Regular, Sustained Exercise Helps in Managing CF, Study Suggests
Physical activity, undertaken regularly over the long term, appears to complement other therapies in managing cystic fibrosis (CF), a study in a group of active and non-active patients found.
Its results also showed that tumor necrosis factor alpha (TNF-alpha) may serve as a biomarker of inflammation to monitor the benefits of exercise — both aerobic and anaerobic (weight lifting).
The study, “Physical Activity Regulates TNFα and IL-6 Expression to Counteract Inflammation in Cystic Fibrosis Patients,” was published in the International Journal of Environmental Research and Public Health.
Chronic inflammation, associated with pro-inflammatory molecules like TNF-alpha, accompanies the progressive loss of lung function that characterizes CF. Numerous studies have shown that exercise reduces chronic inflammation, and regular activity over time is associated with fewer upper respiratory infections.
One of the ways in which exercise counters inflammation is by triggering muscles to release signaling molecules, the most common of which is called interleukin-6 (IL-6).
Researchers in Italy monitored changes in the levels of TNF-alpha and IL-6, while evaluating the anti-inflammatory effects of exercise among CF patients who regularly engaged in exercise and those who did not.
They recruited 85 adults with CF in to participate in their study: 42 who were physically active over the prior three years (mean age, 29.8; 20 men and 22 women), and 43 inactive patients (mean age, 31.1; 22 men and 21 women).
More physically active individuals were seen to have higher IL-6 levels than their less active counterparts, and significantly lower TNF-alpha levels. Active participants also had lower hospitalization rates and non-significant declines in lung function, as measured by forced expiratory volume in one second (FEV1), a standard measure of lung health.
TNF-alpha also appeared to rise and fall, along with resting blood sugar levels, among active participants.
In the less active group, rising TNF-alpha levels corresponded to rising IL-6 levels and to falling adiponectin — a pro-inflammatory hormone — and leptin, a hormone that regulates appetite and body weight. Notably, both adiponectin and leptin produced and secreted by fat cells.
The inverse relationship between TNF-alpha, adiponectin, and leptin in less active adults suggested to the investigators “that the inflammatory status of these latter patients was ongoing and perpetuated” by signaling molecules — cytokines — secreted by muscle and fat tissue.
Study results supported previous findings that physical exercise — a combination of aerobic and anaerobic training — may be a useful complement to other treatment approaches, and that cytokines like TNF-alpha may serve as markers of inflammation.
“Further research is required to deeply investigate how these cytokines modulate inflammation and to test the efficacy of [physical activity] as a useful non-pharmacological [aid] in classical CF patient treatment,” the researchers concluded.
“Improvements in quality of life achieved by implementing not only exercise but also favourable lifestyle factors,” they added, “are anticipated to become more actively promoted for CF patient management in the future.”