Exercises Prevent Epigenetic Aging At Old Age

As quoted “Exercise can not only change your fitness, it changes your mind, your attitude, and also your mood.” A new study speaks about one more chance that exercise can make in your body: Exercise can make you younger epigenetically.

Exercises Prevent Epigenetic Aging At Old Age

Epigenetics is the study of DNA independent heritable phenotype change. An exercise freak can now gain an additional benefit that can be passed down to generations. 

Exercises Prevent Epigenetic Aging At Old Age

Regular exercise can provide immeasurable benefits to our bodies. They are:

  • Makes the body fit and aids weight loss. 
  • Strengthens muscles and bones.
  • Reduces depression, anxiety, and stress.
  • Improves skin health.
  • Lowers the risk of diabetes and  high blood pressure
  • Boosts energy levels.
  • Reduces cancer risk.
  • Enhances brain health and memory.
  • Refines sleep quality.
  • Reduces chronic disease risks and lots more.

It’s time for people who love exercising to celebrate because a new study published in the journal “Aging Cell” says that exercising at the latter part of life stops the epigenetic aging of skeletal muscles. That is, exercise can protect you from aging even hereditarily.

The research performed by Kevin Murach and the team gave a clear view of the relationship between DNA methylation and aging. DNA methylation is an epigenetic mechanism, where methyl groups are added to the DNA molecule.  DNA methylation is found to be at higher levels in people of older ages. Hypermethylation is found to occur as the body ages.

Generally, epigenetic changes which result in aging are histone modifications, DNA methylation, and chromatin remodeling. In this research, the reason for the epigenetic anti-aging is DNA methylation which triggers the production of certain proteins by turning on the genes. The addition of the CH3 group at promoter sites on genes in muscle can result in such actions.

Dr. Murach said that ” DNA methylation occurs systematically throughout the lifespan of a person”. An individual’s chronological age can be accurately predicted with the DNA sample of the same through a series of examinations. The age of DNA can be predicted by the ‘methylation clock.’

Though the correlation between aging and methylation is understood, the relationship between methylation and muscle function is not known. Future studies aim to open the unknown sides of the aging process, he added.

The experiment was carried out with aged mice. Mice of age 22 months were allowed to exercise on a weighted exercise wheel. The weighted exercise wheel can confirm to build up muscles. Naturally, older mice can run for about six to eight kilometers per day, while younger mice can make it up to 10-12 kilometers per day. Two months of keen study on the mouse was performed on the activities with the weighted wheel running. This study found that the epigenetic age of experimental mice was 8 weeks younger than the idle mice of the same age.

Mice do not require external pressure or force to make them perform any exercise. They are naturally interested in physical activity which makes the experiment more approachable. The average lifespan of mice is 2 years, after which they start aging and die gradually. This also depends on the breed of the mice, location, and feeding habits of the mice. But, this study goes a step beyond. By calculating with respect to the average lifespan of mice, the life span of the mice is increased by 10%.

The future study expectations as said by Murach are:

  • Involvement of exercise in reverse methylation.
  • Alteration in muscle function by methylation.
  • The cause of Phenotype variation – specific methylation sites.
  • The consequences of methylation.
  • Aging and associated causes
  • The path and occurrence of aging with respect to methylation.

This paper was written by a team from three institutions, consisting of seven researchers. One of the co-first authors, Kevin Murach, Assistant professor, Department of Health, Human Performance and Recreation at the U of A. The research was funded by Murach’s grant from the National Institute of Health. Co-authors of this research include Yuan Wen, Christopher S. Fry, Christine M. Latham, Stanley J. Watowich,  Cory M. Dungan, Andrea L. Dimet-Wiley, and Camille R. Brightwell.

Murach, a faculty member of the U of A, published this as his fourth paper. He established the Molecular Muscle Mass Regulation Laboratory there, after his arrival in June 2021. This paper was published by him in collaboration with the University of Texas Medical Branch and Ridgeline Therapeutics.

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