Exercise Metabolism and the Molecular Regulation of Skeletal Muscle Adaptation

In the citing paper

“This is principally achieved by an augmentation in mitochondrial volume, FA transport and enzymatic adaptations (e.g., increase hydroacyl-CoA-dehydrogenase) to use fat, and a reduction of cell signals such as ADP and AMP during exercise at submaximal work rates thus reducing the activation of key enzymes (e.g., glycogen phosphorylase and pyruvate dehydrogenase) of carbohydrate metabolism [92,160].”

In the citing paper

“Exercise promotes glucose uptake and glycogen synthesis and increases insulin sensitivity, and this persists long after the cessation of exercise (1, 2).”

In the citing paper

“The induction of PGC1α (peroxisome proliferator–activated receptor gamma coactivator 1α) after exercise can promote mitochondrial biogenesis by driving the expression of nuclear- and mitochondrial-encoded genes.”

In the citing paper

“The enhanced skeletal muscle insulin sensitivity after exercise affords metabolic flexibility and a means for replenishing glycogen to deal with subsequent bouts of intense physical activity (1, 2).”

In the citing paper

“Exercise results in skeletal muscle exposure to acute stresses that stimulate compensatory and adaptive physiological responses (1, 2).”

In the citing paper

“These adaptive responses increase tolerance and protect against subsequent stressors and are considered important for the health-promoting effects of exercise (1, 2).”

In the citing paper

“In particular, PGC1α promotes the expression of NRF (nuclear respiratory factor)–1 and NRF-2, which induce the expression of nuclear-encoded genes, as well as TFAM (mitochondrial transcription factor A), which facilitates mitochondrial DNA transcription and replication (2, 3).”

In the citing paper

“A fundamental hormetic response to exercise is the induction of mitochondrial biogenesis, which serves to enhance respiratory capacity and endurance (2, 3).”

In the citing paper

“It is well established that contracting muscle generates ROS and that this is accompanied by increased antioxidant defense orchestrated by NFE2L2 (2, 7, 36).”

In the citing paper

“These observations confirm the hypothesis that endurance exercise training may affect a specific set of functions (e.g., oxidative metabolism and mitochondrial biogenesis) and overall muscle metabolism [93].”

In the citing paper

“Multiple molecular pathways are activated by exercise and these pathways have been shown to contribute to the adaptive remodelling of skeletal muscle [1,2].”

In the citing paper

“These adaptive processes are driven by transcriptional changes in response to each bout of exercise [2,8].”

In the citing paper

“The transcriptional changes accumulate over time such that the protein expression profile of muscle is changed resulting in an altered phenotype [2,8].”

In the citing paper

“Whilst endurance exercise adaptations are believed to be driven primarily by transcriptional responses [2,8], the muscle growth adaptation to resistance exercise is driven primarily by changes in translation, in particular by increases in mRNA activity (protein produced per unit of mRNA) [85][86][87].”

In the citing paper

“It is a key factor in metabolism of all major biomolecules (lipids, carbohydrates, amino acids) as well as ATP synthesis by the electron transport chain [164, 165]”

In the citing paper

“A higher mitochondrial volume density and improved mitochondrial quality can be seen as consequences of chronic activation of AMPK and expression induction of PGC1α, myocyte-specific enhancer factor 2 (MEF2), NRF-1 and NRF-2, and nuclear expulsion of histone deacetylase 4 and 5 (41, 222, 224).”

In the citing paper

“Additionally, PGC1α is expressed upon muscle contraction-induced activation of p38 MAPK (222).”

In the citing paper

“Both promote considerable health benefits such as increased mitochondrial content and improvements in glycemic control (222).”

In the citing paper

“Acute AMPK activation reduces glycogen and protein synthesis while promoting glucose transport and FAO (222).”

In the citing paper

“Because exercise and ApN share similar signaling pathways [75,76] and the potential of counteracting several facets of this metabolic syndrome, numerous studies attempted to establish relationships between exercise and ApN parameters.”