Constant power output exercise above the lactate threshold is associated with the development of a ‘slow component’ of oxygen uptake (V_O2) kinetics that causes V_O2 to rise to a higher value than would be predicted by extrapolation of the relationship between V_O2 and power output established during moderate exercise. The cause of this loss of efficiency remains to be elucidated, but the recruitment of type II muscle fibres has been proposed as a likely candidate (Whipp, 1994). Therefore, in the present study, we hypothesised that an exercise and dietary regime designed to deplete type I muscle fibres of glycogen would result in a greater contribution of type II muscle fibres to the exercise power output and a larger amplitude of the V_O2 slow component.

Eight male subjects (mean ± S.D. age 20.8 ± 1.6 years; body mass 75.7 ± 7.1 kg;V_O2,max 3.5 ± 1.1 l min^-1) gave written informed consent to participate in this study which was approved by the institutional ethics committee. On day 1, the subjects reported to the laboratory at 08.00 h following an overnight fast, and completed a 9 min exercise bout at a power output calculated to require 85 %V_O2,max on an electrically braked cycle ergometer. Pulmonary V_O2 was determined breath-by-breath and venous and capillary blood samples were drawn immediately before and after exercise for determination of lactate, glucose, glycerol and ammonia concentrations. On day 2, the subjects were fed a 4200 kJ meal (60 % protein, 40 % fat) at 12.00 h and then consumed only water for the rest of the day; at 18.00 h they completed a 2 h exercise bout at 60 %V_O2,max. This diet and exercise regimen has been shown to result in total depletion of the glycogen content of type I muscle fibres (Gollnick et al. 1974). At 08.00 h on day 3, the subjects performed an identical exercise bout to that of day 1. The V_O2 data were fitted with a mono-exponential function from 20 s to 3 min of exercise to determine the time constant of the fundamental response, and the slow component was quantified as the difference in V_O2 between 3 and 9 min of exercise. Data were analysed using the signed ranks Wilcoxon test and expressed as means ± S.D.

The respiratory exchange ratio was significantly blunted by the glycogen depletion regimen (from 0.91 ± 0.15 to 0.82 ± 0.12 at rest, and from 1.04 ± 0.05 to 0.98 ± 0.05 during exercise; P < 0.05). Furthermore, blood [glucose] and [lactate] were significantly reduced, while blood [glycerol] and [ammonia] were significantly increased, during both rest and exercise following the glycogen depletion regimen. The V_O2 was significantly higher (by approximately 140 ml min^-1) throughout exercise following glycogen depletion. However, glycogen depletion did not appreciably influence V_O2 kinetics: neither the time constant of the fundamental response (from 35.4 ± 2.5 to 33.2 ± 4.4 s) nor the amplitude of the slow component (from 404 ± 95 to 376 ± 81 ml min^-1) was significantly altered.

The increased V_O2 throughout exercise following glycogen depletion can be explained by changes in substrate utilisation and/or changes in muscle recruitment. The fact that the amplitude of the V_O2 slow component was unaltered by a protocol designed to cause glycogen depletion of the type I fibre population indicates either that the slow component is not related to the recruitment of type II fibres during heavy exercise, or that glycogen depletion of the type I fibre pool does not significantly alter the pattern of motor unit recruitment during subsequent exercise.