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.     

Increases in \dot{V} O2max with “live high–train low” altitude training: role of ventilatory acclimatization

The purpose of this study was to estimate the percentage of the increase in whole body maximal oxygen consumption ( $ \dot{V} $ O_2max) that is accounted for by increased respiratory muscle oxygen uptake after altitude training. Six elite male distance runners ( $ \dot{V} $ O_2max = 70.6 ± 4.5 ml kg^?1 min^?1) and one elite female distance runner ( $ \dot{V} $ O_2max = 64.7 ml kg^?1 min^?1) completed a 28-day “live high–train low” training intervention (living elevation, 2,150 m). Before and after altitude training, subjects ran at three submaximal speeds, and during a separate session, performed a graded exercise test to exhaustion. A regression equation derived from published data was used to estimate respiratory muscle $ \dot{V} $ O₂ ( $ \dot{V} $ O_2RM) using our ventilation ( $ \dot{V} $ _E) values. $ \dot{V} $ O_2RM was also estimated retrospectively from a larger group of distance runners (n = 22). $ \dot{V} $ O_2max significantly (p < 0.05) increased from pre- to post-altitude (196 ± 59 ml min^?1), while $ \dot{V} $ _E at $ \dot{V} $ O_2max also significantly (p < 0.05) increased (13.3 ± 5.3 l min^?1). The estimated $ \dot{V} $ O_2RM contributed 37 % of Δ $ \dot{V} $ O_2max. The retrospective group also saw a significant increase in $ \dot{V} $ O_2max from pre- to post-altitude (201 ± 36 ml min^?1), along with a 10.8 ± 2.1 l min^?1 increase in $ \dot{V} $ _E, thus requiring an estimated 27 % of Δ $ \dot{V} $ O_2max. Our data suggest that a substantial portion of the improvement in $ \dot{V} $ O_2max with chronic altitude training goes to fuel the respiratory muscles as opposed to the musculature which directly contributes to locomotion. Consequently, the time-course of decay in ventilatory acclimatization following return to sea-level may have an impact on competitive performance.     

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}}}} $ .     

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.     

How long does it take to achieve steady state for an accurate assessment of resting \dot{\text{V}}{\text{O}}_{2} in healthy men?

The time necessary to obtain a steady state for an accurate and reliable assessment of resting $ \dot{V}{\text{O}}_{2} $ remains unclear and was the purpose of this study. Thirty healthy men, aged 17–28 years, visited the laboratory twice for the assessment of resting $ \dot{V}{\text{O}}_{2} $ , which was assessed as follows: (a) 24 h abstention from physical exercise, alcohol, soft drinks and caffeine, (b) fasting for at least 8 h, (c) an acclimation period of 10 min, and (d) 60 min assessment in a supine position. Resting $ \dot{V}{\text{O}}_{2} $ significantly changed during the 60 min (F = 37.4, P < 0.001), exhibiting a monoexponential decrease before reaching an asymptote. Post hoc pairwise comparisons showed that significant differences existed between consecutive means until the 30 min time point, after which there were no significant differences. The $ \dot{V}{\text{O}}_{2} $ response across trials exhibited high test–retest reliability, with within-subject coefficients of variations at each time point ranging from 2.8 to 7.0 % and intraclass correlation coefficients ranging from 0.90 to 0.99. The reliability was higher from the 25 min time point onwards. Based on these findings, the following recommendations are made to promote accurate assessment of resting $ \dot{V}{\text{O}}_{2} $ : (a) initiate the resting $ \dot{V}{\text{O}}_{2} $ measurement with 10 min of acclimation to the assessment apparatus, (b) determine resting $ \dot{V}{\text{O}}_{2} $ for a minimum of 30 min, until an apparent $ \dot{V}{\text{O}}_{2} $ steady state has been achieved; and (c) determine resting $ \dot{V}{\text{O}}_{2} $ for a further 5 min, with the average of this last 5 min of data being regarding as the resting $ \dot{V}{\text{O}}_{2} $ .     

The perceptually regulated exercise test is sensitive to increases in maximal oxygen uptake

The aim of this study was to assess the sensitivity of a perceptually regulated exercise test (PRET) to predict maximal oxygen uptake ( $ \dot{V} $ O₂max) following an aerobic exercise-training programme. Sedentary volunteers were assigned to either a training (TG n = 16) or control (CG n = 10) group. The TG performed 30 min of treadmill exercise, regulated at 13 on the Borg Rating of Perceived Exertion (RPE) Scale, 3× per week for 8 weeks. All participants completed a 12-min PRET to predict $ \dot{V} $ O₂max followed by a graded exercise test (GXT) to measure $ \dot{V} $ O₂max before and after training. The PRET required participants to control the speed and incline on the treadmill to correspond to RPE intensities of 9, 11, 13 and 15. Predictive accuracy of extrapolation end-points RPE19 and RPE20 from a submaximal RPE range of 9–15 was compared. Measured $ \dot{V} $ O₂max increased by 17 % (p < 0.05) from baseline to post-intervention in TG. This was reflected by a similar change in $ \dot{V} $ O₂max predicted from PRET when extrapolated to RPE 19 (baseline $ \dot{V} $ O₂max: 31.3 ± 5.5, 30.3 ± 9.5 mL kg^?1 min^?1; post-intervention $ \dot{V} $ O₂max: 36.7 ± 6.4, 37.4 ± 7.9 mL kg^?1 min^?1, for measured and predicted values, respectively). There was no change in CG (measured vs. predicted $ \dot{V} $ O₂max: 39.3 ± 6.5; 40.3 ± 8.2 and 39.2 ± 7.0; 37.7 ± 6.0 mL kg^?1 min^?1) at baseline and post-intervention, respectively. The results confirm that PRET is sensitive to increases in $ \dot{V} $ O₂max following aerobic training.     

The role of anticipatory postural adjustments in interlimb coordination of coupled arm movements in the parasagittal plane: III. Difference in the energy cost of postural actions during cyclic flexion–extension arm movements, ISO- and ANTI-directionally coupled

When oscillating the upper limbs together in the parasagittal plane, movements coordination is lower (i.e., variability of the interlimb relative phase is higher) in antidirectional (ANTI) than in isodirectional (ISO) coupling. In contrast, we previously observed that for arm movements in the horizontal plane, the coordination was worse in ISO than ANTI and the energetic cost of postural activities was higher in ISO. Having hypothesised that the higher postural cost was one factor responsible for the coordination deficit in horizontal ISO, we measured the oxygen uptake ( $\dot{V}_{{{\text{O}}_{2} }}$ ) in parasagittal movements, expecting that in this case too, the postural cost is higher in the less-coordinated mode (ANTI). Breath-by-breath metabolic ( $\dot{V}_{{{\text{O}}_{ 2} }}$ , $\dot{V}_{{{\text{CO}}_{ 2} }}$ ) and cardiorespiratory (HR, $\dot{V}_{\text{E}}$ ) parameters were measured in seven participants, who performed cyclic flexions–extensions in the parasagittal plane with either one arm or both arms, in ISO or ANTI coupling and at 1.4, 2.2 and 2.6 Hz. In each condition, the intermittent exercise (12 s movement, 12 s rest) lasted 264 s. A force platform recorded the mechanical actions to the ground. The exercise metabolic cost ( $\Updelta \dot{V}_{{{\text{O}}_{ 2} }}$ ) was found to be significantly higher in parasagittal ANTI than ISO. The movement amplitude being equal in the two modes, the ANTI-ISO difference should be ascribed to postural activities. This would confirm that the less-coordinated coupling mode requires the higher postural effort in parasagittal movements too. When rising the movement frequency, $\Updelta \dot{V}_{{{\text{O}}_{ 2} }}$ increased and linearly correlated with the coordination loss. Comparison of parasagittal with horizontal movements showed that $\Updelta \dot{V}_{{{\text{O}}_{ 2} }}$ was lower in parasagittal ANTI than in horizontal ISO (the less-coordinated modes), while it was not different between parasagittal ISO and horizontal ANTI (the more-coordinated modes).     

\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.     

Perceived exertion as a tool to self-regulate exercise in individuals with tetraplegia

The purpose of this investigation was to examine the use of subjective rating of perceived exertion (RPE) as a tool to self-regulate the intensity of wheelchair propulsive exercise in individuals with tetraplegia. Eight motor complete tetraplegic (C5/6 and below; ASIA Impairment Scale = A) participants completed a submaximal incremental exercise test followed by a graded exercise test to exhaustion to determine peak oxygen uptake ( $ \dot{V}O_{{ 2 {\text{peak}}}} $ ) on a wheelchair ergometer. On a separate day, a 20-min exercise bout was completed at an individualised imposed power output (PO) equating to 70 % of $ \dot{V}O_{{ 2 {\text{peak}}}} $ . On a third occasion, participants were instructed to maintain a workload equivalent to the average RPE for the 20-min imposed condition. $ \dot{V}O_{2} $ , heart rate (HR) and PO were measured at 1-min intervals and blood lactate concentration [BLa^?] was measured at 0, 10 and 20 min. No differences (P > 0.17) were found between mean $ \dot{V}O_{2} $ , %  $ \dot{V}O_{{ 2 {\text{peak}}}} $ , HR, % HR_peak, [BLa^?], velocity or PO between the imposed and RPE-regulated trials. No significant (P > 0.05) time-by-trial interaction was present for $ \dot{V}O_{2} $ data. A significant interaction (P < 0.001) for the PO data represented a trend for an increase in PO from 10 min to the end of exercise during the RPE-regulated condition. However, post hoc analysis revealed none of the differences in PO across time were significant (P > 0.05). In conclusion, these findings suggest that RPE can be an effective tool for self-regulating 20 min of wheelchair propulsion in a group of trained participants with tetraplegia who are experienced in wheelchair propulsion.     

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.     

One night of sleep deprivation decreases treadmill endurance performance

The aim was to test the hypothesis that one night of sleep deprivation will impair pre-loaded 30 min endurance performance and alter the cardio-respiratory, thermoregulatory and perceptual responses to exercise. Eleven males completed two randomised trials separated by 7 days: once after normal sleep (496 (18) min: CON) and once following 30 h without sleep (SDEP). After 30 h participants performed a 30 min pre-load at 60% $ \dot{V}{\text{O}}_{2\max } $ followed by a 30 min self-paced treadmill distance test. Speed, RPE, core temperature (T _re), mean skin temperature (T _sk), heart rate (HR) and respiratory parameters ( $ \dot{V}{\text{O}}_{2} $ , $ \dot{V}{\text{CO}}_{2} $ , $ \dot{V}{\text{E}} $ , RER pre-load only) were measured. Less distance (P = 0.016, d = 0.23) was covered in the distance test after SDEP (6037 (759) 95%CI 5527 to 6547 m) compared with CON (6224 (818) 95%CI 5674 to 6773 m). SDEP did not significantly alter T _re at rest or thermoregulatory responses during the pre-load including heat storage (0.8°C) and T _sk. With the exception of raised $ \dot{V}{\text{O}}_{2} $ at 30 min on the pre-load, cardio-respiratory parameters, RPE and speed were not different between trials during the pre-load or distance test (distance test mean HR, CON 174 (12), SDEP 170 (13) beats min^?1: mean RPE, CON 14.8 (2.7), SDEP 14.9 (2.6)). In conclusion, one night of sleep deprivation decreased endurance performance with limited effect on pacing, cardio-respiratory or thermoregulatory function. Despite running less distance after sleep deprivation compared with control, participants’ perception of effort was similar indicating that altered perception of effort may account for decreased endurance performance after a night without sleep.     

Differences in exercise limb blood flow and muscle deoxygenation with age: contributions to O2 uptake kinetics

The adjustments of pulmonary oxygen uptake $ \left( {\mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} } \right), $ limb blood flow (LBF) and muscle deoxygenation (ΔHHb) were examined during transitions to moderate-intensity, knee-extension exercise in seven older (OA; 71 ± 7 year) and seven young (YA; 26 ± 3 year) men. YA and OA performed repeated step transitions from an active baseline (3 W; 100 g) to a similar relative intensity of ~80% estimated lactate threshold (θ_L), and YA also performed the same absolute work rate as the OA (24 W, 800 g). Breath-by-breath $ \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} , $ femoral artery LBF (Doppler ultrasound) and muscle HHb (near-infrared spectroscopy) were measured. Phase 2 $ \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} , $ LBF, and ΔHHb data were fit with a mono-exponential model. $ \tau \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ was greater in OA (58 ± 21 s) than YA_80% (31 ± 9 s) and YA_24W (29 ± 11 s). The increase in LBF per increase in $ \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ was not different between groups (5.3–5.8 L min^?1/L min^?1); however, the τLBF was greater in OA (44 ± 19 s) than YA_24W (18 ± 7 s). The overall adjustment in ΔHHb (τ′ΔHHb) was not different between OA and YA, but was faster than $ \tau \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ in OA. This faster τ′ΔHHb than $ \tau \mathop {{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ resulted in an “overshoot” of the normalized $ \Updelta {\text{HHb}}/\Updelta\mathop{{V}}\limits^{ \cdot } {\text{O}}_{{2\,{\text{p}}}} $ response relative to the steady state level that was significantly greater in OA compared with YA suggesting that the adjustment of microvascular blood flow is slowed in OA thereby requiring a greater reliance on O₂ extraction during the transition to exercise.     

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).     

The verification phase and reliability of physiological parameters in peak testing of elite wheelchair athletes

The purpose of this study was (1) to examine the value of a verification phase (VER) in a peak testing protocol and (2) to assess the reliability of peak physiological variables in wheelchair athletes. On two separate days, eight tetraplegic (TETRA), eight paraplegic (PARA) and eight non-spinal cord-injured (NON-SCI) athletes performed treadmill ergometry, consisting of a graded exercise test to exhaustion (GXT) followed by a VER. Peak oxygen uptake $ \left( {\dot{V}{\text{O}}_{{ 2 {\text{peak}}}} } \right) $ was compared (1) between GXT and VER and (2) between test days. $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ did not differ between GXT and VER (P = 0.27), and coefficients of variation between GXT and VER were in the range of 2.9 and 6.4 % for all subgroups. Coefficients of variation of $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ between test days were 9.3 % (TETRA), 4.5 % (PARA) and 3.3 % (NON-SCI). It is therefore concluded that whilst a VER can be used for a more robust determination of $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ , a deviation of up to ~6 % between GXT and VER should be considered as acceptable. For between-day analyses, relatively large changes in $ \dot{V}{\text{O}}_{{2{\text{peak}}}} $ are required to confirm “true” differences, especially in TETRA athletes. This may be due to their lower aerobic capacity, which results in a larger relative variation compared with the other subgroups.     

A mathematical model for carbon dioxide elimination: an insight for tuning mechanical ventilation

Purpose

The aim is to provide better understanding of carbon dioxide ( $\mathrm{CO}_2$ ) elimination during ventilation for both the healthy and atelectatic condition, derived in a pressure-controlled mode. Therefore, we present a theoretical analysis of $\mathrm{CO}_2$ elimination of healthy and diseased lungs.

Methods

Based on a single-compartment model, $\mathrm{CO}_2$ elimination is mathematically modeled and its contours were plotted as a function of temporal settings and driving pressure. The model was validated within some level of tolerance on an average of 4.9 % using porcine dynamics.

Results

$\mathrm{CO}_2$ elimination is affected by various factors, including driving pressure, temporal variables from mechanical ventilator settings, lung mechanics and metabolic rate.

Conclusion

During respiratory care, $\mathrm{CO}_2$ elimination is a key parameter for bedside monitoring, especially for patients with pulmonary disease. This parameter provides valuable insight into the status of an atelectatic lung and of cardiopulmonary pathophysiology. Therefore, control of $\mathrm{CO}_2$ elimination should be based on the fine tuning of the driving pressure and temporal ventilator settings. However, for critical condition of hypercapnia, airway resistance during inspiration and expiration should be additionally measured to determine the optimal percent inspiratory time (%TI) to maximize $\mathrm{CO}_2$ elimination for treating patients with hypercapnia.     

Short-term high-intensity interval and continuous moderate-intensity training improve maximal aerobic power and diastolic filling during exercise

Purpose

This study examined the effects of short-term high-intensity interval training (HIT) and continuous moderate-intensity training (CMT) on cardiac function in young, healthy men.

Methods

Sixteen previously untrained men (mean age of 25.1 ± 4.1 years) were randomly assigned to HIT and CMT (n = 8 each) and assessed before and after six sessions over a 12-day training period. HIT consisted of 8–12 intervals of cycling for 60 s at 95–100 % of pre-training maximal aerobic power ( $\dot{V}$ O_2max), interspersed by 75 s of cycling at 10 % $\dot{V}$ O_2max. CMT involved 90–120 min of cycling at 65 % pre-training $\dot{V}$ O_2max. Left ventricular (LV) function was determined at rest and during submaximal exercise (heart rate ~105 bpm) using two-dimensional and Doppler echocardiography.

Results

Training resulted in increased calculated plasma volume (PV) in both groups, accompanied by improved $\dot{V}$ O_2max in HIT (HIT: from 39.5 ± 7.1 to 43.9 ± 5.5 mL kg^?1 min^?1; CMT: from 39.9 ± 5.9 to 41.7 ± 5.3 mL kg^?1 min^?1; P < 0.001). Resting LV function was not altered. However, increased exercise stroke volume (P = 0.02) and cardiac output (P = 0.02) were observed, secondary to increases in end-diastolic volume (P < 0.001). Numerous Doppler and speckle tracking indices of diastolic function were similarly enhanced during exercise in both training groups and were related to changes in PV.

Conclusion

Short-term HIT and CMT elicit rapid improvements in $\dot{V}$ O_2max and LV filling without global changes in cardiac performance at rest.     

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.     

Acute supra-therapeutic oral terbutaline administration has no ergogenic effect in non-asthmatic athletes

This study aimed to investigate the effects on a possible improvement in aerobic and anaerobic performance of oral terbutaline (TER) at a supra-therapeutic dose in 7 healthy competitive male athletes. On day 1, ventilatory threshold, maximum oxygen uptake $ (\dot{V}O_{2\max }) $ and corresponding power output were measured and used to determine the exercise load on days 2 and 3. On days 2 and 3, 8 mg of TER or placebo were orally administered in a double-blind process to athletes who rested for 3 h, and then performed a battery of tests including a force–velocity exercise test, running sprint and a maximal endurance cycling test at Δ50 % (50 % between VT and $ \dot{V}{\text{O}}_{2\max } $ ). Lactatemia, anaerobic parameters and endurance performance ( $ \dot{V}{\text{O}}_{ 2} ,\dot{V}E $ and time until exhaustion) were raised during the corresponding tests. We found that TER administration did not improve any of the parameters of aerobic performance (p > 0.05). In addition, no change in $ \dot{V}{\text{O}}_{2} $ kinetic parameters was found with TER compared to placebo (p > 0.05). Moreover, no enhancement of the force–velocity relationship was observed during sprint exercises after TER intake (p > 0.05) and, on the contrary, maximal strength decreased significantly after TER intake (p < 0.05) but maximal power remained unchanged (p > 0.05). In conclusion, oral acute administration of TER at a supra-therapeutic dose seems to be without any relevant ergogenic effect on anaerobic and aerobic performances in healthy athletes. However, all participants experienced adverse side effects such as tremors.     

Changes in arterial blood pressure elicited by severe passive heating at rest is associated with hyperthermia-induced hyperventilation in humans

The arterial blood pressure and ventilatory responses to severe passive heating at rest varies greatly among individuals. We tested the hypothesis that the increase in ventilation seen during severe passive heating of resting humans is associated with a decrease in arterial blood pressure. Passive heating was performed on 18 healthy males using hot water immersion to the level of the iliac crest and a water-perfused suit. We then divided the subjects into two groups: MAP_NOTINC (n = 8), whose mean arterial blood pressure (MAP) at the end of heating had increased by ≤3 mmHg, and MAP_INC (n = 10), whose MAP increased by >3 mmHg. Increases in esophageal temperature (T _es) elicited by the heating were similar in the two groups (+2.3 ± 0.3 vs. +2.4 ± 0.4 °C). Early during heating (increase in T _es was <1.5 °C), MAP, minute ventilation ( $ \dot{V}_{\text{E}} $ ), and end-tidal CO₂ pressure ( $ P_{{{\text{ET}}_{\text{CO2}} }} $ ) were similar between the groups. However, during the latter part of heating (increase in T _es was ≥1.5 °C), the increase in $ \dot{V}_{\text{E}} $ and decrease in $ P_{{{\text{ET}}_{\text{CO2}} }} $ were significantly greater or tended to be greater, while the increase in MAP was significantly smaller in MAP_NOTINC than MAP_INC. Among all subjects, heating-induced changes in $ \dot{V}_{\text{E}} $ significantly and negatively correlated with heating-induced changes in MAP during the latter part of heating (r = ?0.52 to ?0.74, P < 0.05). These results suggest that, in resting humans, 25?50 % of the variation in the magnitude of the arterial blood pressure response to severe passive heating can be explained by the magnitude of hyperthermia-induced hyperventilation.