Markers of clinical and mitochondrial adaptation in response to moderate intensity continuous training: A systematic review and meta-analysis
Fig 3
Mitochondrial biogenesis and dynamics in human skeletal muscle in response to exercise.
Endurance type exercise increases expression of PPARGC1A (PGC-1α) which leads to an elevated level of PGC-1α. This coactivator interacts with transcription factors NRF1 and NRF2 promoting expression of TFAM, a protein integral for the initiation of mitochondrial biogenesis. TFAM is synthesized in the cytosol and imported into the mitochondrial matrix via TOM (Translocase of the Outer Membrane) and TIM (Translocase of the Inner membrane) complexes. Inside the mitochondria, TFAM binds to mtDNA to regulate replication and transcription. Mitochondrial morphology is maintained through dynamic remodeling: fusion is mediated by MFN1/MFN2 (outer membrane) and OPA1 (inner membrane), while fission is directed by the cytosolic protein DRP1 is recruited to the mitochondrial surface where is assembles into a ring-like structure, constricting and dividing the organelle into two distinct mitochondria. Together, these pathways ensure mitochondrial quality and adaptability to the energetic demands imposed by exercise in skeletal muscle cells. Figure generated in BioRender.com [68].