ArticleThe Journal of physiology2001
Myoadenylate deaminase deficiency does not affect muscle anaplerosis during exhaustive exercise in humans.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Effects of AMPD1 gene C34T polymorphism on cardiac index, blood pressure and prognosis in patients with cardiovascular diseases: a meta-analysis.BMC cardiovascular disorders · 2017Pooled it
- Does theGenes · 2026Article
- Muscle AMP deaminase activity was lower in Neandertals than in modern humans.Nature communications · 2025Article
- Review
- Skeletal muscle contraction kinetics and AMPK responses are modulated by the adenine nucleotide degrading enzyme AMPD1.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Mild myopathic phenotype in a patient with homozygous c.416C > T mutation inActa myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Article
- Article
- Shortage of Cellular ATP as a Cause of Diseases and Strategies to Enhance ATP.Frontiers in pharmacology · 2019Article
- Role of the HPRG Component of Striated Muscle AMP Deaminase in the Stability and Cellular Behaviour of the Enzyme.Biomolecules · 2018Review
- Article
- Diagnostic Algorithm for Glycogenoses and Myoadenylate Deaminase Deficiency Based on Exercise Testing Parameters: A Prospective Study.PloS one · 2015Observational
- AMPD1 rs17602729 is associated with physical performance of sprint and power in elite Lithuanian athletes.BMC genetics · 2014Article
- Control of ATP homeostasis during the respiro-fermentative transition in yeast.Molecular systems biology · 2010Article
- C34T mutation of the AMPD1 gene in an elite white runner.BMJ case reports · 2009Article
- The effect of AMPD1 genotype on blood flow response to sprint exercise.European journal of applied physiology · 2008Article
- Uric acid changes in urine and plasma: an effective tool in screening for purine inborn errors of metabolism and other pathological conditions.Journal of inherited metabolic disease · 2007Review
- C34T mutation of the AMPD1 gene in an elite white runner.British journal of sports medicine · 2006Article
- Immunohistochemical analysis of human skeletal muscle AMP deaminase deficiency. Evidence of a correlation between the muscle HPRG content and the level of the residual AMP deaminase activity.Journal of muscle research and cell motility · 2006Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Myoadenylate deaminase (AMPD) deficiency is present in 1--2 % of the population. In theory, this deficiency may alter exercise energy metabolism by impairing the purine nucleotide cycle (PNC) and reducing tricarboxylic acid (TCA) cycle anaplerosis. The role of the PNC in TCA cycle anaplerosis is still a debated issue in physiology. Using patients with the AMPD1 mutation will allow a human 'knockout' approach to answering this question. 2. Muscle AMPD activity and genotype (whole blood AMPD1 analysis) was used to classify participants into three groups: n = 3 with absence of AMPD activity and -/- AMPD1 genotype (homozygous); n = 4 with less than 50 % normal AMPD activity and +/- genotype (heterozygous) and n = 12 with normal AMPD activity and +/+ genotype (control). Biopsies were taken from the vastus lateralis muscle before and after incremental cycle ergometry exercise to exhaustion. The muscle biopsies were analysed for AMPD activity, purine nucleotides/nucleosides and bases, creatine, phosphocreatine, amino acids, and the TCA cycle intermediates malate, citrate and fumarate. 3. Time to exhaustion on the cycle ergometer was not different between groups. Muscle adenosine monophosphate increased significantly with exercise for homozygous subjects as compared with the other groups (P < 0.05). Inosine monophosphate increased significantly after exercise for control (P < 0.05) but not for the homozygous subjects. There were no other between-group differences for any other measured variables. 4. In summary, complete and partial muscle AMPD deficiency did not affect TCA cycle anaplerosis, phosphocreatine hydrolysis, energy charge or exercise performance.
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