The effect of prior heavy exercise on the parameters of the power-duration curve for cycle ergometry.

The tolerable duration (t) of high-intensity cycle ergometry is well characterized by a hyperbolic function of power output (P) with an asymptote (termed the critical power (CP)) and a curvature constant (denoted W'). The purpose of this study was to investigate the effect of prior heavy exercise (W-up) that specifically engenders an acidosis on CP and W'. Eight healthy subjects performed 2 sets of 4 high-intensity square-wave exercise bouts on a bicycle ergometer to estimate CP and W', with (W-up) and without (control) prior exercise, respectively. Exercise intensities of the 4 main bouts were selected in the range of 90% to 135% peak oxygen uptake so as to reach the limit of tolerance between approximately 1.5 and 10 min. The W-up bout was preceded by 6 min cycling at a work rate halfway between the lactate threshold and peak oxygen uptake (mean +/- SD of 153.8 +/- 29.8 W) starting 12 min before the main bout. Blood lactate levels ([La]b) just before the main exercise bouts in W-up conditions were significantly higher than those of the control (4.7 +/- 1.1 and 1.4 +/- 0.4 mEq.L(-1), respectively; p < 0.05). However, there were no significant differences in end-exercise [La]b. W-up increased significantly the tolerable duration at every work rate compared with the control, which was attributable exclusively to increased CP (176.5 +/- 34.3 and 168.7 +/- 31.3 W, respectively; p < 0.05), without any significant change in W' (11.0 +/- 3.2 and 11.0 +/- 3.1 kJ, respectively). It is concluded that the prior heavy exercise improved performance mainly because of an enhanced aerobic component of exercise energetics, as indicated by a higher CP and lower increment in the [La]b.

Central circulatory and peripheral O2 extraction changes as interactive facilitators of pulmonary O2 uptake during a repeated high-intensity exercise protocol in humans.

It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake [Formula: see text] response at the onset of subsequent identical exercise. To clarify the roles of central O(2) delivery and/or peripheral O(2) extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O(2) content difference [Formula: see text] to the [Formula: see text] transient during repeated bouts of high-intensity knee extension (KE) exercise. Nine healthy subjects volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate 70-75% of peak power) separated by 6 min of rest. Throughout the protocol, continuous-wave Doppler ultrasound was used to measure beat-by-beat CO (i.e., via simultaneous measurement of stroke volume and the diameter of the arterial aorta). The phase II [Formula: see text] response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the [Formula: see text] speeding at 10 and 30 s, respectively. After this, the contribution of [Formula: see text] became increasingly more predominant: being responsible to an estimated 64% of the [Formula: see text] speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and [Formula: see text] clearly interact to determine the [Formula: see text] response, the speeding of [Formula: see text] kinetics by prior high-intensity KE exercise is predominantly attributable to increases in [Formula: see text].