Abstract
Skeletal muscle adaptations to resistance and endurance training include increased ribosome and mitochondrial biogenesis, respectively. Such adaptations are believed to contribute to the notable increases in hypertrophy and aerobic capacity observed with each exercise mode. Data from multiple studies suggest the existence of a competition between ribosome and mitochondrial biogenesis, in which the first adaptation is prioritized with resistance training while the latter is prioritized with endurance training. In addition, reports have shown an interference effect when both exercise modes are performed concurrently. This prioritization/interference may be due to the interplay between the 5’ AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin complex 1 (mTORC1) signaling cascades and/or the high skeletal muscle energy requirements for the synthesis and maintenance of cellular organelles. Negative associations between ribosomal DNA and mitochondrial DNA copy number in human blood cells also provide evidence of potential competition in skeletal muscle. However, several lines of evidence suggest that ribosome and mitochondrial biogenesis can occur simultaneously in response to different types of exercise and that the AMPK-mTORC1 interaction is more complex than initially thought. The purpose of this review is to provide in-depth discussions of these topics. We discuss whether a curious competition between mitochondrial and ribosome biogenesis exists and show the available evidence both in favor and against it. Finally, we provide future research avenues in this area of exercise physiology.
Highlights
Research interest in the fields of ribosome and mitochondrial biogenesis has been growing considerably over the last decades
Given the proposed role mechanistic target of rapamycin complex 1 (mTORC1) signaling has on skeletal muscle ribosome biogenesis, it seems plausible that this process is impaired during situations of heightened AMPK signaling. In support of this hypothesis, we have reported that treating C2C12-derived myotubes with 5-aminoimidazole4-carboxamide ribonucleotide (AICAR, a stimulator of AMPK activity) for 6 hours reduced 47S pre-rRNA levels by 16% compared to vehicle-treated cells (Mobley et al, 2016); notably, while a one-way ANOVA with multiple cell culture treatments indicated no difference between the groups in our publication, a direct comparison between AICAR and vehicle-treated cells indicated p < 0.05 between these two conditions
We have provided evidence in favor of the biogenesis competition paradigm, in which ribosome biogenesis is prioritized with resistance training while mitochondrial biogenesis is prioritized with endurance training, or an interference effect is observed when both modes of exercise are performed concurrently
Summary
Research interest in the fields of ribosome and mitochondrial biogenesis has been growing considerably over the last decades. Evidence in multiple cell lines and tissues suggests that increased AMPK signaling facilitates mitochondrial gene expression to provide for mitochondrial biogenesis (Reznick et al, 2007; Yan et al, 2013; Marin et al, 2017) In this regard, endurance exercise studies with rodents and humans have shown AMPK signaling and mRNAs involved in mitochondrial biogenesis increase hours following exercise (Fujii et al, 2000; Atherton et al, 2005; Jorgensen et al, 2005). Aside from upregulating muscle protein synthesis, more recent evidence suggests mTOR signaling regulates ribosome biogenesis across multiple cell lines [reviewed in (Mayer and Grummt, 2006)]. For further information on this topic, readers are encouraged to refer to other excellent reviews (Kim et al, 2019; Von Walden, 2019)
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