Continuous
hypoxia is associated with
insulin resistance, altered
glucose metabolism, and increased sympathetic nervous activity. This study examined the effect of 2 successive exposures to intermittent hypercapnic
hypoxia (IHH) on
glucose metabolism and
insulin sensitivity in neonatal piglets. Piglets were assigned to 2 groups. One group was exposed to 2 x 90 minutes of hypercapnic
hypoxia (8% O(2), 7% CO(2)), intermittently in 6-minute cycles alternating with 6-minute air. The second group was given 2 x 90 minutes of air. Blood pressure, blood
gases,
glucose,
insulin, and
lactate were measured during exposures.
Insulin sensitivity was assessed using the euglycemic clamp before and after the exposures. Piglets in the IHH group exhibited reduced PO(2) (from 111.4 +/- 14.2 to 43.3 +/- 21.7), increased PCO(2) (from 33.6 +/- 1.9 to 49.4 +/- 5.4), and
lactic acidosis. Compared with air, IHH decreased
blood glucose (control [CON] 4.44 +/- 0.72 mmol/L vs IHH 2.67 +/- 1.2 mmol/L, P = .007),
insulin (CON 12.5 +/- 7.4 microU/mL vs IHH 3.6 +/- 3.1 microU/mL, P = .03), and mean arterial pressure (CON 143.0 +/- 7.9 mm Hg vs IHH 112.5 +/- 9.5 mm Hg, P < .001) over 90 minutes. Maximal
insulin-stimulated
glucose disposal was not different between the groups on either day, nor was endogenous
glucose production. Overall, exposure to
hypoxia in an intermittent pattern reduced sympathetic drive as indicated by blood pressure and did not alter
insulin sensitivity, resulting in decreases in
blood glucose and
insulin. We speculate that an intermittent hypoxic stimulus results in failure of initiation of compensatory responses to increased energy requirements that would usually be observed during sustained exposure to
hypoxia.