The Role Of Autonomic Nervous Activity On Metaboreceptor-mediated Pressor Responses In Autism Spectrum Disorder

Hyperactivity of the sympathetic nervous system (SNA) is known to contribute to the development of hypertension and cardiovascular disease. Recent reports indicate that adolescents and young adults with autism spectrum disorder (ASD) experience a higher prevalence of hypertension and cardiometabolic disease than the general population. Limited studies suggest that individuals with ASD may have autonomic dysfunction from heart rate variability (HRV) analysis. However, it is still unclear whether autonomic dysfunction influences blood pressure (BP) response to exercise in ASD. PURPOSE: to compare autonomic function to regulate the BP to exercise and metaboreceptor-mediated pressor response between young adults with and without ASD. METHODS: A total of 21 young adults with and without ASD completed the study. HR from ECG, beat-to-beat arterial BP from Finapres, and stroke volume from Modelflow, muscle SNA from microneurography, were continuously measured during baseline, 2 minutes of handgrip exercise at 35% of maximal contraction, 2 minutes of occlusion on exercising arm (postexercise ischemia; PEI), and recovery. In addition, time and frequency domains of HRV analysis were used from baseline and recovery. RESULTS: ASD had higher resting baseline MSNA (10 ± 2 Control vs. 15 ± 5 ASD, burst/min) and HR (58 ± 2 Control vs. 65 ± 2 ASD, bpm) compared to control. There is an attenuated increase in MSNA from rest to exercise in ASD (Δ12 ± 2 Control, Δ-1 ± 6 ASD, burst/min). While both groups increased HR and BP from rest to exercise, ASD had attenuated pressor response (Δ11 ± 1 control vs Δ6 ± 1 ASD, mmHg). Mean BP stayed elevated similarly during PEI compared to exercise in both groups. While HR decreased significantly to PEI from exercise in control (Δ-6 ± 1 bpm), it stayed elevated in ASD (Δ-2 ± 2 bpm). RMSSD, HF power, and total power were significantly lower in the ASD group during recovery while they tended to be lower at rest. CONCLUSION: The attenuated pressor response to exercise in ASD appeared to be due to lesser sympathetic contribution. Greater tachycardic response in ASD did not contribute to the metaboreceptor-mediated pressor effect. Our findings suggest that individuals with ASD have autonomic dysfunction which may attenuate pressor responses to exercise. This work is supported by National Institute of Health, NIGMS Grant (SC2GM144165 to A.K. Jensen) and SJSU Student Research Fellowship (23-SRF-05-045 to S.S. Wang)