Effects of aging on microvascular oxygen pressures in rat skeletal muscle

Aging alters skeletal muscle vascular geometry and control such that the dynamics of muscular blood flow (Q˙) and O2 delivery (Q˙O2) may be impaired across the rest-exercise transition. If, at the onset of muscle contractions, Q˙ dynamics are slowed disproportionately to those of muscle O2 uptake (V˙O2), microvascular PO2 (PO2m) would be reduced and blood-tissue O2 transfer compromised. This investigation determined the effects of aging on PO2m (a direct reflection of the Q˙O2-to-V˙O2 ratio), at rest and across the rest-contractions transition in the spinotrapezius of young (∼6 months, n = 9) and old (>24 months, n = 10) male Fisher 344/Brown Norway hybrid rats. Phosphorescence quenching techniques were used to quantify PO2m, and test the hypothesis that, across the rest-contractions (twitch, 1 Hz; 4-6 V, 240 s) transition, aging would transiently reduce the Q˙O2-to-V˙O2 ratio causing a biphasic profile in which PO2m fell below steady-state contracting values. Old rats had a lower pre-contraction baseline PO2m than young (27.1 ± 1.9 versus 33.8 ± 1.6 mmHg, P < 0.05, respectively). In addition, in old rats PO2m demonstrated a pronounced difference between the absolute nadir and end-contracting values (2.5 ± 0.9 mmHg), which was absent in young rats. In conclusion, unlike their young counterparts, old rats exhibited a transiently reduced PO2m across the rest-contractions transition that may impair blood-tissue O2 exchange and elevate the O2 deficit, thereby contributing to premature fatigue.