Michael K Stickland1, Craig D Steinback2,3,4,5, Andrew R Steele6, Lindsey F Berthelsen6, Graham M Fraser7, Devin B Phillips1, Desi P Fuhr1, Eric Y L Wong1. 1. Division of Pulmonary Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, T6G 2E1, Canada. 2. Neurovascular Health Lab, Faculty of Kinesiology, Sport, & Recreation, University of Alberta, 1-059D Li Ka Shing Centre for Health Research Innovation, Edmonton, T6G 2E1, Canada. craig.steinback@ualberta.ca. 3. Women and Children's Health Research Institute, University of Alberta, Edmonton, T6G 2E1, Canada. craig.steinback@ualberta.ca. 4. Alberta Diabetes Institute, University of Alberta, Edmonton, T6G 2E1, Canada. craig.steinback@ualberta.ca. 5. Neuroscience and Mental Health Institute, University of Alberta, Edmonton, T6G 2E1, Canada. craig.steinback@ualberta.ca. 6. Neurovascular Health Lab, Faculty of Kinesiology, Sport, & Recreation, University of Alberta, 1-059D Li Ka Shing Centre for Health Research Innovation, Edmonton, T6G 2E1, Canada. 7. Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Abstract
PURPOSE: Obstructive sleep apnea (OSA) is a common disorder (~ 4%) that augments sympathetic nerve activity (SNA) and elevates blood pressure. The relationship between sympathetic vasomotor outflow and vascular responsiveness, termed sympathetic neurovascular transduction (sNVT), has been sparsely characterized in patients with OSA. Therefore, we sought to quantify spontaneous sympathetic bursts and related changes in diastolic pressure. METHODS: Twelve participants with variable severities of OSA were recruited. We collected muscle sympathetic nerve activity (MSNA) (microneurography) and beat-by-beat diastolic pressure (finger photoplethysmography) during normoxia (FiO2 = 0.21) and hyperoxia (FiO2 = 1.0) to decrease MSNA burst frequency. MSNA burst sequences (i.e. singlets, doublets, triplets and quadruplets) were identified and coupled to changes in diastolic pressure over 15 cardiac cycles as an index of sNVT. sNVT slope for each individual was calculated from the slope of the relationship between peak responses in outcome plotted against normalized burst amplitude. RESULTS: sNVT slope was unchanged during hyperoxia compared to normoxia (normoxia 0.0024 ± 0.0011 Δ mmHg total activity [a.u.]-1 vs. hyperoxia 0.0029 ± 0.00098 Δ mmHg total activity [a.u.]-1; p = 0.14). sNVT slope was inversely associated with burst frequency during hyperoxia (r = -0.58; p = 0.04), but not normoxia (r = -0.11; p = 0.71). sNVT slope was inversely associated with the apnea-hypopnea index (AHI) (r = -0.62; p = 0.030), but not after age was considered. CONCLUSIONS: We have demonstrated that the prevailing MSNA frequency is unmatched to the level of sNVT, and this can be altered by acute hyperoxia.
PURPOSE:Obstructive sleep apnea (OSA) is a common disorder (~ 4%) that augments sympathetic nerve activity (SNA) and elevates blood pressure. The relationship between sympathetic vasomotor outflow and vascular responsiveness, termed sympathetic neurovascular transduction (sNVT), has been sparsely characterized in patients with OSA. Therefore, we sought to quantify spontaneous sympathetic bursts and related changes in diastolic pressure. METHODS: Twelve participants with variable severities of OSA were recruited. We collected muscle sympathetic nerve activity (MSNA) (microneurography) and beat-by-beat diastolic pressure (finger photoplethysmography) during normoxia (FiO2 = 0.21) and hyperoxia (FiO2 = 1.0) to decrease MSNA burst frequency. MSNA burst sequences (i.e. singlets, doublets, triplets and quadruplets) were identified and coupled to changes in diastolic pressure over 15 cardiac cycles as an index of sNVT. sNVT slope for each individual was calculated from the slope of the relationship between peak responses in outcome plotted against normalized burst amplitude. RESULTS: sNVT slope was unchanged during hyperoxia compared to normoxia (normoxia 0.0024 ± 0.0011 Δ mmHg total activity [a.u.]-1 vs. hyperoxia 0.0029 ± 0.00098 Δ mmHg total activity [a.u.]-1; p = 0.14). sNVT slope was inversely associated with burst frequency during hyperoxia (r = -0.58; p = 0.04), but not normoxia (r = -0.11; p = 0.71). sNVT slope was inversely associated with the apnea-hypopnea index (AHI) (r = -0.62; p = 0.030), but not after age was considered. CONCLUSIONS: We have demonstrated that the prevailing MSNA frequency is unmatched to the level of sNVT, and this can be altered by acute hyperoxia.
Authors: Craig D Steinback; Graham M Fraser; Charlotte W Usselman; Laura M Reyes; Colleen G Julian; Michael K Stickland; Radha S Chari; Rshmi Khurana; Sandra T Davidge; Margie H Davenport Journal: J Physiol Date: 2019-06-13 Impact factor: 5.182
Authors: Keri S Taylor; Hisayoshi Murai; Philip J Millar; Nobuhiko Haruki; Derek S Kimmerly; Beverley L Morris; George Tomlinson; T Douglas Bradley; John S Floras Journal: Hypertension Date: 2016-10-03 Impact factor: 10.190