Dean E. Mills
Nottingham Trent University
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Featured researches published by Dean E. Mills.
Medicine and Science in Sports and Exercise | 2012
Michael A. Johnson; Dean E. Mills; David McAllister Brown; Katie J Bayfield; Javier T. Gonzalez; Graham R. Sharpe
PURPOSE This study examined the effects of different pressure threshold inspiratory loads on lactate clearance and plasma acid-base balance during recovery from maximal exercise. METHODS Eight moderately trained males (V˙O(2peak) = 4.29 ± 0.46 L·min⁻¹) performed, on different days, four maximal incremental cycling tests (power started at 0 W and increased by 20 W·min⁻¹) of identical duration (exercise time during the first trial was 16.32 ± 1.12 min). During 20-min recovery, subjects either rested passively or breathed through a constant pressure threshold inspiratory load of 10 (ITL10), 15 (ITL15), or 20 (ITL20) cm H2O. Plasma lactate concentration ([La⁻]) was measured, and acid-base balance was quantified using the physicochemical approach, which describes the dependency of [H⁺] on the three independent variables: strong ion difference ([Na⁺] + [K⁺] - [Cl⁻] + [La⁻]), the total concentration of weak acids, and the partial pressure of carbon dioxide. RESULTS Peak exercise responses were not significantly different between trials. During recovery, the area under the plasma [La] curve was not different between trials (pooled mean = 261 ± 60 mEq) and the [La] measured at the end of the 20-min recovery was also similar (passive recovery = 9.2 ± 3.1 mEq·L⁻¹, ITL10 = 9.3 ± 3.1 mEq·L⁻¹, ITL15 = 8.7 ± 2.8 mEq·L⁻¹, ITL20 = 8.7 ± 3.2 mEq·L⁻¹). Similarly, changes in other strong ions contributing to strong ion difference and total concentration of weak acids, partial pressure of carbon dioxide, and, therefore, [H⁺] were not different between trials. CONCLUSIONS These data suggest that, in individuals of moderate endurance training status, inspiratory loading at the intensities used in the present study does not accelerate lactate clearance or modify plasma acid-base balance during recovery from maximal exercise.
Journal of Applied Physiology | 2013
Dean E. Mills; Michael A. Johnson; Martin J. McPhilimey; Neil C. Williams; Javier T. Gonzalez; Yvonne Barnett; Graham R. Sharpe
It is unknown whether the respiratory muscles contribute to exercise-induced increases in plasma interleukin-6 (IL-6) concentration, if this is related to diaphragm fatigue, and whether inspiratory muscle training (IMT) attenuates the plasma IL-6 response to whole body exercise and/or a volitional mimic of the exercise hyperpnea. Twelve healthy males were divided equally into an IMT or placebo (PLA) group, and before and after a 6-wk intervention they undertook, on separate days, 1 h of 1) passive rest, 2) cycling exercise at estimated maximal lactate steady state power (EX), and 3) volitional hyperpnea at rest, which mimicked the breathing and respiratory muscle recruitment patterns achieved during EX (HYPEX). Plasma IL-6 concentration remained unchanged during passive rest. The plasma IL-6 response to EX was reduced following IMT (main effect of intervention, P = 0.039) but not PLA (P = 0.272). Plasma IL-6 concentration increased during HYPEX (main effect of time, P < 0.01) and was unchanged postintervention. There was no evidence of diaphragm fatigue (measured by phrenic nerve stimulation) following each trial. In conclusion, plasma IL-6 concentration is increased during EX and HYPEX and this occurred in the absence of diaphragm fatigue. Furthermore, IMT reduced the plasma IL-6 response to EX but not HYPEX. These findings suggest that the respiratory muscles contribute to exercise-induced increases in plasma IL-6 concentration in the absence of diaphragm fatigue and that IMT can reduce the magnitude of the response to exercise but not a volitional mimic of the exercise hyperpnea.
Medicine and Science in Sports and Exercise | 2015
Dean E. Mills; Michael A. Johnson; Yvonne Barnett; William H. T. Smith; Graham R. Sharpe
PURPOSE Declining inspiratory muscle function and structure and systemic low-level inflammation and oxidative stress may contribute to morbidity and mortality during normal ageing. Therefore, we examined the effects of inspiratory muscle training (IMT) in older adults on inspiratory muscle function and structure and systemic inflammation and oxidative stress, and reexamined the reported positive effects of IMT on respiratory muscle strength, inspiratory muscle endurance, spirometry, exercise performance, physical activity levels (PAL), and quality of life (QoL). METHODS Thirty-four healthy older adults (68 ± 3 yr) with normal spirometry, respiratory muscle strength, and physical fitness were divided equally into a pressure-threshold IMT or sham-hypoxic placebo group. Before and after an 8-wk intervention, measurements were taken for dynamic inspiratory muscle function and inspiratory muscle endurance using a weighted plunger pressure-threshold loading device; diaphragm thickness by using B-mode ultrasonography; plasma cytokine concentrations by using immunoassays; DNA damage levels in peripheral blood mononuclear cells by using comet assays; spirometry, maximal mouth pressures, and exercise performance by using a 6-min walk test; PAL by using a questionnaire and accelerometry; and QoL using a questionnaire. RESULTS Compared with placebo, IMT increased maximal inspiratory pressure (+34% ± 43%, P = 0.008), diaphragm thickness at residual volume (+38% ± 39%, P = 0.03), and peak inspiratory flow (+35% ± 42%, P = 0.049) but did not change other spirometry measures, plasma cytokine concentrations, DNA damage levels in peripheral blood mononuclear cells, dynamic inspiratory muscle function, inspiratory muscle endurance, exercise performance, PAL, or QoL. CONCLUSION These novel data indicate that in healthy older adults, IMT elicits some positive changes in inspiratory muscle function and structure but neither attenuates systemic inflammation and oxidative stress nor improves exercise performance, PAL, or QoL.
Journal of Applied Physiology | 2014
Dean E. Mills; Michael A. Johnson; Martin J. McPhilimey; Neil C. Williams; Javier T. Gonzalez; Yvonne Barnett; Graham R. Sharpe
The influence of oxidative stress, diaphragm fatigue, and inspiratory muscle training (IMT) on the cytokine response to maximum sustainable voluntary ventilation (MSVV) is unknown. Twelve healthy males were divided equally into an IMT or placebo (PLA) group, and before and after a 6-wk intervention they undertook, on separate days, 1 h of (1) passive rest and (2) MSVV, whereby participants undertook volitional hyperpnea at rest that mimicked the breathing and respiratory muscle recruitment patterns commensurate with heavy cycling exercise. Plasma cytokines remained unchanged during passive rest. There was a main effect of time (P < 0.01) for plasma interleukin-1β (IL-1β) and interleukin-6 (IL-6) concentrations and a strong trend (P = 0.067) for plasma interleukin-1 receptor antagonist concentration during MSVV. Plasma IL-6 concentration was reduced after IMT by 27 ± 18% (main effect of intervention, P = 0.029), whereas there was no change after PLA (P = 0.753). There was no increase in a systemic marker of oxidative stress [DNA damage in peripheral blood mononuclear cells (PBMC)], and diaphragm fatigue was not related to the increases in plasma IL-1β and IL-6 concentrations. A dose-response relationship was observed between respiratory muscle work and minute ventilation and increases in plasma IL-6 concentration. In conclusion, increases in plasma IL-1β and IL-6 concentrations during MSVV were not due to diaphragm fatigue or DNA damage in PBMC. Increases in plasma IL-6 concentration during MSVV are attenuated following IMT, and the plasma IL-6 response is dependent upon the level of respiratory muscle work and minute ventilation.
Medicine and Science in Sports and Exercise | 2014
Michael A. Johnson; Dean E. Mills; Pi Brown; Graham R. Sharpe
Medicine and Science in Sports and Exercise | 2017
Dean E. Mills; Kurt Vogel; Michael A. Johnson; Graham R. Sharpe; Jeff S. Coombes; David Briskey
Archive | 2013
Michael A. Johnson; Dean E. Mills; Pi Brown; Graham R. Sharpe
European Respiratory Journal | 2012
Dean E. Mills; Michael A. Johnson; Martin McPhillimey; Neil C. Williams; Javier Ganzalez; Barnett Yvonne; Sharpe Graham
European Respiratory Journal | 2012
Dean E. Mills; Michael A. Johnson; Martin McPhillimey; Neil C. Williams; Javier T. Gonzalez; Yvonne Barnett; Sharpe Graham
European Respiratory Journal | 2011
Dean E. Mills; Graham R. Sharpe; Michael A. Johnson; Yvonne Barnett