Abstract:The purpose of the present study was to examine the effect of unilateral lower limb suspension (ULLS) deconditioning on oxygen uptake kinetics. Eight healthy males underwent ULLS for 20 days and performed a series of 6-min square-wave transitions from rest to 60-W single-leg cycling exercises just before and after ULLS. To characterize the kinetics of the oxygen uptake response, a single exponential model was applied to the data until the end of the fast component omitted the first 15 s of the on-transit using a nonlinear least-squares fitting procedure. The following results were found: (i) the time constant of oxygen uptake was unchanged before and after ULLS; (ii) although there was no significant difference in the baseline and the asymptotic amplitude of the fast component, the asymptote, i.e., the absolute asymptotic amplitude of the fast component (the sum of the baseline and the asymptotic amplitude), and the end exercise oxygen uptake were decreased after ULLS; (iii) the contribution of the slow component to the total response of oxygen uptake was unchanged at pre-and post-ULLS. In conclusion, the asymptote in the fast component and the end exercise oxygen uptake were decreased after 20-d ULLS, though the response speed and the amplitude of the slow component of oxygen uptake were not changed. It is suggested that deconditioning as a result of limb disuse affects oxygen uptake response. In general, to analyze oxygen uptake ( O 2 ) kinetics in exercising humans, O 2 is usually measured at the mouth by means of the breath-by-breath method. The response speed of O 2 to exercise, i.e., the time constant of O 2 kinetics of the fast component in which O 2 increases exponentially and reaches a steady state within 2-3 min after the onset of exercise, is affected by O 2 delivery systems consisted of central and peripheral circulation, and the function of O 2 utilization, such as the activity of oxidative enzymes in the muscle [1,2]. In cases where the intensity of exercise is heavy, O 2 increases moderately after the end of the fast component, and this is known as the slow component. Although the mechanisms remain speculative, it is thought that the recruitment of fast twitch fibers or the added recruitment of muscle fibers, which have not yet participated in muscle contraction, is the primary cause [3].It is known that the fast component of O 2 kinetics is faster in trained than in untrained individuals [4]. This would indicate that because the time to start producing lactic acid obstructing muscular contraction is shortened, burdens of exercise decrease. Further, Carter et al. [5] revealed that the O 2 slow component was attenuated by 6 weeks of endurance training. This would imply that the subjects were able to accomplish the same level of exercise without the mobilization of added muscular fibers or fast twitch fibers. The endurance tolerance of each muscle fiber would be increased. Therefore it is conceivable that endurance training would speed up O 2 kinetics and would lead to the elimination of th...