The dynamic response of pulmonary oxygen uptake (τVO2) at the onset of moderate-intensity exercise is slowed in middle-aged individuals with type 2 diabetes (T2D) (O'Connor et al. 2012, 2015). This effect is attributed to progressive limitations of O2 delivery and/or utilisation. While traditional moderate-intensity continuous training (MICT) is an established strategy which enhances τVO2p (McAnaney et al. 2012), the effects of a time efficient low-volume, high-intensity interval training (LVHIIT) on τVO2p as well as the time course and mechanisms of adaptations of these enhanced VO2 kinetics following either MICT or LVHIIT are unknown. The aim of this study was to assess the rates of adjustment of VO2p and muscle deoxygenation (i.e., deoxygenated haemoglobin and myoglobin, [HHb+Mb]) during the on-transition to moderate-intensity cycling before training and at weeks 3, 6, 9 and 12 of MICT and LVHIIT. Twenty nine middle-aged individuals with T2D (17 men, 12 women; mean ± SD: age 53 ± 10 yr, body mass index 29.8 ± 4.4 kg.m-2) were randomly assigned to MICT (n=11, 50 min of moderate-intensity cycling) or LVHIIT (n=9, 10 x 1 min cycling 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. VO2 kinetics was calculated from continuously measured breath-by-breath VO2 data, whilst the rate of muscle deoxygenation was continuously measured by near-infrared spectroscopy at the vastus lateralis muscle. Time point analysis of VO2 and [HHb+Mb] responses were performed using a two-way ANOVA with repeated-measures, and post-hoc Tukey tests performed when significant differences were returned. Pre-training τVO2p decreased (P<0.05) by a similar magnitude at wk 3 of training in both MICT (from 44 ± 12 to 32 ± 5 s) and LVHIIT (from 42 ± 8 to 32 ± 4 s) with no further changes thereafter. No changes were reported in the control group. The pretraining overall adjustment of Δ[HHb+Mb] was faster than τVO2p in all groups, resulting in Δ[HHb+Mb]/VO2p showing an "overshoot" during the transient relative to the subsequent steady-state level. After 3 wks of training the Δ[HHb+Mb]/VO2p overshoot was attenuated in both MICT and LVHIIT so that the overall adjustment of Δ[HHb+Mb] was similar to τVO2p in both groups. The enhanced VO2 kinetics response consequent to both MICT and LVHIIT in T2D is likely attributed to a training-induced better matching of O2 delivery to utilisation.
|Publication status||Published - 14 Sep 2018|
|Event||Europhysiology 2018 - QEII Centre, London, United Kingdom|
Duration: 14 Sep 2018 → 16 Sep 2018
|Period||14/09/18 → 16/09/18|