Doug McGuff, MD recently posted an article on the effects of resistance training on aging, calling attention to a study published in PLoS ONE showing a reversal of aging in over 500 genes. (Melov S, Tarnopolsky MA, Beckman K, Felkey K, Hubbard A (2007) Resistance Exercise Reverses Aging in Human Skeletal Muscle. PLoS ONE 2(5): e465. doi:10.1371/journal.pone.0000465)
Human aging is associated with skeletal muscle atrophy and functional impairment (sarcopenia). Multiple lines of evidence suggest that mitochondrial dysfunction is a major contributor to sarcopenia. We evaluated whether healthy aging was associated with a transcriptional profile reflecting mitochondrial impairment and whether resistance exercise could reverse this signature to that approximating a younger physiological age. Skeletal muscle biopsies from healthy older (N = 25) and younger (N = 26) adult men and women were compared using gene expression profiling, and a subset of these were related to measurements of muscle strength. 14 of the older adults had muscle samples taken before and after a six-month resistance exercise-training program. Before exercise training, older adults were 59% weaker than younger, but after six months of training in older adults, strength improved significantly (P<0.001) such that they were only 38% lower than young adults. As a consequence of age, we found 596 genes differentially expressed using a false discovery rate cut-off of 5%. Prior to the exercise training, the transcriptome profile showed a dramatic enrichment of genes associated with mitochondrial function with age. However, following exercise training the transcriptional signature of aging was markedly reversed back to that of younger levels for most genes that were affected by both age and exercise. We conclude that healthy older adults show evidence of mitochondrial impairment and muscle weakness, but that this can be partially reversed at the phenotypic level, and substantially reversed at the transcriptome level, following six months of resistance exercise training.
The full paper can be read here.
Towards the end of the intruduction, the paper states,
“We report here that healthy older adults show a gene expression profile in skeletal muscle consistent with mitochondrial dysfunction and associated processes such as cell death, as compared with young individuals. Moreover, following a period of resistance exercise training in older adults, we found that age-associated transcriptome expression changes were reversed, implying a restoration of a youthful expression profile.”
Note they didn’t say resistance training slowed or stopped the age-associated transcriptome (set of genetic instructions for how to build proteins) expression changes – it reversed them. Like Dr. McGuff stated in his article, this is the closest thing there is to a fountain of youth. If everybody regularly engaged in proper strength training we’d have an elderly population far healthier, more independent, and enjoying a much greater all-around quality of life. Barring accidents, diseases and other disasters, most would probably also live significantly longer.
Dr. McGuff also made an interesting observation based on the study that the low-intensity, long-duration aerobic “exercise” so often recommended as healthy activity may actually contribute to aging:
“If we embrace this concept of aging (the gap between maximal and minimal output), and the type of training that enhances this capability; then we must acknowledge that there is a type of exercise which can produce the opposite result. Low intensity, steady state exercise will actually accelerate aging by this definition.”
The explanation that follows is probably one of the strongest arguments I’ve read against traditional low-intensity, long-duration cardio. It’s too long to post here, so I strongly recommend going there and reading it. In a nutshell (and greatly oversimplified) the changes resulting from low-intensity, long-duration exercise may interfere with the type of exercise adaptations the above study has shown to reverse age-associated transcriptome expression changes.