Summary • Muscle contraction with endurance training generates specific mechanical stimuli that promote adaptation, and primary mechanosensors important for "switching on" the adaptation response include stretch, calcium, fuel utilisation, energy status and oxygen stress. • The molecular adaptation response centres on taking a sequence of genetic code from DNA for a specific cell protein and generating a functional gene product (termed gene expression) for physiological processes such as mitochondrial respiration and biogenesis, signalling and catalytic enzymes, and substrate transporters. • The well recognized exercise-induced increase in skeletal muscle mitochondrial content (termed mitochondrial biogenesis) is fundamental to endurance training, and a key regulator of this process is the transcription coactivator PGC-la. • Endurance training mediates changes in the capacity to transport glucose and fatty acids from the blood into the muscle cell by increasing the level of substrate transporters GLUT4 and FAT/CD36, respectively. • Improved capillary to fibre ratio is an important adaptation process following chronic endurance training, and the VEGF protein has been identified as an important angiogenic factor that promotes blood vessel development. • Maximal activation of molecular responses and increased functional protein in skeletal muscle with endurance training occur within days of a repeated exercise stimulus and plateaus shortly thereafter. • The extensive training history of elite endurance athletes will diminish the exercise-induced molecular response to each acute training session and highlights the need for progressive overload and variety to provide a novel stimulus to promote adaptation.
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