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Titolo:
Regulation of skeletal muscle ATP catabolism by AMPD1 genotype during sprint exercise in asymptomatic subjects
Autore:
Norman, B; Sabina, RL; Jansson, E;
Indirizzi:
Huddinge Univ Hosp, Karolinska Inst, Dept Med Lab Sci & Technol, Div Clin Physiol, S-14186 Stockholm, Sweden Huddinge Univ Hosp Stockholm Sweden S-14186 l, S-14186 Stockholm, Sweden Med Coll Wisconsin, Dept Biochem, Milwaukee, WI 53226 USA Med Coll Wisconsin Milwaukee WI USA 53226 iochem, Milwaukee, WI 53226 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 1, volume: 91, anno: 2001,
pagine: 258 - 264
SICI:
8750-7587(200107)91:1<258:ROSMAC>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOADENYLATE DEAMINASE DEFICIENCY; PURINE NUCLEOTIDE CYCLE; HIGH-INTENSITY; EXHAUSTIVE EXERCISE; FIBERS; METABOLISM; FATIGUE; HUMANS; IMP; AMMONIA;
Keywords:
myoadenylate deaminase; adenine nucleotides; inosine monophosphate; adenosine; ammonia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Norman, B Huddinge Univ Hosp, Karolinska Inst, Dept Med Lab Sci & Technol,Div Clin Physiol, S-14186 Stockholm, Sweden Huddinge Univ Hosp StockholmSweden S-14186 Stockholm, Sweden
Citazione:
B. Norman et al., "Regulation of skeletal muscle ATP catabolism by AMPD1 genotype during sprint exercise in asymptomatic subjects", J APP PHYSL, 91(1), 2001, pp. 258-264

Abstract

Deficiency of myoadenylate deaminase, the muscle isoform of AMP deaminase encoded by the AMPD1 gene, is a common myopathic condition associated with alterations in skeletal muscle energy metabolism. However, recent studies have demonstrated that most individuals harboring this genetic abnormality are asymptomatic. Therefore, 18 healthy subjects with different AMPD1 genotypes were studied during a 30-s Wingate test in order to evaluate the influence of this inherited defect in AMPD1 expression on skeletal muscle energy metabolism and exercise performance in the asymptomatic population. Exercise performances were similar across the AMPD1 genotypes, whereas significantdifferences in several descriptors of energy metabolism were observed. Normal homozygotes (NN) exhibited the highest levels of AMP deaminase activities, net ATP catabolism, and IMP accumulation, whereas intermediate values were observed in heterozygotes (MN). Conversely, mutant homozygotes (MM) hadvery low AMP deaminase activities and showed no significant net catabolismof ATP or IMP accumulation. Accordingly, MM also did not show any postexercise increase in plasma ammonia. Unexpectedly, MN consistently exhibited greater increases in plasma ammonia compared with NN despite the relatively lower accumulation of IMP in skeletal muscle. Moreover, time course profilesof postexercise plasma ammonia and blood lactate accumulation also differed across AMPD1 genotypes. Finally, analysis of adenosine in leftover biopsymaterial revealed a modest twofold increase in MN and a dramatic 25-fold increase in MM.

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Documento generato il 15/07/20 alle ore 12:26:16