Abstract: TH-PO397

Differential Expression of Myogenic Regulators Following Aerobic or Combined Exercise in Non-Dialysis CKD

Session Information

Category: Nutrition, Inflammation, and Metabolism

  • 1401 Nutrition, Inflammation, Metabolism

Authors

  • Gould, Douglas W., University of Leicester, Leicester, United Kingdom
  • Watson, Emma L., University of Leicester, Leicester, United Kingdom
  • Graham-Brown, Matthew P.M., University of Leicester, Leicester, United Kingdom
  • Xenophontos, Soteris, University of Leicester, Leicester, United Kingdom
  • Wilkinson, Thomas James, University of Leicester, Leicester, United Kingdom
  • Viana, Joao L., University Institute of Maia, Porto, Portugal
  • Smith, Alice C., University of Leicester, Leicester, United Kingdom
Background

CKD is associated with satellite cell (SC) dysfunction and reduced expression of myogenic regulatory factors (MRFs), which contribute to muscle wasting. SCs are skeletal muscle stem cells responsible for muscle repair and regeneration following ‘injury’. Such ‘injury’ occurs following exercise; this leads to SC activation, a process controlled by the MRFs MyoD and Myogenin. The effect of exercise on the expression of MRFs in CKD is currently unknown.

Methods

19 CKD patients (62±14 years; 12 female; eGFR: 27±7ml/min/kg/1.73m2) completed supervised aerobic exercise (AE) (n=10), or combined aerobic plus resistance exercise (CE) (n=9) 3x/week for 12 weeks. Muscle biopsies were obtained from the vastus lateralis at baseline (B1) and 24h (B2) post the first and final exercise sessions (B3). Gene expression of MyoD and Myogenin were analysed by RT-PCR and data reported as percentage change from B1. Data was analysed using repeated measures ANOVA with post-hoc paired t-tests.

Results

Analysis revealed effects between biopsy time-points (F=5.795, p=.016) and groups (F=4.630, p=.031) for MyoD expression. Post-hoc analysis revealed AE had a negligible effect on MyoD expression with a change of +0.5% (p=.988) at B2 and +14% (p=.511) at B3. Following CE, MyoD was downregulated by -70% (p=.050) at B2, but up regulated by +54% (p=.123) from baseline at B3, which was +429% (p=.012) from B2. No interactions were observed for Myogenin expression (F=.492, p=.615).

Conclusion

We report differential effects of AE and CE on MyoD gene expression in non-dialysis CKD. In the general population, exercise acts as a potent stimulus for SC activation, which is mediated by MRFs. We observed a small increases at both biopsy time points following AE. In contrast, CE suppressed MyoD gene expression following the initial bout of exercise, indicating a possible abnormal response. However, this appeared to be reversed following 12-weeks, where expression was increased above baseline. This demonstrates that regular exercise incorporating resistance training has the potential to overcome CKD induced abnormalities in SC activation.