| dc.description.abstract | Peak oxygen uptake (V̇O2peak) is consistently reduced in individuals with type 2 diabetes (T2D) of all ages compared with non-diabetic (ND) controls. In middle-aged (between 45 to 60 y) individuals with T2D these reductions in V̇O2peak are influenced by a reduced rate of microvascular blood flow adaptations, but it is unknown if these vascular impairments are apparent in older individuals with this disease. In addition, the dynamic response of V̇O2 at the onset of moderate-intensity exercise (V̇O2 kinetics) is blunted (i.e. slowed) in middle-aged, but not older (between 60 to 70 y) people with T2D compared with age-matched corresponding ND controls. This is likely due to the powerful deleterious effect of ageing per se mainly in untrained individuals. Understanding how to ameliorate these impairments and the confounding effects of older age is important given that these limitations may lead to cardiovascular complications and all-cause mortality.
In this regard, an acute bout of heavy-intensity priming exercise (PE) as well as short-term training interventions involving moderate-intensity continuous training (MICT) and/or low-volume high-intensity interval training (HIIT) have been shown to be effective at speeding V̇O2 kinetics and thus, improving exercise tolerance mainly in middle-aged adults with uncomplicated T2D. However, these effects have not been assessed in older individuals living with T2D.
To further explore these important adaptations, Experiment 1 examined the influence of T2D on muscle deoxygenation ([HHb+Mb]) during ramp incremental cycle exercise in older adults. Fourteen older untrained adults with T2D (62.9 ± 2.8 y; 29.0 ± 3.7 kg.m-2; 9 males/5 females) and 14 untrained older ND controls (64.8 ± 3.9 y; 27.1 ± 2.8 kg.m-2; 10 males/4 females) completed the ramp cycle test. Normalised [HHb+Mb] profiles of the vastus lateralis muscle (%[HHb+Mb]) were plotted as a function of relative peak power output (%PO) using a bilinear model. V̇O2peak was significantly reduced in older individuals with T2D compared to ND controls (27.1 ± 5.7 vs. 23.3 ± 4.0 mL.kg-1.min-1), however, no difference was observed in the primary slope of the Δ%[HHb+Mb]/Δ%PO. These findings suggest that in contrast to middle-aged individuals with T2D, a greater rate of fractional O2 extraction in the exercising musculature for a given increase in V̇O2, indicative of reduced O2 delivery, is not a contributing factor to the reduction in V̇O2peak observed in older individuals with T2D compared to older ND controls.
Experiment 2 investigated the effects of a heavy-intensity PE on a subsequent heavy-intensity cycling exercise in older individuals with T2D (62.5 ± 3 y; 29.4 ± 4.5 kg.m-2; 8 males/1 female) and older ND controls (63.3 ± 3.9 y; 28.4 ± 2.3 kg.m-2; 8 males/1 female). No differences were observed between groups for V̇O2 [HHb+Mb] kinetics in the unprimed bout. Following PE, both groups displayed a significant acceleration for the time constant of the V̇O2 primary phase (τV̇O2P) at the onset of exercise (T2D: 40 ± 3 vs. 32 ± 3 s; ND: 43 ± 5 vs. 34 ± 6 s). A significant reduction in the slow component (V̇O2SC) amplitude was also observed in both groups (T2D: 0.3 ± 0.1 vs. 0.2 ± 0.1 L.min-1; ND: 0.3 ± 0.1 vs. 0.2 ± 0.1 L.min-1). This occurred in conjunction with a slower muscle [HHb+Mb] time constant of the primary phase (Δ[HHb+Mb]τp) in both groups, suggesting an improvement in O2 delivery to utilisation within the exercising muscle which may enhance exercise tolerance in both groups.
When initiating high-intensity exercise from an elevated baseline (work-to-work: WtoW), middle-aged individuals with T2D display a sluggish V̇O2 kinetic response compared to that observed during heavy-intensity exercise initiated from an “unloaded” baseline. The objective of Experiment 3 was to further investigate this influence of PE on V̇O2 and [HHb+Mb] kinetics during a subsequent WtoW exercise bout in older adults with T2D (62.2 ± 2.8 y; 30.1 ± 3.3 kg.m-2; 8 males/2 females) and ND controls (64 ± 4.2 y; 27.6 ± 2.5 kg.m-2; 8 males/2 females). No differences were observed between groups for any responses during the unprimed bouts. Following PE, a reduction occurred in both, the τV̇O2P response (T2D: 49 ± 6 vs. 34 ± 4 s; ND: 49 ± 7 vs. 38 ± 9 s) and the amplitude of the V̇O2SC (T2D: 0.2 ± 0.0 vs. 0.1 ± 0.0 L.min-1; ND: 0.2 ± 0.1 vs. 0.1 ± 0.1 L.min-1). No changes were observed for any [HHb+Mb] responses following PE. These results indicate that PE induced a speeding V̇O2 kinetics response due to a faster contribution from the aerobic metabolism via improvements in O2 delivery as well as an alteration in motor unit recruitment, and that these effects were similar in both groups.
Experiment 4 investigated the effects of 12 weeks of MICT and low-volume HIIT on V̇O2 and [HHb+Mb] kinetics during transitions to heavy-intensity cycling exercise initiated from an unloaded baseline. Participants with T2D were randomly assigned to a control (CON) group (53.9 ± 9.4 y; 30.5 ± 3.6 kg.m-2; 4 males/5 females), a MICT group (54.2 ± 9.9 y; 31.3 ± 5.8 kg.m-2; 7 males/3 females; 50 min of moderate-intensity cycling) and a HIIT group (52 ± 10.1 y; 28.8 ± 3.2 kg.m-2; 6 males/3 females; 10 x 1 min high-intensity bouts at ~90% maximal heart rate interspersed by 1 min of unloaded cycling). Exercise groups trained 3 times per week with the intensity adjusted every 3 weeks. After 12 weeks, τV̇O2P was accelerated for both MICT (35±4 vs. 24±4 s) and HIIT (33±5 vs. 26±3 s) groups, with no differences observed in the CON group (32±4 vs. 31±5 s). Additionally, a significant slowing of the Δ[HHb+Mb]τp response occurred in both exercising groups but not in the control group. Taken together, these results indicate that both exercising groups induced similar benefits in V̇O2 kinetics due to improvements in O2 delivery and/or distribution relative to O2 utilisation.
In conclusion, the accumulated data for the first three experiments of this thesis indicate that no apparent differences in pathophysiological mechanisms are evident with respect to peripheral factors for the impaired exercise tolerance observed in older people with and without T2D. In addition, an acute intervention such as heavy-intensity PE may be effective at improving microvascular blood flow to the exercising muscle, thus, improving the aerobic contribution to exercise and, thereby, increasing exercise tolerance in inactive older adults with and without T2D. Finally, given that the magnitude of effects on V̇O2 kinetics subsequent to low-volume HIIT and MICT were similar in Experiment 4, it is possible that low-volume HIIT, with half the time commitment and volume than MICT, may be a more effective intervention to increase both, exercise involvement and adherence in people with uncomplicated T2D. | en |
