Oxygen Uptake During High-Intensity Running: Response Following a Single Bout of Interval Training

Elevated oxygen uptake ((V) over dot O-2) during moderate-intensity running following a bout of interval running training has been studied previously. To further investigate this phenomenon, the (V) over dot O-2 response to high-intensity exercise was examined following a bout of interval running. Well-trained endurance runners were split into an experimental group [maximum oxygen uptake, (V) over dot O-2max 4.73 (0.39) l.min(-1)] and a reliability group [(V) over dot O-2max 4.77 (0.26) l.min(-1)]. The experimental group completed a training session (4 x 800 m at 1 km.h(-1) below speed at (V) over dot O-2max, with 3 min rest between each 800-m interval). Five minutes prior to, and Ih following the training session, subjects completed 6 min 30 s of constant speed, high-intensity running designed to elicit 40% Delta (where Delta is the difference between (V) over dot O-2 at ventilatory threshold and (V) over dot O-2max; tests 1 and 2, respectively). The slow component of (V) over dot O-2 kinetics was quantified as the difference between the (V) over dot O-2 at 6 min and the (V) over dot O-2 at 3 min of exercise, i.e. Delta(V) over dot O2(6-3) The Delta(V) over dot O2(6-3) was the same in two identical conditions in the reliability group [mean (SD): 0.30 (0.10) l.min(-1) vs 0.32 (0.13) l.min(-1)]. In the experimental group, the magnitude of the slow component of (V) over dot O-2 kinetics was increased in test 2 compared with test 1 by 24.9% [0.27 (0.14) l.min(-1) vs 0.34 (0.08) l.min(-1), P < 0.05]. The increase in Delta(V) over dot O2(6-3) in the experimental group was observed in the absence of any significant change in body mass, core temperature or blood lactate concentration, either at the start or end of tests 1 or 2. It is concluded that similar mechanisms may be responsible for the slow component of (V) over dot O-2 kinetics and for the fatigue following the training session. It has been suggested previously that this mechanism may be linked primarily to changes within the active limb, with the recruitment of alternative and/or additional less efficient fibres