Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak Vo(2) with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and Vo(2) kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME conditions (L) for baseline Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) response in phase II was significantly smaller (mean +/- SE: C: 25.1 +/- 3.0 s; L: 21.8 +/- 3.3 s; P < 0.05), and the amplitude of the Vo(2) slow component was significantly greater (C: 240 +/- 47 ml/min; L: 363 +/- 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) kinetics after L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial Vo(2) by nitric oxide. The cause of the larger Vo(2) slow-component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.     

Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise.

We hypothesized that a higher pedal rate (assumed to result in a greater proportional contribution of type II motor units) would be associated with an increased amplitude of the O(2) uptake (Vo(2)) slow component during heavy-cycle exercise. Ten subjects (mean +/- SD, age 26 +/- 4 yr, body mass 71.5 +/- 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of 35, 75, and 115 rpm. The exercise power output was set at 50% of the difference between the pedal rate-specific ventilatory threshold and peak Vo(2), and the baseline power output was adjusted to account for differences in the O(2) cost of unloaded pedaling. The gain of the Vo(2) primary component was significantly higher at 35 rpm compared with 75 and 115 rpm (mean +/- SE, 10.6 +/- 0.3, 9.5 +/- 0.2, and 8.9 +/- 0.4 ml. min(-1). W(-1), respectively; P < 0.05). The amplitude of the Vo(2) slow component was significantly greater at 115 rpm (328 +/- 29 ml/min) compared with 35 rpm (109 +/- 30 ml/min) and 75 rpm (202 +/- 38 ml/min) (P < 0.05). There were no significant differences in the time constants or time delays associated with the primary and slow components across the pedal rates. The change in blood lactate concentration was significantly greater at 115 rpm (3.7 +/- 0.2 mM) and 75 rpm (2.8 +/- 0.3 mM) compared with 35 rpm (1.7 +/- 0.4 mM) (P < 0.05). These data indicate that pedal rate influences Vo(2) kinetics during heavy exercise at the same relative intensity, presumably by altering motor unit recruitment patterns.     

Addition of inspiratory resistance increases the amplitude of the slow component of O2 uptake kinetics.

The contribution of respiratory muscle work to the development of the O(2) consumption (Vo(2)) slow component is a point of controversy because it has been shown that the increased ventilation in hypoxia is not associated with a concomitant increase in Vo(2) slow component. The first purpose of this study was thus to test the hypothesis of a direct relationship between respiratory muscle work and Vo(2) slow component by manipulating inspiratory resistance. Because the conditions for a Vo(2) slow component specific to respiratory muscle can be reached during intense exercise, the second purpose was to determine whether respiratory muscles behave like limb muscles during heavy exercise. Ten trained subjects performed two 8-min constant-load heavy cycling exercises with and without a threshold valve in random order. Vo(2) was measured breath by breath by using a fast gas exchange analyzer, and the Vo(2) response was modeled after removal of the cardiodynamic phase by using two monoexponential functions. As anticipated, when total work was slightly increased with loaded inspiratory resistance, slight increases in base Vo(2), the primary phase amplitude, and peak Vo(2) were noted (14.2%, P < 0.01; 3.5%, P > 0.05; and 8.3%, P < 0.01, respectively). The bootstrap method revealed small coefficients of variation for the model parameter, including the slow-component amplitude and delay (15 and 19%, respectively), indicating an accurate determination for this critical parameter. The amplitude of the Vo(2) slow component displayed a 27% increase from 8.1 +/- 3.6 to 10.3 +/- 3.4 ml. min(-1). kg(-1) (P < 0.01) with the addition of inspiratory resistance. Taken together, this increase and the lack of any differences in minute volume and ventilatory parameters between the two experimental conditions suggest the occurrence of a Vo(2) slow component specific to the respiratory muscles in loaded condition.     

Oxygen uptake kinetics during treadmill running in boys and men.

The purpose of this study was to compare the kinetics of the oxygen uptake (VO(2)) response of boys to men during treadmill running using a three-phase exponential modeling procedure. Eight boys (11-12 yr) and eight men (21-36 yr) completed an incremental treadmill test to determine lactate threshold (LT) and maximum VO(2). Subsequently, the subjects exercised for 6 min at two different running speeds corresponding to 80% of VO(2) at LT (moderate exercise) and 50% of the difference between VO(2) at LT and maximum VO(2) (heavy exercise). For moderate exercise, the time constant for the primary response was not significantly different between boys [10.2 +/- 1.0 (SE) s] and men (14.7 +/- 2.8 s). The gain of the primary response was significantly greater in boys than men (239.1 +/- 7.5 vs. 167.7 +/- 5.4 ml. kg(-1). km(-1); P < 0.05). For heavy exercise, the VO(2) on-kinetics were significantly faster in boys than men (primary response time constant = 14.9 +/- 1.1 vs. 19.0 +/- 1.6 s; P < 0.05), and the primary gain was significantly greater in boys than men (209.8 +/- 4.3 vs. 167.2 +/- 4.6 ml. kg(-1). km(-1); P < 0.05). The amplitude of the VO(2) slow component was significantly smaller in boys than men (19 +/- 19 vs. 289 +/- 40 ml/min; P < 0.05). The VO(2) responses at the onset of moderate and heavy treadmill exercise are different between boys and men, with a tendency for boys to have faster on-kinetics and a greater initial increase in VO(2) for a given increase in running speed.     

Thigh muscle activation distribution and pulmonary VO2 kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans

The mechanisms underlying the oxygen uptake (Vo(2)) slow component during supra-lactate threshold (supra-LT) exercise are poorly understood. Evidence suggests that the Vo(2) slow component may be caused by progressive muscle recruitment during exercise. We therefore examined whether leg muscle activation patterns [from the transverse relaxation time (T2) of magnetic resonance images] were associated with supra-LT Vo(2) kinetic parameters. Eleven subjects performed 6-min cycle ergometry at moderate (80% LT), heavy (70% between LT and critical power; CP), and very heavy (7% above CP) intensities with breath-by-breath pulmonary Vo(2) measurement. T2 in 10 leg muscles was evaluated at rest and after 3 and 6 min of exercise. During moderate exercise, nine muscles achieved a steady-state T2 by 3 min; only in the vastus medialis did T2 increase further after 6 min. During heavy exercise, T2 in the entire vastus group increased between minutes 3 and 6, and additional increases in T2 were seen in adductor magnus and gracilis during this period of very heavy exercise. The Vo(2) slow component increased with increasing exercise intensity (being functionally zero during moderate exercise). The distribution of T2 was more diverse as supra-LT exercise progressed: T2 variance (ms) increased from 3.6 +/- 0.2 to 6.5 +/- 1.7 between 3 and 6 min of heavy exercise and from 5.5 +/- 0.8 to 12.3 +/- 5.4 in very heavy exercise (rest = 3.1 +/- 0.6). The T2 distribution was significantly correlated with the magnitude of the Vo(2) slow component (P < 0.05). These data are consistent with the notion that the Vo(2) slow component is an expression of progressive muscle recruitment during supra-LT exercise.     

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.     

Dynamics of intramuscular 31P-MRS P(i) peak splitting and the slow components of PCr and O2 uptake during exercise.

The dynamics of pulmonary O(2) uptake (Vo(2)) during the on-transient of high-intensity exercise depart from monoexponentiality as a result of a "slow component" whose mechanisms remain conjectural. Progressive recruitment of glycolytic muscle fibers, with slow O(2) utilization kinetics and low efficiency, has, however, been suggested as a mechanism. The demonstration of high- and low-pH components of the exercising skeletal muscle (31)P magnetic resonance (MR) spectrum [inorganic phosphate (P(i)) peak] at high work rates (thought to be reflective of differences between oxidative and glycolytic muscle fibers) is also consistent with this conjecture. We therefore investigated the dynamics of Vo(2) (using a turbine and mass spectrometry) and intramuscular ATP, phosphocreatine (PCr), and P(i) concentrations and pH, estimated from the (31)P MR spectrum. Eleven healthy men performed prone square-wave high-intensity knee extensor exercise in the bore of a whole body MR spectrometer. A Vo(2) slow component of magnitude 15.9 +/- 6.9% of the phase II amplitude was accompanied by a similar response (11.9 +/- 7.1%) in PCr concentration. Only five subjects demonstrated a discernable splitting of the P(i) peak, however, which began from between 35 and 235 s after exercise onset and continued until cessation. As such, the dynamics of the pH distribution in intramuscular compartments did not consistently reflect the temporal features of the Vo(2) slow component, suggesting that P(i) splitting does not uniquely reflect the activity of oxidative or glycolytic muscle fibers per se.     

Muscle oxygenation and pulmonary gas exchange kinetics during cycling exercise on-transitions in humans.

Near-infrared spectroscopy (NIRS) was utilized to gain insights into the kinetics of oxidative metabolism during exercise transitions. Ten untrained young men were tested on a cycle ergometer during transitions from unloaded pedaling to 5 min of constant-load exercise below (VT) the ventilatory threshold. Vastus lateralis oxygenation was determined by NIRS, and pulmonary O2 uptake (Vo --> Vo2) was determined breath-by-breath. Changes in deoxygenated hemoglobin + myoglobin concentration Delta[deoxy(Hb + Mb)] were taken as a muscle oxygenation index. At the transition, [Delta[deoxy(Hb + Mb)]] was unmodified [time delay (TD)] for 8.9 +/- 0.5 s at VT (both significantly different from 0) and then increased, following a monoexponential function [time constant (tau) = 8.5 +/- 0.9 s for VT]. For >VT a slow component of Delta[deoxy(Hb + Mb)] on-kinetics was observed in 9 of 10 subjects after 75.0 +/- 14.0 s of exercise. A significant correlation was described between the mean response time (MRT = TD + tau) of the primary component of Delta[deoxy(Hb + Mb)] on-kinetics and the tau of the primary component of the pulmonary Vo2 on-kinetics. The constant muscle oxygenation during the initial phase of the on-transition indicates a tight coupling between increases in O2 delivery and O2 utilization. The lack of a drop in muscle oxygenation at the transition suggests adequacy of O2 availability in relation to needs.     

Effects of dichloroacetate on VO2 and intramuscular 31P metabolite kinetics during high-intensity exercise in humans.

Traditional control theories of muscle O2 consumption are based on an "inertial" feedback system operating through features of the ATP splitting (e.g., [ADP] feedback, where brackets denote concentration). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilization) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion before exercise. To investigate these suggestions, six men performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an magnetic resonance spectrometer with each of prior DCA or saline control intravenous infusions. O2 uptake (Vo2) was measured breath by breath (by use of a turbine and mass spectrometer) simultaneously with intramuscular phosphocreatine (PCr) concentration ([PCr]), [Pi], [ATP], and pH (by 31P-MRS) and arterialized-venous blood sampling. DCA had no effect on the time constant (tau) of either Vo2 increase or PCr breakdown [tauVo2 45.5 +/- 7.9 vs. 44.3 +/- 8.2 s (means +/- SD; control vs. DCA); tauPCr 44.8 +/- 6.6 vs. 46.4 +/- 7.5 s; with 95% confidence intervals averaging < +/-2 s]. DCA, however, resulted in significant (P < 0.05) reductions in 1). end-exercise [lactate] (-1.0 +/- 0.9 mM), intramuscular acidification (pH, +0.08 +/- 0.06 units), and [Pi] (-1.7 +/- 2.1 mM); 2). the amplitude of the fundamental components for [PCr] (-1.9 +/- 1.6 mM) and Vo2 (-0.1 +/- 0.07 l/min, or 8%); and 3). the amplitude of the Vo2 slow component. Thus, although the DCA infusion lessened the buildup of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise, it did not enhance either tauVo2 or tau[PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.     

Comparison of oxygen uptake kinetics during knee extension and cycle exercise

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

Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise.

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2)kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to approximately 105% of the predetermined Vo2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means +/- SD: MAX1: 1.3 +/- 0.4 mM vs. MAX2: 7.7 +/- 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 +/- 5.5 s vs. MAX2: 33.2 +/- 7.7 s). Rather, the asymptotic "gain" of the primary Vo2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 +/- 0.9 ml.min(-1).W(-1) vs. MAX2: 9.0 +/- 0.7 ml.min(-1).W(-1); P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise.     

Longitudinal changes in aerobic power in older men and women.

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.     

Effects of prior heavy exercise on VO(2) kinetics during heavy exercise are related to changes in muscle activity.

We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.     

Simultaneous determination of the kinetics of cardiac output, systemic O(2) delivery, and lung O(2) uptake at exercise onset in men

We tested whether the kinetics of systemic O(2) delivery (QaO(2)) at exercise start was faster than that of lung O(2) uptake (Vo(2)), being dictated by that of cardiac output (Q), and whether changes in Q would explain the postulated rapid phase of the Vo(2) increase. Simultaneous determinations of beat-by-beat (BBB) Q and QaO(2), and breath-by-breath Vo(2) at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 +/- 3.2 years, maximal aerobic power 333 +/- 61 W). Vo(2) was determined using Gr?nlund's algorithm. Q was computed from BBB stroke volume (Q(st), from arterial pulse pressure profiles) and heart rate (f(h), electrocardiograpy) and calibrated against a steady-state method. This, along with the time course of hemoglobin concentration and arterial O(2) saturation (infrared oximetry) allowed computation of BBB QaO(2). The Q, QaO(2) and Vo(2) kinetics were analyzed with single and double exponential models. f(h), Q(st), Q, and Vo(2) increased upon exercise onset to reach a new steady state. The kinetics of QaO(2) had the same time constants as that of Q. The latter was twofold faster than that of Vo(2). The Vo(2) kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of Vo(2) increase. We suggest that in unsteady states, lung Vo(2) is dissociated from muscle O(2) consumption. The two components of Q and QaO(2) kinetics may reflect vagal withdrawal and sympathetic activation.     

Effects of prior very-heavy intensity exercise on indices of aerobic function and high-intensity exercise tolerance.

A recent bout of high-intensity exercise can alter the balance of aerobic and anaerobic energy provision during subsequent exercise above the lactate threshold (theta(L)). However, it remains uncertain whether such "priming" influences the tolerable duration of subsequent exercise through changes in the parameters of aerobic function [e.g., theta(L), maximum oxygen uptake (Vo(2max))] and/or the hyperbolic power-duration (P-t) relationship [critical power (CP) and the curvature constant (W')]. We therefore studied six men performing cycle ergometry to the limit of tolerance; gas exchange was measured breath-by-breath and arterialized capillary blood [lactate] was measured at designated intervals. On different days, each subject completed 1) an incremental test (15 W/min) for estimation of theta(L) and measurement of the functional gain (DeltaVo(2)/DeltaWR) and Vo(2peak) and 2) four constant-load tests at different work rates (WR) for estimation of CP, W', and Vo(2max). All tests were subsequently repeated with a preceding 6-min supra-CP priming bout and an intervening 2-min 20-W recovery. The hyperbolicity of the P-t relationship was retained postpriming, with no significant difference in CP (241 +/- 39 vs. 242 +/- 36 W, post- vs. prepriming), Vo(2max) (3.97 +/- 0.34 vs. 3.93 +/- 0.38 l/min), DeltaVo(2)/DeltaWR (10.7 +/- 0.3 vs. 11.1 +/- 0.4 ml.min(-1).W(-1)), or the fundamental Vo(2) time constant (25.6 +/- 3.5 vs. 28.3 +/- 5.4 s). W' (10.61 +/- 2.07 vs. 16.13 +/- 2.33 kJ) and the tolerable duration of supra-CP exercise (-33 +/- 11%) were each significantly reduced, despite a less-prominent Vo(2) slow component. These results suggest that, following supra-CP priming, there is either a reduced depletable energy resource or a residual fatigue-metabolite level that leads to the tolerable limit before this resource is fully depleted.     

Muscle capillary blood flow kinetics estimated from pulmonary O2 uptake and near-infrared spectroscopy.

The near-infrared spectroscopy (NIRS) signal (deoxyhemoglobin concentration; [HHb]) reflects the dynamic balance between muscle capillary blood flow (Q(cap)) and muscle O(2) uptake (Vo(2)(m)) in the microcirculation. The purposes of the present study were to estimate the time course of Q(cap) from the kinetics of the primary component of pulmonary O(2) uptake (Vo(2)(p)) and [HHb] throughout exercise, and compare the Q(cap) kinetics with the Vo(2)(p) kinetics. Nine subjects performed moderate- (M; below lactate threshold) and heavy-intensity (H, above lactate threshold) constant-work-rate tests. Vo(2)(p) (l/min) was measured breath by breath, and [HHb] (muM) was measured by NIRS during the tests. The time course of Q(cap) was estimated from the rearrangement of the Fick equation [Q(cap) = Vo(2)(m)/(a-v)O(2), where (a-v)O(2) is arteriovenous O(2) difference] using Vo(2)(p) (primary component) and [HHb] as proxies of Vo(2)(m) and (a-v)O(2), respectively. The kinetics of [HHb] [time constant (tau) + time delay [HHb]; M = 17.8 +/- 2.3 s and H = 13.7 +/- 1.4 s] were significantly (P < 0.001) faster than the kinetics of Vo(2) [tau of primary component (tau(P)); M = 25.5 +/- 8.8 s and H = 25.6 +/- 7.2 s] and Q(cap) [mean response time (MRT); M = 25.4 +/- 9.1 s and H = 25.7 +/- 7.7 s]. However, there was no significant difference between MRT of Q(cap) and tau(P)-Vo(2) for both intensities (P = 0.99), and these parameters were significantly correlated (M and H; r = 0.99; P < 0.001). In conclusion, we have proposed a new method to noninvasively approximate Q(cap) kinetics in humans during exercise. The resulting overall Q(cap) kinetics appeared to be tightly coupled to the temporal profile of Vo(2)(m).     

Effect of age on O(2) uptake kinetics and the adaptation of muscle deoxygenation at the onset of moderate-intensity cycling exercise.

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.     

Left ventricular function during arm exercise: influence of leg cycling and lower body positive pressure.

The purpose of this study was to characterize left ventricular (LV) diastolic filling and systolic performance during graded arm exercise and to examine the effects of lower body positive pressure (LBPP) or concomitant leg exercise as means to enhance LV preload in aerobically trained individuals. Subjects were eight men with a mean age (+/-SE) of 26.8 +/- 1.2 yr. Peak exercise testing was first performed for both legs [maximal oxygen uptake (Vo(2)) = 4.21 +/- 0.19 l/min] and arms (2.56 +/- 0.16 l/min). On a separate occasion, LV filling and ejection parameters were acquired using non-imaging scintography using in vivo red blood cell labeling with technetium 99(m) first during leg exercise performed in succession for 2 min at increasing grades to peak effort. Graded arm exercise (at 30, 60, 80, and 100% peak Vo(2)) was performed during three randomly assigned conditions: control (no intervention), with concurrent leg cycling (at a constant 15% leg maximal Vo(2)) or with 60 mmHg of LBPP using an Anti G suit. Peak leg exercise LV ejection fraction was higher than arm exercise (60.9 +/- 1.7% vs. 55.9 +/- 2.7%; P < 0.05) as was peak LV end-diastolic volume was reported as % of resting value (110.3 +/- 4.4% vs. 97 +/- 3.7%; P < 0.05) and peak filling rate (end-diastolic volume/s; 6.4 +/- 0.28% vs. 5.2 +/- 0.25%). Concomitant use of either low-intensity leg exercise or LBPP during arm exercise failed to significantly increase LV filling or ejection parameters. These observations suggest that perturbations in preload fail to overcome the inherent hemodynamic conditions present during arm exercise that attenuate LV performance.     

Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.

We tested the hypothesis that heavy-exercise phase II oxygen uptake (VO(2)) kinetics could be speeded by prior heavy exercise. Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise; 3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise. The VO(2) responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on the VO(2) kinetic response to subsequent moderate exercise. Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 65.2 +/- 4.1 to 47.0 +/- 3.1 s; P < 0.05), it had no significant effect on either the amplitude or the time constant (from 23.9 +/- 1.9 to 25.3 +/- 2.9 s) of the VO(2) response in phase II. Instead, this "speeding" was due to a significant reduction in the amplitude of the VO(2) slow component. These results suggest phase II VO(2) kinetics are not speeded by prior heavy exercise.