Cargando…

Skeletal muscle autophagy and mitophagy in endurance-trained runners before and after a high-fat meal

OBJECTIVE: We tested the hypothesis that skeletal muscle of endurance-trained male runners would exhibit elevated autophagy and mitophagy markers, which would be associated with greater metabolic flexibility following a high-fat meal (HFM). METHODS: Muscle biopsies were collected to determine differ...

Descripción completa

Detalles Bibliográficos
Autores principales: Tarpey, Michael D., Davy, Kevin P., McMillan, Ryan P., Bowser, Suzanne M., Halliday, Tanya M., Boutagy, Nabil E., Davy, Brenda M., Frisard, Madlyn I., Hulver, Matthew W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5699914/
https://www.ncbi.nlm.nih.gov/pubmed/29097020
http://dx.doi.org/10.1016/j.molmet.2017.10.006
Descripción
Sumario:OBJECTIVE: We tested the hypothesis that skeletal muscle of endurance-trained male runners would exhibit elevated autophagy and mitophagy markers, which would be associated with greater metabolic flexibility following a high-fat meal (HFM). METHODS: Muscle biopsies were collected to determine differences in autophagy and mitophagy protein markers and metabolic flexibility under fasting conditions and 4 h following a HFM between endurance-trained male runners (n = 10) and sedentary, non-obese controls (n = 9). RESULTS: Maximal oxygen consumption (ml·kg·min(−1)) was approximately 50% higher (p < 0.05) in endurance-trained runners compared with sedentary controls (65.8 ± 2.3 and 43.1 ± 3.4, respectively). Autophagy markers were similar between groups. Mitophagy and mitochondrial dynamics protein markers were significantly higher in skeletal muscle of endurance-trained runners compared with sedentary controls in the fasted state, although unaffected by the HFM. Skeletal muscle metabolic flexibility was similar between groups when fasted (p > 0.05), but increased in response to the HFM in endurance-trained athletes only (p < 0.005). Key mitophagy markers, phospho-Pink1(Thr257) and phospho-Parkin(S65) (r = 0.64, p < 0.005), and phospo-Parkin(Ser65) and phospho-Drp1(Ser616) (r = 0.70, p < 0.05) were correlated only within the endurance-trained group. Autophagy and mitophagy markers were not correlated with metabolic flexibility. CONCLUSION: In summary, mitophagy may be enhanced in endurance-trained runners based on elevated markers of mitophagy and mitochondrial dynamics. The HFM did not alter autophagy or mitophagy in either group. The absence of a relationship between mitophagy markers and metabolic flexibility suggests that mitophagy is not a key determinant of metabolic flexibility in a healthy population, but further investigation is warranted.