The effects of low-volume high-intensity interval training on pulmonary oxygen uptake and muscle deoxygentaion kinetics during heavy intensity exercise in type 2 diabetes.

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 (tau_p, τ_p) 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 VO₂τ_p 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 (A_s) 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. (PCB 182)