Augmented exercise pressor response during maximal treadmill exercise is not related to systemic inflammation in stroke survivors

Background Stroke survivors have exercise intolerance that contributes to reduced quality of life and survival. While exaggerated blood pressure responses during exercise have been documented in other chronic diseases, whether stroke patients have abnormal hemodynamic responses during aerobic exercise remains unexplored. Objectives This cross-sectional study aimed to examine whether stroke survivors have exaggerated increases in blood pressure during maximal treadmill exercise and whether these responses may be related to systemic inflammation. Methods Forty-six participants (25 stroke survivors, STROKE, and 21 controls, CON) performed a maximal treadmill exercise test via the modified Naughton protocol while blood pressure was measured manually during each treadmill stage. A linear mixed model was used to compare the slope of rise in heart rate and blood pressure within and between groups. Spearmans rho analysis was performed to explore the relationship between these responses and circulating concentrations of inflammatory biomarkers. Results The STROKE group exhibited a lower VO(2)peak (16.4 +/- 0.8 vs. 30.0 +/- 1.8 ml/kg/min,P< .001) and a greater rate of increase in systolic blood pressure compared to CON (17.4 +/- 1.5 vs. 9.9 +/- 1.4 mmHg/stage,P< .001). We observed no relationship; however, between inflammatory biomarkers and the exaggerated hemodynamic responses in the STROKE group. Conclusion In conclusion, stroke survivors exhibit greater increases in systolic blood pressure during maximal treadmill exercise compared to controls. These responses do not appear to be related to systemic inflammation. Future work should seek to delineate the mechanisms responsible for exaggerated blood pressure responses during exercise in stroke.

Automated summary

Stroke survivors exhibit greater increases in systolic blood pressure during maximal treadmill exercise compared to controls, and these responses do not appear to be related to systemic inflammation. Future work should seek to delineate the mechanisms responsible for exaggerated blood pressure responses during exercise in stroke.