New research published in the journal Heliyon provides insight into the sleeping patterns of obese, snoring mini pigs — finding airflow patterns in their nasal and mouth passageways may affect their breathing.
The science behind this informs a better understanding of human sleep apnea, the study claims.
Necessary background — Snoring is one of the common culprits behind poor sleep.
Doctors link snoring to obstructive sleep apnea. Obstructive sleep apnea (OSA) may occur after humans snore during sleep. Breathing can nearly halt — or stop. This abruptness can wake a person, leading to interrupted sleep.
There's also a strong correlation between obesity and sleep apnea. Studies suggest nearly 45 percent of people categorized as obese suffer from sleep apnea.
Obstructive sleep apnea also appears in some obese animals, including pigs — leading the researchers behind the new study to their subjects.
How they did it — The researchers examined five Yucatan mini pigs aged 9 to 11-months-old. Two of the pigs were obese, with a BMI exceeding 51, while the other non-obese pigs were used as a reference point.
In a statement, first author Zi-Jun Liu, a research professor and principal investigator in the Department of Orthodontics at the University of Washington, described his subjects as "very fat pigs."
These mini pigs, Liu explained, are not so mini. A normal mini pig can weigh 100 pounds.
"To give some context, normal human body mass index (BMI) range around 25-28, with obesity reached at over 30-35. In pigs, normal BMIs range from 30 to 35, with obesity reached over 50," Liu said.
Liu and his colleagues first monitored the pigs sleeping naturally, then sedated the animals in order to more closely monitor their breathing through a face mask.
While the pigs were sedated, the researchers gathered MRI images related to their breathing. They used the images to build a 3-D model of airflow the pigs' pharynx, which is a passageway behind the nose and mouth that allows airflow in and out of the lung.
Unlike in previous studies, which relied on similar subjects to create airflow models, the researchers modeled their research after the Yucatan mini pigs themselves, leading to a more accurate picture of sleep apnea.
You can listen to the pig snores here:
What was discovered — The researchers hypothesized obese pigs have an increased restriction in the pharynx, leading to greater resistance in airflow. The researchers believed this increased resistance led to something called "turbulence," which temporarily blocks the pharyngeal airway, causing sleep apnea.
Hypothetically, a rapid change or narrowing in the shape of the pharyngeal airway — along with high airflow speed — could cause turbulence.
The hypothesis was partly wrong: The researchers did confirm the presence of sleep apnea in the pigs, observing both heavy snoring and multiple sleep apnea episodes every five seconds or so.
But turbulence was not the cause. Instead, the researchers linked sleep apnea to a lack of “air pumping efficiency.” Due to their narrowing of the pharyngeal passageway, the obese pigs experience lower air volume and a temporary collapse of their airways during sleep compared to non-obese pigs.
The pigs' lungs were unable to compensate for this reduced air volume by pumping more air, leading to sleep apnea.
Why it matters — We already knew that restricted airflow leads to sleep apnea, but researchers still didn't fully understand the exact airflow dynamics that contribute to sleep apnea. Now they do.
Furthermore, the researchers selected Yucatan mini pigs for their similarity to humans, hoping they could apply their pig findings to people.
The study states: "Yucatan minipigs were chosen for this study because they have been reported to present with OSA and display similarities in size, architecture, and tissue type between their pharyngeal airways and those of humans."
However, the researchers concede that applying their pig findings to humans might not be that easy. Pigs and humans' airways are still different in a number of ways, such as the tongue base, which is present in humans' airways, but not in pigs.
The study states:
"Therefore, the results of the current study may not be directly applied in human OSA per se. Nevertheless, the results explain how the airway collapse in obese OSA minipigs could occur, which may refer to potential reason of airway collapse in humans."
Over limitations include the study sample size and not studying the pharyngeal muscles, which may also play a role in sleep apnea. Their model also rests on the assumption that "airway tissues are stationary during each phase of respiration" in the pig, which may not be proven.
What's next — These researchers may not have figured out the science of sleep overnight. But their methods do set a new standard for conducting sleep apnea research, especially concerning the significance of airflow.
The study states: "By identifying the presence of an increase in airflow speed and isolating its location, this CFD simulation provides the framework for succeeding OSA research."
Objectives: Obstructive sleep apnea (OSA) is associated with anatomical restrictions of pharyngeal airway, but the mechanism of airflow dynamics in OSA is largely unknown. This study utilized computational flow dynamics (CFD) to build a 3D model of the pharynx and to test the hypothesis that an increased restriction in the pharynx in OSA/obese minipigs leads to higher resistance, which in turn creates turbulence to induce temporary blockage of pharyngeal airway patency.
Design: Of five 9-11-months-old Yucatan minipigs, 3 were non-obese (BMI<35) and two obese (BMI>51). After natural sleep monitoring using BioRadio system, pigs were sedated to collect MRI images and airflow parameters. The MRI images were processed to create 3D configurations of pharynx. These 3D configurations were meshed to create finite element models (FEM) of CFD. The obtained airflow parameters were input into the configurations to identify turbulent airflow and its location.
Results: Heavy snoring and multiple >5s hypopnea/apnea episodes (AHI ¼ 32–35) were identified in both obese minipigs during sleep. Compared to the non-obese/non-OSA controls, obese/OSA minipigs showed much lower respiratory tidal volumes and inspiratory airflow speed. FEM simulation found that turbulence was not present in the pharynx in either model. However, a 25% increase of airflow velocity was observed at the narrowest part of the nasal pharynx in the obese/OSA minipig model.
Conclusions: Despite the narrower pharyngeal airway and the higher velocity of airflow, FEM simulation indicated that turbulence was not produced in the obese/OSA minipigs.