Exercise-Induced Modulation of Lung Injury Responses

Regular physical exercise exerts profound effects on pulmonary host defence and repair mechanisms in the context of lung injury. Through modulation of the innate immune response, exercise can attenuate neutrophil recruitment, diminish pro-inflammatory cytokine release and promote antioxidant defence pathways. Adaptive changes include a shift in alveolar macrophage polarisation towards a reparative phenotype, reduced formation of neutrophil extracellular traps and stabilisation of endothelial barrier function. These effects have been observed across models of acute lung injury, pneumonia and sepsis, and appear to involve metabolic reprogramming in immune cells, including suppression of aerobic glycolysis and enhancement of nuclear factor erythroid 2-related factor 2 signalling. Collectively, these findings suggest that exercise represents a non-pharmacological strategy to modulate the inflammatory–anti-inflammatory and oxidative–antioxidative balance in lung injury, with potential implications for clinical management and rehabilitation of patients at risk of acute respiratory distress.

Research from Nature Portfolio

Recent studies have demonstrated that four weeks of moderate aerobic preconditioning ameliorates sepsis-associated multiple organ dysfunction, including acute lung injury, in rodent models. Trained animals exhibit reduced pulmonary inflammation and vascular permeability, alongside preservation of alveolar architecture. This exercise regimen downregulates pro-inflammatory cytokines and glycolytic enzymes in lung tissue while upregulating anti-inflammatory mediators and antioxidant transcription factors such as Nrf2. These metabolic and immunomodulatory adaptations collectively mitigate lung injury and improve survival, highlighting a key role for exercise-induced metabolic reprogramming in the host defensive response to systemic infection.

Exercise-Induced Modulation of Lung Injury Responses publication trend

The graph below shows the total number of articles in exercise-induced modulation of lung injury responses across all publications each year (not limited to Nature Index journals).

Technical terms

Acute lung injury (ALI): A syndrome characterised by diffuse inflammation, increased vascular permeability and impaired gas exchange in the lungs.

Neutrophil extracellular traps (NETs): Web-like DNA structures released by activated neutrophils that can exacerbate inflammatory tissue damage.

Alveolar macrophages: Resident immune cells in the lung alveoli that orchestrate inflammatory and reparative responses.

Warburg effect: A metabolic shift favouring glycolysis over oxidative phosphorylation even in the presence of oxygen, influencing immune cell activation and function.

References

1. Moderate Exercise Modulates Inflammatory Responses and Improves Survival in a Murine Model of Acute Pneumonia*. Critical Care Medicine (2024).
2. Voluntary running exercise protects against sepsis-induced early inflammatory and pro-coagulant responses in aged mice. Critical Care (2017).
3. Aerobic Exercise Attenuates Acute Lung Injury Through NET Inhibition. Frontiers in Immunology (2020).
4. Aerobic exercise improves LPS-induced sepsis via regulating the Warburg effect in mice. Scientific Reports (2021).