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

ABSTRACT

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 VO₂peak (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.

KEYWORDS:

• Exercise pressor reflex
• neural control of circulation
• rehabilitation
• exercise induced hypertension

Acknowledgments

Our appreciation is extended to the volunteers who participated in this study. We are grateful to the staff of the Atlanta and Baltimore VA GRECCs and Atlanta CVNR for their assistance in this project. Research reported in this publication was supported by the National Heart Lung and Blood Institution (R01 HL135183 PI: J. Park), the National Institute of Diabetes and Digestive and Kidney Diseases (T32DK007656, PI: J. Sands), and the United States (U.S.) Department of Veterans Affairs (Merit Review Award I01CX001065 (PI: J. Park), Career Development Award IK2 RX-000944 (PI: M. Serra), and a Senior Research Career Scientist (PI: A. Ryan)).

Additional information

Funding

This work was supported by the National Institutes of Health [R01 HL13518]; National Institutes of Health [T32DK007656]; U.S. Department of Veterans Affairs [I01CX001065]; U.S. Department of Veterans Affairs [IK2 RX-000944].