The primary objective of this thesis was to examine the influence of alterations in muscle recruitment on pulmonary O2 uptake (VO2) kinetics during exercise above the gas exchange threshold (GET) in young people. In the first experimental chapter, the phase II time constant (τ) slowed over a 2-yr period in 14-16 yr old boys (25 ± 5 s vs. 30 ± 5 s, P = 0.002) and there was a greater relative VO2 slow component amplitude (Rel. A’2 (%)] during heavy-intensity exercise (9 ± 5% vs. 13 ± 4%, P = 0.036). In the second study, ‘work-to-work’ transitions yielded similar phase II VO2 kinetics during unloaded-to-moderate exercise (U→M) between 11-12 yr old boys and teenagers (19 ± 5 s vs. 22 ± 7 s, P = 0.32) but the phase II τ was significantly lengthened in the latter group at the onset of moderate-to-very heavy exercise (M→VH: 30 ± 5 s vs. 45 ± 11 s, P = 0.011). There were no differences in the phase II τ between teenagers and adult men during M→VH exercise (P = 0.46). In the third study, increasing pedal rate from 50 rev•min-1 to 115 rev•min-1 significantly (P 0.05). The fourth study reported that a reduced relative VO2 slow component amplitude in younger boys compared to men (11 ± 4% vs. 16 ± 3%, P = 0.015) coincided with a lower percentage change in the integrated electromyogram (iEMG) of the m. vastus lateralis from minute 2 to minute 6 of exercise (ΔiEMG6-2: 7 ± 25% vs. 49 ± 48%, P = 0.030), suggesting that alterations in motor unit recruitment might be involved in restricting the O2 cost of exercise above the primary amplitude in children compared to adults. The final experimental chapter tested this hypothesis, but no statistically significant differences were reported for the relative VO2 slow component amplitude between 10-12 yr old boys and men (15 ± 7% vs. 19 ± 4%, P = 0.145). In boys, an excess VO2 temporally coincided with a significant increase in the transverse relaxation time (T2) of the m. vastus lateralis from the VO2 slow component time delay (SCtd) to minute 6 of exercise (41.5 ± 2.4 ms vs. 45.2 ± 2.3 ms, P = 0.001), thereby consistent with the notion that delayed muscle fibre activation might contribute to the development of the VO2 slow component in youth. In conclusion, this thesis has demonstrated that maturational changes in the VO2 kinetic response to heavy-intensity exercise are extended into adolescence. During intense submaximal exercise, the recruitment of higher-order (type II) muscle fibres might be principally involved in modulating VO2 kinetics as children mature but this effect is attenuated in teenage subjects engaged in regular endurance training
