The current world marathon record is set by Eilud Kipchoge, a Kenyan marathoner who finished a full 42.195km in only 2:01:09 in the 2022 Berlin Marathon. I, on the other hand, who follows a stereotypical sedentary lifestyle, probably would go less than 10 kms within the same time and would already be exhausted.

For a long time, researchers have wondered what is responsible for such dramatic differences in the physical abilities of elite athletes and ordinary people. The first clue, of course, was the difference in muscle compositions. In 1945, it was experimentally established that exercise and training induce biochemical differences in skeletal muscles [1]. Soon after in 1967, science pin-pointed that exercise could also affect mitochondrial respiration in skeletal muscles [2]. Mitochondria have two membranes. The inner membrane surrounds a partition called cristae. Earlier studies showed no evidence of plasticity in the physical structure of cristae upon exercise. Therefore, it had been long assumed that exercise affects the plasticity of mitochondria, and not of the cristae, towards an increase in the mitochondrial volume and respiration. 

This assumption was questioned in a more recent study by a group of Danish and Swedish scientists [4]. They recruited volunteers who were either 1) obese with a sedentary lifestyle, 2) recreationally active, or 3) elite athletes. All of them donated their leg muscle biopsy samples before and after participating in a short 10-week exercise schedule. Interestingly, the surface area of the cristae of athletes was 150% greater than those of obese sedentary individuals. Also, the density of cristae significantly increased in recreationally active participants after exercise.  In general, density of cristae predicted the maximal oxygen uptake better than the overall volume of mitochondria. All these results suggest that it is the cristae within our mitochondria that have a certain plasticity that appears to correlate with exercise and the activity levels in our lifestyle.

Figure adapted and modified from [6]

Exercise impacts not only the structure of mitochondrial cristae, but also the overall health of mitochondria. This is measured by how effectively mitochondria maintain or re-establish metabolic homeostasis upon changes in metabolic needs [5]. The importance of mitochondrial health is highlighted over the course of aging. Sarcopenia, progressive decrease in muscle mass, is a hallmark of aging responsible for various health implications for the elderly population. Dysfunctional mitochondria, such as those with fragmented morphology or mutations in the mtDNA, are significant contributors to sarcopenia. It is important to note that the mitochondrial functions of elderly people who exercise regularly are similar to those from younger counterparts, suggesting that exercise is key in preserving mitochondrial health over the process of aging [reviewed in 6].

Nearly 1.5% of all medical publications are related to mitochondria. This is far higher than any other organelles including the nucleus in the second place at around 1%. Further, the interest in mitochondria has only been increasing since 1980 [7]. While the role of mitochondria has been and continues to be highlighted in various aspects of health and disease, exercise remains the most potent behavioral therapeutic approach for enhancing mitochondrial health and overall individual longevity.


  1. Palladin, A. V. (1945). The biochemistry of muscle training. Science, 102(2658), 576-578.
  2. Holloszy, J. O. (1967). Biochemical adaptations in muscle: effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. Journal of biological chemistry, 242(9), 2278-2282.
  3. Hoppeler, H., Lüthi, P., Claassen, H., Weibel, E. R., & Howald, H. (1973). The ultrastructure of the normal human skeletal muscle: a morphometric analysis on untrained men, women and well-trained orienteers. Pflügers Archiv, 344, 217-232.
  4. Nielsen, J., Gejl, K. D., Hey‐Mogensen, M., Holmberg, H. C., Suetta, C., Krustrup, P., … & Ørtenblad, N. (2017). Plasticity in mitochondrial cristae density allows metabolic capacity modulation in human skeletal muscle. The Journal of physiology, 595(9), 2839-2847.
  5. Hood, D. A. (2009). Mechanisms of exercise-induced mitochondrial biogenesis in skeletal muscle. Applied Physiology, Nutrition, and Metabolism, 34(3), 465-472.
  6. Memme, J. M., Erlich, A. T., Phukan, G., & Hood, D. A. (2021). Exercise and mitochondrial health. The Journal of physiology, 599(3), 803-817.
  7. Picard, M., Wallace, D. C., & Burelle, Y. (2016). The rise of mitochondria in medicine. Mitochondrion, 30, 105-116.
The following two tabs change content below.
Previous post Letter from the Chair, Dr. Juan Carlos Zuniga-Pflucker – V11I2
Next post Mitochondria-induced inflammation: The dark side of a cell’s “powerhouse”

Leave a Reply

Your email address will not be published. Required fields are marked *


Feed currently unavailable. Check us out on Twitter @immpressmag for more.