科研之友
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摘要
Reactive oxygen species, such as hydrogen peroxide (H2O2), exert a critical regulatory role on skeletal muscle function. Whether acute increases in H2O2 modulate muscle microvascular O-2 delivery-utilization (<(Q)over dot>O-2/ <(V)over dot>O2) matching [i.e., microvascular partial pressure of O-2 (Pmv(O2))] at rest and following the onset of contractions is unknown. The hypothesis was tested that H2O2 treatment (exogenous H2O2) would enhance Pmv(O2) and slow Pmv(O2) kinetics during contractions compared with control. Anesthetized, healthy young Sprague-Dawley rats had their spinotrapezius muscles either exposed for measurement of blood flow (and therefore <(Q)over dot>O-2), <(V)over dot>O-2, and Pmv(O2), or exteriorized for measurement of force production. Electrically stimulated twitch contractions (1 Hz, similar to 7 V, 2-ms pulse duration, 3 min) were evoked following acute superfusion with Krebs-Henseleit (control) and H2O2 (100 mu M). Relative to control, H2O2 treatment elicited disproportionate increases in <(Q)over dot>O2 and <(V)over dot>O2 that elevated Pmv(O2) at rest and throughout contractions and slowed overall Pmv(O2) kinetics (i.e., similar to 85% slower mean response time; P < 0.05). Accordingly, H2O2 resulted in similar to 33% greater overall Pmv(O2), as assessed by the area under the Pmv(O2) curve (P < 0.05). Muscle force production was not altered with H2O2 treatment (P > 0.05), evidencing reduced economy during contractions (similar to 40% decrease in the force/<(V)over dot>O-2 relationship; P < 0.05). These findings indicate that, although increasing the driving force for blood-myocyte O-2 flux (i.e., Pmv(O2)), transient elevations in H2O2 impair skeletal muscle i.e., reduced economy during contractions), which mechanistically may underlie, in part, the reduced exercise tolerance in conditions associated with oxidative stress.
- 出版日期2011-5
