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

Abstract

Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats. Am J Physiol Heart Circ Physiol 283: H926-H932, 2002. First published May 16, 2002 10.1152/ajpheart.00059.2002.-Type I diabetes reduces dramatically the capacity of skeletal muscle to receive oxygen (Q O2). In control (C; n ϭ 6) and streptozotocininduced diabetic (D: n ϭ 6, plasma glucose ϭ 25.3 Ϯ 3.9 mmol/l and C: 8.3 Ϯ 0.5 mmol/l) rats, phosphorescence quenching was used to test the hypothesis that, in D rats, the decline in microvascular PO2 [PmO 2 , which reflects the dynamic balance between O2 utilization (V O2) and Q O2] 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, PmO 2 at rest was lower (C: 31.2 Ϯ 3.2 mmHg; D: 24.3 Ϯ 1.3 mmHg, P Ͻ 0.05) and at the onset of contractions decreased after a shorter delay (C: 13.5 Ϯ 1.8 s; D: 7.6 Ϯ 2.1 s, P Ͻ 0.05) and with a reduced mean response time (C: 31.4 Ϯ 3.3 s; D: 23.9 Ϯ 3.1 s, P Ͻ 0.05). PmO 2 exhibited a marked undershoot of the end-stimulation response in D muscles (D: 3.3 Ϯ 1.1 mmHg, P Ͻ 0.05), which was absent in C muscles. These results indicate an altered V O2-to-Q O2 matching across the rest-exercise transition in muscles of D rats. streptozotocin diabetes; oxygen uptake kinetics; exercise intolerance; muscle oxygen delivery; phosphorescence quenching PULMONARY GAS EXCHANGE DYNAMICS (i.e., oxygen uptake, V O 2 kinetics) at exercise onset are slowed profoundly in diabetic patients (5, 23). Slowed V O 2 kinetics in response to a given metabolic challenge will mandate generation of a greater O 2 deficit and exacerbate intracellular perturbations of phosphocreatine, free ADP, and P i , for example, that accelerate glycogenolysis and utilization of finite glycogen reserves (33). This phenomenon is likely to contribute to the reduced exercise tolerance that is present in the diabetic condition.

Downhill running: a model of exercise hyperemia in the rat spinotrapezius muscle

“…29). However, the oxidative capacity of the spinotrapezius is a modest 14.0 -15.2 m⅐g Ϫ1 ⅐min Ϫ1 , which is only approximately one-third of that of the highly oxidative limb muscles (3,8). From the relationship between citrate synthase activity and exercising flows shown in Ref.…”

Kinetics of O2uptake, leg blood flow, and muscle deoxygenation are slowed in the upper compared with lower region of the moderate-intensity exercise domain

“…However, in our analysis, we average data into 5-or 10-s time bins to reduce variability in the profiles that may obscure any overshoot that might exist during the exercise transient. Also, Poole and colleagues (5,6,11,27) use an exposed, in situ animal muscle preparation to study microvascular PO 2 , whereas we study NIRS-derived HHb changes measured on the skin surface above the quadriceps muscle during human exercise, where the fidelity of the response may not be as great. In general the NIRS-derived HHb signal adapts with an "exponential-like" profile that we find can be fit adequately using a monoexponential model (see Fig.…”

In vivo Ca2+ buffering capacity and microvascular oxygen pressures following muscle contractions in diabetic rat skeletal muscles: fiber-type specific effects

“…These effects impact the fine balance of O 2 delivery-to-O 2 utilization, at least within the spinotrapezius muscle, such that very low Pmv O 2 values are evident at rest and both during and following contractions (6,37,38). It is conceivable that the ϳ60% fast-twitch fibers that comprise the spinotrapezius (13) are driving these aberrant Pmv O 2 profiles.…”