The data show that eight weeks of HIIT training led to a 7% increase in mitochondrial cristae density, demonstrating cristae plasticity.
Importantly, this plasticity was also observed in patients with type 2 diabetes, highlighting its relevance for metabolic health.

This level of precision was necessary to detect training-induced changes in cristae density, as previous data suggested expected increases of <10%. Even in athletes, cristae density is only ~25% higher than in untrained individuals.

In our previous studies, we used a cut-off of 8 profiles to achieve a coefficient of error of 0.10.
To improve precision, significantly more work (x5) was required, moving onto the flatter part of the curve where additional profiles yield marginal gains in accuracy.

Martin and Amalie manually analysed ~11,000 mitochondrial profiles for cristae density using classical stereology: counting intersections with cristae and points with mitochondria.
Each biopsy typically included >100 profiles, with a minimum cut-off of 49 profiles to ensure a CE ≤ 0.05.

Martin performed TEM imaging on 117 muscle biopsies (pre- and post-training), resulting in ~17,000 images.
These were analysed for mitochondrial and lipid droplet parameters, as published here: 🔗 10.1152/ajpcell.00470.2022 and 10.1113/JP284386

At that time, we had biopsies before and after 10 weeks of aerobic training but found no effect of training on cristae density, raising questions about its plasticity.

Until 2017, the prevailing consensus was that mitochondrial cristae density remained unchanged with training. However, in a cross-sectional study, we observed that endurance-trained athletes had a 25% higher cristae density compared to untrained individuals: 10.1113/JP273040