The effect of exercise training on inflammatory responses to acute exercise in patients with COPD: preliminary findings

Future Physiology (Leeds, UK) (2017) Proc Physiol Soc 39, PC29

Poster Communications: The effect of exercise training on inflammatory responses to acute exercise in patients with COPD: preliminary findings

A. R. Jenkins1, N. S. Holden2, A. Jones1

1. Institute for Health, University of Lincoln, Lincoln, United Kingdom. 2. School of Life Sciences, University of Lincoln, Lincoln, United Kingdom.

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Background – Low-grade systemic inflammation is part of the usual aging process. Chronic obstructive pulmonary disease (COPD), a progressive and irreversible lung condition has been characterised as an accelerated aging phenotype. Exercise is highly recommended for these patients, where it is proposed that increases in inflammatory mediators in those unaccustomed to exercise is followed by an induction of an anti-inflammatory environment with regular bouts of exercise. Neutrophils play a key role in inflammation in COPD, not only in the stable state but also in disease progression. The aim of this study was to assess the effects of acute exercise, as part of an exercise training programme, on inflammatory parameters in COPD. Methods – 13 mild-severe COPD patients (FEV1pred, 48 ± 16%) had blood samples taken pre- and post-exercise at the start (Untrained) and end (Trained) of a National Health Service commissioned exercise training programme. Blood neutrophil counts were obtained using an automated haematology analyser (Horiba ABX Pentra 60, Horiba Medical). Established markers of neutrophil activation were assessed in blood neutrophils (CD45+ CD16+) using flow cytometry (BD FACS Verse, BD Biosciences). Preliminary results were analysed using mean differences and Cohen’s d to quantify effect size. Results – Blood neutrophil counts increased moderately post-exercise in both the Untrained and Trained states (Untrained, mean difference ± SD, 0.61 ± 0.55; d = 0.6; Trained, 0.53 ± 0.99; d = 0.5). CD62L expression decreased in a trivial manner following exercise in the Untrained state (-148 ± 3796; d < 0.1) before a moderate decrease was seen post-exercise in the Trained state (-2554 ± 4132; d = 0.5). There were trivial changes in CD11b (94 ± 882; d = 0.1) and CD66b (35 ± 2086; d = 0.1) expression post-exercise in the Untrained state. Small decreases in CD11b (-377 ± 930; d = 0.2) but not CD66b expression (32 ± 1551; d = 0.1) were observed post-exercise in the Trained state. Conclusions – The preliminary findings from this study suggest that exercise training modulates expression of blood neutrophil activation markers (CD62L and CD11b) following acute exercise. Such effects are seen despite acute exercise bouts inducing similar elevations in neutrophil count in both an untrained and trained state. Acute exercise does not appear to exacerbate inflammatory responses in previously sedentary COPD patients but following regular exposure to exercise, each bout may have an important disease modifying potential.



Where applicable, experiments conform with Society ethical requirements.

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