ArticleScientific reports2019
A "human knockout" model to investigate the influence of the α-actinin-3 protein on exercise-induced mitochondrial adaptations.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 37 citations in OpenAlex.
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- COX7A2L genetic variants determine cardiorespiratory fitness in mice and human.Nature metabolism · 2022Article
- Effect of the ACTN-3 gene polymorphism on functional fitness and executive function of elderly.Frontiers in aging neuroscience · 2022Article
- Contextualizing the biological relevance of standardized high-resolution respirometry to assess mitochondrial function in permeabilized human skeletal muscle.Acta physiologica (Oxford, England) · 2021Article
- Effect ofGenes · 2021Observational
- Regulator of Calcineurin (RCAN): Beyond Down Syndrome Critical Region.Molecules and cells · 2020Review
- The Molecular Adaptive Responses of Skeletal Muscle to High-Intensity Exercise/Training and Hypoxia.Antioxidants (Basel, Switzerland) · 2020Review
- Effect ofSports (Basel, Switzerland) · 2020Article
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9 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Research in α-actinin-3 knockout mice suggests a novel role for α-actinin-3 as a mediator of cell signalling. We took advantage of naturally-occurring human "knockouts" (lacking α-actinin-3 protein) to investigate the consequences of α-actinin-3 deficiency on exercise-induced changes in mitochondrial-related genes and proteins, as well as endurance training adaptations. At baseline, we observed a compensatory increase of α-actinin-2 protein in ACTN3 XX (α-actinin-3 deficient; n = 18) vs ACTN3 RR (expressing α-actinin-3; n = 19) participants but no differences between genotypes for markers of aerobic fitness or mitochondrial content and function. There was a main effect of genotype, without an interaction, for RCAN1-4 protein content (a marker of calcineurin activity). However, there was no effect of genotype on exercise-induced expression of genes associated with mitochondrial biogenesis, nor post-training physiological changes. In contrast to results in mice, loss of α-actinin-3 is not associated with higher baseline endurance-related phenotypes, or greater adaptations to endurance exercise training in humans.
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