We hypothesised that: (1) the maximal lactate steady state (MLSS), critical power (CP) and electromyographic fatigue threshold (EMG(FT)) occur at the same power output in cycling exercise, and (2) exercise above the power output at MLSS (P-MLSS) results in continued increases in oxygen uptake (VO(2)), blood lactate concentration ([La]) and integrated electromyogram (iEMG) with time. Eight healthy subjects [mean (SD) age 25 (3) years, body mass 72.1 (8.2) kg] performed a series of laboratory tests for the determination of MLSS, CP and EMG(FT). The CP was determined from four exhaustive trials of between 2 and 15 min duration. The MLSS was determined as the highest power output at which the increase in blood [La] was less than 1.0 mM across the last 20 min of a series of 30-min trials. The EMG(FT) was determined from four trials of 2 min duration at different power outputs. The surface electromyogram was recorded continuously from the vastus lateralis muscle. The CP was significantly higher than the P-MLSS [242 (25) vs. 222 (23) W; P<0.05], although the two variables were strongly correlated (r=0.95; P<0.01). The EMG(FT) could not be determined in 50% of the subjects. Blood [La], VO(2) and minute ventilation all increased significantly with time for exercise at power outputs above the P-MLSS. In conclusion, the P-MLSS, and not the CP, represents the upper limit of the heavy exercise domain in cycling. During exercise above the P-MLSS, there is no association between changes in iEMG and increases in VO(2) and blood [La] with time.

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The purpose of the present study was to examine comprehensively the kinetics of oxygen uptake (VO2) during treadmill running across the moderate, heavy and severe exercise intensity domains. Nine subjects [mean (SD age, 27 (7) years; mass, 69.8 (9.0) kg; maximum VO2, VO2max, 4,137 (697) ml x min(-1)] performed a series of "square-wave" rest-to-exercise transitions of 6 min duration at running speeds equivalent to 80% and 100% of the VO2 at lactate threshold (LT; moderate exercise); and at 20%, 40%, 60%, 80% and 100% of the difference between the VO2 at LT and VO2max (delta heavy and severe exercise). Critical velocity (CV) was also determined using four maximal treadmill runs designed to result in exhaustion in 2-15 min. The VO2 response was modelled using non-linear regression techniques. As expected, the amplitude of the VO2 primary component increased with exercise intensity [from 1,868 (136) ml x min-( 1) at 80% LT to 3,296 (218) ml x min-(1) at 100% delta, P < 0.05]. However, there was a non-significant trend for the "gain" of the primary component to decrease as exercise intensity increased [181 (7) ml x kg(-1) x km(-1) at 80% LT to 160 (6) ml x kg(-1) x km(-1) at 100% delta]. The time constant of the primary component was not different between supra-LT running speeds (mean value range = 17.9-19.1 s), but was significantly shorter during the 80% LT trial [12.7 (1.4) s, P < 0 .05]. The VO2 slow component increased with exercise intensity from 139 (39) ml x min(-1) at 20% delta to 487 (57) ml x min(-1) at 80% delta (P < 0.05), but decreased to 317 (84) ml x min(-1) during the 100% delta trial (P < 0.05). During both the 80% delta and 100% delta trials, the VO2 at the end of exercise reached VOmax [4,152 (242) ml x min(-1) and 4,154 (114) ml x min(-1), respectively]. Our results suggest that the "gain" of the primary component is not constant as exercise intensity increases across the moderate, heavy and severe domains of treadmill running. These intensity-dependent changes in the amplitudes and kinetics of the VO2 response profiles may be associated with the changing patterns of muscle fibre recruitment that occur as exercise intensity increases.

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.

This case study observed the training delivered by a 1500-m runner and the physiological and performance change during a 2-y period. A male international 1500-m runner (personal best 3:38.9 min:s, age 26 y, height 1.86 m, body mass 76 kg) completed 6 laboratory tests and 14 monitored training sessions, during 2 training years. Training distribution and volume was ascertained from training diary and spot-check monitoring of heart rate and accelerometry measurements. Testing and training information were discussed with coach and athlete from which training changes were made. In the first training year, low-intensity training was found to be performed above the prescribed level, which was adjusted with training and coach support in y 2 (training zone < 80% of vVO2max, y 1 = 20%; y 2 = 55%). “Tempo” training was also performed at an excessively high intensity (Δ [blood lactate] 5–25 min of tempo run, y 1 = Δ6.7 mM, y 2 = Δ2.5 mM). From y 1 to 2, there was a concomitant increase in the proportion of training in the high-intensity zone of 100 to 130% vVO2max from 7 to 10%. Values for VO2max increased from 72 to 79 mL · kg−1 · min, economy improved from 210 to 206 mL · kg−1 · min, and 1500-m performance time improved from 3:38.9 to 3:32.4 min:s from the beginning of y 1 to the end of y 2. This case shows a modification in training methodology that was coincident with a greater improvement in physiological capability and furtherance in performance improvement.