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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.

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.

Gastrocnemius muscle phosphocreatine ([PCr]) and hydrogen ion ([H(+)]) were measured using (31)P-magnetic resonance spectroscopy during repeated bouts of 10-s heavy-intensity (HI) exercise and 5-s rest compared with continuous (CONT) HI exercise. Recreationally active male subjects (n = 7; 28 yr ± 9 yr) performed on separate occasions 12 min of isotonic plantar flexion (0.75 Hz) CONT and intermittent (INT; 10-s exercise, 5-s rest) exercise. The HI power output in both CONT and INT was set at 50% of the difference between the power output associated with the onset of intracellular acidosis and peak exercise determined from a prior incremental plantar flexion protocol. Intracellular concentrations of [PCr] and [H(+)] were calculated at 4 s and 9 s of the work period and at 4 s of the rest period in INT and during CONT exercise. [PCr] and [H(+)] (mean ± SE) were greater at 4 s of the rest periods vs. 9 s of exercise over the course of the INT exercise bout: [PCr] (20.7 mM ± 0.6 vs. 18.7 mM ± 0.5; P < 0.01); [H(+)] (370 nM ± 13.50 vs. 284 nM ± 13.6; P < 0.05). Average [H(+)] was similar for CONT vs. INT. We therefore suggest that there is a glycolytic contribution to ATP recovery during the very short rest period (<5 s) of INT and that the greater average power output of CONT did not manifest in greater [H(+)] and greater glycolytic contribution compared with INT exercise.

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity "priming" exercise (Hvy) on pulmonary O(2) uptake (Vo(2p)) kinetics during moderate-intensity exercise (Mod). Breath-by-breath Vo(2p) and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 ± 4 yr) during repetitions of a Mod 1-Hvy-Mod 2 protocol, where each of the 6-min (Mod or Hvy) leg-cycling bouts was separated by 6 min at 20 W. Subjects were exposed to Hypo [fraction of inspired O(2) (Fi(O(2))) = 15%, Mod 2 + Hypo] or "sham" (Fi(O(2)) = 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 + Hypo). On-transient Vo(2p) and [HHb] responses were modeled as a monoexponential. Data were scaled to a relative percentage of the response (0-100%), the signals were time-aligned, and the individual [HHb]-to-Vo(2) ratio was calculated. Compared with control (Mod 1), τVo(2p) and the O(2) deficit (26 ± 7 s and 638 ± 144 ml, respectively) were reduced (P < 0.05) in Mod 2-N (20 ± 5 s and 529 ± 196 ml) and increased (P < 0.05) in Mod 1 + Hypo (34 ± 14 s and 783 ± 184 ml); in Mod 2 + Hypo, τVo(2p) was increased (30 ± 8 s, P < 0.05), yet O(2) deficit was unaffected (643 ± 193 ml, P > 0.05). The modest "overshoot" in the [HHb]-to-Vo(2) ratio (reflecting an O(2) delivery-to-utilization mismatch) in Mod 1 (1.06 ± 0.04) was abolished in Mod 2-N (1.00 ± 0.05), persisted in Mod 2 + Hypo (1.09 ± 0.07), and tended to increase in Mod 1 + Hypo (1.10 ± 0.09, P = 0.13). The present data do not support an "O(2) delivery-independent" speeding of τVo(2p) following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O(2) delivery likely governs the rate of adjustment of Vo(2) at τVo(2p) greater than ∼20 s.

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.

The effect of hyperventilation-induced hypocapnic alkalosis (Hypo) on the adjustment of pulmonary O2 uptake (VO2p) 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) approximately 40 mmHg] and sustained hyperventilation (Hypo; PetCO2 approximately 20 mmHg). Increases in work rate were made instantaneously from baseline (3 W) to Mod (80% estimated lactate threshold). VO2p 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 (Delta[HHb])-, oxy (Delta[O2Hb])-, and total hemoglobin-myoglobin (Delta[HbTot]) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). The kinetics of VO2p, LBF, and Delta[HHb] were modeled using a monoexponential equation by nonlinear regression. The time constants for the phase 2 VO2p (Hypo, 49+/-26 s; Con, 28+/-8 s) and LBF (Hypo, 46+/-16 s; Con, 23+/-6 s) were greater (P<0.05) in Hypo compared with Con. However, the mean response time for the overall Delta[HHb] response was not different between conditions (Hypo, 23+/-5 s; Con, 24+/-3 s), whereas the Delta[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 DeltaVO2p) O2 delivery, which may contribute to the hyperventilation-induced slowing of VO2p (and muscle O2 utilization) kinetics.

The time course and mechanisms of adjustment of pulmonary oxygen uptake (V(O(2))) kinetics (time constant tauV(O(2p))) were examined during step transitions from 20 W to moderate-intensity cycling in eight older men (O; 68 +/- 7 yr) and eight young men (Y; 23 +/- 5 yr) before training and at 3, 6, 9, and 12 wk of endurance training. V(O(2p)) was measured breath by breath with a volume turbine and a mass spectrometer. Changes in deoxygenated hemoglobin concentration (Delta[HHb]) were measured by near-infrared spectroscopy. V(O(2p)) and Delta[HHb] were modeled with a monoexponential model. Training was performed on a cycle ergometer three times per week for 45 min at approximately 70% of peak V(O(2)). Pretraining tauV(O(2p)) was greater (P < 0.05) in O (43 +/- 10 s) than Y (34 +/- 8 s). tauV(O(2p)) decreased (P < 0.05) by 3 wk of training in both O (35 +/- 9 s) and Y (22 +/- 8 s), with no further changes thereafter. The pretraining overall adjustment of Delta[HHb] was faster than tauV(O(2p)) in both O and Y, resulting in Delta[HHb]/V(O(2p)) displaying an "overshoot" during the transient relative to the subsequent steady-state level. After 3 wk of training the Delta[HHb]/V(O(2p)) 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 V(O(2p)) kinetics in O and Y at 3 wk of training was associated with an improved matching of local O(2) delivery to muscle V(O(2)) (as represented by a lower Delta[HHb]/V(O(2p))). The continued overshoot in Delta[HHb]/V(O(2p)) in O may reflect a reduced vasodilatory responsiveness that may limit muscle blood flow distribution during the on-transient of exercise.

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 early time course of adaptation of pulmonary O(2) uptake (Vo(2)(p)) (reflecting muscle O(2) consumption) and muscle deoxygenation kinetics (reflecting the rate of O(2) extraction) were examined during high-intensity interval (HIT) and lower-intensity continuous endurance (END) training. Twelve male volunteers underwent eight sessions of either HIT (8-12 x 1-min intervals at 120% maximal O(2) uptake separated by 1 min of rest) or END (90-120 min at 65% maximal O(2) uptake). Subjects completed step transitions to a moderate-intensity work rate ( approximately 90% estimated lactate threshold) on five occasions throughout training, and ramp incremental and constant-load performance tests were conducted at pre-, mid-, and posttraining periods. Vo(2)(p) was measured breath-by-breath by mass spectrometry and volume turbine. Deoxygenation (change in deoxygenated hemoglobin concentration; Delta[HHb]) of the vastus lateralis muscle was monitored by near-infrared spectroscopy. The fundamental phase II time constants for Vo(2)(p) (tauVo(2)) and deoxygenation kinetics {effective time constant, tau' = (time delay + tau), Delta[HHb]} during moderate-intensity exercise were estimated using nonlinear least-squares regression techniques. The tauVo(2) was reduced by approximately 20% (P < 0.05) after only two training sessions and by approximately 40% (P < 0.05) after eight training sessions (i.e., posttraining), with no differences between HIT and END. The tau'Delta[HHb] ( approximately 20 s) did not change over the course of eight training sessions. These data suggest that faster activation of muscle O(2) utilization is an early adaptive response to both HIT and lower-intensity END training. That Delta[HHb] kinetics (a measure of fractional O(2) extraction) did not change despite faster Vo(2)(p) kinetics suggests that faster kinetics of muscle O(2) utilization were accompanied by adaptations in local muscle (microvascular) blood flow and O(2) delivery, resulting in a similar "matching" of blood flow to O(2) utilization. Thus faster kinetics of Vo(2)(p) during the transition to moderate-intensity exercise occurs after only 2 days HIT and END training and without changes to muscle deoxygenation kinetics, suggesting concurrent adaptations to microvascular perfusion.

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 effects of prior heavy-intensity exercise on O(2) uptake (Vo(2)) kinetics of a second heavy exercise may be due to vasodilation (associated with metabolic acidosis) and improved muscle blood flow. This study examined the effect of prior heavy-intensity exercise on femoral artery blood flow (Qleg) and its relationship with Vo(2) kinetics. Five young subjects completed five to eight repeats of two 6-min bouts of heavy-intensity one-legged, knee-extension exercise separated by 6 min of loadless exercise. Vo(2) was measured breath by breath. Pulsed-wave Doppler ultrasound was used to measure Qleg. Vo(2) and blood flow velocity data were fit using a monoexponential model to identify phase II and phase III time periods and estimate the response amplitudes and time constants (tau). Phase II Vo(2) kinetics was speeded on the second heavy-intensity exercise [mean tau (SD), 29 (10) s to 24 (10) s, P < 0.05] with no change in the phase II (or phase III) amplitude. Qleg was elevated before the second exercise [1.55 (0.34) l/min to 1.90 (0.25) l/min, P < 0.05], but the amplitude and time course [tau, 25 (13) s to 35 (13) s] were not changed, such that throughout the transient the Qleg (and DeltaQleg/DeltaVo(2)) did not differ from the prior heavy exercise. Thus Vo(2) kinetics were accelerated on the second exercise, but the faster kinetics were not associated with changes in Qleg. Thus limb blood flow appears not to limit Vo(2) kinetics during single-leg heavy-intensity exercise nor to be the mechanism of the altered Vo(2) response after heavy-intensity prior exercise.

It has been suggested that, during heavy-intensity exercise, O(2) 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 on-transient time course of femoral artery blood flow (Q(leg)) 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 Q(leg) 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 Q(leg) of 24.5 s were not different. The change (Delta) in .VO2 response to the end of phase 2 of 0.317 l/min was accompanied by a DeltaQ(leg) of 2.35 l/min, giving a DeltaQ(leg)-to-Delta.VO2 ratio of 7.4. A slow-component .VO2 of 0.098 l/min was accompanied by a further Q(leg) increase of 0.72 l/min (DeltaQ(leg)-to-Delta.VO2 ratio = 7.3). Thus the time course of Q(leg) was similar to that of muscle .VO2 (as measured by the phase 2 .VO2 kinetics), and throughout the on-transient the amplitude of the Q(leg) increase achieved (or exceeded) the Q(leg)-to-.VO2 ratio steady-state relationship (ratio approximately 4.9). Additionally, the .VO2 slow component was accompanied by a relatively large rise in Q(leg), with the increased O(2) delivery meeting the increased Vo(2). 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.

The purpose was to examine the adaptation of pulmonary O(2) uptake (Vo(2p)) 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. Vo(2p) 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). Vo(2p) 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 Vo(2p) [phase 2, time constant (tau) of Vo(2p)] and HHb [following the time delay (TD) from exercise onset to the start of an increase in HHb] data. The tauVo(2p) 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 tau HHb following TD was faster (P < 0.05) in O (8 +/- 2 s) than Y (14 +/- 2 s). The slower Vo(2p) 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 Vo(2p) in O. This suggests that the slowed Vo(2p) kinetics in O may be a consequence of a slower adaptation of local muscle blood flow relative to that in Y.

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.

The purpose of this study was to describe the longitudinal (10 yr) decline in aerobic power [maximal O(2) uptake (Vo(2 max))] and anaerobic threshold [ventilatory threshold (T(Ve))] of older adults living independently in the community. Ten years after initial testing, 62 subjects (34 men, mean age 73.5 +/- 6.4 yr; 28 women, 72.1 +/- 5.3 yr) achieved Vo(2 max) criteria during treadmill walking tests to the limit of tolerance, with T(Ve) determined in a subset of 45. Vo(2 max) in men showed a rate of decline of -0.43 ml.kg(-1).min(-1).yr(-1), and the decline in Vo(2 max) was consequent to a lowered maximal heart rate with no change in the maximum O(2) pulse. The women showed a slower rate of decline of Vo(2 max) of -0.19.ml.kg(-1).min(-1).yr(-1) (P < 0.05), again with a lowered HR(max) and unchanged O(2) pulse. In this sample, lean body mass was not changed over the 10-yr period. Changes in Vo(2 max) were not significantly related to physical activity scores. T(Ve) showed a nonsignificant decline in both men and women. Groupings of young-old (65-72 yr at follow-up) vs. old-old (73-90 yr at follow-up) were examined. In men, there were no differences in the rate of Vo(2 max) decline. The young-old women showed a significant decline in Vo(2 max), whereas old-old women, initially at a Vo(2 max) of 19.4 +/- 3.1 ml.kg(-1).min(-1), showed no loss in Vo(2 max). The longitudinal data, vs. cross-sectional analysis, showed a greater decline for men but similar estimates of the rates of change in women. Thus the 10-yr longitudinal study of the cohort of community-dwelling older adults who remained healthy, ambulatory, and independent showed a 14% decline in Vo(2 max) in men, and a smaller decline of 7% in women, with the oldest women showing little change over the 10-yr period.

Phase 2 pulmonary O(2) uptake (Vo(2(p))) kinetics are slowed with aging. To examine the effect of aging on the adaptation of Vo(2(p)) 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 Vo(2(p)) 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). Vo(2(p)) data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb data were filtered and averaged to 5-s bins. Vo(2(p)) data were fit with a monoexponential model for phase 2, 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 Vo(2(p)) 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 Vo(2(p)) (Y: 7 +/- 2 microM x l(-1) x min(-1); O: 13 +/- 4 microM x l(-1) x min(-1)) was greater (P < 0.01) in O compared with Y. The slower Vo(2(p)) kinetics in O compared with Y adults was accompanied by a slower increase of local muscle blood flow and O(2) delivery discerned from a faster and greater muscle deoxygenation relative to Vo(2(p)) in O.

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (Vo -->Vo2p) and deoxygenation of the vastus lateralis muscle was examined during moderate-intensity leg-cycling exercise. Young adults (5 men, 6 women; 23 +/- 3 yr; mean +/- SD) performed repeated transitions on 3 separate days from 20 W to a constant work rate corresponding to 80% of lactate threshold. Breath-by-breath Vo2p was measured by mass spectrometer and volume turbine. Deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin and myoglobin were sampled each second by near-infrared spectroscopy (Hamamatsu NIRO-300). Vo2p data were filtered, interpolated to 1 s, and averaged to 5-s bins; HHb data were averaged to 5-s bins. Phase 2 Vo2p data were fit with a monoexponential model. For HHb, a time delay (TDHHb) from exercise onset to an increase in HHb was determined, and thereafter data were fit with a monoexponential model. The time constant for Vo2p (30 +/- 8 s) was slower (P < 0.01) than that for HHb (10 +/- 3 s). The TDHHb before an increase in HHb was 13 +/- 2 s. The possible mechanisms of the TDHHb are discussed with reference to metabolic activation and matching of local muscle O2 delivery and O2 utilization. After this initial TDHHb, the kinetics of local muscle deoxygenation were faster than those of phase 2 Vo2p (and presumably muscle O2 consumption), reflecting increased O2 extraction and a mismatch between local muscle O2 consumption and perfusion.

This study examined the effect of heavy-intensity warm-up exercise on O(2) uptake (VO(2)) kinetics at the onset of moderate-intensity (80% ventilation threshold), constant-work rate exercise in eight older (65 +/- 2 yr) and seven younger adults (26 +/- 1 yr). Step increases in work rate from loadless cycling to moderate exercise (Mod(1)), heavy exercise, and moderate exercise (Mod(2)) were performed. Each exercise bout was 6 min in duration and separated by 6 min of loadless cycling. VO(2) kinetics were modeled from the onset of exercise by use of a two-component exponential model. Heart rate (HR) kinetics were modeled from the onset of exercise using a single exponential model. During Mod(1), the time constant (tau) for the predominant rise in VO(2) (tau VO(2)) was slower (P < 0.05) in the older adults (50 +/- 10 s) than in young adults (19 +/- 5 s). The older adults demonstrated a speeding (P < 0.05) of VO(2) kinetics when moderate-intensity exercise (Mod(2)) was preceded by high-intensity warm-up exercise (tau VO(2), 27 +/- 3 s), whereas young adults showed no speeding of VO(2) kinetics (tau VO(2), 17 +/- 3 s). In the older and younger adults, baseline HR preceding Mod(2) was elevated compared with Mod(1), but the tau for HR kinetics was slowed (P < 0.05) in Mod(2) only for the older adults. Prior heavy-intensity exercise in old, but not young, adults speeded VO(2) kinetics during Mod(2). Despite slowed HR kinetics in Mod(2) in the older adults, an elevated baseline HR before the onset of Mod(2) may have led to sufficient muscle perfusion and O(2) delivery. These results suggest that, when muscle blood flow and O(2) delivery are adequate, muscle O(2) consumption in both old and young adults is limited by intracellular processes within the exercising muscle.