Pulmonary oxygen uptake (VO2) kinetics are slowed and phase I duration prolonged in older adults during moderate intensity exercise; whether the same is true during heavy exercise in unknown. Conventionally, this slowing has largely been attributed to an age-related reduction in the capacity to both deliver and utilise O2. However, the recent observation of a prolonged phase I duration in older people suggests that slower VO2 kinetics might be an artefact of the inappropriate exclusion of phase I. Furthermore, slower VO2 kinetics in older people has always been reported in combination with a lower peak VO2. Therefore, it remains to be elucidated whether the slowing of VO2 kinetics is attributable to age per se, to the concomitant reduction in aerobic fitness or to a methodological artefact. Fifty younger (24±4 yrs, 28 male) and 15 older (54±3 yrs, 6 male) healthy participants completed repeated bouts of moderate (Mod; 70% gas exchange threshold, GET) and heavy (Hvy; 30% of the difference between the GET and peak VO2) intensity exercise. Pulmonary gas exchange variables were measured throughout. Parameters describing the dynamic VO2 response to the step change in work rate were derived using a mono-exponential model with a time delay, constrained to exclude the visually identified slow component during heavy exercise. The phase I-phase II transition was visually identified (VI) and compared to fixed exclusion time periods ranging from 15s to 40s. Irrespective of age, Phase I duration did not affect the phase II τ during Mod. During Hvy, the phase II τ was significantly slower when fitting started at 15s compared to at the VI phase I duration (Y: 31±9 vs. 29±9; O: 35±11 vs. 30±8 s; P<0.05) but no difference was evident when fitting started at any other phase I duration. Neither the phase II τ (irrespective of phase I duration) nor peak V<O2 were influenced by age during Mod or Hvy. The VO2 slow component was significantly smaller in older participants (O: 9±4 vs. Y: 15±11 %; P<0.05). The age-independence of VO2 kinetics observed here in participants with similar peak VO2 refutes the notion that slowing of VO2 kinetics in older people is attributable to age per se. The apparent age-related slowing in previous studies may be attributable to concomitant reductions in aerobic fitness. Our results do not support a role of Phase I duration in explaining apparent age-related differences: provided a minimum period of 20s was excluded, the phase I duration did not influence phase II τ in young or older people. Finally, the smaller slow component amplitude observed here in older participants agrees with a preferential loss of Type II motor units with age (1), the additional recruitment of which might be linked to development of the slow component (2, 3).