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We examined the effect of heavy-intensity 'priming' exercise on the rate of adjustment of pulmonary O 2 uptake (τV˙O 2p ) initiated from elevated intensities. Fourteen men (separated into two groups: τV˙O 2p ≤25s [Fast] or τV˙O 2p >25s [Slow]) completed step-transitions from 20W to 45% lactate threshold (LT; lower-step, LS) and 45% to 90%LT (upper-step, US) performed (i) without; and (ii) with US preceded by heavy-intensity exercise (HUS). Breath-by-breath V˙O 2p and near-infrared spectroscopy-derived muscle deoxygenation ([HHb+Mb]) were measured. Compared to LS, τV˙O 2p was greater (p<0.05) in US in both Fast (LS, 19±4s; US, 30±4s) and Slow (LS, 25±5s; US, 40±11s) with τV˙O 2p in US being lower (p<0.05) in Fast. In HUS, τV˙O 2p in Slow was reduced (28±8s, p<0.05) and was not different (p>0.05) from LS or Fast group US. In Slow, τ[HHb+Mb] increased (p<0.05) in US relative to HUS; this finding coupled with a reduced τV˙O 2p indicates a priming-induced improvement in matching of muscle O 2 delivery-to-O 2 utilization during transitions from elevated intensities in those with Slow but not Fast V˙O 2p kinetics., (Copyright © 2016 Elsevier B.V. All rights reserved.)

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., (Copyright © 2015 the American Physiological Society.)

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 (V̇O(2peak)), gas exchange threshold (GET), and peak work rate (WR(peak)). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% V̇O(2peak)) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 (V̇O(2p)) 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., (Copyright © 2014 the American Physiological Society.)

Pulmonary O2 uptake (V(O₂p)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate-leg knee-extension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P(ET, CO₂)) ~40 mmHg], i.e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; P(ET, CO₂) ~20 mmHg), i.e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; P(ET, CO₂) ~40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (~5%). The V(O₂p) was measured breath by breath using mass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 V(O₂p) kinetics (τV(O₂p)) was different (P < 0.05) amongst all three conditions (CON, 19 ± 7 s; HYPO, 43 ± 17 s; and NORMO, 30 ± 8 s), while LBF kinetics (τLBF) was slower (P < 0.05) in HYPO (31 ± 9 s) compared with both CON (19 ± 3 s) and NORMO (20 ± 6 s). Similar to previous findings, HYPO was associated with slower V(O₂p) and LBF kinetics compared with CON. In the present study, preventing the fall in end-tidal P(CO₂) (NORMO) restored LBF kinetics, but not V(O₂p) kinetics, which remained 'slowed' relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower V(O₂p) kinetics observed during HYPO.

During step transitions in work rate (WR) within the moderate-intensity (MOD) exercise domain, pulmonary O2 uptake (Vo2p) kinetics are slowed, and Vo2p 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.

This study examines the effects of recovery duration following heavy-intensity "priming" exercise (Hvy) on pulmonary oxygen (O2) uptake (V̇O2p) during subsequent prolonged moderate-intensity exercise (Mod). Nine participants (6 men and 3 women) (27 ± 7 years) each completed 3 repetitions of 2 continuous Mod 1-Hvy-Mod 2 leg-cycling protocols in which Mod 2 lasted 30 min, but was preceded by a recovery duration of either 6 (R6) or 20 (R20) min at 20 W following Hvy; in each case, Mod 1 and Hvy lasted 6 min and were preceded by 6 min at 20 W. V̇O2p, heart rate (HR), and near-infrared spectroscopy (NIRS)-derived muscle deoxygenation ([HHb]) responses were modeled as a monoexponential; additionally, 60-s averages were computed every 6 min in Mod 1 and Mod 2. V̇O2p was elevated (p < 0.05) throughout Mod 2 compared with Mod 1 in both R6 and R20 (by -82 mL·min(-1) or ∼5.0%); this occurred despite a complete recovery of baseline V̇O2p (V̇O2pBsln) following R20. HR and minute ventilation (V̇E), but not [HHb], were also elevated throughout Mod 2. The phase II time constant for V̇O2p (τV̇O2p) was reduced in Mod 2 (22 s (Mod 1), 19 s (Mod 2); p < 0.05), as was the "overshoot" in the normalized [HHb]/O2 uptake ratio (p < 0.05). This study shows that V̇O2p was elevated during Mod following Hvy, regardless of recovery duration; however, a determining role for V̇O2pBsln is precluded. Furthermore, neither V̇O2p, HR, nor V̇E showed any evidence of a readjustment back to no-Hvy conditions during prolonged Mod (p > 0.05). Lastly, regardless of recovery duration, τV̇O2p was reduced to a similar extent with Hvy, likely resulting from an improved matching of local muscle O2 delivery to O2 utilization.

The matching of muscle O(2) delivery to O(2) utilization can be inferred from the adjustments in muscle deoxygenation (Δ[HHb]) and pulmonary O(2) uptake (Vo(2p)). This study examined the adjustments of Vo(2p) and Δ[HHb] during ramp incremental (RI) and constant-load (CL) exercise in adult males. Ten young adults (YA; age: 25 ± 5 yr) and nine older adults (OA; age: 70 ± 3 yr) completed two RI tests and six CL step transitions to a work rate (WR) corresponding to 1) 80% of the estimated lactate threshold (same relative WR) and 2) 50 W (same absolute WR). Vo(2p) was measured breath by breath, and Δ[HHb] of the vastus lateralis was measured using near-infrared spectroscopy. Δ[HHb]-WR profiles were normalized from baseline (0%) to peak Δ[HHb] (100%) and fit using a sigmoid function. The sigmoid slope (d) was greater (P < 0.05) in OA (0.027 ± 0.01%/W) compared with YA (0.017 ± 0.01%/W), and the c/d value (a value corresponding to 50% of the amplitude) was smaller (P < 0.05) for OA (133 ± 40 W) than for YA (195 ± 51 W). No age-related differences in the sigmoid parameters were reported when WR was expressed as a percentage of peak WR. Vo(2p) kinetics compared with Δ[HHb] kinetics for the 50-W transition were similar between YA and OA; however, Δ[HHb] kinetics during the transition to 80% of the lactate threshold were faster than Vo(2p) kinetics in both groups. The greater reliance on O(2) extraction displayed in OA during RI exercise suggests a lower O(2) delivery-to-O(2) utilization relationship at a given absolute WR compared with YA.

The relationship between the adjustment of muscle deoxygenation (∆[HHb]) and phase II VO(2p) was examined in subjects presenting with a range of slow to fast VO(2p) kinetics. Moderate intensity VO(2p) and ∆[HHb] kinetics were examined in 37 young males (24 ± 4 years). VO(2p) was measured breath-by-breath. Changes in ∆[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. VO(2p) and ∆[HHb] response profiles were fit using a mono-exponential model, and scaled to a relative % of the response (0-100%). The ∆[HHb]/∆VO(2p) ratio for each individual (reflecting the matching of O(2) distribution to O(2) utilization) was calculated as the average ∆[HHb]/∆VO(2p) response from 20 to 120 s during the exercise on-transient. Subjects were grouped based on individual phase II VO(2p) time-constant (τVO(2p)): <21 s [very fast (VF)]; 21-30 s [fast (F)]; 31-40 s [moderate (M)]; >41 s [slow (S)]. The corresponding ∆[HHb]/∆VO(2p) were 0.98 (VF), 1.05 (F), 1.09 (M), and 1.22 (S). The larger ∆[HHb]/∆VO(2p) in the groups with slower VO(2p) kinetics resulted in the ∆[HHb]/∆VO(2p) displaying a transient "overshoot" relative to the subsequent steady state level, which was progressively reduced as τVO(2) became smaller (r = 0.91). When τVO(2p) > ~20 s, the rate of adjustment of phase II VO(2p) appears to be mainly constrained by the matching of local O(2) distribution to muscle VO(2). These data suggest that in subjects with "slower" VO(2) kinetics, the rate of adjustment of VO(2) may be constrained by O(2) availability within the active tissues related to the matching of microvascular O(2) distribution to muscle O(2) utilization.

The relationship between the adjustment of muscle deoxygenation (Δ[HHb]) and phase II V(O(2p)) during moderate-intensity exercise was examined before (Mod 1) and after (Mod 2) a bout of heavy-intensity "priming" exercise. Moderate intensity V(O(2p)) and Δ[HHb] kinetics were determined in 18 young males (26 ± 3 yr). V(O(2p)) was measured breath-by-breath. Changes in Δ[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. V(O(2p)) and Δ[HHb] response profiles were fit using a monoexponential model, and scaled to a relative % of the response (0-100%). The Δ[HHb]/Vo(2) ratio for each individual (reflecting the local matching of O(2) delivery to O(2) utilization) was calculated as the average Δ[HHb]/Vo(2) response from 20 s to 120 s during the exercise on-transient. Phase II τV(O(2p)) was reduced in Mod 2 compared with Mod 1 (P < 0.05). The effective τ'Δ[HHb] remained the same in Mod 1 and Mod 2 (P > 0.05). During Mod 1, there was an "overshoot" in the Δ[HHb]/Vo(2) 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 Δ[HHb]/Vo(2) ratio and the smaller τV(O(2p)) from Mod 1 to Mod 2 (r = 0.78; P < 0.05). This study showed that a smaller τV(O(2p)) during a moderate bout of exercise subsequent to a heavy-intensity priming exercise was associated with improved microvascular O(2) delivery during the on-transient of exercise, as suggested by a smaller Δ[HHb]/Vo(2) ratio.

This study sought to determine the effect of the pre-transition work rate (WR) and WR transition magnitude on the adjustment of pulmonary oxygen uptake (VO(2p) kinetics) in older men. Seven men (69 ± 5 years; mean ± SD) each performed 4-6 cycling transitions from 20 W to either a WR corresponding to 90% estimated lactate threshold (full step, FS) or 2 equal-step transitions (lower step, LS; upper step, US) to the same end-exercise WR as in FS. Gas exchange was analysed breath-by-breath and muscle deoxygenation (∆[HHb]) was measured with NIRS. The time constant (τ) for VO(2p) was greater in US (53 ± 17 s) and FS (44 ± 11 s) compared to LS (37 ± 9 s); τVO(2p) for US also trended (p = 0.05) towards being greater than FS. The VO(2p) gain in US (9.97 ± 0.41 mL/min/W) was greater than LS (9.06 ± 1.17; p = 0.06) and FS (9.13 ± 0.54; p < 0.05). The O(2) deficit was greater in US (0.25 ± 0.08 L) than LS (0.19 ± 0.06 L); yet the 'accumulated O(2) deficit' (0.44 ± 0.13 L; O(2) deficit from LS + US) was similar to that of FS (0.42 ± 0.13 L; p = 0.38). The effective Δ[HHb] response time (τ'∆[HHb]) for US (36 ± 12 s) was greater than LS (27 ± 6 s; p = 0.07) and FS (26 ± 4 s; p < 0.05), suggesting that the slowed adjustment of muscle O(2) extraction was associated with the slowed VO(2) kinetics of the US. Despite already slowed VO(2p) kinetics, older men exhibit further slowing when small WR transitions are initiated from an elevated pre-transition WR, yet this results in no cumulative impact on O(2) deficit. This slowing in US compared to LS does not appear to be related to local O(2) availability.

The effect of hyperventilation-induced hypocapnic alkalosis (HYPO) and prior heavy-intensity exercise (HVY) on pulmonary O(2) uptake (VO(2p)) kinetics were examined in young adults (n = 7) during moderate-intensity exercise (MOD). Subjects completed leg cycling exercise during (1) normal breathing (CON, P(ET)CO(2) approximately 40 mmHg) and (2) controlled hyperventilation (HYPO, P(ET)CO(2) approximately 20 mmHg) throughout the protocol, with each condition repeated on four occasions. The protocol consisted of two MOD transitions (MOD1, MOD2) to 80% estimated lactate threshold with MOD2 preceded by HVY (Delta50%); each transition lasted 6 min and was preceded by 20 W cycling. VO(2p) was measured breath-by-breath and concentration changes in oxy- and deoxy-hemoglobin/myoglobin (Delta[HHb]) of the vastus lateralis muscle were measured by near-infrared spectroscopy. Adjustment of VO(2p) and Delta[HHb] were modeled using a mono-exponential equation by non-linear regression. During MOD1, the phase 2 time constant (tau) for VO(2p)(tauVO(2p)) was greater (P < 0.05) in HYPO (45 +/- 24 s) than CON (28 +/- 17 s). During MOD2, tauVO(2p) was reduced (P < 0.05) in both conditions (HYPO: 24 +/- 7 s, CON: 20 +/- 8 s). The Delta[Hb(TOT)] and Delta[O(2)Hb] were greater (P < 0.05) prior to and throughout MOD2. The Delta[HHb] mean response time was similar in MOD1 and MOD2, and between conditions, however, the MOD1 Delta[HHb] amplitude was greater (P < 0.05) in HYPO compared to CON, with no differences between conditions in MOD2. These findings suggest that the speeding of VO(2p) kinetics after prior HVY in HYPO was related, in part, to an increase in microvascular perfusion.

The time-course and mechanisms of adaptation of cardiorespiratory fitness were examined in 8 older (O) (68 +/- 7 yr old) and 8 young (Y) (23 +/- 5 yr old) men pretraining and at 3, 6, 9, and 12 wk of training. Training was performed on a cycle ergometer three times per week for 45 min at approximately 70% of maximal oxygen uptake (Vo(2 max)). Vo(2 max) increased within 3 wk with further increases observed posttraining in both O (+31%) and Y (+18%), (P < 0.05). Maximal cardiac output (Q(max), open-circuit acetylene) and stroke volume were higher in O and Y after 3 wk with further increases after 9 wk of training (P < 0.05). Maximal arterial-venous oxygen difference (a-vO(2 diff)) was higher at weeks 3 and 6 and posttraining compared with pretraining in O and Y (P < 0.05). In O, approximately 69% of the increase in Vo(2 max) from pre- to posttraining was explained by an increased Q(max) with the remaining approximately 31% explained by a widened a-vO(2 diff). This proportion of Q and a-vO(2 diff) contributions to the increase in Vo(2 max) was consistent throughout testing in O. In Y, 56% of the pre- to posttraining increase in Vo(2 max) was attributed to a greater Q(max) and 44% to a widened a-vO(2 diff). Early adaptations (first 3 wk) mainly relied on a widened maximal a-vO(2 diff) (approximately 66%) whereas further increases in Vo(2 max) were exclusively explained by a greater Q(max). In conclusion, with short-term training O and Y significantly increased their Vo(2 max); however, the proportion of Vo(2 max) increase explained by Q(max) and maximal a-vO(2 diff) throughout training showed a different pattern by age group.

The kinetics of pulmonary O(2) uptake (VO(2p)), limb blood flow (LBF) and deoxygenation (DeltaHHb) of the vastus lateralis (VL) and vastus medialis (VM) muscles during the transition to moderate-intensity knee-extension exercise (MOD) was examined. Seven males (27 +/- 5 years; mean +/- SD) performed repeated step transitions (n = 4) from passive exercise to MOD. Breath by breath VO(2p) femoral artery LBF, and VL and VM muscle DeltaHHb were measured, respectively, by mass spectrometer and volume turbine, Doppler ultrasound and near-infrared spectroscopy. Phase 2 VO(2p), LBF, and HHb data were fit with a mono-exponential model. The time constant (tau) of the VO(2p) and LBF response were not different (tauVO(2p), 24 +/- 6 s; tauLBF, 23 +/- 8 s). The DeltaHHb response did not differ between VL and VM in amplitude (VL 6.97 +/- 4.22 a.u.; VM 7.24 +/- 3.99 a.u.), time delay (DeltaHHb(TD): VL 17 +/- 2 s; VM 15 +/- 1 s), time constant (tauDeltaHHb: VL 11 +/- 6 s; VM 13 +/- 4 s), or effective time constant [tau'DeltaHHb (= DeltaHHb(TD) + tauDeltaHHb): VL 28 +/- 7 s; VM 28 +/- 4 s]. Adjustments in DeltaHHb in VL and VM depict a similar balance of regional O(2) delivery and utilization within the quadriceps muscle group. The tau'DeltaHHb and tauVO(2p) were similar, however, the DeltaHHb displayed an "overshoot" relative to the steady-state levels reflecting a slower alteration of microvascular blood flow (O(2) delivery) relative to O(2) utilization, necessitating a greater reliance on O(2) extraction.

The lack of estrogen in postmenopausal women not using hormone replacement therapy (HRT), compared with those using HRT, may reduce submaximal blood flow during exercise and result in an oxygen delivery limitation constraining oxygen uptake (VO(2) have been changed to V in the abstract, but will appear correctly in the body of the paper.) kinetics. The adaptation of pulmonary VO(2) (VO(2p)) during the transition to exercise in older women was examined in this study. Thirty-one healthy postmenopausal women (mean age, 61 +/- 6 years), 15 not using HRT and 16 using HRT, performed repeated exercise transitions (6 min) on a cycle, to work rates corresponding to 80% of estimated ventilatory threshold (moderate-intensity exercise) and to Delta50 (heavy-intensity exercise). There was no difference in moderate-intensity tauVO(2p) between non-HRT (40 +/- 9 s) and HRT (41 +/- 9 s) women. Similarly, there was no difference in heavy-intensity tauVO(2p) between non-HRT (44 +/- 8 s) and HRT (45 +/- 8 s) women. Thus, HRT did not affect the slowing of VO(2) kinetics of older women.

The adaptation of pulmonary oxygen uptake (VO(2)(p)) kinetics during the transition to moderate-intensity exercise is slowed in older compared with younger adults; however, this response is faster following a prior bout of heavy-intensity exercise. We have examined VO(2)(p) kinetics, pyruvate dehydrogenase (PDH) activation, muscle metabolite contents, and muscle deoxygenation in older adults [n = 6; 70 +/- 5 (67-74) yr] during moderate-intensity exercise (Mod(1)) and during moderate-intensity exercise preceded by heavy-intensity warm-up exercise (Mod(2)). The phase 2 VO(2)(p) time constant (tauVO(2)(p)) was reduced (P < 0.05) in Mod(2) (29 +/- 5 s) compared with Mod(1) (39 +/- 14 s). PDH activity was elevated (P < 0.05) at baseline prior to Mod(2) (2.1 +/- 0.6 vs. 1.2 +/- 0.3 mmol acetyl-CoA x min(-1) x kg wet wt(-1)), and the delay in attaining end-exercise activity was abolished. Phosphocreatine breakdown during exercise was reduced (P < 0.05) at both 30 s and 6 min in Mod(2) compared with Mod(1). Near-infrared spectroscopy-derived indices of muscle oxygenation were elevated both prior to and throughout Mod(2), while muscle deoxygenation kinetics were not different between exercise bouts consistent with elevated perfusion and O(2) availability. These results suggest that in older adults, faster VO(2)(p) kinetics following prior heavy-intensity exercise are likely a result of prior activation of mitochondrial enzyme activity in combination with elevated muscle perfusion and O(2) availability.

The effect of prior exercise on pulmonary O(2) uptake (Vo(2)(p)), 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)] performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Delta50%, 8 min; HVY 2) KE exercise. Vo(2)(p) was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O(2)Hb)-, deoxy (HHb)-, and total (Hb(tot)) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 Vo(2)(p), 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 + tau) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 Vo(2)(p) kinetics [HVY 1: 42 s (6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the Vo(2)(p) slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O(2)Hb and Hb(tot) were elevated throughout the on-transient following prior heavy-intensity exercise. The tauLBF [HVY 1: 39 s (7); HVY 2: 47 s (21); P = 0.48] 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 microM (10); HVY 2: 25 microM (10); P < 0.001] and the HHb-to-Vo(2)(p) ratio [(HHb/Vo(2)(p)) HVY 1: 14 microM x l(-1) x min(-1) (6); HVY 2: 17 microM x l(-1) x min(-1) (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 tauVo(2)(p) was the result of both elevated local O(2) availability and greater O(2) extraction evidenced by the greater HHb amplitude and HHb/Vo(2)(p) ratio following prior heavy-intensity exercise.

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 (thetaL) performed as a single step (S3) and in two equal steps (S1, 3 W to approximately 45% thetaL; S2, approximately 45% thetaL to approximately 90% thetaL). The time constants (tau) of pulmonary oxygen uptake (Vo2), leg blood flow (LBF), heart rate (HR), and muscle deoxygenation (HHb) were greater (P < 0.05) in S2 (tauVo2, approximately 52 s; tauLBF, approximately 39 s; tauHR, approximately 42 s; tauHHb, approximately 33 s) compared with S1 (tauVo2, approximately 24 s; tauLBF, approximately 21 s; tauHR, approximately 21 s; tauHHb, approximately 16 s), while the delay before an increase in HHb was reduced (P < 0.05) in S2 (approximately 14 s) compared with S1 (approximately 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 S1 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.

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 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 VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 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 VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. 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 VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.

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 (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p 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, tauVO2p 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.

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2 ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 +/- 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 +/- 0.21 and 2.75 +/- 0.27 cm x s(-1) x mmHg(-1) (p < 0.05) during hypoxic and 1.69 +/- 0.17 and 2.80 +/- 0.14 cm x s(-1) x mmHg(-1) (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 +/- 0.67 and 10.89 +/- 2.55 L min(-1) m mHg(-1) and 3.31 +/- 0.50 and 7.86 +/- 1.43 L x min(-1) x mmHg(-1)) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 +/- 1.29 and 49.00 +/- 1.56 mmHg CO2 during hypoxic and hyperoxic rebreathing) was likely not due to PCO2 or perfusion pressure, since PETCO2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage.

It remains unclear whether an overshoot in skeletal muscle deoxygenation (HHb; reflecting a microvascular kinetic mismatch of O2 delivery to consumption) contributes to the slowed adjustment of oxidative energy provision at the onset of exercise. We progressively reduced the fractional inspired O2 concentration (F(I,O2)) to investigate the relationship between slowed pulmonary O2 uptake (V(O2)) kinetics and the dynamics and spatial distribution of absolute[HHb]. Seven healthy men performed 8 min cycling transitions during normoxia (F(I,O2) = 0.21),moderate hypoxia (F(I,O2) = 0.16) and severe hypoxia (F(I,O2)= 0.12). V(O2) uptake was measured using a flowmeter and gas analyser system. Absolute [HHb] was quantified by multichannel,time-resolved near-infrared spectroscopy from the rectus femoris and vastus lateralis (proximal and distal regions), and corrected for adipose tissue thickness. The phase II V(O2) time constant was slowed (P

The goal of this study was to examine the time-course of changes in oxygen uptake kinetics (τVO(2p)) during step-transitions from 20 W to moderate-intensity cycling in response to endurance-training in older (O) and young (Y) women. Six O (69 ± 7 years) and 8 Y (25 ± 5 years) were tested pre-training, and at 3, 6, 9, and 12 weeks of training. VO(2p) was measured breath-by-breath using a mass spectrometer. Changes in deoxygenated-hemoglobin concentration of the vastus lateralis (∆[HHb]) were measured by near-infrared spectroscopy in Y (but this was not possible in O). VO(2p) and ∆[HHb] were modeled with a mono-exponential. Training was performed on a cycle-ergometer three times per week for 45 min at ~70% of VO(2 peak). Pre-training τVO(2p) was greater (p < 0.05) in O (55 ± 16 s) than Y (31 ± 8 s). After 3 weeks training, τVO(2p) decreased (p < 0.05) in both O (35 ± 12 s) and Y (22 ± 4 s). A pre-training "overshoot" in the normalized ∆[HHb]/VO(2p) ratio relative to the subsequent steady-state level (interpreted as a mismatch of local O(2) delivery to muscle VO(2)) was observed in Y. Three weeks of training resulted in that "overshoot" being abolished. Thus there was a training-induced speeding of VO(2) kinetics in O and Y. In the Y this appeared to be the result of improved matching of local O(2) delivery to muscle VO(2). In O, inadequate systemic O(2) distribution (as indirectly expressed by the arterial-venous O(2) difference/VO(2p) ratio) seemed to play a role for the initial slower rate of adjustment in VO(2p). [ABSTRACT FROM AUTHOR]

The adjustments of pulmonary oxygen uptake V O2p 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 V O2p femoral artery LBF (Doppler ultrasound) and muscle HHb (near-infrared spectroscopy) were measured. Phase 2V O2p LBF, and ΔHHb data were fit with a mono-exponential model. τ V O2p 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 V O2p 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 τ V O2p in OA. This faster τ'ΔHHb than τ V O2p resulted in an "overshoot" of the normalized ΔHHb/Δ V O2p 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 O(2) extraction during the transition to exercise. [ABSTRACT FROM AUTHOR]

The adaptation of pulmonary oxygen uptake (VO2p) kinetics during the transition to moderate-intensity exercise is slowed in older compared with younger adults; however, this response is faster following a prior bout of heavy-intensity exercise. We have examined VO2p kinetics, pyruvate dehydrogenase (PDH) activation, muscle metabolite contents, and muscle deoxygenation in older adults In = 6; 70 ± 5 (67-74) yr] during moderate-intensity exercise (Mod1) and during moderate-intensity exercise preceded by heavy-intensity warm-up exercise (Mod2). The phase 2 VO2p time constant (τVO2p) was reduced (P < 0.05) in Mod2 (29 ± 5 s) compared with Mod1 (39 ± 14 s). PDH activity was elevated (P < 0.05) at baseline prior to Mod2 (2.1 ± 0.6 vs. 1.2 ± 0.3 mmol acetyl-CoA∙min-1∙kg wet wt-1), and the delay in attaining end-exercise activity was abolished. Phosphocreatine breakdown during exercise was reduced (P < 0.05) at both 30 s and 6 mm in Mod2 compared with Mod1. Near-infrared spectroscopyderived indices of muscle oxygenation were elevated both prior to and throughout Mod2, while muscle deoxygenation kinetics were not different between exercise bouts consistent with elevated perfusion and O2 availability. These results suggest that in older adults, faster VO2p kinetics following prior heavy-intensity exercise are likely a result of prior activation of mitochondrial enzyme activity in combination with elevated muscle perfusion and 02 availability. [ABSTRACT FROM AUTHOR]

Abstract: Eight men were exposed to progressive isocapnic hypoxia for 10min to test the hypothesis that (i) cerebral and muscle tissue would follow similar deoxygenation profiles during an acute hypoxic ventilatory response (AHVR) test; and (ii) strong cerebrovascular responsiveness to hypoxia would be related to attenuated cerebral deoxygenation. End-tidal O2 concentration was reduced from normoxia (∼102mmHg) to ∼45mmHg while arterial oxygen saturation (%) declined from 98±1% to 77±7% (P <0.001). Near-infrared spectroscopy (NIRS)-derived local cerebral tissue (frontal lobe) deoxyhemoglobin increased 5.55±2.22μM, while oxyhemoglobin and tissue oxygenation index decreased 2.57±1.99μM and 6.2±3.4%, respectively (all P <0.001). In muscle (m. vastus lateralis) the NIRS changes from the initial normoxic level were non-significant. Cerebral blood velocity (V mean, transcranial Doppler) in the middle cerebral artery increased from 53.4±10.4 to 60.6±11.6cms−1 (P <0.001). In relation to the decline in % the mean rate of increase of V mean and AHVR were 0.33±0.19cms−1 %−1 and 0.52±0.20lmin−1 %−1, respectively. We conclude that cerebral, but not muscle, tissue shows changes reflecting a greater deoxygenation during acute hypoxia. However, the changes in NIRS parameters were not related to cerebrovascular responsiveness or ventilatory chemosensitivity during graded hypoxia. [Copyright &y& Elsevier]

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]

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]

A response to the "Letter to the Editor" entitled "Interpreting the confidence intervals of model parameters of breath-by-breath pulmonary O2 uptake" by Maria Pia Francescato and colleagues which appeared in the March 2015 issue of the journal is presented.