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Diabetes, Vol 42, Issue 7 956-965, Copyright © 1993 by American Diabetes Association
Regulation of glucose uptake and metabolism by working muscle. An in vivo analysis
BA Zinker, DB Lacy, D Bracy, J Jacobs and DH Wasserman
Department of Molecular Physiology and Biophysics, Vanderbilt School of Medicine, Nashville, TN 37232-0615.
To assess the mechanisms whereby muscular work stimulates glucose uptake
and metabolism in vivo, dogs were studied during rest (-40-0 min), moderate
exercise (0-90 min), and exercise recovery (90-180 min) with plasma glucose
clamped at 5.0, 6.7, 8.3, and 10.0 mM (n = 5 at 5.0 mM and n = 4 at all
other levels) using a variable glucose infusion. Basal insulin was
maintained with somatostatin and insulin replacement. Whole-body glucose
uptake, limb glucose uptake, and oxidative and nonoxidative glucose plus
lactate metabolism, were assessed with tracers ([3H]glucose and
[14C]glucose) and arteriovenous differences. The combined effects of
glucose and exercise on the increment above resting values for limb glucose
uptake, arteriovenous glucose difference, LGO, LGNO, and rate of glucose
disappearance were synergistic (approximately 112, 90, 125, 76, and 90%
greater than the additive values, respectively). Neither exercise nor
recovery affected the Km for limb glucose uptake (4.7 +/- 1.1, 4.8 +/- 0.4,
and 5.2 +/- 0.3 mM during rest, exercise, and recovery, respectively), but
both conditions increased the Vmax (44 +/- 16, 217 +/- 30, and 118 +/- 14
mumol/min during rest, exercise, and recovery, respectively). Similarly,
the Km for arteriovenous glucose differences were unaffected by exercise
recovery (4.9 +/- 0.6, 5.0 +/- 0.4, and 5.3 +/- 0.3 mM during rest,
exercise, and recovery, respectively), but the maximum rose (272 +/- 50,
650 +/- 78, and 822 +/- 111 microM during rest, exercise, and recovery,
respectively). The LGO was unchanged by glycemia at rest (15 +/- 4
mumol/min at 10.0 mM). The Km for LGO during exercise was 5.1 +/- 0.3 mM,
and the Vmax was 163 +/- 15. The capacity for LGO returned to basal during
recovery. LGNO increased gradually with increasing glycemia during rest,
exercise, and recovery and did not approach saturation (38 +/- 13, 105 +/-
36, and 132 +/- 45 mumol/min during rest, exercise, and recovery,
respectively, at 10.0 mM). In general, the LGNO was elevated at every
glucose level during exercise (approximately twofold) and recovery
(approximately threefold) compared with rest. Arterial free fatty acid and
glycerol levels decreased with increasing glycemia within all periods. Free
fatty acids were suppressed by a greater amount during exercise compared
with rest and recovery.(ABSTRACT TRUNCATED AT 400 WORDS)

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Copyright © 1993 by the American Diabetes Association.
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