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The pulmonary O2 uptake (V̇o2p) response to ramp-incremental (RI) exercise increases linearly with work rate (WR) after an early exponential phase, implying that a single time constant (τ) and gain (G) describe the response. However, variability in τ and G of V̇o2p kinetics to different step increments in WR is documented. We hypothesized that the "linear" V̇o2p-WR relationship during RI exercise results from the conflation between WR-dependent changes in τ and G. Nine men performed three or four repeats of RI exercise (30 W/min) and two step-incremental protocols consisting of four 60-W increments beginning from 20 W or 50 W. During testing, breath-by-breath V̇o2p was measured by mass spectrometry and volume turbine. For each individual, the V̇o2p RI response was characterized with exponential functions containing either constant or variable τ and G values. A relationship between τ and G vs. WR was determined from the step-incremental protocols to derive the variable model parameters. τ and G increased from 21 ± 5 to 98 ± 20 s and from 8.7 ± 0.6 to 12.0 ± 1.9 ml·min(-1)·W(-1) for WRs of 20-230 W, respectively, and were best described by a second-order (τ) and a first-order (G) polynomial function of WR (lowest Akaike information criterion score). The sum of squared residuals was not different (P > 0.05) when the V̇o2p RI response was characterized with either the constant or variable models, indicating that they described the response equally well. Results suggest that τ and G increase progressively with WR during RI exercise. Importantly, these relationships may conflate to produce a linear V̇o2p-WR response, emphasizing the influence of metabolic heterogeneity in determining the apparent V̇o2p-WR relationship during RI exercise.

Skeletal muscle deoxygenated hemoglobin and myoglobin concentration ([HHb]), assessed by near-infrared spectroscopy (NIRS), is commonly used as a surrogate of regional O2 extraction (reflecting the O2 delivery-to-consumption ratio, Q̇/V̇o2). However, [HHb] change (Δ[HHb]) is also influenced by capillary-venous heme concentration, and/or small blood vessel volume (reflected in total heme; [THb]). We tested the hypotheses that Δ[HHb] is associated with O2 extraction, and insensitive to [THb], over a wide range of Q̇/V̇o2 elicited by passive head-up tilt (HUT; 10-min, 15° increments, between -10° and 75°). Steady-state common femoral artery blood flow (FBF) was measured by echo-Doppler, and time-resolved NIRS measured [HHb] and [THb] of vastus lateralis (VL) and gastrocnemius (GS) in 13 men. EMG confirmed muscles were inactive. During HUT in VL [HHb] increased linearly (57 ± 10 to 101 ± 16 μM; P < 0.05 above 15°) and was associated (r(2) ∼ 0.80) with the reduction in FBF (618 ± 75 ml/min at 0° to 268 ± 52 ml/min at 75°; P < 0.05 above 30°) and the increase in [THb] (228 ± 30 vs. 252 ± 32 μM; P < 0.05 above 15°). GS response was qualitatively similar to VL. However, there was wide variation within and among individuals, such that the overall limits of agreement between Δ[HHb] and ΔFBF ranged from -35 to +19% across both muscles. Neither knowledge of tissue O2 saturation nor vascular compliance could appropriately account for the Δ[HHb]-ΔFBF dissociation. Thus, under passive tilt, [HHb] is influenced by Q̇/V̇o2, as well as microvascular hematocrit and/or tissue blood vessel volume, complicating its use as a noninvasive surrogate for muscle microvascular O2 extraction.

During constant-power output (PO) exercise above lactate threshold (LT), pulmonary O2 uptake (...) features a developing slow component (...). This progressive increase in O2 cost of exercise is suggested to be related to the effects of muscle fatigue development. We hypothesized that peripheral muscle fatigue as assessed by contractile impairment would be associated with the ... Eleven healthy men were recruited to perform four constant-PO tests at an intensity corresponding to ~Δ60 (very heavy, VH) where Δ is 60% of the difference between LT and peak ... The VH exercise was completed for each of 3, 8, 13, and 18 min (i.e., VH3, VH8, VH13, VH18) with each preceded by 3 min of cycling at 20 W. Peripheral muscle fatigue was assessed via pre- vs. postexercise measurements of quadriceps torque in response to brief trains of electrical stimulation delivered at low (10 Hz) and high (50 Hz) frequencies. During exercise, breath-by-breath ... was measured by mass spectrometry and volume turbine. The magnitude of ... increased (P < 0.05) from 224 ± 81 ml/min at VH3 to 520 ± 119, 625 ± 134, and 678 ± 156 ml/min at VH8, VH13, and VH18, respectively. The ratio of the low-to-high frequency (10/50 Hz) response was reduced (P < 0.05) at VH3 (-12 ± 9%) and further reduced (P < 0.05) at VH8 (-25 ± 11%), VH13 (-42 ± 19%), and VH18 (-46 ± 16%), mirroring the temporal pattern of ... development. The reduction in 10/50 Hz ratio was correlated (P < 0.001, r² = 0.69) with ... amplitude. The temporal and quantitative association of decrements in muscle torque production and ... suggest a common physiological mechanism between skeletal muscle fatigue and loss of muscle efficiency. [ABSTRACT FROM AUTHOR]

The pulmonary O2 uptake (...O2p) response to ramp-incremental (RI) exercise increases linearly with work rate (WR) after an early exponential phase, implying that a single time constant (τ) and gain (G) describe the response. However, variability in τ and G of ...O2p kinetics to different step increments in WR is documented. We hypothesized that the "linear" ...O2p-WR relationship during RI exercise results from the conflation between WR-dependent changes in τ and G. Nine men performed three or four repeats of RI exercise (30 W/min) and two step-incremental protocols consisting of four 60-W increments beginning from 20 W or 50 W. During testing, breath-by-breath ...O2p was measured by mass spectrometry and volume turbine. For each individual, the ...O2p RI response was characterized with exponential functions containing either constant or variable τ and G values. A relationship between τ and G vs. WR was determined from the step-incremental protocols to derive the variable model parameters. τ and G increased from 21 ± 5 to 98 ± 20 s and from 8.7 ± 0.6 to 12.0 ±1.9 ml⋅min-1 ⋅W-1 for WRs of 20-230 W, respectively, and were best described by a second-order (τ) and a first-order (G) polynomial function of WR (lowest Akaike information criterion score). The sum of squared residuals was not different (P > 0.05) when the ...O2p RI response was characterized with either the constant or variable models, indicating that they described the response equally well. Results suggest that τ and G increase progressively with WR during RI exercise. Importantly, these relationships may conflate to produce a linear ...O2p-WR response, emphasizing the influence of metabolic heterogeneity in determining the apparent ...O2p-WR relationship during RI exercise. [ABSTRACT FROM AUTHOR]

The present study compared peak muscle deoxygenation ([HHb]peak) responses at three quadriceps sites during occlusion (OCC), ramp incremental (RI), severe- (SVR) and moderate-intensity (MOD) exercise. Seven healthy men (25 ± 4 yr) each completed a stationary cycling RI (20 W/min) test to determine [HHb]peak [at distal and proximal vastus lateralis (VLD and VLP) and rectus femoris (RF)], peak V̇o2 (V̇o2peak), gas exchange threshold (GET), and peak work rate (WRpeak). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% V̇o2peak) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 (V̇o2p) monitored continuously. Additionally, [HHb] and total hemoglobin ([Hb]tot) were monitored at rest and during subsequent OCC (250 mmHg). Site-specific adipose tissue thickness was assessed (B-mode ultrasound), and its relationship with resting [Hb]tot was used to correct absolute [HHb]. For VLD and RF, [HHb]peak was higher (P > 0.05) during OCC (VLD = 111 ± 38, RF = 114 ± 26 µM) than RI (VLD 64 ± 14, RF = 85 ± 20) and SVR (VLD = 63 ± 13, RF = 81 ± 18). [HHb]peak was similar (P > 0.05) across these conditions at the VLP (OCC = 67 ± 17, RI = 69 ± 17, SVR = 63 ± 17 µM). [HHb] peaked and then decreased prior to exercise cessation during SVR at all three muscle sites. [HHb]peak during MOD was consistently lower than other conditions at all sites. A “[HHb] reserve” exists during intense cycling at the VLD and RF, likely implying either sufficient blood flow to meet oxidative demands or insufficient diffusion time for complete equilibration. In VLP this [HHb] reserve was absent, suggesting that a critical PO2 may be challenged during intense cycling. [ABSTRACT FROM AUTHOR]

During step transitions in work rate (WR) within the moderate-intensity (MOD) exercise domain, pulmonary O2 uptake (V̇O2p) kinetics are slowed, and V̇O2p gain (ΔVO2p/ΔWR) is greater when exercise is initiated from an elevated metabolic rate. High-intensity interval training (HIT) has been shown to speed VO2p kinetics when step transitions to MOD exercise are initiated from light-intensity baseline metabolic rates. The effects of HIT on step transitions initiated from elevated metabolic rates have not been established. Therefore, this study investigated the effects of HIT on VO2p kinetics during transitions from low and elevated metabolic rates, within the MOD domain. Eight young, untrained men completed 12 sessions of HIT (spanning 4 wk). HIT consisted of 8-12 1-min intervals, cycling at a WR corresponding to 110% of pretraining maximal WR (WRmax). Pre-, mid- and posttraining, subjects completed a ramp-incremental test to determine maximum O2 uptake, WRmax, and estimated lactate threshold (θL). Participants additionally completed double-step constant-load tests, consisting of step transitions from 20 W → Δ45% θL [lower step (LS)] and Δ45 → 90% θL [upper step (US)]. HIT led to increases in maximum O2 uptake (P < 0.05) and WRmax (P < 0.01), and τVO2p of both lower and upper MOD step transitions were reduced by ∼40% (LS: 24 s → 15 s; US: 45 s → 25 s) (P < 0.01). However, the time course of adjustment of local muscle deoxygenation was unchanged in the LS and US. These results suggest that speeding of VO2p kinetics in both the LS and US may be due, in part, to an improved matching of muscle O2 utilization to microvascular O2 delivery within the working muscle following 12 sessions of HIT, although muscle metabolic adaptations cannot be discounted. [ABSTRACT FROM AUTHOR]

The relationship between the adjustment of muscle deoxygenation (Δ[HHb]) and phase II Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. during moderate-intensity exercise was examined before (Mod 1) and after (Mod 2) a bout of heavy-intensity "priming" exercise. Moderate intensity Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. and Δ[HHb] kinetics were determined in 18 young males (26 ± 3 yr). Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. was measured breath-by-breath. Changes in Δ[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. and Δ[HHb] response profiles were fit using a monoexponential model, and scaled to a relative % of the response (0-100%). The Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. ratio for each individual (reflecting the local matching of O2 delivery to O2 utilization) was calculated as the average Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. response from 20 s to 120 s during the exercise on-transient. Phase II Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. was reduced in Mod 2 compared with Mod 1 (P < 0.05). The effective τΔ[HHb] remained the same in Mod 1 and Mod 2 (P > 0.05). During Mod 1, there was an "overshoot" in the Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. ratio (1.08; P < 0.05) that was not present during Mod 2 (1.01; P > 0.05). There was a positive correlation between the reduction in the Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. ratio and the smaller Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. from Mod 1 to Mod 2 (r = 0.78; P < 0.05). This study showed that a smaller Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. during a moderate bout of exercise subsequent to a heavy-intensity priming exercise was associated with improved microvascular O2 delivery during the on-transient of exercise, as suggested by a smaller Due to image rights restrictions, multiple line equation(s) cannot be graphically displayed. ratio. [ABSTRACT FROM AUTHOR]

The effect of hyperventilation-induced hypocapnic alkalosis (Hypo) on the adjustment of pulmonary O2 uptake (V̇o2p) and leg femoral conduit artery ("bulk") blood flow (LBF) during moderate-intensity exercise (Mod) was examined in eight young male adults. Subjects completed four to six repetitions of alternate-leg knee-extension exercise during normal breathing [Con; end-tidal partial pressure of CO2 (PETCO2) ~40 mmHg] and sustained hyperventilation (Hypo; PETCO2 ~20 mmHg). Increases in work rate were made instantaneously from baseline (3 W) to Mod (80% estimated lactate threshold). V̇o2p was measured breath by breath by mass spectrometry and volume turbine, and LBF (calculated from mean femoral artery blood velocity and femoral artery diameter) was measured simultaneously by Doppler ultrasound. Concentration changes of deoxy (Δ[HHb])-, oxy (Δ[O2Hb])-, and total hemoglobin-myoglobin (Δ[HbTot) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). The kinetics of V̇o2p, LBF, and Δ[HHb] were modeled using a monoexponential equation by nonlinear regression. The time constants for the phase 2 V̇o2p (Hypo, 49 ± 26 s; Con, 28 ± 8 s) and LBF (Hypo, 46 ± 16 s: Con, 23 ± b s) were greater (P < 0.05) in Hypo compared with Con. However, the mean response time for the overall Δ[HHb] response was not different between conditions (Hypo, 23 ± 5 s; Con, 24 ± 3 s), whereas the Δ[HHb] amplitude was greater (P < 0.05) in Hypo (8.05 ± 7.47 a.u.) compared with Con (6.69 ± 6.31 a.u.). Combined, these results suggest that hyperventilation-induced hypocapnic alkalosis is associated with slower convective (i.e., slowed femoral 'artery and microvascular blood flow) and diffusive (i.e., greater fractional O2 extraction for a given ΔV̇2p) O2 delivery, which may contribute to the hyperventilation-induced slowing of V̇o2p (and muscle O2 utilization) kinetics. [ABSTRACT FROM AUTHOR]

The time course and mechanisms of adjustment of pulmonary oxygen uptake (Vo2) kinetics (time constant τVo2p) were examined during step transitions from 20 W to moderate-intensity cycling in eight older men (0; 68 ± 7 yr) and eight young men (Y; 23 ± S yr) before training and at 3, 6, 9, and 12 wk of endurance training. Vo2p, was measured breath by breath with a volume turbine and a mass spectrometer. Changes in deoxygenated hemoglobin concentration (Δ[HHb]) were measured by nearinfrared spectroscopy. Vo2p, and Δ[HHb] were modeled with a monoexponential model. Training was performed on a cycle ergometer three times per week for 45 mm at ∼70% of peak Vo2. Pretraining τVo2p was greater (P < 0.05) in 0 (43 ± 10 s) than Y (34 ± 8 s). τVo2p decreased (P < 0.05) by 3 wk of training in both 0 (35 ± 9 s) and Y (22 ± 8 s), with no further changes thereafter. The pretraining overall adjustment of Δ[HHb] was faster than τVo2p in both O and Y, resulting in Δ[HHb]/Vo2p displaying an "overshoot" during the transient relative to the subsequent steady-state level. After 3 wk of training the Δ[HHb]/Vo2p overshoot was attenuated in both O and Y. With further training, this overshoot persisted in O but was eliminated after 6 wk in Y. The training-induced speeding of Vo2p, kinetics in O and Y at 3 wk of training was associated with an improved matching of local O2 delivery to muscle Vo2 (as represented by a lower Δ[HHb]/Vo2p). The continued overshoot in Δ[HHb]/Vo2p in O may reflect a reduced vasodilatory responsiveness that may limit muscle blood flow distribution during the on-transient of exercise. [ABSTRACT FROM AUTHOR]

The effect of prior exercise on pulmonary O2 uptake (VO2p), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee- extension KE) exercise was examined. Seven subjects [27 (5) yr; mean (SD)1 performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Δ50%, 8 mm; HVY 2) KE exercise. VO2p, was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O2Hb)-, deoxy (HHb)-, and total (Hbtot) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 VO2p, LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb - MRT = TD + τ) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 VO2p kinetics [HVY 1: 42s(6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY I: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the VO2p slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O2Hb and Hbtot were elevated throughout the on-transient following prior heavy-intensity exercise. The τLBF [HVY 1: 39 s (7); HVY 2: 47 s(21); P = 0.481 and HHb-MRT [HVY 1: 23 s (4); HVY 2: 21 s (7); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 μM (10); HVY 2: 25 μM (10); P < 0.0011 and the HHb-to-VO2p ratio [(HHb/VO2p) HVY 1: 14 μM·1-1·min-1 (6); HVY 2: 17 μM·1-1·min-1 (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 πVO2p was the result of both elevated local O2 availability and greater O2 extraction evidenced by the greater HHb amplitude and HHb/O2p ratio following prior heavy-intensity exercise. [ABSTRACT FROM AUTHOR]

Six male subjects [23 yr (SD 4)] performed repetitions (6-8) of two-legged, moderate-intensity, knee-extension exercise during two separate protocols that included step transitions from 3 W to 90% estimated lactate threshold (θL) performed as a single step (S3) and in two equal steps (S1, 3 W to ∼45% θL; S2, ∼45% θL to ∼90% θL). The time constants (τ) of pulmonary oxygen uptake (Vo2), leg blood flow (LBF), heart rate (HR), and muscle deoxygenation (HHb) were greater (P < 0.05) in S2 (τVo2, ∼52 s; θLBF, ∼ 39 s; θHR, ∼42 s; θHHb, ∼33 s) compared with S1 (#x03B8;Vo2, ∼24 s; θLBF, ∼21 s; θHR, ∼21 s; θHHb, ∼16 s), while the delay before an increase in HHb was reduced (P < 0.05) in S2 (∼ 14 s) compared with S1 (∼20 s). The Vo2 and HHb amplitudes were greater (P < 0.05) in S2 compared with S1, whereas the LBF amplitude was similar in S2 and S1. Thus the slowed Vo2 response in S2 compared with S 1 is consistent with a mechanism whereby Vo2 kinetics is limited, in part, by a slowed adaptation of blood flow and/or O2 transport when exercise was initiated from a baseline of moderate-intensity exercise. [ABSTRACT FROM AUTHOR]

It has been suggested that, during heavy-intensity exercise, O2 delivery may limit oxygen uptake (Vo2) kinetics; however, there are limited data regarding the relationship of blood flow and Vo2 kinetics for heavy-intensity exercise. The purpose was to determine the exercise un-transient time course of femoral artery blood flow (Qleg) in relation to Vo2 during heavy-intensity, single-leg, knee-extension exercise. Five young subjects performed five to eight repeats of heavy-intensity exercise with measures of breath-by-breath pulmonary Vo2 and Doppler ultrasound femoral artery mean blood velocity and vessel diameter. The phase 2 time frame for Vo2 and Qleg was isolated and fit with a monoexponent to characterize the amplitude and time course of the responses. Amplitude of the phase 3 response was also determined. The phase 2 time constant for Vo2 of 29.0 s and time constant for Qleg of 24.5 s were not different. The change (A) in Vo2 response to the end of phase 2 of 0.317 1/min was accompanied by a ΔQleg of 2.35 1/min, giving a ΔQleg-to-ΔVo2 ratio of 7.4. A slow-component Vo2 of 0.098 l/min was accompanied by a further Qleg increase of 0.72 l/min (ΔQleg-to-ΔVo2 ratio = 7.3). Thus the time course of Qleg was similar to that of muscle Vo2 (as measured by the phase 2 Vo2 kinetics), and throughout the on-transient the amplitude of the Qleg increase achieved (or exceeded) the Qleg-to-Vo2 ratio steady-state relationship (ratio ∼4.9). Additionally, the Vo2 slow component was accompanied by a relatively large rise in Qleg, with the increased O2 delivery meeting the increased Vo2. Thus, in heavy-intensity, single-leg, knee-extension exercise, the amplitude and kinetics of blood flow to the exercising limb appear to be closely linked to the Vo2 kinetics. [ABSTRACT FROM AUTHOR]

The purpose was to examine the adaptation of pulmonary O2 uptake (VO2p)and deoxygenation of the vastus lateralis muscle at the onset of heavy-intensity, constant-load cycling exercise in young (Y; 24 ± 4 yr; mean ± SD; n = 5) and older (O; 68 ± 3 yr; n = 6) adults. Subjects performed repeated transitions on 4 separate days from 20 W to a work rate corresponding to heavy-intensity exercise. VO2p was measured breath by breath. The concentration changes in oxyhemoglobin, deoxyhemoglobin (HHb), and total hemoglobin/myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). VO2p data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb-near-infrared spectroscopy data were filtered and averaged to 5-s bins. A monoexponential model was used to fit VO2p [phase 2, time constant (τ) of VO2p] and HHb [following the time delay (TD) from exercise onset to the start of an increase in HHb] data. The τVO2p was slower (P < 0.001) in O (49 ± 8 s) than Y (29 ± 4 s). The HHb TD was similar in O (8 ± 3 s) and Y (7 ± 1 s); however, the τ HHb following TD was faster (P < 0.05) in O (8 ± 2 s) than Y (14 ± 2 s). The slower VO2p kinetics and faster muscle deoxygenation in O compared with Y during heavy-intensity exercise imply that the kinetics of muscle perfusion are slowed relatively more than those of VO2p in O. This suggests that the slowed VO2p kinetics in O may be a consequence of a slower adaptation of local muscle blood flow relative to that in Y. [ABSTRACT FROM AUTHOR]

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (τ&Vdot;o2) was examined in young adults exhibiting relatively fast (FK; τ&Vdot;o2 < 30 s; n = 6) and slow (SK; τ&Vdot;o2 > 30 s; n = 6) &Vdot;o2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak &Vdot;o2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. &Vdot;o2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respec- tively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). τ&Vdot;o2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 ± 5 s vs. 26 ± 5 s, respectively) and SK (30 ± 8 s vs. 45 ± 11 s, respectively); linear regression analysis showed a greater ‘speeding’ of &Vdot;o2 kinetics in subjects exhibiting a greater Mod1 τ&Vdot;o2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Modl. The delay before the increase in HHb was reduced (P < 0.05) in Mod2, whereas the HHb mean response time was reduced (P < 0.05) in FK (Mod2, 22 ± 3 s; Mod1 32 ± 11 s) but not different in SK (Mod2, 36 ± 13 s; Mod1, 34 ± 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of &Vdot;o2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked. [ABSTRACT FROM AUTHOR]

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 ± 3 yr) and older (n = 5; 68 ± 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hbtot) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; τ) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 ± 9 µM; young subjects: 9 ± 8 µM) and Hbtot (older subjects: 12 ± 8 µM; young subjects: 14 ± 10 µM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, τVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 ± 7 s) than no warm-up (38 ± 5 s), whereas in young subjects, τVO2p was similar in no warm-up (26 ± 7 s) and heavy warm-up (25 ± 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery. [ABSTRACT FROM AUTHOR]

Phase 2 pulmonary O2 up take (VO2p) kinetics are slowed with aging. To examine the effect of aging on the adaptation of VO2p, and deoxygenation of the vastus lateralis muscle at the onset of moderate-intensity constant-load cycling exercise, young (Y) (n = 6; 25 ± 3 yr) and older (O) (n = 6; 68 ± 3 yr) adults performed repeated transitions from 20 W to work rates corresponding to moderate-intensity (80% estimated lactate threshold) exercise. Breath-by-breath VO2p was measured by mass spectrometer and volume turbine. Deoxy (HHb)-, oxy-, and total Hb and/or myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). VO2p data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb data were filtered and averaged to 5-s bins. VO2p data were fit with a monoexponential model for phase2, and HHb data were analyzed to determine the time delay from exercise onset to the start of an increase in HHb and thereafter were fit with a single-component exponential model. The phase 2 time constant for VO2p was slower (P < 0.01) in O (Y: 26 ± 7 s, O: 42 ± 9 s), whereas the delay before an increase in HHb (Y: 12 ± 2 s; O: 11 ± 1 s) and the time constant for HHb after the time delay (Y: 13 ± 10 s; O: 9 ± 3 s) were similar in Y and O. However, the increase in HHb for a given increase in VO2p (Y: 7 ± 2 µM·l-1·min-1; O: 13 ± 4 µM·l-1·min-1) was greater (P < 0.01) in O compared with Y. The slower VO2p kinetics in O compared with Y adults was accompanied by a slower increase of local muscle blood flow and O2 delivery discerned from a faster and greater muscle deoxygenation relative to VO2p in O. [ABSTRACT FROM AUTHOR]

Examines the temporal relationship between kinetics of pulmonary oxygen uptake with deoxygenation of the vastus lateralis muscle during moderate intensity leg-cycling exercise. Result of sampling by infrared spectroscopy; Mismatch of local muscle oxygen consumption with perfusion; Adaptation of pulmonary oxygen uptake.