Key result
Priming exercise significantly reduced the primary phase time constant of pulmonary oxygen uptake kinetics from 48 seconds to 32 seconds in middle-aged individuals with type 2 diabetes.
Why the study?
Pulmonary oxygen uptake kinetics during submaximal efforts are slower in middle-aged people with type 2 diabetes, partly due to muscle oxygen supply limitations. This study examined whether high-intensity priming exercise would speed kinetics during subsequent high-intensity cycling.
Does high-intensity priming exercise accelerate pulmonary oxygen uptake kinetics during subsequent high-intensity cycling in middle-aged individuals with type 2 diabetes?
Does high-intensity priming exercise accelerate pulmonary oxygen uptake kinetics during subsequent high-intensity cycling in middle-aged individuals with type 2 diabetes?
Absolute Event Rate: 32% vs 48%
p-value: p=<0.001
A prior bout of high-intensity priming exercise normalizes the slowed oxygen uptake kinetics typically seen in middle-aged individuals with type 2 diabetes during subsequent high-intensity exercise.
Longer τp in T2D may reflect oxygen supply limits; hypothesis-generating and should not yet change practice.
Background: The primary phase time constant of pulmonary oxygen uptake kinetics ( V·O2 τ p ) during submaximal efforts is longer in middle-aged people with type 2 diabetes (T2D), partly due to limitations in oxygen supply to active muscles. This study examined if a high-intensity “priming” exercise (PE) would speed V·O2 τ p during a subsequent high-intensity cycling exercise in T2D due to enhanced oxygen delivery. Methods: Eleven (4 women) middle-aged individuals with type 2 diabetes and 11 (4 women) non-diabetic controls completed four separate cycling bouts each starting at an ‘unloaded’ baseline of 10 W and transitioning to a high-intensity constant-load. Two of the four cycling bouts were preceded by priming exercise. The dynamics of pulmonary V·O2 and muscle deoxygenation (i.e. deoxygenated haemoglobin and myoglobin concentration [HHb + Mb]), were calculated from breath-by-breath and near-infrared spectroscopy data at the vastus lateralis, respectively. Results: At baseline V·O2 τ p, was slower ( p < 0.001) in the type 2 diabetes group (48 ± 6 s) compared to the control group (34 ± 2 s) but priming exercise significantly reduced V·O2 τ p ( p < 0.001) in type 2 diabetes (32 ± 6 s) so that post priming exercise it was not different compared with controls (34 ± 3 s). Priming exercise reduced the amplitude of the V·O2 slow component (A s ) in both groups (type 2 diabetes: 0.26 ± 0.11 to 0.16 ± 0.07 L/min; control: 0.33 ± 0.13 to 0.25 ± 0.14 L/min, p < 0.001), while [HHb + Mb] kinetics remained unchanged. Conclusion: These results suggest that in middle-aged men and women with T2D, PE speeds V·O2 τ p likely by a better matching of O 2 delivery to utilisation and reduces the V·O2 A s during a subsequent high-intensity exercise.
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Rocha et al. (2022) studied Type 2 diabetes (n=22). Priming exercise vs. Unprimed exercise (no prior priming bout) was evaluated on Primary phase time constant of pulmonary oxygen uptake kinetics (VO2 τp) (p=<0.001). Priming exercise significantly reduced the primary phase time constant of pulmonary oxygen uptake kinetics from 48 seconds to 32 seconds in middle-aged individuals with type 2 diabetes.
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