Age-related declines in energy metabolism, muscle strength, and physical performance have been linked to lower mitochondrial respiratory capacity. This study investigates whether mitochondrial respiration in peripheral blood mononuclear cells (PBMC) is associated with substrate utilization during submaximal exercise, muscle strength, and physical function in healthy older adults.
Methods
The researchers quantified PBMC mitochondrial respiratory capacity using high-resolution respirometry to assess ROUTINE, LEAK, and MAX states. They measured postprandial substrate oxidation during steady-state treadmill walking at 60% of VO2max through indirect calorimetry, calculating fat and carbohydrate oxidation rates with standard stoichiometric equations. Metabolic flexibility was defined as a lower respiratory exchange ratio (RER) and higher relative fat oxidation at a fixed workload. Muscle strength was evaluated using handgrip dynamometry and one-repetition maximum leg extension, while physical function was assessed through gait speed and five-repetition chair rise time. The study analyzed associations with linear and logistic regression, adjusting for age, sex, skeletal muscle index, physical activity, and high-sensitive C-reactive protein concentrations.
Results
The study involved fifty community-dwelling older adults (22 men, 28 women; average age 70 ± 4 years). The results indicated that higher ROUTINE respiration correlated with RER (rho = -0.335, p = 0.020), fat utilization (rho = -0.334, p = 0.019), grip strength (rho = 0.302, p = 0.033), and gait speed (rho = 0.324, p = 0.022). Adjusted regression analyses confirmed that ROUTINE respiration was associated with greater fat oxidation (β = 0.212, 95% CI 0.049; 0.375), lower RER (β = -0.160, 95% CI -0.300; -0.020), and higher gait speed (β = 0.153, 95% CI 0.028; 0.277). Cluster analysis revealed high- and low-respiration phenotypes, with the low-respiration group showing lower counter-movement jump (CMJ) height (OR: 0.204, 95% CI 0.055; 0.763) and quadriceps strength (OR: 0.373, 95% CI 0.155; 0.897).
What this study does not show
This study does not establish a direct causal relationship between mitochondrial respiration and improved physical performance outcomes, nor does it assess the long-term effects of enhancing mitochondrial respiration on physical function.
Evidence scorecard
- Analytic validity: established
- Clinical validity: partial
- Clinical utility: not established
The evidence is based on primary research involving unclassified human status.