The effect of acute intermittent hypoxia on postprandial triglyceride levels in humans: a randomized crossover trial

Abstract

Background Obstructive sleep apnea (OSA), a sleep disorder frequently observed in individuals living with obesity, consists of repeated involuntary breathing obstructions during sleep, leading to intermittent hypoxia (IH). In humans, acute continuous hypoxia slightly increases plasma triglycerides (TG). However, no study yet compared the postprandial TG response of individuals with or without OSA under intermittent hypoxia. Methods Using a randomized crossover design, seven individuals diagnosed with moderate OSA and eight healthy individuals without OSA were given a meal after which they were exposed for 6 h to normoxia or intermittent hypoxia (e.g., 15 hypoxic events per hour). Blood lipid levels were measured hourly during each session. Results Peak postprandial TG concentrations tended to be 22% higher under IH irrespective of group (IH × time interaction, p = 0.068). This trend toward higher total plasma TG was attributable to increased levels of denser TG-rich lipoproteins such as very low-density lipoproteins (VLDL) and chylomicrons (CM) remnants. Irrespective of group, the postprandial TG concentrations in denser TG-rich lipoproteins was 20% higher under IH (IH × time interaction, p = 0.036), although IH had virtually no impact on denser TG-rich lipoprotein concentrations in the OSA group. Conclusion Acute intermittent hypoxia tends to negatively affect postprandial TG levels in healthy individuals, which is attributable to an increase in denser TG-carrying lipoprotein levels such as VLDL and CM remnants. This altered postprandial TG response to acute intermittent hypoxia was not observed in individuals with OSA.

Physiological Responses to Hypoxia on Triglyceride Levels

“…CPAP withdrawal increased nocturnal NEFA but not TG levels. In line with this observation, Morin et al (2021) recently showed no difference in postprandial TG in individuals with OSA exposed to 6 h of IH or ambient air, in a crossover design.…”

“…Recent evidence also suggests that the gastrointestinal tract seems to cope well with hypoxia exposure. More precisely, no difference was observed in the circulating CM-TG of healthy individuals after 6 h of normobaric hypoxia (FiO 2 = 100%) after a meal ( Morin et al, 2021 ).…”

“…The same group also investigated the effect of acute intermittent hypoxia (IH) on postprandial TG levels in healthy young men in 2 independent studies with conflicting results despite using similar IH protocols. In one study, no difference in postprandial TG levels between IH and normoxia exposure was observed ( Mahat et al, 2016 ), while in the other, a marginal transient increase in postprandial TG levels was observed after 3 h of IH exposure ( Morin et al, 2021 ). This discrepancy is not readily explainable, but we speculate that it could be the result of higher postprandial peaks in TG levels achieved in the latter study.…”

“…More recently, a study reported that prandial TG concentrations associated with denser lipoproteins (CM remnants and VLDL) were increased by 6 h of normobaric hypoxia ( Mauger et al, 2019 ). Acute IH was also shown to negatively affect postprandial TG levels in healthy individuals, due to an increase in denser TRL levels such as VLDL and CM remnants ( Morin et al, 2021 ). These results support the concept that hypoxia disturbs the prandial/postprandial metabolism of denser TRL.…”

The Effect of Acute Intermittent and Continuous Hypoxia on Plasma Circulating ßOHB Levels Under Different Feeding Statuses in Humans

“…Under hypoxic conditions, oxygen availability becomes limited and oxidative phosphorylation is hampered ( Solaini et al, 2010 ). Experiments in humans studying the metabolic responses to hypoxia in continuous and intermittent forms, and under fed or fasted state, showed that hypoxia significantly increases plasma NEFA concentrations ( Jun et al, 2011 ; Mahat et al, 2016 , 2018 ; Chopra et al, 2017 ; Mauger et al, 2019 ; Morin et al, 2021 ), which should translate into an increased ketogenesis. In this regard, limited studies conducted in rodents have reported that circulating ßOHB levels significantly increase in response to acute hypoxic exposure ( D’Alecy et al, 1990 ; Jun et al, 2012 ; Rising and D’Alecy, 1989 ).…”