Understanding the molecular mechanisms that promote the muscle adaptive response to exercise, therefore, has relevance from a basic science, clinical, and applied sport perspective ( 45). These adaptations also contribute to the beneficial effects of exercise in the prevention and treatment of chronic diseases, including type 2 diabetes and cardiovascular disease ( 18, 19, 34). An enhanced capacity for substrate transport and oxidation contributes to improved metabolic control during exercise at a given workload and enhanced functional capacity ( 21, 22). Skeletal muscle mitochondrial biogenesis is a classic adaptation to endurance exercise training ( 20, 21), as commonly demonstrated by increased expression, content, and/or activity of mitochondrial proteins. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. Exercise activated p38 MAPK and AMPK in the cytosol. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery.
Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest.
Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response.
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