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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00059.2002
Submitted on January 23, 2002
Accepted on May 7, 2002
1 Kinesiology, Anatomy & Physiology, Kansas State University, Manhattan, KS, USA
2 Medicine, University of California-San Diego, La Jolla, CA, USA
3 Physiology, Kirksville College of Osteopathic Medicine, Kirksville, MO, USA
* To whom correspondence should be addressed. E-mail: bbehnke{at}vet.ksu.edu.
Type I diabetes reduces dramatically the capacity of skeletal muscle to recieve oxygen (QO2). In control (C, n=6) and streptozotocin-induced diabetic (D, n=6, plasma glucose, 25.3 ± 3.9 mmol/L) rats, phosphorescence-quenching was used to test the hypothesis that, in D rats, the decline in microvascular PO2 (PO2m, which reflects the dynamic balance between O2 utilization (VO2) and QO2) of the spinotrapezius muscle following the onset of electrical stimulation (1 Hz) would be faster compared to that of C rats. PO2m data were fit with a 1 or 2 exponential process (contingent on the presence of an undershoot) with independent time delays using least squares regression analysis. In D rats, PO2m at rest was lower (C, 31.2±3.2; D, 24.3±1.3 mmHg, p<0.05) and at the onset of contractions decreased following a shorter delay (C, 13.5±1.8; D, 7.6±2.1 s, p<0.05) and with a reduced mean response time (C, 31.4±3.3; D, 23.9±3.1 s, p<0.05). PO2m exhibited a marked undershoot of the steady-state response in D (D, 3.3±1.1 mmHg, p<0.05) which was absent in C muscles. These results indicate an altered VO2-to-QO2 matching across the rest-exercise transition in muscles of diabetic rats.
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