Key points The arterial baroreflex controls vasoconstrictor muscle sympathetic nerve activity (MSNA) in a negative feedback manner by increasing or decreasing activity during spontaneous blood pressure falls or elevations, respectively. Spontaneous sympathetic baroreflex sensitivity is commonly quantified as the slope of the relationship between MSNA burst incidence or strength and beat‐to‐beat variations in absolute diastolic blood pressure. We assessed the relationships between blood pressure inputs related to beat‐to‐beat blood pressure change or blood pressure rate‐of‐change (variables largely independent of absolute pressure) and MSNA at rest and during exercise and mental stress. The number of participants with strong linear relationships between MSNA and beat‐to‐beat diastolic blood pressure change variables or absolute diastolic blood pressure were similar at rest, although during stress the beat‐to‐beat diastolic blood pressure change variables were superior. Current methods may not fully characterize the capacity of the arterial baroreflex to regulate MSNA. Abstract Spontaneous sympathetic baroreflex sensitivity (sBRS) is commonly quantified as the slope of the relationship between variations in absolute diastolic blood pressure (DBP) and muscle sympathetic nerve activity (MSNA) burst incidence or strength. This relationship is well maintained at rest but not during stress. We assessed whether sBRS could be calculated at rest and during stress (static handgrip, rhythmic handgrip, mental stress) using blood pressure variables that quantify relative change: beat‐to‐beat DBP change (ΔDBP), ΔDBP rate‐of‐change (ΔDBP rate), pulse pressure (PP) and PP rate‐of‐change (PP rate). Sixty‐six healthy participants underwent continuous measures of blood pressure (finger photoplethysmography) and multi‐unit MSNA (microneurography). At rest, absolute DBP (91%), ΔDBP (97%) and ΔDBP rate (97%) each yielded higher proportions of participants with strong linear relationships (r ≥ 0.6) with MSNA burst incidence compared to PP (57%) and PP rate (56%) and produced similar sBRS slopes (DBP: −4.5 ± 2.0 bursts 100 heartbeats–1/mmHg; ΔDBP: −5.0 ± 2.1 bursts 100 heartbeats–1/ΔmmHg; ΔDBP rate: −4.9 ± 2.2 bursts 100 heartbeats–1/ΔmmHg s–1; P > 0.05). During stress, ΔDBP (74%) and ΔDBP rate (74%) yielded higher proportions of strong linear relationships with MSNA burst incidence than absolute DBP (43%), PP (46%) and PP rate (49%) (all P < 0.05). The absolute DBP associated with a 50% chance of a MSNA burst (T50) was shifted rightward during static handgrip (Δ+15 ± 11 mmHg, P < 0.001) and mental stress (Δ+11 ± 7 mmHg, P < 0.001); however, the ΔDBP T50 was shifted rightward during static handgrip (Δ+2.5 ± 3.7 mmHg, P = 0.009) but not mental stress (Δ0.0 ± 4.4 mmHg, P = 0.99). These findings suggest that calculating sBRS using absolute DBP alone may not adequately characterize arterial baroreflex regulation of MSNA, particularly during stress.

This thesis investigated the effects of high intensity interval training (HIIT) and continuous moderate intensity training (CMIT) on maximal exercise capacity (VO2max), resting and exercising hemodynamics, and clinical symptoms in eighteen men and women with Parkinson's Disease. Participants were randomized to HIIT (n=9), or CMIT (n=9) groups and completed two pre-training visits. Participants completed clinical questionnaires and performed a progressive exercise test to determine VO2max. Measurements of arterial stiffness and wave reflection characteristics were recorded. Continuous hemodynamic measurements were recorded during a 2-minute isometric handgrip contraction followed by 3-minutes of post-exercise circulatory occlusion. Participants then completed 10 weeks (3x/week; 1 hour/session) of HIIT or CMIT at the Guelph YMCA followed by the same two days of post-testing. HIIT provided clinically relevant improvements in VO2max, UPDRS part III, and BDI-II scores which were greater compared to CMIT. Both exercise protocols provided no improvements in fatigue and resting or exercising hemodynamics. iii Acknowledgements I would like to start by acknowledging the incredible support my family and friends provided me not only throughout the past two-year journey, but throughout my entire life. Thank you so much for your selflessness and encouragement. I am forever grateful and will continue to push forward, knowing I have you all by my side. Thank you. Secondly, I would like to acknowledge my advisor, Dr. Philip Millar. When I first began this two-year journey, I did not know what to expect, where to start and how to truly think like a scientist. However, after working with you, I have learned to be more independent, persistent, and communicative. Thank you for always being available to your students and putting in countless hours of your time towards us, even when you had other commitments. You are a great role model and your passion for research is contagious.I would also like to acknowledge my committee members Dr. Lori Vallis and Dr. Jamie Burr. Thank you for your continuous help throughout the entire two-year process. Thank you for being so flexible with your time, especially during the numerous testing visits. I also want to thank all of your lab members for their time and flexibility. Without the support from you all, the study would not be where it is today.Finally, I would like to thank my lab mates, Anthony, Jordan, Massimo, Andre, Muhammad, Joseph, and Mitchell. Thank you for all the help and support during this process. I am very lucky to have had such dependable and kind peers. A special thanks to Anthony and Jordan for being great role models and always being there when I had any questions or issues.

The sympathetic arterial baroreflex regulates blood pressure through negative feedback changes in vasoconstrictor muscle sympathetic nerve activity (MSNA). Spontaneous sympathetic baroreflex sensitivity (BRS) is quantified using a weighted linear regression relating absolute diastolic blood pressure (DBP) with occurrence (burst incidence [BI]) or strength (burst amplitude [BA]) of a multi‐unit MSNA burst. Such as assessment generally produces strong negative linear relationships between DBP and MSNA at rest, but are often weakened or absent during sympathoexcitatory stimuli, such as exercise or mental stress. We hypothesized that sympathetic BRS would be better represented during stress by using the change in DBP between two subsequent cardiac cycles (DBP change) rather than the absolute DBP value (absolute DBP). We retrospectively examined 64 participants whom underwent continuous recordings of heart (ECG), blood pressure (Finometer), and MSNA (microneurography). Each participant completed a 2–5 min resting baseline followed by one or more of the following protocols: rhythmic handgrip (RHG; n=24; 3 min at 40% maximal voluntary contraction [MVC]), static handgrip (SHG; n=16; 2 min at 30% MVC), mental stress (MS; n=28; 2 min serial subtraction). At rest, we observed a similar number of strong negative linear relationships (r>0.6) with BI (52/64 vs. 59/64, p=0.12) and BA (41/64 vs. 49/64, p=0.18) using the absolute and change methods. In participants possessing strong relationships across both methods (BI: n=49; BA: n=32), we observed differences in sympathetic BRS of BI (−4.7±1.8 bursts/100 heartbeats/mmHg vs. −5.4±2.0 bursts/100 heartbeats/ΔmmHg, p=0.03) and BA (−2.9±1.0 AU/mmHg vs. −2.5±1.3 AU/ΔmmHg, p=0.06), and modest correlations between methods for BRS of BI (r=0.32) and for BRS of BA (r=0.42). During stress, the absolute and change methods yielded a similar proportion of strong negative linear relationships with BI during RHG (6/24 vs. 10/24, p=0.36), but a higher number using the DBP change method during SHG (7/16 vs. 15/16, p=0.006) and MS (16/28 vs. 24/28, p=0.04). Similarly, the change method identified a greater proportion of strong negative linear relationships with BA during RHG (0/24 vs. 12/24, p<0.001), SHG (0/16 vs. 14/16, p<0.001), and MS (9/28 vs. 20/28, p=0.007). The DBP change method more consistently identified strong negative linear relationships with MSNA BI and BA. The modest relationships between methods at rest may highlight the importance of beat‐to‐beat DBP changes in arterial baroreflex regulation of muscle sympathetic outflow.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada (NSERC); NSERC Discovery Grant; Canada Foundation for InnovationThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.