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Abstract: PO2062

Association of Self-Reported and Objective Measures of Physical Activity with Leg Muscle Mitochondrial Oxidative Capacity in CKD

Session Information

Category: Health Maintenance, Nutrition, and Metabolism

  • 1300 Health Maintenance, Nutrition, and Metabolism

Authors

  • Bae, Se Ri, University of California Davis, Davis, California, United States
  • Kim, Tae Youn, University of California Davis, Davis, California, United States
  • Gamboa, Jorge, Vanderbilt University Department of Medicine, Nashville, Tennessee, United States
  • Vargas, Chenoa R., University of California Davis, Davis, California, United States
  • Liu, Sophia, University of Washington, Seattle, Washington, United States
  • Patel, Kushang V., University of Washington, Seattle, Washington, United States
  • de Boer, Ian H., University of Washington Department of Medicine, Seattle, Washington, United States
  • Kestenbaum, Bryan R., University of Washington Department of Medicine, Seattle, Washington, United States
  • Roshanravan, Baback, University of California Davis Department of Internal Medicine, Sacramento, California, United States
Background

Chronic kidney disease (CKD) is associated with skeletal muscle dysfunction leading to lower muscle mitochondrial oxidative capacity and decreased physical performance. However, the influence of physical activity (PA) on muscle mitochondrial function remains unknown.

Methods

We included participants from the CKD Mitochondrial Energetics and Dysfunction (CKD-MEND) study. Muscle mitochondrial oxidative capacity (ATPmax) in the leg muscle was measured using in vivo 31Phosphorus Magnetic Resonance Spectroscopy. We measured self-reported PA using the adjusted Human Activity Profile (HAP) score and objective PA using an Actigraph accelerometer. Linear regressions were used to test associations between CKD status and ATPmax adjusting for confounders.

Results

We included 36 participants with CKD (mean eGR=38) and 19 controls. Mean age was 61±13 years, 51% male, and 25% had diabetes. Diabetes and CKD were independently associated with lower ATPmax (-0.12 mM/s, p<.01 and -0.19 mM/s, p<.01, respectively). Accelerometry counts per minute (r=.58, p<.01) was more strongly correlated with ATPmax than HAP scores (r=.46, p<.01) with no interaction by CKD status (p=.9). Accelerometry counts explained 43% of the difference in ATPmax between CKD and controls and HAP scores 15% after adjustment.

Conclusion

Objective PA was more strongly associated with ATPmax and explained more of the differences in ATPmax between CKD and controls than self-reported PA. Further studies should demonstrate if exercise interventions can improve muscle ATPmax in CKD.

Funding

  • NIDDK Support