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Randomized Controlled Trial
. 2021 Aug;9(15):e14932.
doi: 10.14814/phy2.14932.

Blood glucose concentration is unchanged during exposure to acute normobaric hypoxia in healthy humans

Affiliations
Randomized Controlled Trial

Blood glucose concentration is unchanged during exposure to acute normobaric hypoxia in healthy humans

Jason S Chan et al. Physiol Rep. 2021 Aug.

Abstract

Normal blood [glucose] regulation is critical to support metabolism, particularly in contexts of metabolic stressors (e.g., exercise, high altitude hypoxia). Data regarding blood [glucose] regulation in hypoxia are inconclusive. We aimed to characterize blood [glucose] over 80 min following glucose ingestion during both normoxia and acute normobaric hypoxia. In a randomized cross-over design, on two separate days, 28 healthy participants (16 females; 21.8 ± 1.6 years; BMI 22.8 ± 2.5 kg/m2 ) were randomly exposed to either NX (room air; fraction of inspired [FI ]O2 ~0.21) or HX (FI O2 ~0.148) in a normobaric hypoxia chamber. Measured FI O2 and peripheral oxygen saturation were both lower at baseline in hypoxia (p < 0.001), which was maintained over 80 min, confirming the hypoxic intervention. Following a 10-min baseline (BL) under both conditions, participants consumed a standardized glucose beverage (75 g, 296 ml) and blood [glucose] and physiological variables were measured at BL intermittently over 80 min. Blood [glucose] was measured from finger capillary samples via glucometer. Initial fasted blood [glucose] was not different between trials (NX:4.8 ± 0.4 vs. HX:4.9 ± 0.4 mmol/L; p = 0.47). Blood [glucose] was sampled every 10 min (absolute, delta, and percent change) following glucose ingestion over 80 min, and was not different between conditions (p > 0.77). In addition, mean, peak, and time-to-peak responses during the 80 min were not different between conditions (p > 0.14). There were also no sex differences in these blood [glucose] responses in hypoxia. We conclude that glucose regulation is unchanged in young, healthy participants with exposure to acute steady-state normobaric hypoxia, likely due to counterbalancing mechanisms underlying blood [glucose] regulation in hypoxia.

Keywords: acute hyperglycemia; acute hypoxia; blood [glucose] regulation; insulin sensitivity.

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Figures

FIGURE 1
FIGURE 1
Changes in the fraction of inspired oxygen (FIO2; %), peripheral oxygen saturation (SpO2; %), heart rate (min−1), and mean arterial pressure (MAP; mmHg) in response to varying levels of oxygen over 80 min following glucose ingestion. The data from normoxic (black) and hypoxic (grey) conditions collected before (BL; transparent grey box) and after a glucose load. The baseline (BL) measures were obtained following 10 min in the chamber in each oxygen condition, but were fasted (transparent grey box). Participants then consumed the 75 g glucose beverage, under both oxygen conditions (see Figure 2). (a) Mean FIO2 values at baseline were lower in hypoxia (14.8 ± 0.6%) compared to normoxia (20.4 ± 0.5%; Table 1), and stable throughout the 80‐min protocol. (b) Mean SpO2 values at baseline were lower in hypoxia (88.6 ± 3.7%) compared to normoxia (96.8 ± 2.2%; Table 1). SpO2 values were stable throughout the 80‐min protocol in normoxia, but significantly higher than baseline during the hypoxia protocol. (c) Mean heart rate (HR) values at baseline were higher in hypoxia (79.0 ± 8.9 min−1) compared to normoxia (72.0 ± 11.3 min−1; Table 1). HR significantly increased from baseline in both normoxia and hypoxia trials. (d) Average MAP values at baseline were not different between hypoxia (88.2 ± 7.6 mmHg) and normoxia (86.8 ± 8.0 mmHg; Table 1). MAP values were relatively stable throughout the 80‐min protocol in normoxia and hypoxia, but were significantly reduced near the end of the hypoxia trial only. All p values for main effects (Time and Condition), and interaction (Time × Condition) indicated on each graph. *represents values different from baseline for that (or both) oxygen condition(s) over time. Values are reported as mean ± SD
FIGURE 2
FIGURE 2
Blood [glucose] response at baseline and following a 75 g, 296 ml of standardized glucose beverage under both normoxic (black) and hypoxic (grey) conditions. (a) Absolute blood [glucose] values in response to glucose ingestion were not significantly different between normoxia and hypoxia. (b) Delta blood [glucose] values in response to glucose ingestion were not significantly different between normoxia and hypoxia. (c) Percent change blood [glucose] values in response to glucose ingestion were not significantly different between normoxia and hypoxia. All p values for main effects (Time and Condition), and interaction (Time × Condition) indicated on each graph. *represents values different from baseline for that (or both) oxygen condition(s) over time. Values are reported as mean ± SD
FIGURE 3
FIGURE 3
Average and peak blood [glucose], and time‐to‐peak [glucose] for all participants in both normoxic (black) and hypoxic (grey) conditions. (a) 80‐min average blood [glucose] was not significantly different between normoxia and hypoxic conditions (p = 0.21). (b) Absolute peak blood [glucose] was not significantly different between normoxia and hypoxic conditions (p = 0.14). (c) Time‐to‐peak [glucose] (from b) in minutes were not significantly different between normoxia and hypoxic conditions (p = 1.0). Values are reported as mean ± SD. NSD, no statistical difference

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