This NIH-supported study explores that how sleep and exercise may influence the inflammation with caused by age related genetic mutations in a blood stem cells. As the people age some of a blood stem cells acquires mutations that allows them to multiply more rapidly than normal cells. This process is called clonal hematopoiesis can increase inflammation throughout the body. Persistent inflammation is important because it can contribute to atherosclerosis the buildup of fatty plaques inside arteries which raises the risk of heart attacks and strokes.

The research team lead by a Dr Cameron McAIpine at Icahn School of Medicine at Mount Sinai, examined whether lifestyle habits such as regular physical activity and good sleep could affect this process. Their findings were published in Nature on June 10, 2026

First the researchers analyzed data from more than 90000 participants in the UK Bio bank and the NIH,s All of Us Research Program. They compared people’s daily levels of moderate-to-vigorous physical activity with genetic changes found in their blood cells. The results showed that individuals who were more physically active were less likely to have clonal hematopoiesis involving certain common genes. However exercise did not appear to reduce clonal hematopoiesis involving certain common genes. However exercise did not appear to reduce clonal hematopoiesis linked to mutation a person carries.

The scientists then studied mice with mutations in four genes Jak2, Trp53, and Dnmt3a. Poor sleep increased the accumulation of altered blood cells in mice with Jack2 and Tet2 mutations, but not in mice with the other mutations. Exercise reduced this accumulation. These results reinforce the idea that lifestyle factors can affect some genetic mutations more strongly than others.

The Study also looked at artery plaque buildup. Mice with clonal hematopoiesis developed more plaque but poor sleep made the condition worse when certain mutations were present. Exercise in contrast reduced plaque buildup in several cases. Again the Dnmt 3a mutation showed little response to sleep or exercise changes

The research focused closely on the Jak2 mutation. They found that poor sleep increased activity in the inflammation a molecular system I n immune cells that promotes inflammation. This increased inflammation worsened opaque buildup. Exercise activated neurons in a brain region called the locus coreless increasing levels of the hormones noradrenaline. Noradrenaline helped reduced inflammation and therefore reduced artery plaque.

Overall the research shows that healthy sleep and regular exercise may protect cardiovascular health for some people with age related blood cells mutations. However the benefits are not identical for everyone. In the future genetic information may help doctors tailor lifestyle advice and treatments more precisrely.