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics should not be considered the direct cause, but rather a marker, of impaired exercise tolerance. For a given ATP turnover rate, faster (or slower) [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics are associated with smaller (or greater) muscle [PCr] decreases. The latter, however, should not be taken per se responsible for the higher (or lower) exercise tolerance, but should be considered within the general concept of “metabolic stability”. Good muscle metabolic stability at a given ATP turnover rate (~power output) is associated with relatively smaller decreases, compared to rest, in [PCr] and in the Gibbs free energy of ATP hydrolysis, as well as with relatively smaller increases in [Pi], [ADP_free], [AMP_free], and [IMP_free], metabolites directly related to fatigue. Disturbances in muscle metabolic stability can affect muscle function in various ways, whereas good metabolic stability is associated with less fatigue and higher exercise tolerance. Smaller [PCr] decreases, however, are strictly associated with a faster [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics. Thus, faster [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics may simply be an “epiphenomenon” of a relatively higher metabolic stability, which would then represent the relevant variable in terms of fatigue and exercise tolerance.     

Influence of blood donation on the incidence of plateau at \dot{V}{\text{O}} 2max

Purpose

The purpose of this study was to examine the effects of reductions in blood volume and associated oxygen-carrying capacity on the incidence of plateau at $\dot{V}{\text{O}}$ _2max.

Methods

Fifteen well-trained athletes (age 23.3 ± 4.5; mass 77.4 ± 13.1 kg, height 180.1 ± 6.0 cm) completed three incremental cycle tests to volitional exhaustion, of which the first was defined as familiarisation, with the remaining two trials forming the experimental conditions of pre- (UBL) and post-(BLE) blood donation (~450 cm³). The work rate for the incremental tests commenced at 100 W for 60 s followed by a ramp of 0.42 W s^?1, with cadence being held constant at 80 rpm. Throughout all trials, $\dot{V}{\text{O}}$ ₂ was determined on a breath-by-breath basis using a pre-calibrated metabolic cart. The criteria for plateau determination was a ? $\dot{V}{\text{O}}$ ₂ ≤ 50 ml min^?1 over the final two consecutive 30 s sampling periods.

Results

Despite a significant (P = 0.0028) 9.4 % reduction in haemoglobin concentration and 10.8 % (P = 0.016) reduction in erythrocyte count between UBL and BLE, there was no change in plateau incidence. However, significant differences were observed for both $\dot{V}{\text{O}}$ _2max (P = 0.0059) 51.3 ± 7.6 (UBL) 48.4 ± 7.9 ml kg^?1 min^?1 (BLE) and gas exchange threshold arrival time 383.4 ± 85.2 s (UBL) 349.2 ± 71.4 s (BLE) (P = 0.0028).

Conclusion

These data suggest that plateau at $\dot{V}{\text{O}}$ _2max is unaffected by O₂ availability lending support to the notion of the plateau being dependent on the anaerobic capacity and the classically orientated concept of $\dot{V}{\text{O}}$ _2max.     

Cardiac output but not stroke volume is similar in a Wingate and \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} test in young men

Wingate test (WT) training programmes lasting 2?C3?weeks lead to improved peak oxygen consumption. If a single 30?s WT was capable of significantly increasing stroke volume and cardiac output, the increase in peak oxygen consumption could possibly be explained by improved oxygen delivery. Thus, we investigated whether a single WT increases stroke volume and cardiac output to similar levels than those obtained at peak exercise during a graded cycling exercise test (GXT) to exhaustion. Fifteen healthy young men (peak oxygen consumption 45.0?±?5.3?ml?kg^?1?min^?1) performed one WT and one GXT on separate days in randomised order. During the tests, we estimated cardiac output using inert gas rebreathing (nitrous oxide and sulphur hexafluoride) and subsequently calculated stroke volume. We found that cardiac output was similar (18.2?±?3.3 vs. 17.9?±?2.6?l?min^?1; P?=?0.744), stroke volume was higher (127?±?37 vs. 94?±?15?ml; P?<?0.001), and heart rate was lower (149?±?26 vs. 190?±?12 beats?min^?1; P?<?0.001) at the end (27?±?2?s) of a WT as compared to peak exercise during a GXT. Our results suggest that a single WT produces a haemodynamic response which is characterised by similar cardiac output, higher stroke volume and lower heart rate as compared to peak exercise during a GXT.     

Factors determining the time course of {\dot{V}}\hbox{O}_{2\max} decay during bedrest: implications for {\dot{V}}\hbox{O}_{2\max} limitation

The aim of this study was to characterize the time course of maximal oxygen consumption VO2(max) changes during bedrests longer than 30 days, on the hypothesis that the decrease in VO2(max) tends to asymptote. On a total of 26 subjects who participated in one of three bedrest campaigns without countermeasures, lasting 14, 42 and 90 days, respectively, VO2(max) maximal cardiac output (Qmax) and maximal systemic O2 delivery (QaO2max) were measured. After all periods of HDT, VO2max, Qmax, and QaO2max were significantly lower than before. The VO2max decreased less than qmax after the two shortest bedrests, but its per cent decay was about 10% larger than that of Qmax after 90-day bedrest. The VO2max decrease after 90-day bedrest was larger than after 42- and 14-day bedrests, where it was similar. The Qmax and QaO2max declines after 90-day bedrest was equal to those after 14- and 42-day bedrest. The average daily rates of the VO2max, Qmax, and QaO2max decay during bedrest were less if the bedrest duration were longer, with the exception of that of VO2max in the longest bedrest. The asymptotic VO2max decay demonstrates the possibility that humans could keep working effectively even after an extremely long time in microgravity. Two components in the VO2max decrease were identified, which we postulate were related to cardiovascular deconditioning and to impairment of peripheral gas exchanges due to a possible muscle function deterioration.     

Skeletal muscle \dot{V} {\text{O}_2} kinetics from cardio-pulmonary measurements: assessing distortions through O2 transport by means of stochastic work-rate signals and circulatory modelling

During non-steady-state exercise, dynamic changes in pulmonary oxygen uptake ( $\dot{V} {\text{O}_{\text{2pulm}}}$ ) are dissociated from skeletal muscle $ \dot{V} {\text{O}_2}$ ( $\dot{V} {\text{O}_{\text{2musc}}}$ ) by changes in lung and venous O₂ concentrations (CvO₂), and the dynamics and distribution of cardiac output (CO) between active muscle and remaining tissues ( $ \dot{Q}_{\text{rem}}$ ). Algorithms can compensate for fluctuations in lung O₂ stores, but the influences of CO and CvO₂ kinetics complicate estimation of $\dot{V} {\text{O}_{\text{2musc}}}$ from cardio-pulmonary measurements. We developed an algorithm to estimate $\dot{V} {\text{O}_{\text{2musc}}}$ kinetics from $\dot{V} {\text{O}_{\text{2pulm}}}$ and heart rate (HR) during exercise. 17 healthy volunteers (28 ± 7 years; 71 ± 12 kg; 7 females) performed incremental exercise using recumbent cycle ergometry ( $\dot{V} {\text{O}_{\text{2peak}}}$ 52 ± 8 ml min^?1 kg^?1). Participants completed a pseudo-random binary sequence (PRBS) test between 30 and 80 W. $\dot{V} {\text{O}_{\text{2pulm}}}$ and HR were measured, and CO was estimated from HR changes and steady-state stroke volume. $\dot{V} {\text{O}_{\text{2musc}}}$ was derived from a circulatory model and time series analyses, by solving for the unique combination of venous volume and the perfusion of non-exercising tissues that provided close to mono-exponential $\dot{V} {\text{O}_{\text{2musc}}}$ kinetics. Independent simulations showed that this approach recovered the $\dot{V} {\text{O}_{\text{2musc}}}$ time constant (τ) to within 7 % (R ² = 0.976). Estimates during PRBS were venous volume 2.96 ± 0.54 L; $ \dot{Q}_{\text{rem}}$ 3.63 ± 1.61 L min^?1; τHR 27 ± 11 s; τ $\dot{V} {\text{O}_{\text{2musc}}}$ 33 ± 8 s; τ $\dot{V} {\text{O}_{\text{2pulm}}}$ 43 ± 14 s; $\dot{V} {\text{O}_{\text{2pulm}}}$ time delay 19 ± 8 s. The combination of stochastic test signals, time series analyses, and a circulatory model permitted non-invasive estimates of $\dot{V} {\text{O}_{\text{2musc}}}$ kinetics. Large kinetic dissociations exist between muscular and pulmonary $\dot{V} {\text{O}_{\text{2}}}$ during rapid exercise transients.     

Effect of high-intensity interval training and detraining on extra {\dot{{V}}\hbox{O}_{2}} and on the {\dot{{V}}\hbox{O}_{2}} slow component

To examine the effect of 6-week of high-intensity interval training (HIT) and of 6-week of detraining on the VO2/Work Rate (WR) relationship and on the slow component of VO2, nine young male adults performed on cycle ergometer, before, after training and after detraining, an incremental exercise (IE), and a 6-min constant work rate exercise (CWRE) above the first ventilatory threshold (VT1). For each IE, the slope and the intercept of the VO2/WR relationship were calculated with linear regression using data before VT1. The difference between VO2max measured and VO2max expected using the pre-VT1 slope was calculated (extra VO2). The difference between VO2 at 6th min and VO2 at 3rd min during CWRE (DeltaVO2(6'-3')) was also determined. HIT induced significant improvement of most of the aerobic fitness parameters while most of these parameters returned to their pre-training level after detraining. Extra VO2 during IE was reduced after training (130 +/- 100 vs. -29 +/- 175 ml min(-1), P = 0.04) and was not altered after detraining compared to post-training. DeltaVO2(6'-3') during CWRE was unchanged by training and by detraining. We found a significant correlation (r2 = 0.575, P = 0.02) between extra VO2 and DeltaVO2(6'-3') before training. These results show that an alteration of extra VO2 can occur without any change in the VO2 slow component, suggesting a possible dissociation of the two phenomena. Moreover, the fact that extra VO2 did not change after detraining could indicate that this improvement may remain after the loss of other adaptations.     

Reliability of peak \dot V{\text{O}}_2 and maximal cardiac output assessed using thoracic bioimpedance in children

The purpose of this study was to evaluate the reliability of a thoracic electrical bioimpedance based device (PhysioFlow) for the determination of cardiac output and stroke volume during exercise at peak oxygen uptake (peak in children. The reliability of peak is also reported. Eleven boys and nine girls aged 10–11 years completed a cycle ergometer test to voluntary exhaustion on three occasions each 1 week apart. Peak was determined and cardiac output and stroke volume at peak were measured using a thoracic bioelectrical impedance device (PhysioFlow). The reliability of peak cardiac output and stroke volume were determined initially from pairwise comparisons and subsequently across all three trials analysed together through calculation of typical error and intraclass correlation. The pairwise comparisons revealed no consistent bias across tests for all three measures and there was no evidence of non-uniform errors (heteroscedasticity). When three trials were analysed together typical error expressed as a coefficient of variation was 4.1% for peak 9.3% for cardiac output and 9.3% for stroke volume. Results analysed by sex revealed no consistent differences. The PhysioFlow method allows non-invasive, beat-to-beat determination of cardiac output and stroke volume which is feasible for measurements during maximal exercise in children. The reliability of the PhysioFlow falls between that demonstrated for Doppler echocardiography (5%) and CO₂ rebreathing (12%) at maximal exercise but combines the significant advantages of portability, lower expense and requires less technical expertise to obtain reliable results.     

Times to exhaustion at 100% of velocity at\dot V{\text{O}}_{\text{2}} max and modelling of the time-limit / velocity relationship in elite long-distance runners

The aim of this study was to measure running times to exhaustion (Tlim) on a treadmill at 100% of the minimum velocity which elicits _{max max} in 38 elite male long - distance runners _max = 71.4 ± 5.5 ml.kg^–1.min^–1 and _max = 21.8 ± 1.2 km.h^–1). The lactate threshold (LT) was defined as a starting point of accelerated lactate accumulation around 4 mM and was expressed in _max. Tlim value was negatively correlated with _max (r = -0.362, p< 0.05) and _max (r = –0.347, p< 0.05) but positively with LT (%v _max) (r = 0.378, p < 0.05). These data demonstrate that running time to exhaustion at _max in a homogeneous group of elite male long-distance runners was inversely related to _max and experimentally illustrates the model of Monod and Scherrer regarding the time limit-velocity relationship adapted from local exercise for running by Hughson et al. (1984) .     

Predicting {\dot{V}}{\text{O}}_{2{\text{max}}} with an objectively measured physical activity in Japanese men

The present study investigated the use of the accelerometer-determined physical activity (PA) variables as the objective PA variables for estimating [(V)\dot]\textO _{2 \textmax} \dot{V}{\text{O}}_{{ 2 {\text{max}}}} in Japanese adult men. One hundred and twenty-seven Japanese adult men aged from 20 to 69 years were recruited as subjects of the present study. Maximal oxygen uptake ( [(V)\dot]\textO _{2 \textmax} \dot{V}{\text{O}}_{{ 2 {\text{max}}}} ) was measured with a maximal incremental test on a bicycle ergometer. Daily step counts (SC) and the amount spent in moderate to vigorous PA (MVPA) and vigorous PA (VPA) were measured using accelerometer-based activity monitors worn at the waist for seven consecutive days. The non-exercise models were derived using hierarchical linear regression analysis, and cross-validated using two separate cross-validation procedures. SC, MVPA, and VPA were significantly related to [(V)\dot]\textO _{2 \textmax} \dot{V}{\text{O}}_{{ 2 {\text{max}}}} (partial correlation coefficient r = 0.58, r = 0.42, and r = 0.51, respectively) after adjusting for age. Two models were developed by multiple regression to estimate [(V)\dot]\textO _{2 \textmax} \dot{V}{\text{O}}_{{ 2 {\text{max}}}} using data of age, SC, VPA, and either BMI (the coefficient of determination (R ²) = 0.71, standard error of estimate (SEE) = 4.2 ml kg⁻¹ min⁻¹), or waist circumference (R ² = 0.74, SEE = 3.9 ml kg⁻¹ min⁻¹). All regression models demonstrated a high level of cross-validity supported by the minor shrinkage of R ² and increment of SEE in the PRESS procedure, and by small constant errors for subgroups of age, SC, and [(V)\dot]\textO _{2 \textmax} . \dot{V}{\text{O}}_{{ 2 {\text{max}}}} . This study demonstrated that combining SC with VPA, but not with MVPA, was useful in predicting [(V)\dot]\textO _{2 \textmax} \dot{V}{\text{O}}_{{ 2 {\text{max}}}} variance and improved the ability of the regression models to accurately predict [(V)\dot]\textO _{2 \textmax} \dot{V}{\text{O}}_{{ 2 {\text{max}}}} .     

Effect of an increase in{\text{Hb}}_{{\text{O}}_{\text{2}} } affinity on the calculated capillary recruitment of an isolated rat heart

The effect of an increase in hemoglobin O₂ affinity on myocardial O₂ delivery was studied in a blood perfused working rat heart preparation. In a first series of experiments P₅₀ ( for which saturation is 50%) was lowered by use of carbon monoxide. The heart was alternatively perfused with the blood sample of P₅₀=32 mm Hg and the blood sample of P₅₀=17 mm Hg. O₂ capacity of both samples was kept the same by appropriate hemodilution. In a second serie of experiments change of P₅₀ was obtained by the use of adult human erythrocytes containing hemoglobin creteil with a P₅₀ of 13.6 mm Hg. As P₅₀ decreased from 25 to 10 mm Hg, coronary sinus ( ) diminished from 26±2 to 18±2 mm Hg (–29±2%), coronary sinus O₂ content ( ) increased by 15±3%, myocardial oxygen consumption did not change significantly. The percentage of increase of coronary flow was 23±4%.Analysis of these results with a simple mathematical model of O₂ delivery suggest that increase in affinity is corrected by a simultaneous increase in coronary flow and capillary recruitment.This study was supported by contracts 74-7-0274 from D.G.R.S.T., 76-1-1755 from I.N.S.E.R.M. and a grant from the University of Paris VII