Impact Of Prolonged Sitting On Peripheral Blood Mononuclear Cell Mitochondrial Function In Older Adults

Prolonged sitting (PS) has been identified as an independent risk factor for the development of cardiovascular diseases (CVDs). Interestingly, recent studies suggest that PS may contribute to CVD development by promoting systemic inflammation and oxidative stress. Therefore, assessing the effects of PS on peripheral blood mononuclear cells (PBMCs) may provide important insights into the impacts of PS on CVD development. However, no studies have examined PS-mediated changes in PBMC content and function. PURPOSE: Therefore, the purpose of this study was to examine acute PS-mediated changes in PBMC content and mitochondrial function in older adults. METHODS: Six healthy older adults (73.76 ± 4.25 years) participated in 2.5 hours of PS. Blood samples (10 mL) were collected before and after PS. PBMCs were isolated via centrifugation, PBMC content was assessed with an automated cell counter, and PBMC mitochondrial function was assessed by high-resolution respirometry. RESULTS: Interestingly, although acute PS significantly increased PBMC content (114,312 ± 31,831 vs. 127,685 ± 36,144 cell/mL; p < 0.05), mitochondrial complex I state 3 respiration (4.64 ± 1.17 vs. 3.73 ± 1.11 pmol/s-1/cell-1; p < 0.05) and complex I + II state 3 respiration (11.31 ± 1.91 vs. 9.00 ± 2.09 pmol/s-1/cell-1; p < 0.05) were significantly decreased. Furthermore, the respiratory control ratio (complex I + II state 3 / state 4) was significantly lower after PS (3.76 ± 0.85 vs. 2.86 ± 0.42, p < 0.05), which indicates a reduction in mitochondrial efficiency. However, complex IV respiration was not changed after PS (51.38 ± 7.23 vs. 50.24 ± 7.94 pmol/s-1/cell-1; p = 0.48), which indicates no change in mitochondrial content. CONCLUSION: These findings suggest that even a single bout of PS may increase systemic inflammation, which may contribute to cardiovascular disease risks in older adults.