{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T08:57:25Z","timestamp":1781081845456,"version":"3.54.1"},"reference-count":30,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,10,13]],"date-time":"2004-10-13T00:00:00Z","timestamp":1097625600000},"content-version":"vor","delay-in-days":6314,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[1987,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The forearm ischemic exercise test (FIET) is a very important clinical tool for evaluation of patients suspected to have a metabolic disorder of muscle function. Failure to elevate lactate in blood washed out from ischemically exercised muscles confirms an abnormality of glycolytic metabolism. A normal increase of lactate on FIET is assumed to rule out a disorder of glycolytic metabolism. Two patients with low levels of muscle phosphorylase are presented who produced a normal elevation of lactate on FIET. This suggests that, although the FIET is capable of identifying patients with absence of myophosphorylase, the test cannot identify patients with a partial expression of that disorder. Evaluation of the blood samples for ammonia in addition to lactate can be a significant help in confirming that the exercise performed by the patient was an adequate challenge for the glycolytic pathway. In addition, failure to elevate ammonia on ischemic exercise can identify a relatively new disorder of muscle metabolism.<\/jats:p>","DOI":"10.1002\/mus.880100609","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T07:43:53Z","timestamp":1104565433000},"page":"546-551","source":"Crossref","is-referenced-by-count":21,"title":["Ischemic exercise test: Failure to detect partial expression of Mcardle's disease"],"prefix":"10.1002","volume":"10","author":[{"given":"Robert G.","family":"Taylor","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James S.","family":"Lieberman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret M.","family":"Portwood","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2004,10,13]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00423246"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1136\/pgmj.53.617.161"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-7125(16)31673-X"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1976.00500090042008"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/mus.880090305"},{"key":"e_1_2_1_7_2","first-page":"83","article-title":"Disorders of glycogen metabolism of muscle","volume":"1","author":"DiMauro S","year":"1984","journal-title":"CRC Crit Rev Clin Neurobiol"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM196301172680306"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9343(70)80003-1"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.644316"},{"key":"e_1_2_1_11_2","first-page":"103","article-title":"Observations on the oxygen content of venous blood from the arm vein and on the oxygen consumption of resting human muscle","volume":"4","author":"Holling HE","year":"1939","journal-title":"Clin Sci"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1002\/mus.880030302"},{"key":"e_1_2_1_13_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198502073120609"},{"key":"e_1_2_1_14_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.6587566"},{"key":"e_1_2_1_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/clinchem\/13.4.314"},{"key":"e_1_2_1_16_2","first-page":"13","article-title":"Myopathy due to a defect in muscle glycogen breakdown","volume":"10","author":"McArdle B","year":"1951","journal-title":"Clin Sci"},{"key":"e_1_2_1_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(63)90137-2"},{"key":"e_1_2_1_18_2","doi-asserted-by":"publisher","DOI":"10.1002\/mus.880070706"},{"key":"e_1_2_1_19_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.45.6.791"},{"key":"e_1_2_1_20_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.20.12.1171"},{"key":"e_1_2_1_21_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(61)90075-4"},{"key":"e_1_2_1_22_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM196606092742301"},{"key":"e_1_2_1_23_2","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.1983.04050060074014"},{"key":"e_1_2_1_24_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198105283042206"},{"key":"e_1_2_1_25_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI109995"},{"key":"e_1_2_1_26_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI103983"},{"key":"e_1_2_1_27_2","doi-asserted-by":"publisher","DOI":"10.1002\/mus.880080608"},{"key":"e_1_2_1_28_2","doi-asserted-by":"publisher","DOI":"10.1002\/mus.880080704"},{"key":"e_1_2_1_29_2","doi-asserted-by":"publisher","DOI":"10.1016\/0009-8981(74)90223-X"},{"key":"e_1_2_1_30_2","doi-asserted-by":"publisher","DOI":"10.1016\/0303-8467(85)90102-7"},{"key":"e_1_2_1_31_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00430955"}],"container-title":["Muscle &amp; 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