The Daily Telegraph reports that “vigorous daily exercise could repair damage caused by a heart attack”.
It has long been known that the heart muscle can increase in size in response to regular exercise increasing its workload. This has been thought to just be due to the existing heart muscle cells getting bigger.
However, this new study has found that in healthy adult rats, this increase in size is also, in part, due to the generation of new heart muscle cells from dormant stem cells in the heart tissue.
The researchers also identified some of the proteins that appear to be prompting this cell generation.
As this was a study in rats with healthy hearts it is not yet clear whether exercise has the same generative effect in in humans, or in damaged heart tissue.
If these findings are to be harnessed to develop new treatments for humans, this is most likely to involve using the proteins that the researchers have identified to prompt dormant stem cells into action. Tests of this approach have been started in animals, and these will need to be successful before any tests could begin in humans.
The study was carried out by researchers from Liverpool John Moores University and the Magna Graecia University in Italy. It was funded by the British Heart Foundation, the European Community, the FIRB-Futuro-in-Ricerca program, and the Italian Ministry of Health.
The study was published in the peer-reviewed European Heart Journal.
The Telegraph reports that this research is early stage, and was in rats. While rats and humans share many biological similarities, there are also – self-evidently, some important differences.
So, while the news report suggests that the findings may apply to humans with heart muscle damage, it is not yet clear whether this is the case.
This was animal research assessing whether exercise might induce heart stem cells to produce new heart muscle cells.
It is known that if an animal does a lot of exercise, its heart muscle increases in size to cope with the increased workload.
This was thought to be due to the existing heart muscle cells getting bigger, and the researchers wanted to investigate whether new heart muscle cells might also be being made from the stem cells that exist in adult heart tissue. Stem cells are essentially biological “building blocks” that have the ability to develop into a wide range of specialised cells, including heart muscle cells (myocytes).
As humans and other animals share many aspects of their biology, findings from animal studies give researchers an idea about how human biology may work. However, these hypotheses do need testing, as there can be differences between the species.
The researchers exercised male adult rats on a treadmill for 30 minutes a day, four days a week for up to four weeks. They also had a group of similar adult male rats that were not exercised.
They then looked at the effect of the exercise programme on heart tissue, and particularly the stem cells in their heart tissue.
This included looking at whether new heart or blood vessel cells were being made by the stem cells.
They also looked at how any changes to the stem cells might come about by looking at whether growth factor proteins were being produced by the existing heart tissue that could be prompting the stem cells to become active.
As expected, the researchers found that, in response to the exercise programme, the rats’ heart muscles got bigger, due in part to the existing heart muscle cells getting bigger. However, they also found that new heart muscle cells had been formed, with about a 7% increase in the number of heart cells seen in the rats that did the highest-intensity exercise.
New capillaries (small blood vessels) also formed to increase blood flow to the new heart tissue.
The researchers found that there was an increase in the number of stem cells in the hearts of the exercised rats, although the number decreased after the first two weeks of exercise. This was suggested, in part, to be because they had developed into new heart muscle or capillary cells, and in part because the heart had adapted to its new workload. The stem cells in the exercised rats had increased activity of genes, which lead to them developing into heart muscle or capillary cells.
The researchers found that the existing heart muscle cells in exercised rats produced more of a certain group of growth factor proteins than they did in control rats. Exposing heart stem cells in the laboratory to these proteins made the stem cells divide more, and start down the pathway of development of heart muscle and capillary cells. This suggested that these proteins might be what are inducing stem cells to produce more heart muscle cells and capillary cells in the hearts of the exercised rats.
The researchers concluded that intensity-controlled exercise training prompts heart muscle remodelling both through increasing the size of existing heart muscle cells, and by leading to differentiation of heart stem cells into new heart muscle cells and capillary cells.
They say that these findings highlight the “regenerative capacity of the adult heart” provided by the heart stem cells, and identify proteins which could potentially be used to induce regeneration and repair in damaged heart tissue.
These findings suggest that, at least in adult rats, exercise can lead heart stem cells to become active and generate new heart muscle and capillary tissue.
This challenges the previous view that change in heart muscle size in adult animals in response to exercise is only a result of the increasing size of existing muscle cells.
The study has investigated the effects of exercise in healthy rats, and it is not yet clear whether exercise would have the same effect in rats with heart muscle damage.
If the findings are to be harnessed to help treat human heart muscle damage, this is most likely to involve using the proteins that have been found to prompt this regeneration.
The authors of the paper report that further animal research into this possibility is ongoing.
This animal research will need to show positive results before any such new treatments could be tested on humans.