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1 Department of Kinesiology and Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506-5802; 2 Department of Medicine, University of California, La Jolla, California 92093-0623; and 3 Department of Physiology, Kirksville College of Osteopathic Medicine, Kirksville, Missouri 63501
Type I diabetes reduces
dramatically the capacity of skeletal muscle to receive oxygen
(
O2). 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 [PmO2, which
reflects the dynamic balance between O2 utilization (
O2) and
O2] 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 altered
O2-to-O2
matching across the rest-exercise transition in muscles of D rats.
streptozotocin diabetes; oxygen uptake kinetics; exercise intolerance; muscle oxygen delivery; phosphorescence quenching
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