Even a modest workout can dramatically improve heart health if done every day, new Harvard research has shown.
Regular movement drives cells into a rhythm of regeneration, which helps to fight inflammation and decay that can lead to fatigue and heart disease, they found.
In a series of experiments, mice made more than four times as many new heart muscle cells when they exercised daily compared to their peers who moved less.
The findings has implications for the rehabilitation of heart attack patients and protecting the hearts of people as they age.
Every little helps: Regular movement drives cells into a rhythm of regeneration, which helps to fight inflammation and decay that can lead to fatigue and heart disease, they found
Senior author Professor of medicine Dr Anthony Rosenzweig at Harvard Medical School in Boston said: ‘Maintaining a healthy heart requires balancing the loss of heart muscle cells due to injury or ageing with the regeneration or birth of new heart muscle cells.
‘Our study suggests exercise can help tip the balance in favour of regeneration.’
Fellow senior author Harvard Professor of Stem Cell and Regenerative Biology Dr Richard Lee added: ‘Our study shows that you might be able to make your heart younger by exercising more every day.’
The human heart has a relatively low capacity to regenerate itself with young adults renewing around one per cent of their heart muscle cells every year.
Yet that rate decreases with age and losing heart cells is linked to heart failure.
The researchers explained any interventions that increases new heart cell formation have potential to prevent heart failure.
Postdoctoral Fellow Dr Ana Vujic from the Harvard Department of Stem Cell and Regenerative Biology (HSCRB) explained: ‘We wanted to know whether there is a natural way to enhance the regenerative capacity of heart muscle cells.
‘So we decided to test the one intervention we already know to be safe and inexpensive: exercise.’
To test the effects of exercise, the researchers gave one group of healthy mice voluntary access to a treadmill and when left to their own devices ran around five kilometres each day.
The other healthy group had no such gym membership, and remained sedentary.
Their heart regeneration was measured by administering a labelled chemical that was incorporated into newly made DNA as cells prepared to divide.
By following the labelled DNA in the heart muscle, the researchers could see where new cells were being produced.
Exercising mice made over four-and-a-half times the number of new heart muscle cells than the mice without treadmill access.
But while the results were certainly significant, scientists then set out to explore whether they were relevant when the heart was damaged.
Dr Vujic added: ‘We also wanted to test this in the disease setting of a heart attack, because our main interest is healing.’
After experiencing a heart attack, mice with treadmill access still ran five kilometres a day, voluntarily.
Compared to their sedentary counterparts, the exercising mice showed an increase in the area of heart tissue where new muscle cells were made.
The study also pinpointed which biological mechanisms linked exercise with increased regenerative activity in the heart.
It identified a specific biological pathway that is required for exercise to turn on cardiac regeneration.
Prof Rosenzweig added: ‘Now we need to find the signals that are sufficient to turn this pathway on.’
Prof Lee said: ‘If we can turn on these pathways at just the right time, in the right people, then we can improve recovery after a heart attack.’
The study was published in the journal Nature Communications.