{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T22:32:05Z","timestamp":1774564325768,"version":"3.50.1"},"reference-count":48,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2004,6,1]],"date-time":"2004-06-01T00:00:00Z","timestamp":1086048000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>During constant work-rate exercise above the lactic acidosis threshold, oxygen consumption fails to plateau by 3 minutes, but continues to rise slowly. This slow component correlates closely with the rise in lactate in normal subjects. We investigated if oxygen consumption during constant work-rate exercise could rise after 3 minutes in the absence of a rise in lactate. We studied five patients with McArdle's disease, one patient with phosphofructokinase deficiency and six normal subjects. Subjects performed two 6-minute duration constant work-rate exercise tests at 40 and 70% of peak oxygen consumption. During low-intensity exercise, oxygen consumption reached steady state by 3 minutes in both groups. Lactate rose slightly in control subjects but not in patients. During high-intensity exercise, oxygen consumption rose from the third to the sixth minute by 144 (21\u2013607) ml\/minute (median and range) in control subjects and by 142 (73\u2013306) ml\/minute in patients (p = not significant, Mann-Whitney U test). Over the same period, lactate (geometric mean and range) rose from 2.68 (1.10\u20135.00) to 5.39 (2.70\u201310.00) mmol\/L in control subjects, but did not rise in patients (1.20 [0.64\u20131.60] to 0.70 [0.57\u20131.20] mmol\/L). We conclude that the slow component of oxygen consumption during heavy exercise is not dependent on lactic acidosis.<\/jats:p>","DOI":"10.1164\/rccm.200307-974oc","type":"journal-article","created":{"date-parts":[[2004,4,12]],"date-time":"2004-04-12T20:24:42Z","timestamp":1081801482000},"page":"1238-1244","source":"Crossref","is-referenced-by-count":12,"title":["Gas Exchange Responses to Constant Work-Rate Exercise in Patients with Glycogenosis Type V and VII"],"prefix":"10.1093","volume":"169","author":[{"given":"Hean-Yee","family":"Ong","sequence":"first","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Conor S.","family":"O'Dochartaigh","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sharon","family":"Lovell","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victor H.","family":"Patterson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karlman","family":"Wasserman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. Paul","family":"Nicholls","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marshall S.","family":"Riley","sequence":"additional","affiliation":[{"name":"Department of Medicine, Royal Victoria Hospital; Department of Neurology, Royal Victoria Hospital; Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland; and Division of Respiratory and Critical Care Physiology and Medicine, Harbor-UCLA Medical Center, Torrance, 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