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Purpose: We tested the hypothesis that incremental ramp cycling exercise performed in the supine position (S) would be associated with an increased reliance on muscle deoxygenation (deoxy[heme]) in the deep and superficial vastus lateralis (VLd and VLs, respectively) and the superficial rectus femoris (RFs) when compared to the upright position (U)., Methods: 11 healthy men completed ramp incremental exercise tests in S and U. Pulmonary [Formula: see text]O 2 was measured breath-by-breath; deoxy[heme] was determined via time-resolved near-infrared spectroscopy in the VLd, VLs and RFs., Results: Supine exercise increased the overall change in deoxy[heme] from baseline to maximal exercise in the VLs (S: 38 ± 23 vs. U: 26 ± 15 μM, P < 0.001) and RFs (S: 36 ± 21 vs. U: 25 ± 15 μM, P < 0.001), but not in the VLd (S: 32 ± 23 vs. U: 29 ± 26 μM, P > 0.05)., Conclusions: The present study supports that the impaired balance between O 2 delivery and O 2 utilization observed during supine exercise is a regional phenomenon within superficial muscles. Thus, deep muscle defended its O 2 delivery/utilization balance against the supine-induced reductions in perfusion pressure. The differential responses of these muscle regions may be explained by a regional heterogeneity of vascular and metabolic control properties, perhaps related to fiber type composition.

We hypothesized that the performance of prior heavy exercise would speed pulmonary oxygen uptake (V̇o 2 ) kinetics (i.e., as described by the time constant, [Formula: see text]) and reduce the amplitude of muscle deoxygenation (deoxy[heme]) kinetics in the supine (S) but not upright (U) body position. Seventeen healthy men completed heavy-intensity constant-work rate exercise tests in S and U consisting of two bouts of 6-min cycling separated by 6-min cycling at 20 W. Pulmonary V̇o 2 was measured breath by breath; total and deoxy[heme] were determined via time-resolved near-infrared spectroscopy (NIRS) at three muscle sites. Priming exercise reduced [Formula: see text] in S ( bout 1 : 36 ± 10 vs. bout 2 : 28 ± 10 s, P < 0.05) but not U ( bout 1 : 27 ± 8 s vs. bout 2 : 25 ± 7 s, P > 0.05). Deoxy[heme] amplitude was increased after priming in S ( bout 1 : 25-28 μM vs. bout 2 : 30-35 μM, P < 0.05) and U ( bout 1 : 13-18 μM vs. bout 2 : 17-25 μM, P > 0.05), whereas baseline total[heme] was enhanced in S ( bout 1 : 110-179 μM vs. bout 2 : 121-193 μM, P < 0.05) and U ( bout 1 : 123-186 μM vs. bout 2 : 137-197 μM, P < 0.05). Priming exercise increased total[heme] in both S and U, likely indicating enhanced diffusive O 2 delivery. However, the observation that after priming the amplitude of the deoxy[heme] response was increased in S suggests that the reduction in [Formula: see text] subsequent to priming was related to a combination of both enhanced intracellular O 2 utilization and increased O 2 delivery. NEW & NOTEWORTHY Here we show that oxygen uptake (V̇o 2 ) kinetics are slower in the supine compared with upright body position, an effect that is associated with an increased amplitude of skeletal muscle deoxygenation in the supine position. After priming in the supine position, the amplitude of muscle deoxygenation remained markedly elevated above that observed during upright exercise. Hence, the priming effect cannot be solely attributed to enhanced O 2 delivery, and enhancements to intracellular O 2 utilization must also be contributory.

This study compared the brachial artery blood flow (Q̇ BA ) and microvascular oxygen delivery responses during handgrip exercise above vs. below critical force (CF; the isometric analog of critical power). Q̇ BA and microvascular oxygen delivery are important determinants of oxygen utilization and metabolite accumulation during exercise, both of which increase progressively during exercise above CF. However the Q̇ BA and microvascular oxygen delivery responses above vs. below CF remain unknown. We hypothesized that Q̇ BA , deoxygenated-heme (deoxy-[heme]; an estimate of microvascular fractional oxygen extraction), and total-heme concentrations (total-[heme]; an estimate of changes in microvascular hematocrit) would demonstrate physiological maximums above CF despite increases in exercise intensity. Seven men and six women performed 1) a 5-min rhythmic isometric-handgrip maximal-effort test (MET) to determine CF and 2) two constant target-force tests above (severe-intensity; S1 and S2) and two constant target-force tests below (heavy-intensity; H1 and H2) CF. CF was 189.3 ± 16.7 N (29.7 ± 1.6%MVC). At end-exercise, Q̇ BA was greater for tests above CF (S1: 418 ± 147 mL/min; S2: 403 ± 137 mL/min) compared to tests below CF (H1: 287 ± 97 mL/min; H2: 340 ± 116 mL/min; all p < 0.05) but was not different between S1 and S2. Further, end-test Q̇ BA during both tests above CF was not different from Q̇ BA estimated at CF (392 ± 37 mL/min). At end-exercise, deoxy-[heme] was not different between tests above CF (S1: 150 ± 50 μM; S2: 155 ± 57 μM), but was greater during tests above CF compared to tests below CF (H1: 101 ± 24 μM; H2: 111 ± 21 μM; all p < 0.05). At end-exercise, total-[heme] was not different between tests above CF (S1: 404 ± 58 μM; S2: 397 ± 73 μM), but was greater during tests above CF compared to H1 (352 ± 58 μM; p < 0.01) but not H2 (371 ± 57 μM). These data suggest limb blood flow limitations exist and maximal levels of muscle microvascular oxygen delivery and extraction occur during exercise above, but not below, CF., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

New Findings: What is the central question of this study? Does the presence and extent of heterogeneity in the ratio of O 2 delivery to uptake across human muscles relate specifically to different muscle activation patterns? What is the main finding and its importance? During ramp incremental knee-extension and cycling exercise, the profiles of muscle deoxygenation (deoxy[haemoglobin + myoglobin]) and diffusive O 2 potential (total[haemoglobin + myoglobin]) in the vastus lateralis corresponded to different muscle activation strategies. However, this was not the case for the rectus femoris, where muscle activation and deoxygenation profiles were dissociated and might therefore be determined by other structural and/or functional attributes (e.g. arteriolar vascular regulation and control of red blood cell flux)., Abstract: Near-infrared spectroscopy has revealed considerable heterogeneity in the ratio of O 2 delivery to uptake as identified by disparate deoxygenation {deoxy[haemoglobin + myoglobin] (deoxy[Hb + Mb])} values in the exercising quadriceps. However, whether this represents a recruitment phenomenon or contrasting vascular and metabolic control, as seen among fibre types, has not been established. We used knee-extension (KE) and cycling (CE) incremental exercise protocols to examine whether differential muscle activation profiles could account for the heterogeneity of deoxy[Hb + Mb] and microvascular haemoconcentration (i.e. total[Hb + Mb]). Using time-resolved near-infrared spectroscopy for the quadriceps femoris (vastus lateralis and rectus femoris) during exhaustive ramp exercise in eight participants, we tested the following hypotheses: (i) the deoxy[Hb + Mb] (i.e. fractional O 2 extraction) would relate to muscle activation levels across exercise protocols; and (ii) KE would induce greater total[Hb + Mb] (i.e. diffusive O 2 potential) at task failure (i.e. peak O 2 uptake) than CE irrespective of muscle site. At a given level of muscle activation, as assessed by the relative integrated EMG normalized to maximal voluntary contraction (%iEMG max ), the vastus lateralis deoxy[Hb + Mb] profile was not different between exercise protocols. However, at peak O 2 uptake and until 20% iEMG max for CE, rectus femoris exhibited a lower deoxy[Hb + Mb] (83.2 ± 15.5 versus 98.2 ± 19.4 μm) for KE than for CE (P < 0.05). The total[Hb + Mb] at peak O 2 uptake was not different between exercise protocols for either muscle site. These data support the hypothesis that the contrasting patterns of convective and diffusive O 2 transport correspond to different muscle activation patterns in vastus lateralis but not rectus femoris. Thus, the differential deoxygenation profiles for rectus femoris across exercise protocols might be dependent upon specific facets of muscle architecture and functional haemodynamic events., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

The purpose of this study was to determine the effects of assuming constant tissue scattering properties on tissue oxygenation measurements during a vascular occlusion test (VOT). Twenty-one subjects (21.8 ± 1.9 yr) completed a VOT [1 min baseline (BL), 5 min of tissue ischemia (TI), and 3 min of vascular reperfusion (VR)]. Absolute concentrations of oxygenated heme (oxy-[heme]), deoxygenated heme (deoxy-[heme]), total heme (total [heme), tissue oxygen saturation (S t O 2 ), and heme difference [heme] diff ) were measured using frequency domain near-infrared spectroscopy (FD-NIRS) while 1 ) continuously measuring and incorporating tissue scattering ([Formula: see text]) and 2 ) assuming scattering remained constant. FD-NIRS measured [Formula: see text] increased during TI at 692 nm ( P < 0.001) and decreased at 834 nm ( P < 0.001). During VR, [Formula: see text] decreased at 692 nm ( P < 0.001) and increased at 834 nm ( P < 0.001). When assuming constant scattering, oxy-[heme] was significantly less at TI peak ( P < 0.05) while deoxy-[heme] and S t O 2 were significantly altered at BL, TI peak , and VR peak (all P < 0.001). Total [heme] did not change during the VOT. Absolute changes in deoxy-[heme], oxy-[heme], and S t O 2 in response to TI and VR were significantly exaggerated (all P < 0.001) and the rates of change during TI ( slope 1 ) and VR ( slope 2 ) in deoxy-[heme], oxy-[heme], S t O 2 , and [heme] diff were significantly increased (all P < 0.05) when constant tissue scattering was assumed. These findings demonstrate the need for caution when interpreting NIRS data without continuously measuring tissue optical properties. Further, assuming tissue optical properties remain constant may have important consequences to experimental data and clinical conclusions made using NIRS. NEW & NOTEWORTHY NIRS measurements provide significant experimental and clinical insight. We demonstrate that absolute changes in tissue oxygenation measurements made with NIRS are overestimated and the kinetic responses of NIRS measurements are exaggerated by varying degrees among individuals if tissue scattering characteristics are assumed to remain constant during vascular occlusion tests.

Relative perfusion of active muscles is greater during knee extension ergometry (KE) than cycle ergometry (CE). This provides the opportunity to investigate the effects of increased O 2 delivery (Q̇o 2 ) on deoxygenation heterogeneity among quadriceps muscles and pulmonary oxygen uptake (V̇o 2 ) kinetics. Using time-resolved near-infrared spectroscopy, we hypothesized that compared with CE the superficial vastus lateralis (VL), superficial rectus femoris, and deep VL in KE would have 1 ) a smaller amplitude of the exercise-induced increase in deoxy[Hb + Mb] (related to the balance between V̇o 2 and Q̇o 2 ); 2 ) a greater amplitude of total[Hb + Mb] (related to the diffusive O 2 conductance); 3 ) a greater homogeneity of regional muscle deoxy[Hb + Mb]; and 4 ) no difference in pulmonary V̇o 2 kinetics. Eight participants performed square-wave KE and CE exercise from 20 W to heavy work rates. Deoxy[Hb + Mb] amplitude was less for all muscle regions in KE ( P < 0.05: superficial, KE 17-24 vs. CE 19-40; deep, KE 19 vs. CE 26 μM). Furthermore, the amplitude of total[Hb + Mb] was greater for KE than CE at all muscle sites ( P < 0.05: superficial, KE, 7-21 vs. CE, 1-16; deep, KE, 11 vs. CE, -3 μM). Although the amplitude and heterogeneity of deoxy[Hb + Mb] were significantly lower in KE than CE during the first minute of exercise, the pulmonary V̇o 2 kinetics was not different for KE and CE. These data show that the microvascular Q̇o 2 to V̇o 2 ratio, and thus tissue oxygenation, was greater in KE than CE. This suggests that pulmonary and muscle V̇o 2 kinetics in young healthy humans are not limited by Q̇o 2 during heavy-intensity cycling.

Limb blood flow increases linearly with exercise intensity; however, invasive measurements of muscle microvascular blood flow during incremental exercise have demonstrated submaximal plateaus. We tested the hypotheses that 1) brachial artery blood flow (Q̇ BA ) would increase with increasing exercise intensity until task failure, 2) blood flow index of the flexor digitorum superficialis (BFI FDS ) measured noninvasively via diffuse correlation spectroscopy would plateau at a submaximal work rate, and 3) muscle oxygenation characteristics (total-[heme], deoxy-[heme], and percentage saturation) measured noninvasively with near-infrared spectroscopy would demonstrate a plateau at a similar work rate as BFI FDS . Sixteen subjects (23.3 ± 3.9 yr, 170.8 ± 1.9 cm, 72.8 ± 3.4 kg) participated in this study. Peak power (P peak ) was determined for each subject (1.8 ± 0.4 W) via an incremental handgrip exercise test. Q̇ BA , BFI FDS , total-[heme], deoxy-[heme], and percentage saturation were measured during each stage of the exercise test. On a subsequent testing day, muscle activation measurements of the FDS (RMS FDS ) were collected during each stage of an identical incremental handgrip exercise test via electromyography from a subset of subjects ( n = 7). Q̇ BA increased with exercise intensity until the final work rate transition ( P < 0.05). No increases in BFI FDS or muscle oxygenation characteristics were observed at exercise intensities greater than 51.5 ± 22.9% of P peak . No submaximal plateau in RMS FDS was observed. Whereas muscle activation of the FDS increased until task failure, noninvasively measured indices of perfusive and diffusive muscle microvascular oxygen delivery demonstrated submaximal plateaus. NEW & NOTEWORTHY Invasive measurements of muscle microvascular blood flow during incremental exercise have demonstrated submaximal plateaus. We demonstrate that indices of perfusive and diffusive microvascular oxygen transport to skeletal muscle, measured completely noninvasively, plateau at submaximal work rates during incremental exercise, even though limb blood flow and muscle recruitment continued to increase.

N-acetylcysteine (NAC; antioxidant and thiol donor) supplementation has improved exercise performance and delayed fatigue, but the underlying mechanisms are unknown. One possibility isNACsupplementation increases limb blood flow during severe-intensity exercise. The purpose was to determine ifNACsupplementation affected exercising arm blood flow and muscle oxygenation characteristics. We hypothesized thatNACwould lead to higher limb blood flow and lower muscle deoxygenation characteristics during severe-intensity exercise. Eight healthy nonendurance trained men (21.8 ± 1.2 years) were recruited and completed two constant power handgrip exercise tests at 80% peak power until exhaustion. Subjects orally consumed either placebo (PLA) orNAC(70 mg/kg) 60 min prior to handgrip exercise. Immediately prior to exercise, venous blood samples were collected for determination of plasma redox balance. Brachial artery blood flow (BABF) was measured via Doppler ultrasound and flexor digitorum superficialis oxygenation characteristics were measured via near-infrared spectroscopy. FollowingNACsupplementaiton, plasma cysteine (NAC: 47.2 ± 20.3 μmol/L vs.PLA: 9.6 ± 1.2 μmol/L;P = 0.001) and total cysteine (NAC: 156.2 ± 33.9 μmol/L vs.PLA: 132.2 ± 16.3 μmol/L;P = 0.048) increased. Time to exhaustion was not significantly different (P = 0.55) betweenNAC(473.0 ± 62.1 sec) andPLA(438.7 ± 58.1 sec). RestingBABFwas not different (P = 0.79) withNAC(99.3 ± 31.1 mL/min) andPLA(108.3 ± 46.0 mL/min).BABFwas not different (P = 0.42) during exercise or at end-exercise (NAC: 413 ± 109 mL/min;PLA: 445 ± 147 mL/min). Deoxy-[hemoglobin+myoglobin] and total-[hemoglobin+myoglobin] were not significantly different (P = 0.73 andP = 0.54, respectively) at rest or during exercise between conditions. We conclude that acuteNACsupplementation does not alter oxygen delivery during exercise in men., (© 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.)

We investigated whether muscle and ventilatory responses to incremental ramp exercise would be influenced by aerobic fitness status by means of a cross-sectional study with a large subject population. Sixty-four male students (age: 21.2 ± 3.2 years) with a heterogeneous peak oxygen uptake (51.9 ± 6.3 mL·min(-1)·kg(-1), range 39.7-66.2 mL·min(-1)·kg(-1)) performed an incremental ramp cycle test (20-35 W·min(-1)) to exhaustion. Breath-by-breath gas exchange was recorded, and muscle activation and oxygenation were measured with surface electromyography and near-infrared spectroscopy, respectively. The integrated electromyography (iEMG), mean power frequency (MPF), deoxygenated [hemoglobin and myoglobin] (deoxy[Hb+Mb]), and total[Hb+Mb] responses were set out as functions of work rate and fitted with a double linear function. The respiratory compensation point (RCP) was compared and correlated with the breakpoints (BPs) (as percentage of peak oxygen uptake) in muscle activation and oxygenation. The BP in total[Hb+Mb] (83.2% ± 3.0% peak oxygen uptake) preceded (P < 0.001) the BP in iEMG (86.7% ± 4.0% peak oxygen uptake) and MPF (86.3% ± 4.1% peak oxygen uptake), which in turn preceded (P < 0.01) the BP in deoxy[Hb+Mb] (88.2% ± 4.5% peak oxygen uptake) and RCP (87.4% ± 4.5% peak oxygen uptake). Furthermore, the peak oxygen uptake was significantly (P < 0.001) positively correlated to the BPs and RCP, indicating that the BPs in total[Hb+Mb] (r = 0.66; P < 0.001), deoxy[Hb+Mb] (r = 0.76; P < 0.001), iEMG (r = 0.61; P < 0.001), MPF (r = 0.63; P < 0.001), and RCP (r = 0.75; P < 0.001) occurred at a higher percentage of peak oxygen uptake in subjects with a higher peak oxygen uptake. In this study a close relationship between muscle oxygenation, activation, and pulmonary oxygen uptake was found, occurring in a cascade of events. In subjects with a higher aerobic fitness level this cascade occurred at a higher relative intensity.

Exposure to a microgravity environment decreases the maximal rate of O2 uptake (VO(2max)) in healthy individuals returning to a gravitational environment. The magnitude of this decrease in VO(2max) is, in part, dependent on the duration of microgravity exposure, such that long exposure may result in up to a 38% decrease in VO(2max). This review identifies the components within the O(2) transport pathway that determine the decrease in postmicrogravity VO(2max) and highlights the potential contributing physiological mechanisms. A retrospective analysis revealed that the decline in VO(2max) is initially mediated by a decrease in convective and diffusive O(2) transport that occurs as the duration of microgravity exposure is extended. Mechanistically, the attenuation of O(2) transport is the combined result of a deconditioning across multiple organ systems including decreases in total blood volume, red blood cell mass, cardiac function and mass, vascular function, skeletal muscle mass, and, potentially, capillary hemodynamics, which become evident during exercise upon re-exposure to the head-to-foot gravitational forces of upright posture on Earth. In summary, VO(2max) is determined by the integration of central and peripheral O(2) transport mechanisms, which, if not maintained during microgravity, will have a substantial long-term detrimental impact on space mission performance and astronaut health.

Near-infrared assessment of skeletal muscle is restricted to superficial tissues due to power limitations of spectroscopic systems. We reasoned that understanding of muscle deoxygenation may be improved by simultaneously interrogating deeper tissues. To achieve this, we modified a high-power (∼8 mW), time-resolved, near-infrared spectroscopy system to increase depth penetration. Precision was first validated using a homogenous optical phantom over a range of inter-optode spacings (OS). Coefficients of variation from 10 measurements were minimal (0.5-1.9%) for absorption (μa), reduced scattering, simulated total hemoglobin, and simulated O2 saturation. Second, a dual-layer phantom was constructed to assess depth sensitivity, and the thickness of the superficial layer was varied. With a superficial layer thickness of 1, 2, 3, and 4 cm (μa = 0.149 cm(-1)), the proportional contribution of the deep layer (μa = 0.250 cm(-1)) to total μa was 80.1, 26.9, 3.7, and 0.0%, respectively (at 6-cm OS), validating penetration to ∼3 cm. Implementation of an additional superficial phantom to simulate adipose tissue further reduced depth sensitivity. Finally, superficial and deep muscle spectroscopy was performed in six participants during heavy-intensity cycle exercise. Compared with the superficial rectus femoris, peak deoxygenation of the deep rectus femoris (including the superficial intermedius in some) was not significantly different (deoxyhemoglobin and deoxymyoglobin concentration: 81.3 ± 20.8 vs. 78.3 ± 13.6 μM, P > 0.05), but deoxygenation kinetics were significantly slower (mean response time: 37 ± 10 vs. 65 ± 9 s, P ≤ 0.05). These data validate a high-power, time-resolved, near-infrared spectroscopy system with large OS for measuring the deoxygenation of deep tissues and reveal temporal and spatial disparities in muscle deoxygenation responses to exercise., (Copyright © 2015 the American Physiological Society.)

The conventional continuous wave near-infrared spectroscopy (CW-NIRS) has enabled identification of regional differences in muscle deoxygenation following onset of exercise. However, assumptions of constant optical factors (e.g., path length) used to convert the relative changes in CW-NIRS signal intensity to values of relative concentration, bring the validity of such measurements into question. Furthermore, to justify comparisons among sites and subjects, it is essential to correct the amplitude of deoxygenated hemoglobin plus myoglobin [deoxy(Hb+Mb)] for the adipose tissue thickness (ATT). We used two time-resolved NIRS systems to measure the distribution of the optical factors directly, thereby enabling the determination of the absolute concentrations of deoxy(Hb+Mb) simultaneously at the distal and proximal sites within the vastus lateralis (VL) and the rectus femoris muscles. Eight subjects performed cycle exercise transitions from unloaded to heavy work rates (>gas exchange threshold). Following exercise onset, the ATT-corrected amplitudes (A(p)), time delay (TD(p)), and time constant (τ(p)) of the primary component kinetics in muscle deoxy(Hb + Mb) were spatially heterogeneous (intersite coefficient of variation range for the subjects: 10-50 for A(p), 16-58 for TD(p), 14-108% for τ(p)). The absolute and relative amplitudes of the deoxy(Hb+Mb) responses were highly dependent on ATT, both within subjects and between measurement sites. The present results suggest that regional heterogeneity in the magnitude and temporal profile of muscle deoxygenation is a consequence of differential matching of O(2) delivery and O(2) utilization, not an artifact caused by changes in optical properties of the tissue during exercise or variability in the overlying adipose tissue.

We investigated the effects of prior heavy exercise on the spatial heterogeneity of muscle deoxygenation kinetics and the relationship to the pulmonary O(2) uptake (pVO(2)) kinetics during subsequent heavy exercise. Seven healthy men completed two 6-min bouts of heavy work rate cycling exercise, separated by 6 min of unloaded exercise. The changes in the concentration of deoxyhemoglobin/myoglobin (Delta deoxy-[Hb+Mb]) were assessed simultaneously at 10 different sites on the rectus femoris muscle using multichannel near-infrared spectroscopy. Prior exercise had no effect on either the time constant or the amplitude of the primary component pVO(2), whereas it reduced the amplitude of the slow component (SC). Delta deoxy-[Hb+Mb] across all 10 sites for bout 2 displayed a shorter time delay (mean and SD for subjects: 13.5 +/- 1.3 vs. 9.3 +/- 1.4 s; P < 0.01) and slower primary component time constant (tau: 9.3 +/- 1.3 vs. 17.8 +/- 1.0 s; P < 0.01) compared with bout 1. Prior exercise significantly reduced both the intersite coefficient of variation (CV) of the tau of Delta deoxy-[Hb+Mb] (26.6 +/- 11.8 vs. 13.7 +/- 5.6%; P < 0.01) and the point-by-point heterogeneity [root mean square error (RMSE)] during the primary component in the second bout. However, neither the change in the CV for tau nor RMSE of Delta deoxy-[Hb+Mb] correlated with the reduction in the SC in pVO(2) kinetics during subsequent heavy exercise. In conclusion, prior exercise reduced the spatial heterogeneity of the primary component of muscle deoxygenation kinetics. This effect was not correlated with alterations in the pVO(2) response during subsequent heavy exercise.

It is unclear whether measurement of limb or conduit artery blood flow during recovery from exercise provides an accurate representation of flow to the muscle capillaries where gas exchange occurs. To investigate this, we: (a) examined the kinetic responses of femoral artery blood flow (QFA), estimated muscle capillary blood flow (Qcap) and estimated muscle oxygen uptake (VO2m) following cessation of exercise; and (b) compared these responses to verify the adequacy of O2 delivery during recovery. Pulmonary VO2 (VO2p) was measured breath by breath, QFA was measured using Doppler ultrasonography, and deoxy-haemoglobin/myoglobin (deoxy-[Hb/Mb]) was estimated by near-infrared spectroscopy over the rectus femoris in nine healthy subjects during a series of transitions from moderate knee-extension exercise to rest. The time course of Qcap was estimated by rearranging the Fick equation [i.e. Qcap(t) alpha VO2m(t)/deoxy-[Hb/Mb](t)], using the primary component of Vo2p to represent VO2m and deoxy-[Hb/Mb] as a surrogate for arteriovenous O2 difference. There were no significant differences among the overall kinetics of VO2m (tau, 31.4+/-8.2 s), QFA [mean response time (MRT), 34.5+/-20.4 s] and Qcap (MRT, 31.7+/-14.7 s). The VO2m kinetics were also significantly correlated (P<0.05) with those of both QFA and Qcap. Both QFA and Qcap appear to be coupled with VO2m during recovery from moderate knee-extension exercise, such that extraction falls (thus cellular energetic state is not further compromised) throughout recovery.

Inability to directly measure microvascular oxygen distribution and extraction in striated muscle during a contraction/relaxation cycle limits our understanding of oxygen transport to and utilization by contracting muscle. We examined muscle microvascular hemoglobin concentration (total [Hb/Mb]) and oxygenation within the contraction-relaxation cycle to determine if microvascular RBC volume would be preserved and if oxygen extraction continued during the actual contraction phase. Eight subjects performed dynamic knee extension exercise (40 contractions/min) at moderate ( approximately 30% of peak work rate) and heavy ( approximately 80% of peak) work rates. Total hemoglobin/myoglobin (total [Hb/Mb]) and deoxy-hemoglobin/myoglobin (deoxy-[Hb/Mb]) were measured in the rectus femoris using NIRS to determine if microvascular total [Hb/Mb] would be preserved during the contraction, and to estimate microvascular oxygen extraction, respectively. Mean values during the relaxation (RP) and contractile phases and the peak values during the contractile phase for both moderate and heavy exercise were calculated. Total [Hb/Mb] increased from rest to steady-state exercise (6.36+/-5.08 microM moderate; 5.72+/-4.46 microM heavy exercise, both P<0.05), but did not change significantly within the contraction/relaxation cycle. Muscle contractions were associated with a significant (1.29+/-0.98 microM moderate; 2.16+/-2.12 microM heavy exercise, P<0.05) increase in deoxy-[Hb/Mb] relative to RP. We conclude that (a) microvascular RBC volume is preserved during muscle contractions (i.e., RBCs are present in the capillaries), and (b) the cyclical pattern of deoxygenation/oxygenation during the respective contraction/relaxation phases of the contraction cycle suggests that oxygen extraction is not restricted to the relaxation phase but continues to occur during muscle contractions.

Utilization of near-infrared spectroscopy (NIRS) in clinical exercise testing to detect microvascular abnormalities requires characterization of the responses in healthy individuals and theoretical foundation for data interpretation. We examined the profile of the deoxygenated hemoglobin signal from NIRS {deoxygenated hemoglobin + myoglobin [deoxy-(Hb+Mb)] approximately O(2) extraction} during ramp exercise to test the hypothesis that the increase in estimated O(2) extraction would be close to hyperbolic, reflecting a linear relationship between muscle blood flow (Q(m)) and muscle oxygen uptake (Vo(2)(m)) with a positive Q(m) intercept. Fifteen subjects (age 24 +/- 5 yr) performed incremental ramp exercise to fatigue (15-35 W/min). The deoxy-(Hb+Mb) response, measured by NIRS, was fitted by a hyperbolic function [f(x) = ax/(b + x), where a is the asymptotic value and b is the x value that yields 50% of the total amplitude] and sigmoidal function {f(x) = f(0) + A/[1 + e(-(-c+dx))], where f(0) is baseline, A is total amplitude, and c is a constant dependent on d, the slope of the sigmoid}, and the goodness of fit was determined by F test. Only one subject demonstrated a hyperbolic increase in deoxy-(Hb+Mb) (a = 170%, b = 193 W), whereas 14 subjects displayed a sigmoidal increase in deoxy-(Hb+Mb) (f(0) = -7 +/- 7%, A = 118 +/- 16%, c = 3.25 +/- 1.14, and d = 0.03 +/- 0.01). Computer simulations revealed that sigmoidal increases in deoxy-(Hb+Mb) reflect a nonlinear relationship between microvascular Q(m) and Vo(2)(m) during incremental ramp exercise. The mechanistic implications of our findings are that, in most healthy subjects, Q(m) increased at a faster rate than Vo(2)(m) early in the exercise test and slowed progressively as maximal work rate was approached.

To test the hypothesis that, during exercise, substantial heterogeneity of muscle hemoglobin and myoglobin deoxygenation [deoxy(Hb + Mb)] dynamics exists and to determine whether such heterogeneity is associated with the speed of pulmonary O(2) uptake (pVo(2)) kinetics, we adapted multi-optical fibers near-infrared spectroscopy (NIRS) to characterize the spatial distribution of muscle deoxygenation kinetics at exercise onset. Seven subjects performed cycle exercise transitions from unloaded to moderate [GET) work rates and the relative changes in deoxy(Hb + Mb), at 10 sites in the quadriceps, were sampled by NIRS. At exercise onset, the time delays in muscle deoxy(Hb + Mb) were spatially inhomogeneous [intersite coefficient of variation (CV), 3~56% for GET]. The primary component kinetics (time constant) of muscle deoxy(Hb + Mb) reflecting increased O(2) extraction were also spatially inhomogeneous (intersite CV, 6~48% for GET) and faster (P < 0.05) than those of phase 2 pVo(2). However, the degree of dynamic intersite heterogeneity in muscle deoxygenation did not correlate significantly with phase 2 pVo(2) kinetics. In conclusion, the dynamics of quadriceps microvascular oxygenation demonstrates substantial spatial heterogeneity that must arise from disparities in the relative kinetics of Vo(2) and O(2) delivery increase across the regions sampled.

In humans at exercise onset, intramuscular phosphocreatine decreases immediately, whereas muscle oxygen (O2) uptake seems to rise after a delay of up to 15 s which is inconsistent with models of metabolic control. Novel microcirculatory investigations reveal that elevated capillary-to-myocyte O2 flux in rat muscle is, in fact, initiated simultaneously with contractions.

The time course of muscle oxygen desaturation (StO2 kinetics) following exercise onset reflects the dynamic interaction between muscle blood flow and muscle oxygen consumption. In patients with peripheral arterial disease (PAD), muscle StO2 kinetics are slowed during walking exercise; potentially reflecting altered muscle oxygen consumption relative to blood flow. This study evaluated whether StO2 kinetics measured using near infrared spectroscopy (NIRS) would be slowed in PAD during low work rate calf exercise compared with healthy subjects under conditions in which blood flow did not differ. Eight subjects with PAD and eight controls performed 3 min of calf exercise at 5, 10, 30, and 50% of maximal voluntary contraction (MVC). Calf blood flow responses were measured by plethysmography. Power outputs were similar between groups for all work rates. In PAD, the time constants of StO2 kinetics were significantly slower than controls during 5% MVC (13.5 +/- 1.7 vs. 6.9 +/- 1.2 s, P < 0.05) and 10% MVC work rates (14.5 +/- 2.7 vs. 6.8 +/- 1.1 s, P < 0.05). Blood flow assessed when exercise was interrupted after 30 s did not differ between PAD and control subjects at these work rates. In contrast, the StO2 time constants were not different between groups during 30 and 50% MVC work rates, where blood flow responses in PAD subjects were lower as compared with controls. Thus in PAD, the slowed StO2 kinetic responses under conditions of unimpaired calf blood flow reflect slowed muscle oxygen consumption in PAD skeletal muscle during low work rate plantar flexion exercise as compared with healthy skeletal muscle.

The aim of this study was to examine the effects of assuming constant reduced scattering coefficient (mu'(s)) on the muscle oxygenation response to incremental exercise and its recovery kinetics. Fifteen subjects (age: 24 +/- 5 yr) underwent incremental cycling exercise. Frequency domain near-infrared spectroscopy (NIRS) was used to estimate deoxyhemoglobin concentration {[deoxy(Hb+Mb)]} (where Mb is myoglobin), oxyhemoglobin concentration {[oxy(Hb+Mb)]}, total Hb concentration (Total[Hb+Mb]), and tissue O(2) saturation (Sti(O(2))), incorporating both continuous measurements of mu'(s) and assuming constant mu'(s). When measuring mu'(s), we observed significant changes in NIRS variables at peak work rate Delta[deoxy(Hb+Mb)] (15.0 +/- 7.8 microM), Delta[oxy(Hb+Mb)] (-4.8 +/- 5.8 microM), DeltaTotal[Hb+Mb] (10.9 +/- 8.4 microM), and DeltaSti(O(2))(-11.8 +/- 4.1%). Assuming constant mu'(s) resulted in greater (P < 0.01 vs. measured mu'(s)) changes in the NIRS variables at peak work rate, where Delta[deoxy(Hb+Mb)] = 24.5 +/- 15.6 microM, Delta[oxy(Hb+Mb)] = -9.7 +/- 8.2 microM, DeltaTotal[Hb+Mb] = 14.8 +/- 8.7 microM, and DeltaSti(O(2))= -18.7 +/- 8.4%. Regarding the recovery kinetics, the large 95% confidence intervals (CI) for the difference between those determine measuring mu'(s) and assuming constant mu'(s) suggested poor agreement between methods. For the mean response time (MRT), which describes the overall kinetics, the 95% confidence intervals were MRT - [deoxy(Hb+Mb)] = 26.7 s; MRT - [oxy(Hb+Mb)] = 11.8 s, and MRT - Sti(O(2))= 11.8 s. In conclusion, mu'(s) changed from light to peak exercise. Furthermore, assuming a constant mu'(s) led to an overestimation of the changes in NIRS variables during exercise and distortion of the recovery kinetics.

Critical power (CP) is lower at faster rather than slower pedalling frequencies and traditionally reported in watts (W). Faster pedalling frequencies also engender a greater metabolic rate (VO2) at low work rates, but with progressive increases in power output, the initial difference in VO2 between fast and slower pedalling frequencies is reduced. We tested the hypothesis that CP represents a unique metabolic rate for any given individual which would be similar at different pedalling frequencies. Eleven collegiate athletes (five cross-country runners, END; six sprinters, SPR), aged 18-23 years, performed exhaustive rides at either 60 or 100 r.p.m. on separate days for the determination of the pedal rate-specific CP. The VO2 at CP (CP-VO2) was determined from an 8 min ride at the CP for each pedal frequency. The group mean CP was significantly lower at 100 r.p.m. (189 +/- 50 W) compared to 60 r.p.m. (207 +/- 53 W, P < 0.05). However, the group mean CP-VO2 values at 60 (2.53 +/- 0.60 l min(-1)) and 100 r.p.m. (2.58 +/- 0.53 l min(-1)) were not significantly different. Critical power was significantly higher in the END athletes (242 +/- 50 W at 60 r.p.m.; 221 +/- 56 W at 100 r.p.m.) compared to SPR athletes at both pedal frequencies (177 +/- 38 W at 60 r.p.m.; 162 +/- 27 W at 100 r.p.m., P < 0.05), but the CP-VO2 was not (P > 0.05). However, when the CP-VO2 was scaled to body weight, the END athletes had a significantly greater CP-VO2 (41.3 +/- 4.1 ml min(-1) kg(-1) at 60 r.p.m.; 40.8 +/- 5.5 ml min(-1) kg(-1) at 100 r.p.m.) compared to the SPR athletes at both pedal frequencies (27.7 +/- 4.6 ml min(-1) kg(-1) at 60 r.p.m.; 29.4 +/- 2.8 ml min(-1) kg(-1) at 100 r.p.m., P < 0.05). We conclude that CP represents a specific metabolic rate (VO2) which can be achieved at different combinations of power outputs and pedalling frequencies.

An increase in muscle contraction frequency could limit muscle blood flow QM compromising the matching of QM and muscle oxygen uptake VO2M. This study examined the effects of pedal cadence on skeletal muscle oxygenation at low, moderate and peak exercise. Nine healthy subjects [24.7+/-6.3 years (SD)] performed incremental cycling exercise at 60 and 100 rpm. Pulmonary VO2(VO2P) was measured breath-by-breath and vastus lateralis oxygenation was determined by near-infrared spectroscopy (NIRS). The deoxyhemoglobin signal ([HHb]) from NIRS was used to estimate microvascular O2 extraction (i.e., [HHb] proportional, variant VO2M/QM). The VO2P and [HHb] for low, moderate and at peak exercise were determined. The VO2P at 60 rpm (low=0.64+/-0.13, moderate=2.03+/-0.38 and peak=3.39+/-0.84 l/min) were lower (P<0.01) than at 100 rpm (1.29+/-0.23, 2.14+/-0.39 and 3.54+/-0.88 l/min, respectively). There was a progressive increase in [HHb] from low to peak exercise. However, there was no significant difference (ANOVA, P=0.94) for the 60 (in microM, low=24.0+/-9.5, moderate=30.5+/-13.8 and peak=36.7+/-16.5) and 100 contractions/min (in microM, low=25.7+/-11.6, moderate=32.1+/-14.0 and peak=35.4+/-16.5). We conclude that vastus lateralis O2 extraction was similar at 60 and 100 cpm, suggesting that the VO2M/QM in the microcirculation was not altered and, presumably, no impairment of QM occurred with the increase in pedal frequency.

This study examined the relationship between muscle recruitment patterns using surface electromyography (EMG) and the excess O(2) uptake (Ex.V(O(2))) that accompanies slow (SR, 8 W min(-1)) but not fast (FR, 64 W min(-1)) ramp increases in work rate (WR) during exercise on a cycle ergometer. Nine subjects (2 females) participated in this study (25 +/- 2 years, +/- S.E.M.). EMG was obtained from the vastus lateralis and medialis and analysed in the time (root mean square, RMS) and frequency (median power frequency, MDPF) domain. Results for each muscle were averaged to provide an overall response and expressed relative to a maximal voluntary contraction (%MVC). Delta.V(O(2))/DeltaWR was calculated for exercise below (S(1)) and above (S(2)) the lactate threshold (LT) using linear regression. The increase in RMS relative to the increase in WR for exercise below the LT (DeltaRMS/DeltaWR-S(1)) was determined using linear regression. Due to non-linearities in RMS above the LT, DeltaRMS/DeltaWR-S(2) is reported as the difference in RMS (DeltaRMS) and the difference in WR (DeltaWR) at end-exercise and the LT. SR was associated with a higher (P < 0.05) Delta.V(O(2))/DeltaWR (S(1), 9.3 +/- 0.3 ml min(-1) W(-1); S(2), 12.5 +/- 0.6 ml min(-1) W(-1)) than FR (S(1), 8.5 +/- 0.4 ml min(-1) W(-1); S(2), 7.9 +/- 0.4 ml min(-1) W(-1)) but a similar DeltaRMS/DeltaWR-S(1) (SR, 0.11 +/- 0.01% W(-1); FR, 0.10 +/- 0.01 % W(-1)). Ex.V(O(2)) was greater (P < 0.05) in SR (3.6 +/- 0.7 l) than FR (-0.7 +/- 0.4 l) but was not associated with a difference in either DeltaRMS/DeltaWR-S(2) (SR, 0.14 +/- 0.01% W(-1); FR, 15 +/- 0.02 % W(-1)) or MDPF (SR, 2.6 +/- 5.9 %; FR, -15.4 +/- 4.5 %). The close matching between power output and RMS during SR and FR suggests that the Ex.V(O(2)) of heavy exercise is not associated with the recruitment of additional motor units since Ex.V(O(2)) was observed during SR only. Compared to the progressive decrease in MDPF observed during FR, the MDPF remained relatively constant during SR suggesting that either (i) there was no appreciable recruitment of the less efficient type II muscle fibres, at least in addition to those recruited initially at the onset of exercise, or (ii) the decrease in MDPF associated with fatigue was offset by the addition of a higher frequency of type II fibres recruited to replace the fatigued motor units.

ObjectivesNovel protocols were used to focus on dynamic cardiorespiratory function during submaximal exercise and on the recovery from 1-min pulses of exercise in children who had undergone Fontan corrections for single-ventricle lesions.BackgroundParticularly in children, maximal oxygen uptake (VO2max), which is commonly used to assess the functional capability of patients after the Fontan procedure, is highly effort dependent and not physiologic and leads to uncomfortable metabolic and cardiorespiratory stress. Alternative approaches include the measurement of dynamic responses during progressive exercise and recovery after short bursts of exercise. These strategies yield mechanistic insight into cardiorespiratory impairment and can be used to gauge limitations in daily life activity.MethodsSixteen patients (mean [+/-SD] age 12.2 +/- 2.4 years; 9 boys) and 10 age-matched control subjects (mean age 12.2 +/- 2.4 years; 6 boys) performed two separate cycle ergometer tests in which gas exchange was measured on a breath by breath basis: 1) Progressive exercise was used to determine the dynamic relation among VO2, carbon dioxide production (VCO2), ventilation (VE), heart rate (HR) and work rate (WR). 2) A 1-min constant WR test was used to determine the recovery time for gas exchange and HR.ResultsPeak VO2 and anaerobic threshold were reduced in patients who underwent the Fontan procedure compared with control subjects by 57% and 52%, respectively (p < 0.001). Dynamic relations during progressive exercise--deltaVO2/deltaHR and deltaVO2/deltaWR--were decreased (p < 0.001) and deltaVE/deltaVCO2 was increased (p < 0.005) in the Fontan group patients. Recovery times for HR and VO2 were prolonged in the Fontan group patients by 154% and 69%, respectively (p < 0.01).ConclusionsThe results demonstrate that submaximal gas exchange responses to progressive exercise and recovery times after brief high intensity exercise are abnormal in patients after the Fontan procedure. These observations complement the findings of reduced VO2max observed here and by others. We speculate that the mechanisms for these responses are related to 1) a pervasive reduction in stroke volume for both low and high intensity exercise, 2) an abnormal linkage of ventilation to tissue carbon dioxide production, and 3) increased dependence on anaerobic metabolism in skeletal muscles. The prolonged recovery of HR and VO2 provides a possible mechanism for reduced physical activity.

The article focuses on the application of near-infrared spectroscopy (NIRS) in investigating the convective and diffusive components of oxygen (O2) transport at maximal oxygen uptake (VO˙ 2max). The topics include the O2 cascade from ambient air to muscle mitochondria, a proposed model for evaluating convective and diffusive O2 transport, and the use of NIRS as a noninvasive method to monitor muscle oxygenation.

The article focuses on the suitability of near-infrared spectroscopy (NIRS) for calculating the convective and diffusive components of O2 transport at VO˙ 2max. Topics include a comparison of invasive results with NIRS data in patients with mitochondrial myopathies, highlighting discrepancies in convective O2 transport estimations, and advocating for the use of NIRS StO2 as a surrogate for venous SO2.

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O2 uptake (p&Vdot;o2) kinetics and 2) to characterize the muscle blood flow, muscle &Vdot;o2 (m&Vdot;o2), and p&Vdot;o2 kinetics during KE to investigate the rate-limiting factor(s) of p&Vdot;o2 on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to p&Vdot;o2 during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and m&Vdot;o2 at the onset of KE. First, the gain (amplitude/work rate) of the primary component of p&Vdot;o2 for both moderate and heavy exercise was higher during KE (∼12 ml·W-1·min-1) compared with CE (∼10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of m&Vdot;o2 during heavy KE [25.8 ± 9.0 s (SD)] was not significantly different from that of the phase 11 p&Vdot;o2. Moreover, the slow component of p&Vdot;o2 evident for the heavy KE reflected the gradual increase in m&Vdot;o2. The initial LBF kinetics after onset of KE were significantly faster than the phase 11 p&Vdot;o2 kinetics (moderate: time constant LBF = 8.0 ± 3.5 s, p&Vdot;o2 = 32.7 ± 5.6 s, P < 0.05; heavy: LBF = 9.7 ± 2.0 s, p&Vdot;o2 = 29.9 ± 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of p&Vdot;o2. These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of p&Vdot;o2, consistent with an intramuscular limitation to &Vdot;o2 kinetics, i.e., a microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia. [ABSTRACT FROM AUTHOR]

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2) kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to ∼105% of the predetermined VO2 peak, separated by 3 × 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means ± SD: MAX1: 1.3 ± 0.4 mM vs. MAX2:7.7 ± 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 ± 5.5 s vs. MAX2:33.2 ± 7.7 s). Rather, the asymptotic "gain" of the primary VO2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 ± 0.9 ml·min-1·W-1 vs. MAX2:9.0 ± 0.7 l·min-1·W-1; P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise. [ABSTRACT FROM AUTHOR]

Technical limitations have precluded measurement of the V˙O2 profile within contracting muscle (mV˙O2) and hence it is not known to what extent V˙O2 dynamics measured across limbs in humans or muscles in the dog are influenced by transit delays between the muscle microvasculature and venous effluent. Measurements of capillary red blood cell flux and microvascular PO2 (PO2m) were combined to resolve the time course of mV˙O2 across the rest-stimulation transient (1 Hz, twitch contractions). mV˙O2 began to rise at the onset of contractions in a close to monoexponential fashion (time constant, J=23.2±1.0 sec) and reached it's steady-state value at 4.5-fold above baseline. Using computer simulation in healthy and disease conditions (diabetes and chronic heart failure), our findings suggest that: (1) mV˙O2 increases essentially immediately (<2 sec) following exercise onset; (2) within healthy muscle the J blood flow (thus O2 delivery, JQ˙O2m) is faster than JmV˙O2 such that oxygen delivery is not limiting, and 3) a faster PO2m fall to a PO2m value below steady-state values within muscle from diseased animals is consistent with a relatively sluggish Q˙O2m response compared to that of mV˙O2. [ABSTRACT FROM AUTHOR]

Exposure to a microgravity environment decreases the maximal rate of O2 uptake (...O2max) in healthy individuals returning to a gravitational environment. The magnitude of this decrease in ...O2max is, in part, dependent on the duration of microgravity exposure, such that long exposure may result in up to a 38% decrease in ...O2max. This review identifies the components within the O2 transport pathway that determine the decrease in postmicrogravity ...O2max and highlights the potential contributing physiological mechanisms. A retrospective analysis revealed that the decline in ...O2max is initially mediated by a decrease in convective and diffusive O2 transport that occurs as the duration of microgravity exposure is extended. Mechanistically, the attenuation of O2 transport is the combined result of a deconditioning across multiple organ systems including decreases in total blood volume, red blood cell mass, cardiac function and mass, vascular function, skeletal muscle mass, and, potentially, capillary hemodynamics, which become evident during exercise upon re-exposure to the head-to-foot gravitational forces of upright posture on Earth. In summary, ...O2max is determined by the integration of central and peripheral O2 transport mechanisms, which, if not maintained during microgravity, will have a substantial long-term detrimental impact on space mission performance and astronaut health. [ABSTRACT FROM AUTHOR]

Abstract: A computer model was developed to provide a theoretical framework for interpreting the dynamics of muscle capillary O2 exchange in health and disease. We examined the effects of different muscle oxygen uptake () and CvO2 profiles on muscle blood flow () kinetics (). Further, we simulated and responses to predict the CvO2 profile and the underlying dynamics of capillary O2 exchange (). Exponential equations describing , CvO2 and responses in vivo were used in the simulations. The results indicated that kinetics were relatively insensitive to CvO2 parameters, but directly associated with kinetics. The biphasic response produced a substantial fall in CvO2 within the first 15–20s of the exercise transition (phase 1 of ). These results revealed that the main determinant of CvO2 (or O2 extraction) kinetics was the dynamic interaction of and kinetics during phase 1 of . [Copyright &y& Elsevier]

It has recently been reported that the ‘gain’ of Phase II increase in pulmonary oxygen uptake (i.e. the ‘fundamental’ increase in &Vdot;O2 per unit increase in work rate; Gp) does not attain the anticipated value of ∼10 ml min-1 W-1 following the onset of high-intensity exercise. In the present study, we hypothesised that Gp would fall significantly below 10 ml min-1 W-1 only when the work rate exceeded the so-called ‘critical power’ (CP). Seven healthy males completed several ‘square-wave’ transitions from ‘unloaded’ cycling to work rates requiring 60 and 90% of the gas exchange threshold (GET), 40 and 80% of the difference between the GET and &Vdot;O2 peak (i.e. below and above the CP, respectively), and 100, 110 and 120% of &Vdot;O2 peak. Pulmonary &Vdot;O2 was measured breath-by-breath and &Vdot;O2 kinetics were determined using non-linear regression techniques. The asymptotic Gp was significantly lower at work rates above (7.2–8.6 ml min-1 W-1) compared to work rates below (9.3–9.7 ml min-1 W-1) the CP (P < 0.05). We conclude that the gain of Phase II increase in &Vdot;O2 becomes significantly reduced when the work rate exceeds the CP. [Copyright &y& Elsevier]