P. gingivalis infection suppresses PGC-1α expression, reducing muscle endurance capacity after training in rats

Porphyromonas gingivalis, a major pathogen in periodontitis, is increasingly recognized for its systemic inflammatory effects, contributing to conditions like inflammatory arthritis and Alzheimer's disease. The impact of this chronic low-grade inflammation on skeletal muscle function and exercise adaptation remains less explored. PGC-1α is a master regulator of mitochondrial biogenesis and a critical factor in enhancing muscle endurance capacity in response to training. Understanding how P. gingivalis infection influences PGC-1α expression is key to elucidating its potential to impair exercise benefits.

Twenty 8-week-old Wistar rats were randomly divided into two groups. The P. g-group received sonicated P. gingivalis via intraperitoneal administration, while the Control-group received saline. After three weeks of administration, both groups underwent a treadmill exercise protocol. Gastrocnemius muscles and blood samples were collected 24 hours after the exercise session. Researchers measured the expression of PGC-1α and TNF-α in the gastrocnemius muscle (likely via qPCR or Western blot, though not specified) and serum IgG antibody titers against P. gingivalis to confirm infection.

Serum IgG antibody titers against P. gingivalis were significantly higher in the P. g-group compared to the Control-group, confirming a robust systemic immune response to the infection. Concurrently, TNF-α expression in the skeletal muscle was also significantly higher in the P. g-group, indicating localized inflammation. This inflammatory state correlated with a crucial metabolic change:

PGC-1α expression, a key regulator of mitochondrial biogenesis and exercise adaptation, was significantly lower in the P. g-group than in the Control-group. A clear negative correlation was observed between PGC-1α and TNF-α expression, suggesting that P. gingivalis-induced inflammation, potentially mediated by TNF-α, directly suppresses PGC-1α activity. These findings collectively indicate that P. gingivalis infection induces systemic and local inflammation that impairs the molecular machinery essential for improving muscle endurance.