AJP - Endocrinology and Metabolism, Vol 273, Issue 1 E220-E225, Copyright © 1997 by American Physiological Society
Exercise-stimulated glucose transport in skeletal muscle is nitric oxide dependent
C. K. Roberts, R. J. Barnard, S. H. Scheck and T. W. Balon
Department of Physiological Science, University of California, Los Angeles 90024, USA.
It has been suggested that there are separate insulin-stimulated and
contraction-stimulated glucose transport pathways in skeletal muscle. This
study examined the effects of nitric oxide on glucose transport in rat
skeletal muscle by use of an isolated sarcolemmal membrane preparation and
the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester
(L-NAME), administered in the drinking water (1 mg/ml). Female
Sprague-Dawley rats were divided into five groups: control, acute exercise,
acute exercise+L-NAME, insulin stimulated, and insulin stimulated+L-NAME.
Exercise (45 min of exhaustive treadmill running) increased glucose
transport (37 +/- 2 to 76 +/- 5 pmol.mg-1.15 s-1) and this increase was
completely inhibited by L-NAME (40 +/- 4 pmol.mg-1.15 s-1). A maximum dose
of insulin increased glucose transport (87 +/- 10 pmol.mg-1.15 s-1), and
adding L-NAME had no effect (87 +/- 11 pmol.mg-1.15 s-1). In addition,
exercise, but not exercise+L-NAME, increased sarcolemma GLUT-4 content.
This study confirms that there are separate pathways for contraction- and
insulin-stimulated glucose transport. More importantly, although exercise
and insulin both significantly increased glucose transport, L-NAME had no
effect on insulin-stimulated glucose transport but blocked the
exercise-stimulated transport. We conclude that nitric oxide is involved in
the signal transduction mechanism to increase glucose transport during
exercise.
