An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle

TLDR

Low‑volume high‑intensity interval training is known to boost skeletal muscle mitochondrial capacity, but the underlying mechanisms remain poorly understood. The study aimed to identify the molecular pathways driving mitochondrial biogenesis in human skeletal muscle following a single bout of high‑intensity interval training. Eight healthy men performed four 30‑second all‑out cycling bursts separated by four minutes of rest, with vastus lateralis biopsies taken before, immediately after, and at 3 and 24 hours post‑exercise to assess signaling and gene expression. Acute high‑intensity interval training activated cytosolic p38 MAPK and AMPK, increased nuclear PGC‑1α at 3 hours, upregulated mitochondrial gene expression, and ultimately elevated mitochondrial protein content and enzyme activity by 24 hours, confirming that nuclear PGC‑1α mediates exercise‑induced mitochondrial biogenesis.

Abstract

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. 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.