Of Mice, Muscles, Older Adults and RSV

As the global population ages, respiratory viral infections have become a significant health concern, leading to severe morbidity and increased mortality in this demographic. Skeletal muscle loss is ordinarily a feature of aging and age-related health conditions. However, in the setting of severe respiratory infections, susceptible older adults experience faster muscle deterioration. But the mechanisms contributing to accelerated muscle loss are not well established.

Using an aged mice model, researchers demonstrated the pathophysiological mechanisms during respiratory syncytial virus (RSV) infection in a study published in Geroscience.J. Sophie Sagawe, Ph.D., from the National Heart and Lung Institute in London and team investigated how aging impacts inflammatory responses and subsequent muscle degradation.

The research on aged mice identified specific pathways through which RSV infection exacerbates muscle loss. Key findings included increased disease severity, as aged mice exhibited more severe illness, characterized by greater weight loss. The aged mice also had higher viral loads and delayed viral clearance. Additionally, they had reduced feeding and heightened airway inflammation during RSV infection compared with their younger counterparts.

Muscle wasting was another noticeable change. Significant decreases in both leg muscle weight and muscle fiber size were observed in aged mice post-infection. This loss of muscle mass aligns with previous literature highlighting the risks of sarcopenia, the medical term for age-related muscle loss.

Aged mice demonstrated increased expression of key atrophy-related genes, specifically Atrogin-1 and MuRF-1. These enzymes are known to promote muscle protein breakdown, suggesting that RSV infection triggers a catabolic response that is more pronounced in older mice. Furthermore, aged mice failed to elevate muscle protein synthesis rates during infection, indicating a disruption in the balance of muscle turnover, which is critical for muscle maintenance.

The study also showed a correlation between the increased expression of markers of atrophy with elevated levels of interleukin-6 in the lungs, linking systemic inflammation to localized muscle degradation.

The implications of this research are significant for both clinical practice and further scientific inquiry. Muscle wasting is a natural process exacerbated by chronic disease and inactivity. The data gathered from aged mice helps thje understanding of the relationship between aging, inflammation and muscle health. Recognizing that respiratory infections can intensify muscle loss opens avenues for targeted interventions in elderly patients.

The identification of elevated IL-6 and other atrophy-promoting factors suggests potential therapeutic targets. Interventions that aim to modulate the inflammatory response may help mitigate muscle loss during respiratory infections in older adults.