4.4 Article

Priming exercise accelerates pulmonary oxygen uptake kinetics during work-to-work cycle exercise in middle-aged individuals with type 2 diabetes

Journal

EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
Volume 121, Issue 2, Pages 409-423

Publisher

SPRINGER
DOI: 10.1007/s00421-020-04518-y

Keywords

Near-infrared spectroscopy; Oxygen extraction; Cycling; Oxygen uptake slow component; Electromyography

Funding

  1. Health Research Board [HRA_POR/2073/274]

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This study found that high-intensity priming exercise can accelerate the pulmonary oxygen uptake kinetics time constant in type 2 diabetes patients, likely by eliminating the oxygen delivery limitation present in the unprimed condition, and reducing the oxygen uptake slow component possibly due to changes in muscle fiber activation.
Purpose The time constant of phase II pulmonary oxygen uptake kinetics ((V)over dotO(2) tau(p)) is increased when high-intensity exercise is initiated from an elevated baseline (work-to-work). A high-intensity priming exercise (PE), which enhances muscle oxygen supply, does not reduce this prolonged (V)over dotO(2) tau(p) in healthy active individuals, likely because (V)over dotO(2) tau(p) is limited by metabolic inertia (rather than oxygen delivery) in these individuals. Since (V)over dotO(2) tau(p) is more influenced by oxygen delivery in type 2 diabetes (T2D), this study tested the hypothesis that PE would reduce (V)over dotO(2) tau(p) in T2D during work-to-work cycle exercise. Methods Nine middle-aged individuals with T2D and nine controls (ND) performed four bouts of constant-load, high-intensity work-to-work transitions, each commencing from a baseline of moderate-intensity. Two bouts were completed without PE and two were preceded by PE. The rate of muscle deoxygenation ([HHb + Mb]) and surface integrated electromyography (iEMG) were measured at the right and left vastus lateralis, respectively. Results Subsequent to PE, (V)over dotO(2) tau(p) was reduced (P = 0.001) in T2D (from 59 +/- 17 to 37 +/- 20 s) but not ( P = 0.24) in ND (44 +/- 10 to 38 +/- 7 s). The amplitude of the (V)over dotO(2) slow component ((V)over dotO(2) tau(p2) A(s)) was reduced (P = 0.001) in both groups (T2D: 0.16 +/- 0.09 to 0.11 +/- 0.04 l/min; ND: 0.21 +/- 0.13 to 0.13 +/- 0.09 l/min). This was accompanied by a reduction in Delta iEMG from the onset of (V)over dotO(2) slow component to end-exercise in both groups (P < 0.001), while [HHb + Mb] kinetics remained unchanged. Conclusions PE accelerates (V)over dotO(2) tau(p) in T2D, likely by negating the O-2 delivery limitation extant in the unprimed condition, and reduces the (V)over dotO(2)A(s) possibly due to changes in muscle fibre activation.

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