Norita Gildea1, Joel Rocha2, Donal O'Shea3,4, Simon Green5, Mikel Egaña6. 1. Department of Physiology, School of Medicine, Trinity College Dublin, Dublin 2, Ireland. 2. Division of Sport and Exercise Sciences, Abertay University, Dundee, UK. 3. Department of Endocrinology, St. Columcille's Hospital, Dublin, Ireland. 4. Department of Endocrinology and Diabetes Mellitus, St. Vincent's University Hospital, Dublin, Ireland. 5. Schools of Health Sciences and Medicine, Western Sydney University, Sydney, Australia. 6. Department of Physiology, School of Medicine, Trinity College Dublin, Dublin 2, Ireland. megana@tcd.ie.
Abstract
PURPOSE: The time constant of phase II pulmonary oxygen uptake kinetics ([Formula: see text]) 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 [Formula: see text] in healthy active individuals, likely because [Formula: see text] is limited by metabolic inertia (rather than oxygen delivery) in these individuals. Since [Formula: see text] is more influenced by oxygen delivery in type 2 diabetes (T2D), this study tested the hypothesis that PE would reduce [Formula: see text] 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, [Formula: see text] 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 [Formula: see text] slow component ([Formula: see text]2 As) 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 ΔiEMG from the onset of [Formula: see text] slow component to end-exercise in both groups (P < 0.001), while [HHb + Mb] kinetics remained unchanged. CONCLUSIONS: PE accelerates [Formula: see text] in T2D, likely by negating the O2 delivery limitation extant in the unprimed condition, and reduces the [Formula: see text]As possibly due to changes in muscle fibre activation.
PURPOSE: The time constant of phase II pulmonary oxygen uptake kinetics ([Formula: see text]) 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 [Formula: see text] in healthy active individuals, likely because [Formula: see text] is limited by metabolic inertia (rather than oxygen delivery) in these individuals. Since [Formula: see text] is more influenced by oxygen delivery in type 2 diabetes (T2D), this study tested the hypothesis that PE would reduce [Formula: see text] 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, [Formula: see text] 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 [Formula: see text] slow component ([Formula: see text]2 As) 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 ΔiEMG from the onset of [Formula: see text] slow component to end-exercise in both groups (P < 0.001), while [HHb + Mb] kinetics remained unchanged. CONCLUSIONS: PE accelerates [Formula: see text] in T2D, likely by negating the O2 delivery limitation extant in the unprimed condition, and reduces the [Formula: see text]As possibly due to changes in muscle fibre activation.
Authors: Fred J Dimenna; Jonathan Fulford; Stephen J Bailey; Anni Vanhatalo; Daryl P Wilkerson; Andrew M Jones Journal: Respir Physiol Neurobiol Date: 2010-04-22 Impact factor: 1.931
Authors: Fred J Dimenna; Daryl P Wilkerson; Mark Burnley; Stephen J Bailey; Andrew M Jones Journal: Respir Physiol Neurobiol Date: 2009-08-08 Impact factor: 1.931