Intramyocellular Oxygen Availability Does Not Limit Oxidative Capacity In Vivo In Young Or Older Adults

Phosphorus magnetic resonance spectroscopy (31P MRS) is commonly used to measure post-contraction intramyocellular phosphocreatine (PCr) recovery kinetics (kPCr), which reflect the maximal rate of mitochondrial energy production in vivo. However, mitochondrial respiration and thus kPCr are slowed if intramyocellular oxygen availability (PO2) falls below its critical threshold (< 0.35 Torr). Presently, it is not known whether O2 is limited during oxidative capacity measurements or if there are age-related differences in PO2 that contribute to potential age-related differences in kPCr. PURPOSE: Determine whether intramyocellular PO2 limits oxidative capacity in vivo in young or older muscle. METHODS: 12 young (35 ± 3 yr, mean ± SD; moderate-vigorous physical activity [MVPA]: 254 ± 144 min·week-1, 7 female) and 8 older (71 ± 1 yr, MVPA: 306 ± 149 min·week-1, 5 female) adults completed a 24-s knee extensor maximal contraction protocol (0.5 Hz, 120°·s-1), 10 min of recovery, and 8 min of cuff ischemia while supine in a 3 T MR scanner. Simultaneous measurements of PCr (by 31P MRS) and deoxygenated myoglobin (dMb, by 1H MRS) were acquired from the vastus lateralis muscle throughout and used to calculate kPCr (s-1) and PO2 (Torr), respectively. Oxygen availability was quantified as PO2 during the final 4 s of contractions. Group differences were evaluated by unpaired t tests and the relationships between PO2 and kPCr were evaluated by linear regression. RESULTS: Compared with the older muscle (0.021 ± 0.003 s-1), kPCr was greater in the younger muscle (0.025 ± 0.005 s-1, p = 0.02). PO2 remained above 0.35 Torr in older (2.1 ± 1.1 Torr) and younger (1.4 ± 1.0 Torr) muscle and did not differ by age (p = 0.16). PO2 was not linearly related to kPCr in the older (r2 = 0.08, p = 0.49), young (r2 = 0.22, p = 0.12) or combined (r2 = 0.02, p = 0.51) groups. CONCLUSIONS: These data indicate that, during a contraction protocol designed to quantify muscle oxidative capacity, intracellular PO2 remained above critical and thus did not limit kPCr. The lack of association between PO2 and kPCr confirms this by showing that oxidative capacity was independent of O2 availability, provided PO2 is above the minimum threshold. Lastly, the lower kPCr observed here in older muscle reflects its lower mitochondrial capacity and not a limitation in O2 availability in vivo. Funding: NIH R01 AG058607