Examinando por Autor "Carriel-Nesvara, Alfonso"

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  • Miniatura
    Ítem
    Impact of different exercise modalities on mitophagy in human skeletal muscle
    (Elsevier, 2025) Muñoz-Medina, Cristóbal; Carriel-Nesvara, Alfonso; Botella, Javier; Castro-Sepúlveda, Mauricio
    Exercise induces profound mitochondrial adaptations in skeletal muscle, with different modalities uniquely influencing different branches of mitochondrial quality control (MQC). This review examines how endurance, resistance, and high-intensity interval training (HIIT) regulate mitophagy, the selective degradation of damaged mitochondria, in skeletal muscle (SkM). Research in rodents has shown that endurance exercise upregulates mitophagy primarily through the AMPK/PGC-1α signaling axis, promoting mitochondrial turnover and ensuring metabolic efficiency. In humans, high-intensity exercise increases mitophagy to a larger extent when compared to traditional endurance exercises. On the other hand, resistance exercise triggers alternative MQC mechanisms, including potential mitochondrial ejection. Collectively, these results suggest that mitophagy and MQC pathways are regulated in human SkM following exercise, but the specific molecular pathways seem to be specific to each exercise mode. Future studies should aim at disentangling the multiple mitophagy and MQC pathways in human SkM following exercise.
  • Miniatura
    Ítem
    The role of the circadian clock in regulating mitochondrial dynamics and their impact on skeletal muscle function and metabolism
    (The Physiological Society, 2025-06-25) Carriel-Nesvara, Alfonso; Muñoz-Medina, Cristóbal; Deldicque, Louise; Castro-Sepúlveda, Mauricio
    Disruptions in both circadian clock and mitochondrial dynamics in the skeletal muscle (SkM) have been associated with insulin resistance and sarcopenia. Emerging evidence, in resting conditions and in response to metabolic challenges like exercise, suggests the intricate interplay between the circadian clock, mitochondrial dynamics and SkM function. However the molecular mechanisms that connect the circadian clock to mitochondrial dynamics and SkM function remain poorly understood. This review focuses on the role of circadian clock proteins, particularly brain and muscle Arnt-like protein-1 (BMAL1), in regulating mitochondrial dynamics and examines how their dysregulation contributes to metabolic and SkM deterioration. By exploring their interaction we aim to identify potential therapeutic targets that could improve metabolic health and muscle function.