Aaron Nevin1, Norita Gildea1, Adam McDermott1, Joel Rocha2, Domenico Crognale1, Simon Green3, Donal O’Shea4, Mikel Egana1 1Department of Physiology, Trinity College Dublin, Dublin, Ireland. 2Division of Sport and Exercise Sciences, Abertay University, Dundee, United Kingdom. 3School of Science and Health and School of Medicine, University of Western Sydney, Sydney, Australia.4Endocrinology, St Columcille’s and St Vincent’s Hospitals, Dublin, Ireland. We tested the hypothesis that a 12 week intervention involving low-volume high-intensity interval training (LVHIIT) would increase the speed of the adjustment of the primary phase (taup, τp) of pulmonary oxygen uptake (VO2) and/or reduce the amplitude of the slow component of VO2 during high-intensity cycling in type 2 diabetes (T2D) to a similar extend as a traditional moderate-intensity continuous training (MICT) intervention. Twenty eight middle-aged participants with T2D (17 men, mean ± SD: age 53 ± 10 yr, body mass index 30.0 ± 4.0 kg.m-2) were randomly assigned to MICT (n=10, 50 min of moderate-intensity cycling) or LVHIIT (n=9, 10 x 1 min at ~90% maximal heart rate interspersed by 1 min of ‘unloaded’ cycling) or to a non-exercising control group (n=9). Exercising groups trained 3 times/week and every 3 weeks exercise intensity was adjusted. Before and after the intervention participants completed two bouts of constant-load cycling corresponding to 50% between their ventilatory threshold and peak VO2 power outputs (i.e. 50%Δ) previously established during a ramp incremental test. VO2 kinetics were calculated from continuously measured breath-by-breath VO2 data, whilst the rates of muscle deoxygenation (i.e., deoxygenated haemoglobin and myoglobin, [HHb+Mb]) were continuously measured by near-infrared spectroscopy at the vastus lateralis muscle. VO2 and Δ[HHb+Mb] responses were modelled using a bi-exponential model. Time point analysis of VO2 and [HHb+Mb] responses were performed using a two-way ANOVA. Values are mean ± SD. The VO2τp were speeded by a similar magnitude in both MICT (Pre: 33.6 ± 5.1, Post: 24.7 ± 5.1 s; P < 0.05) and LVHIIT (Pre: 30.7 ± 5.3, Post: 26.4 ± 2.7 s; P < 0.05) but no effect was observed for the same parameter for the control group. Similarly, the overall mean response time of the VO2 response (fitted by a mono-exponential model) in both training groups was significantly speeded, but not in the control group. The amplitude of the VO2 slow component (As) was reduced in the MICT group only. There were no changes between or within group pre and post intervention for muscle deoxygenation parameters. In middle-aged individuals with T2D, MICT and LVHIIT enhanced VO2 kinetics responses during high intensity exercise likely consequent to a training-induced increase in muscle blood flow and/or improved muscle perfusion to metabolic rate.