Introduction: Concussion, a form of mild traumatic brain injury (TBI), has an estimated annual incidence of 1-4 million cases in the US alone. Studies have documented impairments in cerebral vascular function following concussion which often coincide with other neurocognitive symptoms but, in some cases, persist despite symptom resolution. However, the majority of these studies were performed 3 months or less post-concussion. Therefore, we tested the hypothesis that cerebral vasodilator function is impaired in adults who had a concussion 6 months prior and are asymptomatic relative to healthy age- and sex- matched controls with no known history of concussion. Methods: Six adults (3 Male/3 Female, 26 ± 5 years) with a history of diagnosed concussion ~6 months prior to the study visit (average, 6 ± 1 months) and six controls (3 Male/3 Female, 28 ± 5 years) without a known history of concussion were recruited. Beat-to-beat blood pressure (finger photoplethysomography), middle cerebral artery blood velocity (MCAv; transcranial Doppler ultrasound) and partial pressure of end-tidal carbon dioxide (P ET CO 2 ; capnography) were measured continuously during two-minutes of quiet supine rest and throughout a rebreathing protocol designed to increase P ET CO 2 up to +15mmHg. Cerebral vascular conductance index (CVCi) was calculated as mean MCAv divided by mean arterial pressure (MAP) on a beat-to-beat basis. Cerebrovascular reactivity was assessed as the percent change in MCAv or CVCi at increasing levels of P ET CO 2 (Δ3,6,9,12,15 mmHg P ET CO 2 ) and the gain of the relationship between MCAv or CVCi and P ET CO 2 . Results: Resting MAP (P=0.33), MCAv (control: 76 ± 6 cm/sec; TBI: 74 ± 8 cm/sec, P=0.82), and CVCi (control: 0.91 ± 0.08 cm/sec/mmHg; TBI: 0.86 ± 0.11 cm/sec/mmHg, P=0.72) were not different between groups. The CO2 rebreathing protocol increased MCAv and CVCi in both groups (main effect of time; P<0.001 for both). However, the percent change in MCAv and CVCi did not differ between control and TBI participants throughout the rebreathing protocol (Interaction, P=0.13 and P=0.26, respectively). Likewise, the MCAv (control: 3.5 ± 0.4 cm/sec/mmHg; TBI: 4.0 ± 0.6 cm/sec/mmHg, P=0.51) and CVCi (P=0.72) gains were not different between groups. Conclusion: These preliminary findings suggest that individuals six-months post-concussion who are asymptomatic do not exhibit impaired cerebral vasodilator function. This project was supported by the Henry M Jackson Foundation HU0001-18-2-0016. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Approximately 1 million people in the United States are living with multiple sclerosis (MS) with nearly 75% of those being female. MS is a progressive demyelinating neurological disease of the central nervous system associated with a high prevalence of orthostatic hypotension. Our laboratory has previously shown that individuals with MS have a reduced ability to increase mean arterial pressure during simulated hypotension which was attributed to a blunted vascular response. The purpose of this project was to investigate how spontaneous bursts of muscle sympathetic nerve activity (MSNA) induce end-organ response(s) and ultimately evoke a change in blood pressure (BP) on a heartbeat-to-heartbeat basis in females with MS, a process known as sympathetic transduction to BP. We tested the hypothesis that females with MS have reduced resting sympathetic transduction to BP compared to sex-, height-, weight-, age- and race-matched healthy controls. Beat-to-beat BP (Finometer) and MSNA (peroneal microneurography) were continuously recorded during 10 minutes of quiet supine rest in 9 females with relapsing-remitting MS (age: 39.6 ± 3.3 years; Expanded Disability Status Scale < 6.0) and 10 healthy female controls (age: 35.4 ± 2.1 years). Total vascular conductance (TVC) was estimated using modelflow. Sympathetic transduction was determined by identifying the peak change in diastolic BP and the nadir reduction of TVC over 10 cardiac cycles following spontaneous MSNA bursts using signal averaging. No differences were detected in resting mean arterial pressure (MS: 88 ± 3 mmHg; controls: 85 ± 2; P = 0.42) or MSNA burst frequency (MS: 26 ± 3 bursts/min; controls: 19 ± 3 bursts/min; P = 0.11) between groups. Peak increases in diastolic BP following MSNA bursts were lower in females with MS (1.2 ± 0.2 mmHg) compared to controls (2.5 ± 0.6 mmHg; P = 0.039). Whereas no differences were observed in nadir reductions in TVC (MS: -1.7 ± 0.5 ml/min/mmHg; controls: -3.0 ± 0.8 ml/min/mmHg; P = 0.11). These preliminary data suggest that sympathetic transduction to BP is blunted in females with MS. Reduced sympathetic transduction to BP may contribute to the high occurrence of orthostatic hypotension in this clinical population. Further investigation is warranted to help better understand the potential mechanism(s) underlying lower sympathetic transduction in females with MS. This work was supported by American Heart Association Predoctoral Fellowship (Award #915655, Trotter) and American College of Sports Medicine Doctoral Research Grant (Award # 19-01141, Trotter) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.