SUMMARY1. At work rates which do not result in a sustained increase in blood lactate ([L-]), oxygen uptake (Po2) approaches the steady state with first-order kinetics. However, when [L-] is increased, at least two kinetic components are required to characterize the Jo response dynamics. The purpose of the present investigation was to determine whether these more-complex kinetics are best represented as: (a) two components which operate throughout the exercise or (b) a delayed slow component which is consequent to the lactic acidaemia and which does not influence the early development of the 02 deficit.2. Six healthy subjects underwent an incremental ramp test on a cycle ergometer, to the limit of tolerance, for determination of the maximum V0 (uV0) and estimation ()of the threshold for lactic acidaemia (0L) non-invasively. Subjects then performed, on different days, two to four repetitions of square-wave exercise from a baseline of unloaded pedalling ('O' Watts (W)) to work rates (WR) <0L (90% OL) and > OL (half-way between 0L and VO2). Ventilatory and pulmonary gas exchange variables were determined breath-by-breath. For each subject, the VO2 transitions were averaged prior to fitting a least-squares algorithm to the on-and off-transient responses.3. The < OL test resulted in a mono-exponential VO2 response, with a time constant of 31-3 and 31-5 s for the on-and off-transients, respectively. 4. The V02 responses to the > OL test were fitted to three competing models: (a) a single exponential for the entire period; (b) a double exponential for the entire period; and (c) an initial single exponential with a subsequent phase of delayed onset. Model (c) yielded a significantly lower residual mean-squares error than methods (a) and (b), with a time constant for the initial component of 40-2 s for the on-transient and 32-9 s for the off-transient and a subsequent phase of Po2 increase for the ontransient which averaged 230 ml min-'. The AVQ2/AWR for the early kinetics of the > OL test were not different from the < OL test (9-6 and 9-5 ml min-' W-1, respectively).

Despite a fraction of the time commitment, run SIT induces similar body composition, VO(2max), and performance adaptations as ET, but with no effect on Q(max). These data suggest that adaptations with ET are of central origin primarily, whereas those with SIT are more peripheral

We investigated whether values for passive resistive torque, dorsiflexion strength, and active mobility of the ankle joint varied with age in a randomly selected sample of middle-aged and elderly males and females. The main effects of sex and age group were significant, without an interaction effect, on values for passive resistive torque and voluntary strength. The trends indicated that females had lower values for both variables and that passive torque increased and strength decreased with respect to age. Dorsiflexion range of motion also showed a highly significant trend to decrease across age groups, and more so for females than males. Mean values for middle-aged men vs old men went from 20.0 to 13.5 degrees, while corresponding values for women decreased from 20.7 degrees of dorsiflexion to 10.1. Functional ankle movement thus becomes limited with age, but could be improved by strengthening weak dorsiflexor muscles.

Cross-sectional studies have compared the oxygen uptake (VO2) kinetics during the on-transient of moderate intensity exercise in older and younger adults. The slower values in the older adults may have been due to an age-related reduction in the capacity for O2 transport or alternatively a reduced intramuscular oxidative capacity. We studied: (1) the effects of ageing on VO2 kinetics in older adults on two occasions 9 years apart, and (2) the effect of hyperoxia on VO2 kinetics at the second test time. After a 9 year period, follow-up testing was undertaken on seven older adults (78 +/- 5 years, mean +/- S.D.). They each performed six repeats of 6 min bouts of constant-load cycle exercise from loadless cycling to 80% of their ventilatory threshold. They breathed one of two gas mixtures (euoxia: inspired O2 fraction, FI,O2, 0.21; hyperoxia: FI,O2, 0.70) on different trials determined on a random basis. Breath-by-breath VO2 data were time aligned and ensemble averaged. VO2 kinetics, modelled with a single exponential from phase 2 onset (+20 s) to steady state and described by the exponential time constant (tau) were compared with data collected from the same adults 9 years earlier. One-way repeated measures analysis of variance revealed that tau was slowed significantly with age (from 30 +/- 8 to 46 +/- 10 s), but was unaffected by hyperoxia (43 +/- 15 s). We concluded that: (1) in older adults studied longitudinally over a 9 year period, the on-transient VO2 kinetics are slowed, in agreement with, but to a greater extent, than from cross-sectional data; and (2) the phase 2 time constant (tau) for these older adults was not accelerated by hyperoxic breathing. Thus the expected hyperoxia-induced increase in the capacity for O2 transport was not associated with faster on-transient VO2 kinetics suggesting either that O2 transport may not limit VO2 kinetics during the 8th decade, or that O2 transport was not improved with hyperoxia.