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Intermittent hypoxia : activation of the sympathetic nervous system

University of British Columbia

BACKGROUND: Individuals with obstructive sleep apnea (OSA) are reported to have elevated muscle sympathetic nerve activity (MSNA). In this complicated pathological condition numerous factors can be implicated in the elevated sympathetic activity; however periodic exposures to hypoxia appear to be the primary cause. In laboratory interventions with healthy humans, it is well documented that acute hypoxia increases MSNA, which persists after removal of the hypoxic stimulus. The effect of long term exposure of to intermittent hypoxia (IH) on MSNA is unknown. PURPOSE: The present study was undertaken to address the effect of long term IH on MSNA during an acute hypoxic exposure and during the following normoxic recovery period. Concurrent vastus lateralis oxygenation, cerebral oxygenation, ventilatory and cardiovascular measurements were acquired to examine the relationship between the various physiological systems and how they are altered in response to IH. HYPOTHESIS: Ten days of IH will augment the rise in MSNA during hypoxia and recovery. METHODS: Eleven healthy males underwent two experimental sessions, consisting of 4 stages: 10 minutes baseline, 5-7 minutes hypoxic ventilatory response (HVR), 20 minutes isocapnic hypoxia (80% arterial oxygen saturation; SaO₂), and 20 minutes normoxic recovery. Experimental days were separated by 10 days of IH where 1 hour of isocapnic hypoxia (SaO₂ = 80%) was administered. During both experimental sessions the following parameters were collected: 1) MSNA was acquired from peroneal nerve recordings. Total MSNA was calculated as the product of burst frequency and burst amplitude; 2) blood pressure (BP); 3) heart rate (HR) was acquired from electrocardiogram; 4) vastus lateralis and cerebral tissue oxygenation were monitored with near infrared spectroscopy (NIRS); 5) ventilatory measures; and 6) isocapnic and hypoxic stimuli was assessed by end-tidal carbon dioxide (P[sub et]CO₂) and SaO₂, respectively. RESULTS: Total MSNA, burst frequency and burst amplitude increased during hypoxia (p<0.01). Post IH, burst frequency was higher (p<0.01), total MSNA trended towards higher values (p=0.06), there was no effect on burst amplitude (p=0.82), and the HVR increased significantly from 0.30 ± 0.03 to 0.61 ± 0.12 L min⁻¹ %SaO₂⁻¹ (means ± SE, p<0.01). Those subjects with the greatest rise in burst frequency during the hypoxic exposure demonstrated the greatest increase in HVR post IH (r = 0.91, p<0.05); this relationship did not exist pre IH (r = 0.39, p>0.05). During the hypoxic exposure HR, BP, and minute ventilation all increased (p<0.05) and returned to baseline during recovery; however, there was no effect of IH. For both the vastus lateralis and cerebral tissue, indices of tissue oxygenation significantly decreased (p<0.05) during the hypoxic exposure and returned to baseline values during recovery. Cerebral tissue oxygenation was unaffected by 10 days of IH. Vastus lateralis total haemoglobin (tHb) increase from baseline post IH (p=0.03), where as pre IH values for tHb did not. However, tHb values were not statistically different between trials (p=0.49). There was no difference between P[sub et]CO₂ or SaO₂ values in each experimental session (p>0.05). CONCLUSION: Exposure to 10 days of IH significantly increases MSNA and augments the ventilatory response to hypoxia. The enhanced MSNA is mediated primarily through an increase in burst frequency, which shows a strong relationship to HVR post IH. This suggests that concurrent adaptations to the ventilatory and neurovascular control systems may occur with IH. Although our subjects only experienced brief IH, our data support the hypothesis that repeated exposures to IH in OSA could contribute to the sustained increases in MSNA observed in the absence of hypoxic stimuli.

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2010-02-05

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http://hdl.handle.net/2429/19680

Human Kinetics

University of British Columbia

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