Credit: Greg McFall/Flikr
The appeal of freediving may lie in its freedom. Freedivers, without cumbersome scuba gear and noisy regulators, easily glide through tranquil waters toward coral or rocky reefs with scenes unobstructed by bubble trails. With dives often exceeding five minutes, they get to see up close and personal the colorful marine life that typically flees from noisy scuba divers. Freedivers can extend their time underwater by hyperventilating—breathing in and out rapidly—before diving. This allows more oxygen into the lungs, but if the dive is not planned and executed well, it can also have dangerous results.
Oxygen is key to our survival: It’s used to make ATP, a molecule that fuels everything we do. When we breathe in, oxygen in the air travels into our lungs, goes into our blood and finally makes it to our cells, where ATP is produced. Carbon dioxide (CO2) is also made during ATP production. As we make more and more ATP, CO2 builds up. To get rid of this accumulated CO2, CO2 flows from the cells to the blood and then into the lungs, where we eventually exhale it.
The presence of CO2 in our lungs means there is less room for oxygen. Hyperventilating can cut the amount of CO2 in half, allowing more space for oxygen. With this additional oxygen, freedivers can stay underwater a little longer, but they can misjudge when they need to head to the surface for air.
Low oxygen level is not what prompts us to breathe. Rather it’s the accumulation of CO2. Under normal breathing, the buildup of CO2 signals us to breathe before oxygen becomes too low. However, hyperventilating reduces CO2, and the signal to breathe comes later. Without a timely signal, a freediver may dive too long and allow too much oxygen to be consumed. As the diver finally heads to the surface, oxygen can become too low for the brain to maintain consciousness. The consequences can be fatal.
Cassondra Williams, PhD, is a postdoctoral fellow at Scripps Institution of Oceanography.
Credit: Melissa Bates
In 1963, President John Kennedy’s wife, Jackie, gave birth to a little boy three weeks early. The baby survived only 39 hours before dying of hyaline membrane disease, more commonly known as respiratory distress syndrome. The first successful treatments began in 1991, and now nearly 99 percent of babies like the Kennedy baby survive prematurity. Physicians are even able to treat babies born as much as 16 weeks early. This also means that the first large-scale group of people with hyaline membrane disease to survive being born prematurely is only 24 years old. What does the future hold for this population?
Hyaline membrane disease is caused by a deficiency in the molecule surfactant. Surfactant is produced in the lung starting shortly before birth and is critical for the lungs to inflate and the lungs’ surface to stay dry. To treat the disease, premature babies are given surfactant derived from animals. In addition to surfactant, supplemental oxygen is given and babies are placed on mechanical ventilators.
We recently found that adults who had been born prematurely had important, but unexpected, changes in their physiology. For example, unlike their peers who were born at full term, prematurely born adults couldn’t increase their breathing in a low-oxygen environment. We also discovered that their exercise capacity and the ability of their lungs to take up oxygen were reduced. We were really struck by this because these prematurely born adults looked just as healthy as adults born at term, until they were stressed with exercise or a low-oxygen environment.
Although we studied minor stresses in a healthy population, we think that our experiments offer a clue that a bigger problem exists on the horizon. Soon, this young population will begin to age. We’ve already found that their physiology is different. Given the current success in treating premature infants now, it is absolutely vital that we shift some of our scientific focus to figuring out whether their different physiology puts them at higher risk of age-related diseases, such as high blood pressure, pulmonary hypertension and diabetes, in the future.
Melissa Bates, PhD, is an assistant professor of human physiology at the University of Iowa.
Correction (10/22/15): An earlier version had said that the baby was born in 1967. The correct year was 1963, and the post has been revised.
June 21 officially marked the first day of summer, bringing in long hot days of fun in the sun. Summer is also the time when air quality alerts start popping up, warning us to avoid breathing in bad air and limit activities outside. These alerts can put a damper on our outdoor plans, but why is poor air quality unhealthy for lung physiology?
The inside surface of our lungs is covered by a fluid called lung-lining fluid that helps keep the lungs clean. The fluid traps pollutants and particles, which are swept out by fine hairs that also line the lungs. Cells from the immune system drift around in the fluid, too. These cells can neutralize pollutants by ingesting and destroying them.
Air quality alerts are triggered by high levels of particulates and a chemical called ozone. When the temperature heats up, exhaust from cars, power plants and other sources turns into ozone. This is the same molecule making up the ozone layer that shields Earth from the sun’s radiation. Ozone high above protects our health, but on the ground, it can worsen it. Ozone dissolves in the lung-lining fluid, reacting with molecules in the fluid and on the surface of the lungs’ cells. The lung cells react by releasing molecules that attract and activate immune cells, leading to inflammation.
The American Lung Association describes ozone’s effect like a sunburn in the lungs. Symptoms of breathing in too much ozone include coughing, shortness of breath and difficulty breathing. The effects of ozone may be more severe among children and the elderly and in people with respiratory ailments such as asthma. The good news is that these effects are reversible and if you stop breathing ozone, symptoms can improve in a few hours. So, mind the poor air quality warning when you see it. Avoiding bad air is good for you and your lungs!
Maggie Kuo, PhD, is the former Communications and Social Media Coordinator for APS. Catch more of her writing in the Careers Section of Science Magazine.
What is breathing? The simple explanation is that animals, including humans, breathe in oxygen and exhale carbon dioxide. But a recent discovery has blown the lid off this paradigm by showing that respiration is not so simple.
In vertebrate animals, oxygen is breathed in through the lungs, bound to red blood cells and then transported through the blood to every part of the body. When the body uses up oxygen, carbon dioxide is produced as a waste product and is transported through the blood to the lungs to be exhaled.
The Stamler lab from Cleveland recently published in the journal Proceedings of the National Academy of Sciences that nitric oxide is a third essential component in respiration.
It turns out that a tiny block (called bCys93) on the surface of every red blood cell is devoted to carrying nitric oxide. Nitric oxide has many roles in the body, but no one knew exactly why it attached to red blood cells. Stamler’s group mutated this block so that it could not bind nitric oxide. Remarkably, mice with this mutation could not carry oxygen normally through the bloodstream. When the mice were challenged with a low-oxygen environment akin to a high-altitude mountain climb, normal mice were able to accommodate the stress, but the mutated mice were not. In other words, nitric oxide is essential for oxygen to be delivered to the body.
The results of this study suggest that it might be beneficial to include nitric oxide in blood bags for transfusions to improve oxygen uptake following blood transfusion. But it’s also time to upgrade biology textbooks with a new respiratory cycle: breathe in, breathe out and don’t forget the nitric oxide!
Source: “Hemoglobin βCys93 is essential for cardiovascular function and integrated response to hypoxia,” Rongli Zhang, PNAS, DOI: 10.1073/pnas.1502285112
Emily Johnson, PhD, is an APS member and a former volunteer editor for the I Spy Physiology blog.