The Effect of Acute Continuous Hypoxia on Triglyceride Levels in Constantly Fed Healthy Men

Abstract

Introduction Elevated plasma triglyceride (TG) concentrations are an important contributor to deleterious metabolic alterations. Evidence in animals suggest that acute exposure to an environment with reduced oxygen inhibits plasma TG clearance and causes important rise in plasma TG, especially in the postprandial state. The objective of this study was to characterize the effects of an acute exposure to normobaric hypoxia on prandial TG levels in 2 distinct lipoprotein subtypes in healthy humans: chylomicrons which are secreted by the intestine and carry dietary lipids, and denser TG carriers (mainly VLDL), which are secreted by the liver and carry endogenous lipids. Plasma lipolytic activity was also assessed. It was hypothesized that hypoxia would reduce prandial plasma lipolytic activity and raise prandial TG levels in both lipoprotein subtypes. Methods Using a randomized crossover design, 9 healthy young men were studied for 6 h in a constantly fed state while being exposed to either normobaric hypoxia (FiO 2 = 0.12) and normoxic conditions on two different days. Prandial glucose, TG, non-esterified fatty acid (NEFA), and post-heparin plasma lipolytic activity were measured during each session. Results Six hours of exposure to hypoxia marginally increase prandial glycemia (+5%, p = 0.06) while increasing insulinemia by 40% ( p = 0.04). Hypoxia induced a 30% rise in prandial NEFA levels and tended to slightly increased total prandial TG levels by 15% ( p = 0.11). No difference was observed in TG concentrations and metabolism of chylomicrons between conditions. However, TG in the VLDL containing fraction decreased significantly overtime under normoxia but not under hypoxia (time × condition interaction, p = 0.02). No difference was observed in post-heparin plasmatic lipolytic activity between conditions. Conclusion Acute hypoxia in healthy men tends to increase prandial VLDL-TG levels. These results lend support to the increased blood lipid levels reported in animals exposed acutely to lower partial pressures of oxygen.

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

“…Assuming that lipid absorption is not affected by hypoxia, the present study suggests that hypoxia may also impair the clearance of TRL-TG as shown by the accumulation of buoyant TRL TG under IH in the control group. Taken together, recent [ 27 ] and current results suggest that alteration in plasma TG under hypoxia in healthy individuals seems to occur only in the prandial and postprandial states and that the intensity of the lipid challenge, measured in terms of peak triglyceridemia, may be a critical factor for these effects to be observed. Our initial hypothesis that individuals with OSA would display an altered postprandial triglyceridemia was confirmed based on the fact that plasma TG were still on average significantly higher in the OSA group 6-h post meal ingestion under normoxia.…”

“…This divergence could possibly be attributed to the fact that, for unclear reasons, higher average peak postprandial TG concentrations were achieved in the present study (~ 3 mmol/L) compared to the previous one (~ 2 mmol/L). The higher postprandial triglyceridemia achieved in the present study could also be responsible for the fact that we observed a trend toward an increase in the TG content of buoyant TRL, an effect that was not seen in a previous study we conducted in healthy young men in prandial state under continuous hypoxia (in which plasma TG concentrations around 1.8 mmol/L were achieved on average) [ 27 ]. This last study allowed us to hypothesize that hypoxia, in healthy individuals, may increase the hepatic production of VLDL-TG in response to an increase in lipid influx in the form of elevated plasma NEFA and chylomicron remnants.…”

“…Most recent studies investigating the effects of hypoxia in humans, either continuous or intermittent, have reported that hypoxia induces increases in plasma NEFA [ 4 , 25 , 27 ]. In line with these observations, the current study shows that postprandial NEFA levels increase over time under IH compared to normoxia in the CTL group (IH × time, p = 0.058), but not in the OSA group.…”

“…Recent studies in humans suggest that the effects of acute hypoxia, either intermittent or continuous, on plasma TG are much less robust than its impact on plasma NEFA [ 4 , 25 – 27 ]. We reported that an acute 6-h exposure to IH does not increase postprandial plasma TG in a group of healthy young men similar to our CTL group [ 25 ].…”

“…We have reported that 6 h of IH at rest did not change postprandial TG levels in healthy individuals [ 25 ]. We also showed that an acute 6-h exposure to continuous (i.e., not intermittent) normobaric hypoxia does not impact circulating TG levels in the fasted state [ 26 ], but may slightly rise prandial lipemia in the constantly fed state [ 27 ]. In individuals with OSA, on the other hand, the effect of chronic exposure to intermittent hypoxia may lead to deleterious alterations in lipid metabolism and lipemia.…”