Author(s): KUNIMATSU, N., LIU, J., TSUKAMOTO, H., OGOH, S., Institution: TOYO UNIVERSITY, Country: JAPAN, Abstract-ID: 1307

INTRODUCTION:
Exercise is well known to reduce cardiovascular disease risk [1]. However, it has been suggested that even healthy young adults who exhibit exaggerated blood pressure responses during exercise have an increased risk of developing hypertension later in life [2]. The physiological mechanism of individual differences in blood pressure response to exercise remains unknown. Based on the Selfish Brain hypothesis, which proposes that the brain actively regulates systemic blood pressure to maintain cerebral perfusion [3], we hypothesized that individual differences in posterior cerebral perfusion, particularly in brainstem regions involved in blood pressure regulation, contribute to variability in exercise-induced blood pressure responses.
METHODS:
To test this hypothesis, twenty-seven young healthy adults (7 males and 20 females, age: 21 ± 1 years; height: 163.5 ± 7.9 cm; weight: 56.9 ± 9.1 kg; mean ± standard deviation [SD]) performed a 3-minute handgrip exercise at 30% maximal voluntary contraction. Vertebral artery (VA) diameter and blood velocity were assessed using ultrasound before and during the exercise to evaluate posterior cerebral circulation. Arterial blood pressure was continuously monitored. VA blood flow was calculated, and a cerebrovascular resistance index (CVRi) was derived from systolic blood pressure (SBP) and VA blood flow. Correlations between exercise-induced changes in SBP and changes in CVRi or VA blood flow were analyzed.
RESULTS:
Exercise-induced SBP responses varied widely among individuals (Δ SBP, 17 ± 18 mmHg; range, -35 to 60 mmHg). The magnitude of SBP increase was positively correlated with CVRi (r = 0.543, P = 0.006). In contrast, VA blood flow was maintained irrespective of the magnitude of SBP response (r = 0.020, P = 0.921).
CONCLUSION:
These findings suggest that individual differences in exercise-induced blood pressure responses in young adults may reflect a compensatory mechanism aimed at preserving posterior cerebral perfusion when VA resistance increases, supporting the concept that variability in exercise pressor responses is driven, at least in part, by cerebrovascular regulatory mechanisms.
REFERENCES:
[1] Nosarev et al., 2014 Front Cell Dev Biol
[2] Paton et al., 2009 Exp Physiol
[3] Schultz et al., 2015 J Am Coll Cardiol