It is presently unclear how the fast and slow components of pulmonary oxygen uptake (VO(2)) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (VO(2) equal to 50% of the difference between LT and peak VO(2)) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in VO(2) was similar in the two positions, but VO(2) kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of VO(2) to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component of VO(2), without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exercise VO(2) was the same in the two positions. The changes in VO(2) kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component for VO(2) but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.

For high-intensity cycle ergometer exercise, the relation between power (P) and its tolerable duration (t) has been well characterized by the hyperbolic relationship: (P-thetaF) t = W', or P = W' (1/t)+thetaF, where thetaF may be termed the 'fatigue threshold'. The curvature constant (W') reflects a constant amount of work which is postulated to be equivalent to a finite energy store that relates to the oxygen-deficit: phosphagen pool, anaerobic glycolysis and oxygen stores. Compared to thetaF, the physiological nature of W' has received little consideration. The purpose of this study was therefore to establish the parameters of the power-duration curve (thetaF and W') for subjects in normal glycogen (NG) and glycogen depleted (GD) states. Seven healthy male subjects (aged 22 to 41 years) each performed four high-intensity square-wave exercise bouts on an electrically braked cycle ergometer under two different muscular glycogen content conditions, i.e. NG and GD states. Subjects performed the following exercise on the evening before the trial day to induce the GD state. Initially, they performed a 75-min cycling exercise at 60% of VO2max. After a 5-min rest period, they subsequently repeated a 1-min cycling bout at 115% of VO2max (separated by 1-min rest periods) until the subject could no longer maintain the prescribed pedal rate for the full minute. Subjects then reported to the laboratory after an overnight fast and performed a single high-intensity exercise bout. The GD procedure was repeated four times at 1-week intervals. In the GD state, the respiratory exchange ratio (RER) (VO2/VCO2) value during a recumbent control period prior to the trial was significantly lower than that in the NG state [GD: 0.84+/-0.02, NG: 0.94+/-0.04, mean +/- SD]. There was no significant difference for thetaF between GD and NG state [NG: 197.1+/-31.9 W, GD: 190.6+/-28.2 W]. W' in contrast was significantly reduced by the GD procedure [NG: 12.83+/-2.21 kJ, GD: 10.33+/-2.41 kJ]. The present results indicate that the muscular glycogen store seems to be an important determinant of the curvature constant (W') of the power-duration curve for cycle ergometry.

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.

It has been repeatedly demonstrated that the tolerable duration (t) of high-intensity cycling is well characterized as a hyperbolic function of power (P) with an asymptote that has been termed the "fatigue threshold" and with a curvature constant. This hyperbolic P-t relationship has also been confirmed in running and swimming, when speed (V) is used instead of P; that is, (V - V(F)). t = D', where V(F) is the V at the fatigue threshold, and D' is the curvature constant. Therefore, we theoretically analyzed herein the consequences of an athlete performing the initial part of an endurance event at a V different from the constant rate that would allow the performance time to be determined by the hyperbolic V-t relationship. We considered not only the V-t constraints that limit the athlete's ability to make up the time lost by too slow an early pace but also the consequences of a more rapid early pace. Our analysis demonstrates that both the V(F) and D' parameters of the athlete's V-t curve play an important role in the pace allocation strategy of the athlete. That is, 1) when the running V during any part of the whole running distance is below V(F), the athlete can never attain the goal of achieving the time equivalent to that of running the entire race at constant maximal V (i.e., that determined by one's own best V-t curve); and 2) the "endurance parameter ratio" D'/V(F) is especially important in determining the flexibility of the race pace that the athlete was able to choose intentionally.

For high-intensity cycle ergometer exercise, the tolerable duration (t) is well characterized as a hyperbolic function of power output, P : t = W'/(P-thetaF), where thetaF may be termed the "fatigue threshold." The purpose of this study was to determine the effect of oral creatine (Cr) supplementation on the curvature constant parameter (W') of the power-duration curve. A double-blind research method and a cross-over design were employed for creatine/placebo supplementation. Eight healthy male subjects (aged 18 to 22 years) each performed four or five high-intensity square-wave exercise bouts on an electrically braked cycle ergometer after 5 d of Cr monohydrate (CR: 20 g of Cr with artificial sweetener/d) or placebo (PL: 6 g of glucose/d) supplementation. Each subject performed a single high-intensity exercise trial per day for four or five successive days to determination the P-t hyperbolic relation. After 6 weeks (the washout time of Cr from the muscles), each subject performed the other condition (i.e., PL or CR) and repeated the same experimental procedure. There was no significant difference for thetaF between PL and CR conditions (PL: 214.4 +/- 23.6, CR: 207.0 +/- 19.8 W, mean +/- SD). In contrast, W' was significantly increased by the Cr supplementation (PL: 10.9 +/- 2.7, CR: 13.7 +/- 3.0 kJ; p<0.05). The results indicated that Cr and/or PCr content in muscles seems to be one of the important determinants of the curvature constant parameter (W') of the power-duration hyperbolic curve for cycle ergometry.

The tolerable duration of high-intensity, constant-load cycle ergometry is a hyperbolic function of power, with an asymptote termed critical power (CP) and a curvature constant (W') with units of work. It has been suggested that continued exercise after exhaustion may only be performed below CP, where predominantly aerobic energy transfer can occur and W' can be partially replenished. To test this hypothesis, six volunteers each performed cycle-ergometer exercise with breath-by-breath determination of ventilatory and pulmonary gas exchange variables. Initially, four exercise tests to exhaustion were made: 1). a ramp-incremental and 2). three high-intensity constant-load bouts at different work rates, to estimate lactate (theta(L)) and CP thresholds, W', and maximum oxygen uptake (Vo2 max). Subsequently, subjects cycled to the limit of tolerance (for approximately 360 s) on three occasions, each followed by a work rate reduction to 1). 110% CP, 2). 90% CP, and 3). 80% theta(L) for a 20-min target. W' averaged 20.9 +/- 2.35 kJ or 246 +/- 30 J/kg. After initial fatigue, 110% CP was tolerated for only 30 +/- 12 s. Each subject completed 20 min at 80% theta(L), but only two sustained 20 min at 90% CP; the remaining four subjects fatigued at 577 +/- 306 s, with oxygen consumption at 89 +/- 8% Vo2 max. The results support the suggestion that replenishing W' after fatigue necessitates a sub-CP work rate. The variation in subjects' responses during 90% CP was unexpected but consistent with mechanisms such as reduced CP consequent to prior high-intensity exercise, variation in lactate handling, and/or regional depletion of energy substrates, e.g., muscle glycogen.

We conclude that the work equivalent of W' is not affected by power variations during exhausting cycle ergometry, at least in the P range of 100-134% of CP.

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O(2) uptake (VO(2)) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal VO(2)) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 +/- 0.3, 5.6 +/- 0.9, and 6.7 +/- 1.4 meq/l, respectively. An "effective" time constant (tau) of VO(2) with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the VO(2) kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) VO(2) kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the VO(2) slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of VO(2) kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.