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[O.sub.2]). In control (C; n = 6) and streptozotocin-induced diabetic (D: n = 6, plasma glucose = 25.3 [+ or -] 3.9 mmol/l and C: 8.3 [+ or -] 0.5 mmol/l) rats, phosphorescence quenching was used to test the hypothesis that, in D rats, the decline in microvascular P[O.sub.2] [[MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII], which reflects the dynamic balance between [O.sub.2] utilization (V[O.sub.2]) and Q[O.sub.2]] of the spinotrapezius muscle after the onset of electrical stimulation (1 Hz) would be faster compared with that of C rats. [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] 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, [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] at rest was lower (C: 31.2 [+ or -] 3.2 mmHg; D: 24.3 [+ or -] 1.3 mmHg, P < 0.05) and at the onset of contractions decreased after a shorter delay (C: 13.5 [+ or -] 1.8 s; D: 7.6 [+ or -] 2.1 s, P < 0.05) and with a reduced mean response time (C: 31.4 [+ or -] 3.3 s; D: 23.9 [+ or -] 3.1 s, P < 0.05). [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] exhibited a marked undershoot of the end-stimulation response in D muscles (D: 3.3 [+ or -] 1.1 mmHg, P < 0.05), which was absent in C muscles. These results indicate an altered V[O.sub.2]-to-Q[O.sub.2] matching across the rest-exercise transition in muscles of D rats. streptozotocin diabetes; oxygen uptake kinetics; exercise intolerance; muscle oxygen delivery; phosphorescence quenching