Plasticity of microvascular oxygenation control in rat fast-twitch muscle: effects of experimental creatine depletion.

Aging, heart failure and diabetes each compromise the matching of O2 delivery (Q˙O2)-to-metabolic requirements (O2 uptake, V˙O2) in skeletal muscle such that the O2 pressure driving blood-myocyte O2 flux (microvascular PO2, PmvO2) is reduced and contractile function impaired. In contrast, β-guanidinopropionic acid (β-GPA) treatment improves muscle contractile function, primarily in fast-twitch muscle (Moerland and Kushmerick, 1994). We tested the hypothesis that β-GPA (2% wt/BW in rat chow, 8 weeks; n=14) would improve Q˙O2-to-V˙O2 matching (elevated PmvO2) during contractions (4.5V @ 1Hz) in mixed (MG) and white (WG) portions of the gastrocnemius, both predominantly fast-twitch). Compared with control (CON), during contractions PmvO2 fell less following β-GPA (MG -54%, WG -26%, P<0.05), elevating steady-state PmvO2 (CON, MG: 10±2, WG: 9±1; β-GPA, MG 16±2, WG 18±2 mmHg, P<0.05). This reflected an increased Q˙O2/V˙O2 ratio due primarily to a reduced V˙O2 in β-GPA muscles. It is likely that this adaptation helps facilitate the β-GPA-induced enhancement of contractile function in fast-twitch muscles.