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

Abstract

Type I diabetes reduces dramatically the capacity of skeletal muscle to receive oxygen (Q˙o 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 Po 2 [PmO2 , which reflects the dynamic balance between O2 utilization (V˙o 2) andQ˙o 2] of the spinotrapezius muscle after the onset of electrical stimulation (1 Hz) would be faster compared with that of C rats. PmO2 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, PmO2 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). PmO2 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 alteredV˙o 2-to-Q˙o 2matching across the rest-exercise transition in muscles of D rats.