Geoff B Coombs1, Diana Vucina2, Hannah G Caldwell3, Otto F Barak4,5, Tanja Mijacika6, Amanda H X Lee7, Zoe K Sarafis7, Jordan W Squair7, Andrei V Krassioukov7, Aaron A Phillips8, Zeljko Dujic6, Philip N Ainslie3. 1. Centre for Heart, Lung and Vascular Health, Faculty of Health and Social Development, University of British Columbia Okanagan, 1147 Research Rd, Kelowna, BC, Canada. geoff.coombs91@gmail.com. 2. Department of Neurology, Clinical Hospital Center Split, Spinciceva 1, Split, Croatia. 3. Centre for Heart, Lung and Vascular Health, Faculty of Health and Social Development, University of British Columbia Okanagan, 1147 Research Rd, Kelowna, BC, Canada. 4. Faculty of Medicine, University of Novi Sad, Hajduk Veljkova 3, 21137, Novi Sad, Serbia. 5. Faculty of Sports and Physical Education, University of Novi Sad, Novi Sad, Serbia. 6. Department of Integrative Physiology, University of Split School of Medicine, Soltanska 2, HR-21000, Split, Croatia. 7. International Collaboration on Repair Discoveries, Faculty of Medicine, University of British Columbia, 818 West 10th Avenue, Vancouver, Canada. 8. Departments of Physiology and Pharmacology, Cardiac Sciences, Clinical Neurosciences, Hotchkiss Brain Institute, Libin Cardiovascular Institute, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, Canada.
Abstract
STUDY DESIGN: Experimental study. OBJECTIVES: Compromised cerebrovascular function likely contributes to elevated neurological risk in spinal cord injury (SCI). Passive heating offers many cardiovascular and neurological health benefits; therefore, we aimed to determine the effects of an acute bout of heating on cerebrovascular function in chronic SCI. METHODS: Persons with cervical SCI (n = 15) and uninjured controls (CON; n = 15) completed 60 min of lower limb hot water immersion (40 °C). Assessments of middle cerebral (MCA) and posterior cerebral artery (PCA) velocities, pulsatilities, and neurovascular coupling (NVC) were performed using transcranial Doppler ultrasound. Duplex ultrasonography was used to index cerebral blood flow via the internal carotid artery (ICA), and carotid-femoral pulse-wave velocity (PWV) was measured using tonometry. The NVC response was quantified as the peak hyperemic value during 30-s cycles of visual stimulation. RESULTS: Mean arterial pressure changed differentially with heating [mean (standard deviation); SCI: +6(14) mmHg, CON: -8(12) mmHg; P = 0.01]. There were no differences in any intracranial artery measures (all P > 0.05), except for small (~10%) increases in MCA conductance in CON after heating vs. SCI (interaction P = 0.006). Resting ICA flow was greater in SCI vs. CON (P = 0.03) but did not change with heating in either group (interaction P = 0.34). There were also no between-group differences in the NVC response (ΔPCA conductance) pre- [SCI: 29(19)% vs. CON: 30(9)%] or post-heating [SCI 30(9)% vs. 25(9)%; interaction P = 0.22]. CONCLUSIONS: Mild acute heating does not impair or improve cerebrovascular function in SCI or CON. Thus, further study of the effects of chronic heating interventions are warranted.
STUDY DESIGN: Experimental study. OBJECTIVES: Compromised cerebrovascular function likely contributes to elevated neurological risk in spinal cord injury (SCI). Passive heating offers many cardiovascular and neurological health benefits; therefore, we aimed to determine the effects of an acute bout of heating on cerebrovascular function in chronic SCI. METHODS:Persons with cervical SCI (n = 15) and uninjured controls (CON; n = 15) completed 60 min of lower limb hot water immersion (40 °C). Assessments of middle cerebral (MCA) and posterior cerebral artery (PCA) velocities, pulsatilities, and neurovascular coupling (NVC) were performed using transcranial Doppler ultrasound. Duplex ultrasonography was used to index cerebral blood flow via the internal carotid artery (ICA), and carotid-femoral pulse-wave velocity (PWV) was measured using tonometry. The NVC response was quantified as the peak hyperemic value during 30-s cycles of visual stimulation. RESULTS: Mean arterial pressure changed differentially with heating [mean (standard deviation); SCI: +6(14) mmHg, CON: -8(12) mmHg; P = 0.01]. There were no differences in any intracranial artery measures (all P > 0.05), except for small (~10%) increases in MCA conductance in CON after heating vs. SCI (interaction P = 0.006). Resting ICA flow was greater in SCI vs. CON (P = 0.03) but did not change with heating in either group (interaction P = 0.34). There were also no between-group differences in the NVC response (ΔPCA conductance) pre- [SCI: 29(19)% vs. CON: 30(9)%] or post-heating [SCI 30(9)% vs. 25(9)%; interaction P = 0.22]. CONCLUSIONS: Mild acute heating does not impair or improve cerebrovascular function in SCI or CON. Thus, further study of the effects of chronic heating interventions are warranted.
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