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.     

Relationship of pulmonary diffusing capacity (D L ) and cardiac output (\dot Q_c ) in exercise

The present study was designed to investigate the interrelationships of pulmonary diffusing capacity for CO ( \(D_{L_{{\text{CO}}} } \) ), pulmonary capillary blood flow ( \(\dot Q_c \) ), oxygen uptake ( \(\dot V_{{\text{O}}_{\text{2}} } \) ), and related functions in exercise. Six young adult men were tested on a bicycle ergometer on 9–20 occasions at various intensities of exercise up to the maximal level that could be sustained for 5 min. Measurements at each exercise level included work load (kgm/min), heart rate (HR), minute ventilation (V _I ), \(\dot Q_c \) , \(D_{L_{{\text{CO}}} } \) , and \(\dot V_{{\text{O}}_{\text{2}} } \) . Using regression analysis, it was established that \(\dot Q_c \) and D _{L CO} increased linearly with \(\dot V_{{\text{O}}_{\text{2}} } \) throughout the work range in each subject and no tendency toward a plateau was observed. While the maximal value varied from subject to subject, there was no difference between individuals in the coefffcient describing the relationship of D _L and \(\dot Q_c \) to \(\dot V_{{\text{O}}_{\text{2}} } \) . Combining all subjects, D _L was found to increase linearly with \(\dot Q_c \) the regression equation being: $$D_L = 26.4 + 1.03{\text{ }}\dot Q_c ,{\text{ }}r = .79$$ These results suggest that high-intensity short-duration exercise (5 min) is probably not limited by either of these functions in normals.     

Energy cost of arm stroke,leg kick,and the whole stroke in competitive swimming styles

In male elite swimmers \(\dot V_{{\text{O}}_{\text{2}} } \) at a given velocity in freestyle and backstroke was on average 1 to 2 l x min^?1 lower as compared with breaststroke and butterfly. Except for breaststroke, swimming with arm strokes only demanded a lower \(\dot V_{{\text{O}}_{\text{2}} } \) at a given submaximal velocity than the whole stroke. In freestyle and backstroke the submaximal \(\dot V_{{\text{O}}_{\text{2}} } \) of leg kick at a given velocity was clearly higher than the whole stroke. The highest velocity during maximal swimming was always attained with the whole stroke, and the lowest with the leg kick, except for breast stroke, where the leg kick was most powerful. At a given submaximal \(\dot V_{{\text{O}}_{\text{2}} } \) , heart rate and \(\dot V_{\text{E}} :\dot V_{{\text{O}}_{\text{2}} } \) tended to be higher during swimming with arm strokes only as compared with the whole stroke. Highest values for \(\dot V_{{\text{O}}_{\text{2}} } \) , heart rate and blood lactate during maximal exercise were almost always attained when swimming the whole stroke, and lowest when swimming with arm strokes only. At higher velocities body drag was 0.5 to 0.9 kp lower when arms or legs were supported by a cork plate as compared with body drag without support.     

Indirect determination of maximal aerobic power output during work with one or two limbs

The cardiac frequency (f _H ) and oxygen intake ( \(\dot V_{O_2 } \) ) responses to submaximal and maximal work with 1- and 2-arms and 1- and 2-legs on suitably modified bicycle ergometers in relation to the prediction of maximal aerobic power output ( \(\dot V_{{\text{O}}_{{\text{2max}}} }\) ) have been examined in 12 healthy male subjects. The results showed that the physiological responses to the different forms of submaximal and maximal exercise were distinct and dependent upon the effective muscle mass used to perform the work. The observed \(\dot V_{{\text{O}}_{{\text{2max}}} }\) of 1-limb could be converted to respective 2-limb value with a coefficient of variation ranging from 4 to 7%, but maximal work with the arms gave no guide to that of the legs. Extrapolation of the \(\dot V_{O_2 } \) /f _H curve to the f _{H max} in 1-leg (175 beats/min) and 2-arm (165 beats/min) resulted in an overestimation of \(\dot V_{{\text{O}}_{{\text{2max}}} }\) of +70 ± 200 ml · min^?1 and +70 ± 240 ml · min^?1; but in 1-arm work (153 beats/min), \(\dot V_{{\text{O}}_{{\text{2max}}} }\) was underestimated by ?70 ± 270 ml · min^?1. The bias in predictions for the 3 forms of exercise could be removed by applying the appropriate regression equations relating predicted to observed \(\dot V_{{\text{O}}_{{\text{2max}}} }\) , but the overall accuracy of the extrapolation method was limited to ± 8%, ± 15% and ± 23% in 1-leg, 2-arm and 1-arm work respectively. It was concluded that maximal work with the upper and lower limbs should be treated separately and if an accuracy of greater than ± 8 to ± 23% is required in situations where through injury, two limb exercise cannot be performed, attempts should be made to ascertain the \(\dot V_{{\text{O}}_{{\text{2max}}} }\) of a single limb directly.     

Plasma catecholamine concentration during dynamic exercise involving different muscle groups

The change in plasma catecholamine concentration (ΔC) has been studied in four healthy male subjects during work, involving different muscle groups, whilst breathing air and 45% oxygen. The results show that during arm and (1- and 2-) leg(s) work ΔC was more closely associated with relative (expressed as a % of \(\dot V_{{\text{O}}_{{\text{2max}}} }\) ) than absolute work load; a rise in C occurred at ～ 60% \(\dot V_{{\text{O}}_{{\text{2max}}} }\) in all 3 forms of exercise. However, in arm and 1-leg work the curves relating ΔC to % \(\dot V_{{\text{O}}_{{\text{2max}}} }\) were displaced to the right indicating the independence of the two variables. Further, breathing 45% oxygen reduced ΔC but was without effect on either \(\dot V_{O_2 } \) at a given work load or \(\dot V_{{\text{O}}_{{\text{2max}}} }\) . For a given \(\dot V_{O_2 } \) , ΔC was inversely related to the effective muscle (plus bone) volume used to perform the work and associated with change of blood lactic acid (LA) concentration, but again the use of exercise involving different muscle groups indicated that the changes in C and LA were essentially independent. This was also true of the changes of C with cardiac output but not cardiac frequency (f _H ). Plasma C changed as a curvilinear function of f _H , the association between the two variables being independent of type of exercise and inspired O₂ concentration within the range used in this study. This suggests that the rise in C and f _H in exercise may be closely related to circulatory stress and may reflect the degree of vasoconstriction present in ‘non-active’ tissues and efficacy of the body's ability to maintain the integrity of systemic blood pressure in the face of increased demands of the exercising muscles for blood and the transport of oxygen.     

The steady state response of brainstem respiratory neuron activity to various levels ofP_{A{\text{, CO}}_2 } andP_{A{\text{, O}}_2 }

Extracellular recordings were made of 52 respiratory neurons in the brainstem of cats, anesthetized (chloralose-urethane), vagotomized and artificially ventilated. Phrenic nerve activity was recorded and quantified as an index of the output of the respiratory neuronal organization in the brainstem. The unit activity was quantified by using the modal spike frequency as a possible indication of the activating effect of one unit on other respiratory neurons (Smolders and Folgering, 1979). Inspiratory neurons showed the strongest reaction to changes in \(P_{A{\text{, CO}}_2 }\) and/or \(P_{A{\text{, O}}_2 }\) . Expiratory neurons and frequency modulated neurons responded less to changes in chemical drive. Phase spanning neurons did not show any consistent response. Four out of ten continuously firing neurons without any respiratory rhytmicity increased their firing frequency when \(P_{A{\text{, CO}}_2 }\) was increased. Apart from the increase in modal spike frequency, the respiratory neuronal organization also reacted with an increase in active units (recruitment) when the chemical drive was increased. The relationship between quantified phrenic nerve activity and spike frequency was independent of the stimulus (hypercapnia or hypoxia). A model was developed in which the increase in modal frequency of a unit arouses other units: when the chemical drive increases, progressively more units tend to be recruited into the respiratory neuronal organization in the brainstem.     

Experimental study of the performance of competition swimmers

The purpose of this study was to consider which characteristics are related to a high velocity in water during swimming. The study was performed on 13 of the best competition swimmers of the region of Lyon (France). The collected data were: \(\dot V_{O_2 } \) max, measured during leg-work ( \(\dot V_{O_2 } \) max LW), during arm-work ( \(\dot V_{O_2 } \) max AW), and the hydrodynamic resistances measured when the swimmers were towed at the speed of 1.80 m/sec. The cardiac output was measured for four of the subjects. The swimmers were characterized by a mean \(\dot V_{O_2 } \) max LW of 56 ml/kg/min and by a high value of the ratio \(\frac{{\dot V_{O_2 } \max {\text{ }}AW}}{{\dot V_{O_2 } \max {\text{ }}LW}}\) which reached 99% for three of them. There was a very high correlation (r = 0.90 and 0.91) between the mean speed calculated from the best performances in competition swims of 400 m and 1500 m and a value which is thought to express the aerobic energy available to the swimmer: $$\dot V_{O_2 } \max water:\dot V_{O_2 } \max {\text{ }}AW + \frac{{\dot V_{O_2 } \max {\text{ }}LW - \dot V_{O_2 } \max {\text{ }}AW}}{6}$$      

Prediction of peak oxygen uptake from differentiated ratings of perceived exertion during wheelchair propulsion in trained wheelchair sportspersons

Purpose

To assess the validity of predicting peak oxygen uptake ( $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ ) from differentiated ratings of perceived exertion (RPE) obtained during submaximal wheelchair propulsion.

Methods

Three subgroups of elite male wheelchair athletes [nine tetraplegics (TETRA), nine paraplegics (PARA), eight athletes without spinal cord injury (NON-SCI)] performed an incremental speed exercise test followed by graded exercise to exhaustion ( $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ test). Oxygen uptake ( $ {\dot{\text{V}}}{\text{O}}_2$ ), heart rate (HR) and differentiated RPE (Central RPE_C, Peripheral RPE_P and Overall RPE_O) were obtained for each stage. The regression lines for the perceptual ranges 9–15 on the Borg 6–20 scale ratings were performed to predict $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ .

Results

There were no significant within-group mean differences between measured $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ (mean 1.50 ± 0.39, 2.74 ± 0.48, 3.75 ± 0.33 L min^?1 for TETRA, PARA and NON-SCI, respectively) and predicted $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ determined using HR or differentiated RPEs for any group (P > 0.05). However, the coefficients of variation (CV %) between measured and predicted $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ using HR showed high variability for all groups (14.3, 15.9 and 9.7 %, respectively). The typical error ranged from 0.14 to 0.68 L min^?1 and the CV % between measured and predicted $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ using differentiated RPE was ≤11.1 % for TETRA, ≤7.5 % for PARA and ≤20.2 % for NON-SCI.

Conclusions

Results suggest that differentiated RPE may be used cautiously for TETRA and PARA athletes when predicting $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ across the perceptual range of 9–15. However, predicting $ {\dot{\text{V}}}{\text{O}}_{{\text{2peak}}}$ is not recommended for the NON-SCI athletes due to the large CV %s (16.8, 20.2 and 18.0 %; RPE_C, RPE_P and RPE_O, respectively).     

Détermination expérimentale du coefficient moyen d'échange de chaleur par évaporation en air calme

The authors have determined the coefficient of evaporative heat loss of the human body (h _e) by means of humidity steps in low air movement (V _a≤0,2 m/s). Such a determination requires a fully wetted skin and this implies therefore some loss of dripping sweat. The collection of this dripping sweat allows the determination of the total evaporation: this evaporation exists on the skin surface and around the drops during their fall from the skin to the oil pan where dripping sweat is collected. An estimation of this dripping sweat evaporation allows to assess the skin evaporation and, consequently, the evaporative coefficienth _e. In these experimental conditions: ( \(E = S - SNE - 0,005{\text{ }}SNE{\text{ }}(P_{S_{H_2 O} } - P_{a_{H_2 O} } )\) ) whereE is the skin evaporative rate (g/h);S = total sweat rate (g/h);SNE = the nonevaporative sweat rate (g/h); \(P_{S_{H_2 O} } \) = the partial pressure of satured water (at \(\bar T_S \) ) on skin (mb) and \(P_{a_{H_2 O} } \) the partial pressure of water vapor in ambient air (mb). The coefficient of evaporative heat loss in low air movement thus found, is 5,18±0,22 W/m² · mb.     

The effects of breathing a helium–oxygen gas mixture on maximal pulmonary ventilation and maximal oxygen consumption during exercise in acute moderate hypobaric hypoxia

To test the hypothesis that maximal exercise pulmonary ventilation ( $ \dot{V}{\text{E}}_{ \max } $ ) is a limiting factor affecting maximal oxygen uptake ( $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ ) in moderate hypobaric hypoxia (H), we examined the effect of breathing a helium–oxygen gas mixture (He–O₂; 20.9% O₂), which would reduce air density and would be expected to increase $ \dot{V}{\text{E}}_{ \max } $ . Fourteen healthy young male subjects performed incremental treadmill running tests to exhaustion in normobaric normoxia (N; sea level) and in H (atmospheric pressure equivalent to 2,500 m above sea level). These exercise tests were carried out under three conditions [H with He–O₂, H with normal air and N] in random order. $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ and arterial oxy-hemoglobin saturation (SaO₂) were, respectively, 15.2, 7.5 and 4.0% higher (all p < 0.05) with He–O₂ than with normal air ( $ \dot{V}{\text{E}}_{ \max } $ _, 171.9 ± 16.1 vs. 150.1 ± 16.9 L/min; $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ , 52.50 ± 9.13 vs. 48.72 ± 5.35 mL/kg/min; arterial oxyhemoglobin saturation (SaO₂), 79 ± 3 vs. 76 ± 3%). There was a linear relationship between the increment in $ \dot{V}{\text{E}}_{ \max } $ and the increment in $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ in H (r = 0.77; p < 0.05). When subjects were divided into two groups based on their $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ , both groups showed increased $ \dot{V}{\text{E}}_{ \max } $ and SaO₂ in H with He–O₂, but $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ was increased only in the high $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ group. These findings suggest that in acute moderate hypobaric hypoxia, air-flow resistance can be a limiting factor affecting $ \dot{V}{\text{E}}_{ \max } $ ; consequently, $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ is limited in part by $ \dot{V}{\text{E}}_{ \max } $ , especially in subjects with high $ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $ .     

Maximum oxygen consumption and catecholamines in thyroidectomized dogs

Comparisons have been made in 7 dogs between maximum oxygen consumption recorded before (N dogs) and after thyroidectomy (T dogs). The comparisons were performed under two conditions 1) during severe cold stress (C \(V_{O_2 }\) max), 2) during a short period of exhaustive work (Ex \(\dot V_{O_2 }\) max). Heart rate, plasma catecholamine and substrate concentrations (glucose, lactic acid, FFA) were measured under each condition.

1. Thyroidectomy induced a more substantial decrease in C \(\dot V_{O_2 }\) max than in Ex \(\dot V_{O_2 }\) max.
2. At C \(\dot V_{O_2 }\) max, average plasma epinephrine and norepinephrine concentrations rose to a higher level in T dogs than in N dogs. In T dogs, correlations were found between plasma epinephrine concentrations and C \(\dot V_{O_2 }\) max values, and between plasma norepinephrine concentrations and C \(\dot V_{O_2 }\) max values. At Ex \(V_{O_2 }\) max, average plasma norepinephrine concentrations were similar in N dogs and in T dogs, and average plasma epinephrine concentrations were not significantly different from each other.
3. At Ex \(\dot V_{O_2 }\) max, average plasma concentrations of the various substrates were not significantly different in N dogs and T dogs. At C \(\dot V_{O_2 }\) max, plasma FFA levels were higher in T dogs.

It may be concluded that in dogs, thyroidectomy affects mechanisms which are more specifically involved in heat production than in muscular exercise. The increased catecholamine secretion in response to cold which occured in T dogs appeared merely to limit the decrease in heat production. It seems possible that increased catecholamine secretion compensates for the decreased sensitivity of β receptors to catecholamine but it cannot fully account for the effects of thyroidectomy.     

Interaction of central and peripheral respiratory drives in cats II. Peripheral and central interaction of hypoxia and hypercapnia

In cats anesthetized with chloralose-urethane the blood supply to the right carotid body was performed by an extracorporal circuit containing a supporting pump and a membrane oxygenator. Inlet and outlet of the circuit were connected to the central and the peripheral end, resp., of the dissected right common carotid artery. By exposure of the circuit blood to different gas mixtures in the membrane oxygenator, \(P_{O_2 } \) and \(P_{CO_2 } \) (referred to as \(P_{gl,O_2 } \) and \(P_{gl,CO_2 } \) ) could be adjusted independently from the gas tensions in the systemic blood. The animals breathed oxygen containing different concentrations of CO₂ in order to obtain selected levels of \(P_{a,CO_2 } \) . The left carotid nerve was dissected. The steady state respiratory responses to isolated and combined hypoxic and hypercapnic stimuli were evaluated.

1. The ventilatory response to severe peripheral hypoxia ( \(P_{gl,CO_2 } \) 33 mmHg) decreased significantly, when \(P_{gl,CO_2 } \) was raised from 30–35 mmHg to 55–60mmHg.
2. This decrease was slightly but not significantly enhanced when \(P_{gl,CO_2 } \) was raised from 21–42mmHg.
3. At constant \(P_{a,CO_2 } \) (28–36mmHg in different animals), the ventilatory response to peripheral hypoxia ( \(P_{gl,CO_2 } \) 63, 47, or 33 mmHg) in general slightly decreased when \(P_{gl,CO_2 } \) was stepwise increased (21–56mmHg).

Under the experimental conditions described above a hypo-additive interaction of respiratory drives could be demonstrated at the level of integration of peripheral and central afferents. At the level of the peripheral chemoreceptors alone a hyper-additive interaction of hypoxic and hypercapnic stimuli could not be confirmed.     

Central leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weight

Previous studies showed that leptin-deficient (ob/ob) mice develop obesity and impaired ventilatory responses to CO₂ $ \left( {{{\dot{V}}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}}} \right) $ . In this study, we examined if leptin replacement improves chemorespiratory responses to hypercapnia (7?% CO₂) in ob/ob mice and if these effects were due to changes in body weight or to the direct effects of leptin in the central nervous system (CNS). $ {\dot{V}_{{{\text{E}}\,}}}{\text{ - C}}{{\text{O}}_{{2}}} $ was measured via plethysmography in obese leptin-deficient- (ob/ob) and wild-type- (WT) mice before and after leptin (10???g/2???l?day) or vehicle (phosphate buffer solution) were microinjected into the fourth ventricle for four consecutive days. Although baseline $ {\dot{V}_{\text{E}}} $ was similar between groups, obese ob/ob mice exhibited attenuated $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ compared to WT mice (134?±?9 versus 196?±?10?ml?min^?1). Fourth ventricle leptin treatment in obese ob/ob mice significantly improved $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ (from 131 ± 15 to 197 ± 10?ml?min^?1) by increasing tidal volume (from 0.38?±?0.03 to 0.55?±?0.02?ml, vehicle and leptin, respectively). Subcutaneous leptin administration at the same dose administered centrally did not change $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ in ob/ob mice. Central leptin treatment in WT had no effect on $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ . Since the fourth ventricle leptin treatment decreased body weight in ob/ob mice, we also examined $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ in lean pair-weighted ob/ob mice and found it to be impaired compared to WT mice. Thus, leptin deficiency, rather than obesity, is the main cause of impaired $ {\dot{V}_{{{\text{E}}\,}}}{ - }\,{\text{C}}{{\text{O}}_{{2}}} $ in ob/ob mice and leptin appears to play an important role in regulating chemorespiratory response by its direct actions on the CNS.     

The validity of the Moxus Modular metabolic system during incremental exercise tests: impacts on detection of small changes in oxygen consumption

Purpose

We investigated the accuracy of the Moxus Modular Metabolic System (MOXUS) against the Douglas Bag Method (DBM) during high-intensity exercise, and whether the two methods agreed when detecting small changes in $\dot{V}{\text{O}}_{2}$ between two consecutive workloads ( $\Delta {\dot{{V}}\text{O}}_{ 2}$ ).

Methods

Twelve trained male runners performed two maximal incremental running tests while gas exchange was analyzed simultaneously by the two systems using a serial setup for four consecutive intervals of 30 s on each test. Comparisons between methods were performed for $\dot{V}{\text{O}}_{2}$ , ${\dot{{V}}}_{\text{E}}$ , fractions of expired O₂ (FeO₂) and CO₂ (FeCO₂) and $\Delta {\dot{{V}}\text{O}}_{ 2}$ .

Results

The MOXUS produced significant higher (mean ± SD, n = 54) readings for $\dot{V}{\text{O}}_{2}$ (80 ± 200 mL min^?1, p = 0.005) and ${\dot{{V}}}_{\text{E}}$ (2.9 ± 4.2 L min^?1, p < 0.0001), but not FeO₂ (?0.01 ± 0.09). Log-transformed 95 % limits of agreement for readings between methods were 94–110 % for $\dot{V}{\text{O}}_{2}$ , 97–108 % for $\dot{V}_{\text{E}}$ and 99–101 % for FeO₂. $\Delta \dot{V}{\text{O}}_{2}$ for two consecutive measurements was not different between systems (120 ± 110 vs. 90 ± 190 mL min^?1 for MOXUS and DBM, respectively, p = 0.26), but agreement between methods was very low (r = 0.25, p = 0.12).

Discussion

Although it was tested during high-intensity exercise and short sampling intervals, the MOXUS performed within the acceptable range of accuracy reported for automated analyzers. Most of the differences between equipments were due to differences in $\dot{V}_{\text{E}}$ . Detecting small changes in $\dot{V}{\text{O}}_{2}$ during an incremental test with small changes in workload, however, might be beyond the equipment’s accuracy.     

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.     

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.     

Faster \dot{V}{\text{O}}_{ 2} kinetics after eccentric contractions is explained by better matching of O2 delivery to O2 utilization

Purpose

This study examined the impact of eccentric exercise-induced muscle damage on the rate of adjustment in muscle deoxygenation and pulmonary O₂ uptake ( \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) kinetics during moderate exercise.

Methods

Fourteen males (25 ± 3 year; mean ± SD) completed three step transitions to 90 % θ_L before (Pre), 24 h (Post24) and 48 h after (Post48) eccentric exercise (100 eccentric leg-press repetitions with a load corresponding to 110 % of the participant’s concentric 1RM). Participants were separated into two groups: phase II \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) time constant (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) ≤ 25 s (fast group; n = 7) or τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\)  > 25 s (slow group; n = 7). \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) and [HHb] responses were modeled as a mono-exponential.

Results

In both groups, isometric peak torque (0°/s) at Post24 was decreased compared to Pre (p < 0.05) and remained depressed at Post48 (p < 0.05). τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) was designed to be different (p < 0.05) at Pre between the Fast (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ; 19 ± 4 s) and Slow (32 ± 6 s) groups. There were no differences among time points (τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) : Pre, 19 ± 4 s; Post24, 22 ± 3 s; Post48, 20 ± 4 s) in the Fast group. In Slow, there was a speeding (p < 0.05) from the Pre (32 ± 6 s) to the Post24 (25 ± 6) but not Post48 (31 ± 6), resulting in no difference (p > 0.05) between groups at Post24. This reduction of τ \(\dot{V}{\text{O}}_{{2{\text{p}}}} \,\) was concomitant with the abolishment (p < 0.05) of an overshoot in the [HHb]/ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ratio.

Conclusion

We propose that the sped \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) kinetics observed in the Slow group coupled with an improved [HHb]/ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ratio suggest a better matching of local muscle O₂ delivery to O₂ utilization following eccentric contractions.     

The determinants of performance in master swimmers: an analysis of master world records

Human performances in sports decline with age in all competitions/disciplines. Since the effects of age are often compounded by disuse, the study of master athletes provides the opportunity to investigate the effects of age per se on the metabolic/biomechanical determinants of performance. For all master age groups, swimming styles and distances, we calculated the metabolic power required to cover the distance (d) in the best performance time as: $ E _{\text{maxR}}^{\prime } = C \times d/{\text{BTP}} = C \times v_{\max } , $ where C is the energy cost of swimming in young elite swimmers, v _max?=?d/BTP is the record speed over the distance d, and BTP was obtained form “cross-sectional data” (http://www.fina.org). To establish a record performance, $ E_{\text{maxR}}^{\prime } $ must be equal to the maximal available metabolic power $ (E_{\text{maxA}}^{\prime } ) $ . This was calculated assuming a decrease of 1% per year at 40–70?years, 2% at 70–80?years and 3% at 80–90?years (as indicated in the literature) and compared to the $ E_{\text{maxR}}^{\prime } $ values, whereas up to about 55?years of age $ E_{\text{maxR}}^{\prime } = E_{\text{maxA}}^{\prime } ,$ for older subjects $ E_{\text{maxA}}^{\prime } > E_{\text{maxR}}^{\prime } ,$ the difference increasing linearly by about 0.30% (backstroke), 1.93% (butterfly), 0.92% (front crawl) and 0.37% (breaststroke) per year (average over the 50, 100 and 200?m distances). These data suggest that the energy cost of swimming increases with age. Hence, the decrease in performance in master swimmers is due to both decrease in the metabolic power available $ (E_{\text{maxA}}^{\prime } ) $ and to an increase in C.     

Pulmonary O2 uptake kinetics during moderate-intensity exercise transitions initiated from low versus elevated metabolic rates: insights from manipulations in cadence

Introduction

The rate of adjustment (τ) of phase II pulmonary O₂ uptake ( \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) ) is slower when exercise transitions are initiated from an elevated baseline work rate (WR) and metabolic rate (MR). In this study, combinations of cycling cadence (40 vs. 90 rpm) and external WR were used to examine the effect of prior MR on τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) .

Methods

Eleven young men completed transitions from 20 W (BSL) to 90 % lactate threshold, with transitions performed as two steps of equal ?WR (LS, lower step; US, upper step), while maintaining a cadence of (1) 40 rpm, (2) 90 rpm, and (3) 40 rpm but with the WRs elevated to match the higher \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) associated with 90 rpm cycling (40_MATCH); transitions lasted 6 min. \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) was measured breath-by-breath using mass spectrometry and turbinometry; vastus lateralis muscle deoxygenation [HHb] was measured using near-infrared spectroscopy. \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) and HHb responses were modeled using nonlinear least squares regression analysis.

Results

\(\dot{V}{\text{O}}_{{2{\text{p}}}}\) at BSL, LS and US was similar for 90 rpm and 40_MATCH, but greater than in 40 rpm. Compared to 90 rpm, τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) at 40 rpm was shorter (p < 0.05) in LS (18 ± 5 vs. 28 ± 8 s) but not in US (26 ± 8 vs. 33 ± 9 s), and at 40_MATCH, τ \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) was lower (p < 0.05) (19 ± 6 s) in LS but not in US (34 ± 13 s) despite differing external WR and ?WR.

Conclusions

A similar overall adjustment of [HHb] and \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) in LS and US across conditions suggested dynamic matching between microvascular blood flow and O₂ utilization. Prior MR (rather than external WR per se) plays a role in the dynamic adjustment of pulmonary (and muscle) \(\dot{V}{\text{O}}_{{2{\text{p}}}}\) .