Periods of Acute Exercise Do Not Significantly Alter Concentrations of Inflammatory Mediators in COPD

October 10, 2020

While researchers found short periods of acute exercise did not significantly increase circulating concentrations of fibrinogen and C-reactive protein in patients with COPD, they did observe increases in total leukocyte and blood neutrophil counts.

A short period of acute exercise does not seem to significantly alter circulating concentrations of inflammatory mediators such as fibrinogen and C-reactive protein (CRP) in patients with chronic obstructive pulmonary disease (COPD), according to a recent study.

However, the study did find that a short period of exercise can increase white blood cell subsets post-exercise, as researchers observed rises in leukocyte and neutrophil counts.

The results came from 40 patients whose responses were assessed at the start and end of an 8-week, conventional community pulmonary rehabilitation program. At the beginning of the program, patients did not exhibit significant changes in fibrinogen (P = .242), CRP, (P = .476), lymphocytes (P = .165), or eosinophils (P = .268) after an acute period of exercise. Meanwhile, researches did observe substantial increases in total leukocyte (P = .004) and blood neutrophil (P<.001) counts after an acute bout of exercise at the beginning of the program.

“This study implies that acute exercise does not appear to worsen selected key systemic inflammatory markers in COPD patients as characterized by a lack of increase in established biomarkers of exacerbations in the initial stages of pulmonary rehabilitation (fibrinogen and CRP),” the authors wrote.

Comparing fibrinogen at the start and end of the program, researchers observed a significant change (P = .045), but they found no significant differences in CRP (P = .483), leukocyte count (P = .159), neutrophil count (P=.279), eosinophil count (P=.155), and lymphocyte count (P = .119) in response to exercise.

As fibrinogen response was greater at the end of the program, researchers posed the finding “potentially reflects the progressive nature of exercise training within pulmonary rehabilitation whereby the absolute intensity and/or duration of exercise in the beginning of the course may not be sufficient to induce an inflammatory response of fibrinogen. Therefore, it may be deemed that exercise needs to be strenuous and/or prolonged in nature to induce increases in fibrinogen concentration.”

According to investigators, future research should aim to determine at what point in a pulmonary rehabilitation program fibrinogen responds to acute exercise change.

The study also analyzed markers of neutrophil activation (CD11b, CD62L, CD66b) and neutrophil phenotypes (mature, CD16high/ CD62Lhigh; suppressive, CD16high/CD62Llow; immature, CD16low/CD62Lhigh; progenitor, CD16low/CD62Llow). At the beginning of the program, there were no significant changes in blood neutrophil surface CD11b (P=.470), CD62L (P=.352), or CD66b (P = .334) expression.

The researchers noted that mature (P=.414), suppressive (P=.073), and progenitor (P=.210) neutrophil phenotypes were also not significantly impacted by the period of acute exercise, although the immature neutrophil subset (P<.001) was significantly increased.

Reference: Jenkins AR, Holden NS, and Jones AW. Inflammatory responses to acute exercise during pulmonary rehabilitation in patients with COPD. Eur J Appl Physiol. Published online August 7, 2020. doi:10.1007/s00421-020-04452-z