HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kono, N. Articles by Tarui, S. Search for Related Content PubMed PubMed Citation Articles by Kono, N. Articles by Tarui, S.

Metabolic basis of improved exercise tolerance

Muscle phosphorylase deficiency after glucagon administration

From the Second Department of Internal Medicine, Osaka University Medical School, Fukushima-ku, Osaka, and the Department of Neurology (Dr. Kang), National Toneyama Hospital, Toneyama, Toyonaka, Japan.

A 26-year-old girl with muscle phosphorylase deficiency had exercise intolerance and experienced an occasional "second wind" phenomenon. Muscle glycogen concentration was about three times the normal level, whereas each glycolytic intermediate below the phosphorylase step was equivalent to only 10% of a normal level. Semi-ischemic forearm exercise tests disclosed no elevation of the venous lactate or pyruvate level, but they showed remarkable increases of serum creatine kinase and ammonia. Glucagon administration markedly augmented exercise tolerance. Forearm exercise after glucagon injection significantly increased venous lactate. Thus, the beneficial effect of glucagon is attributable to blood glucose utilization by muscle.

Address correspondence and reprint requests to Dr. Kono, The Second Department of Internal Medicine, Osaka University Medical School, Fukushima-ku, Osaka, Japan 553.

Supported in part by Grants-in-Aid for Scientific Research (nos. 544085, 557548, 57480399, 57480400, 59480214, and 59870040) and for Special Project Research (nos. 56120009.57113009, and 58105008) from the Ministry of Education, Science and Culture of Japan; Grant (no. 82-39) from NCNMMD of the Ministry of Health and Welfare of Japan; and Basic Research Grant from the Muscular Dystrophy Association of the United States.

Accepted for publication March 8, 1984.

This article has been cited by other articles:

				H. Fukui, S.-i. Taniguchi, Y. Ueta, A. Yoshida, A. Ohtahara, I. Hisatome, and C. Shigemasa Enhanced Activity of the Purine Nucleotide Cycle of the Exercising Muscle in Patients with Hyperthyroidism J. Clin. Endocrinol. Metab., May 1, 2001; 86(5): 2205 - 2210. [Abstract] [Full Text]

				S. Baqué, J. J. Guinovart, and A. M. Gómez-Foix Overexpression of Muscle Glycogen Phosphorylase in Cultured Human Muscle Fibers Causes Increased Glucose Consumption and Nonoxidative Disposal J. Biol. Chem., February 2, 1996; 271(5): 2594 - 2598. [Abstract] [Full Text] [PDF]