Aging impacts microvascular oxygen pressures during recovery from contractions in rat skeletal muscle

Aging-induced alterations in peripheral circulatory control during contractions reduce the microvascular partial pressure of O(2) (P(O)(2)mv; which reflects the dynamic balance in the O(2) delivery-to-O(2) uptake ratio), resulting in exaggerated intramuscular metabolic disturbances and premature fatigue. However, the extent to which this altered P(O)(2)mv during contractions is associated with prolongated muscle metabolic recovery is not known. We tested the hypothesis that the aging-induced speeding of the P(O)(2)mv on-kinetics would presage slowed P(O)(2)mv off-kinetics. The spinotrapezius muscle was exposed in six young (6-8 months) and seven old (26-28 months) male Fischer 344xBrown Norway F1-hybrid rats. The P(O)(2)mv kinetic profile was measured via phosphorescence quenching at rest, during electrically stimulated contractions (1Hz, 7-9V, 2ms pulse duration, 180s), and throughout recovery (180s). Aged rats which evidenced faster P(O)(2)mv on-kinetics (reduced mean response time (MRTon), young: 27.3+/-3.6s, old: 19.2+/-1.6s; P<0.05) exhibited markedly slowed P(O)(2)mv off-kinetics (increased MRToff, young: 46.5+/-5.9s, old: 84.8+/-7.9s; P<0.05). Accordingly, a greater degree of P(O)(2)mv on-off asymmetry (MRToff-MRTon) in the aged muscle was observed (young: 19.1+/-4.5s, old: 65.6+/-8.6s; P<0.01). We conclude that aging-induced speeding of the P(O)(2)mv on-kinetics does indeed presage a slowed P(O)(2)mv off-kinetics, which likely compromises muscle metabolic recovery and may reduce subsequent contractile performance. Moreover, the greater degree of P(O)(2)mv on-off asymmetry in the aged muscle suggests a mechanistic link between impaired microvascular oxygenation and altered muscle metabolic responses during exercise transitions.