Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats

Type I diabetes reduces dramatically the capacity of skeletal muscle to receive oxygen ((Q)over dotO(2)). In control (C; n=6) and streptozotocin-induced diabetic (D: n=6, plasma glucose = 25.3+/-3.9 mmol/l and C: 8.3+/-0.5 mmol/l) rats, phosphorescence quenching was used to test the hypothesis that, in D rats, the decline in microvascular PO2 [Pm-O 2, which reflects the dynamic balance between O-2 utilization ((V)over dotO(2)) and (Q)over dotO(2)] of the spinotrapezius muscle after the onset of electrical stimulation (1 Hz) would be faster compared with that of C rats. PmO 2 data were fit with a one or two exponential process (contingent on the presence of an undershoot) with independent time delays using least-squares regression analysis. In D rats, Pm-O 2 at rest was lower (C:31.2+/-3.2 mmHg; D: 24.3+/-1.3 mmHg, P<0.05) and at the onset of contractions decreased after a shorter delay (C: 13.5 +/- 1.8 s; D: 7.6 +/- 2.1 s, P<0.05) and with a reduced mean response time (C: 31.4+/-3.3 s; D: 23.9+/-3.1 s, P<0.05). Pm-O 2 exhibited a marked undershoot of the end-stimulation response in D muscles (D: 3.3 +/- 1.1 mmHg, P<0.05), which was absent in C muscles. These results indicate an altered (V)over dotO(2)-to-(Q)over dotO(2) matching across the rest-exercise transition in muscles of D rats.