Abstract
Heart failure with preserved ejection fraction (HFpEF) is a major clinical problem, with limited treatments. HFpEF is characterized by a distinct, but poorly understood, skeletal muscle pathology, which could offer an alternative therapeutic target. In a rat model, we identified impaired myonuclear accretion as a mechanism for low myofiber growth in HFpEF following resistance exercise. Acute caloric restriction rescued skeletal muscle pathology in HFpEF, whereas cardiac therapies had no effect. Mechanisms regulating myonuclear accretion were dysregulated in patients with HFpEF. Overall, these findings may have widespread implications in HFpEF, indicating combined dietary with exercise interventions as a beneficial approach to overcome skeletal muscle pathology.
Original language | English |
---|---|
Pages (from-to) | 223-240 |
Number of pages | 18 |
Journal | JACC: Basic to Translational Science |
Volume | 9 |
Issue number | 2 |
Early online date | 1 Jan 2024 |
DOIs | |
Publication status | Published - Feb 2024 |
Keywords
- HFpEF
- diet
- exercise training
- mitochondria
- skeletal muscle