Endurance exercise is a powerful metabolic stimulus affecting the dynamic regulation of mitochondria. However, despite the fundamental role of mitochondria for health, the effects of different exercises on mitochondrial adaptations are still debated.
Twenty-eight men completed one of two 8-week training interventions - Moderate Intensity Continuous Training (MICT; 90 min at ~ 40 % Wmax, Mean W = 127 ± 38, ∆ lactate 0.44 ± 0.24 mmol/L) or very high-intensity Sprint Interval Training (SIT; 6 x 30-s all-out sprints interspersed by 4 min of rest, Mean W = 579 ± 107, ∆ lactate 9.86 ± 1.88 mmol/L). Skeletal muscle samples were collected from the vastus lateralis before and after the first exercise session, as well as pre and post training.
Our RNAseq results suggest a highly coordinated transcriptional response that was largely shared across the two different exercise prescriptions. However, only SIT was characterised by activation of transcriptional pathways associated with mitochondrial stress and the unfolded protein response, combined with structural mitochondrial disturbances (measured via transmission electron microscopy), suggesting increased activation of mitochondrial quality control pathways. This was supported by a significant increase in phosphorylation of ULK1 at serine 555 (p-ULK1 s555) only following SIT. Whole-muscle proteomics demonstrated that SIT also increased proteins involved in mitochondrial protein quality control, while MICT increased proteins involved in the TCA cycle and OXPHOS. Our single-fibre proteomics revealed only a few fibre-specific differences. Only SIT led to an increase in mitochondrial respiratory function, while only MICT was characterised by increased mitochondrial content and complex I protein abundance.
In conclusion, our study provides mechanistic insights regarding how modulating the exercise prescription impacts transient molecular signalling, and subsequent long-term mitochondrial remodelling. These findings provide a strong basis for individualised exercise prescription to achieve specific mitochondrial adaptations at the skeletal muscle level.