Decades-old questions about how the heart adapts to high altitudes are starting to be answered.
Dr Mike Stembridge, Reader in Cardiovascular Environmental Physiology at the Cardiff School of Sport and Health, has conducted several studies in this area at Pyramid lab, which is 5050m above sea level close to Mount Everest.
He explained that once someone has acclimatised to high altitude, cardiac output tends to stay the same, whether at rest or during exercise, as it is at sea level. They will, however, have a higher heart rate and a lower stroke volume. “This lower stroke volume has puzzled scientists and medics alike for decades,” he said.
Dr Stembridge and his team used speckle-tracking echocardiography to examine left ventricular twist, which is impaired when oxygen delivery is compromised, and untwisting velocity, that is related to changes in left ventricular stiffness.
Systolic (dys)function
Explaining his team’s experiments, Dr Stembridge said they took baseline measurements in the lab before taking their subjects “up into the mountains”.
About five years ago, they and another group showed that hypoxia does increase LV twist, but disagreed over whether this indicated normal systolic function with shortened functional reserve, or subendocardial systolic dysfunction. “The idea of dysfunction came from the principle that the sub-endocardium would receive less oxygen due to the way oxygen diffuses across the myocardium,” said Dr Stembridge, describing the endocardium as the “breaking force” on left ventricular twist. “At high altitude, perhaps the epicardium is well oxygenated, but the endocardium becomes slightly hypoxic, and therefore doesn’t function properly.”
A further study from Dr Stembridge’s team concluded that the twist increase could be related to sympathetic nervous system activity. He said: “Along with the increase in twist, we got increases in S’ and ejection fraction with hypoxic exposure in the lab as well as at altitude. We think this is most likely related to sympathetic nervous system activation. We haven't found any evidence of regional or global systolic dysfunction. But we still have this decreased stroke volume.”
Diastolic (dys)function
Dr Stembridge explained that altitude induces a decrease in blood volume. This leads to a reduction in plasma, and an increase in haemoglobin mass. Concomitant to changes in blood volume is an increase in pulmonary artery pressure, called hypoxic pulmonary vasoconstriction.
“The pulmonary vasculature constricts in response to hypoxia, rather than dilating,” said Dr Stembridge, adding that this led to a higher afterload on the right ventricle (RV), lower ejection, and reduced diastolic filling.
“We haven't unearthed any evidence of direct diastolic dysfunction which, although has a logical appeal, given how oxygen sensitive the myocardium is, doesn't appear in healthy individuals to necessarily play a role,” said Dr Stembridge.
High altitude natives
Researchers have also studied “high altitude natives” from Nepal and Peru to understand how they are better equipped to cope with hypoxia.
Dr Stembridge said levels of LV twist were similar in Sherpas at high altitude to “lowlanders” at sea levels. This indicated a potential generational adaptation in the way the nervous system controls cardiovascular function, he said. The Sherpa participants also had a smaller LV than the lowlanders, a trend that was confirmed in a control group of people who were born and raised at high altitude but now lived in Kathmandu.
In summary, Dr Stembridge said that there was no heartbreak at high altitude. Systolic function was preserved, and the LV twist was increased via sympathetic nerve activity.
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