Renaud Tamisier1,2, Can Ozan Tan3, Jean-Louis Pepin1,2, Patrick Levy1,2, J Andrew Taylor3. 1. Université Grenoble Alpes, HP2; Inserm U1042, Grenoble, France. 2. CHU de Grenoble, Clinique Physiologie, Sommeil et Exercice, Grenoble, France. 3. Cardiovascular Research Laboratory, Spaulding Rehabilitation Hospital, and Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA.
Abstract
STUDY OBJECTIVES: To test the hypothesis that greater resting sympathetic activity in obstructive sleep apnea (OSA) syndrome would not induce a lesser sympathetic neurovascular transduction. DESIGN: Case-controlled cohort study. PARTICIPANTS: 33 patients with newly diagnosed OSA without comorbidities and 14 healthy controls. INTERVENTIONS: 6 months of continuous positive airway pressure (CPAP) treatment for OSA patients and follow-up for 9 healthy controls. MEASUREMENTS AND RESULTS: We assessed resting sympathetic outflow and sympathetic neurovascular transduction. Sympathetic activity was directly measured (microneurography) at rest and in response to sustained isometric handgrip exercise. Neurovascular transduction was derived from the relationship of sympathetic activity and blood pressure to leg blood flow during exercise. Despite an elevated sympathetic activity of ∼50% in OSA compared to controls, neurovascular transduction was not different (i.e., absence of tachyphylaxis). After six months of CPAP, there were significant declines in diastolic pressure, averaging ∼4 mm Hg, and in sympathetic activity, averaging ∼20% with no change in transduction. CONCLUSIONS: Greater sympathetic activity in obstructive sleep apnea does not appear to be associated with lesser neurovascular transduction. Hence, elevated sympathetic outflow without lesser transduction may underlie the prevalent development of hypertension in this population that is well controlled by continuous positive airway pressure treatment.
STUDY OBJECTIVES: To test the hypothesis that greater resting sympathetic activity in obstructive sleep apnea (OSA) syndrome would not induce a lesser sympathetic neurovascular transduction. DESIGN: Case-controlled cohort study. PARTICIPANTS: 33 patients with newly diagnosed OSA without comorbidities and 14 healthy controls. INTERVENTIONS: 6 months of continuous positive airway pressure (CPAP) treatment for OSA patients and follow-up for 9 healthy controls. MEASUREMENTS AND RESULTS: We assessed resting sympathetic outflow and sympathetic neurovascular transduction. Sympathetic activity was directly measured (microneurography) at rest and in response to sustained isometric handgrip exercise. Neurovascular transduction was derived from the relationship of sympathetic activity and blood pressure to leg blood flow during exercise. Despite an elevated sympathetic activity of ∼50% in OSA compared to controls, neurovascular transduction was not different (i.e., absence of tachyphylaxis). After six months of CPAP, there were significant declines in diastolic pressure, averaging ∼4 mm Hg, and in sympathetic activity, averaging ∼20% with no change in transduction. CONCLUSIONS: Greater sympathetic activity in obstructive sleep apnea does not appear to be associated with lesser neurovascular transduction. Hence, elevated sympathetic outflow without lesser transduction may underlie the prevalent development of hypertension in this population that is well controlled by continuous positive airway pressure treatment.
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