Abstract

ObjectiveResearch suggests that one physiological effect of concussion is a disruption in regulation of autonomic nervous system control that affects the balance between parasympathetic and sympathetic output. While changes in heart rate after concussion have been observed, the nature of the heart rate change during progressive exercise has not been well evaluated in acutely symptomatic patients. Additionally, little is known about the relationship between HR and RPE in this population.MethodsWe compared changes in heart rate and perceived effort during graded treadmill exertion in recently concussed patients to elucidate the effect of brain injury on cardiovascular response to exercise. Resting HR, HR on exercise initiation, and changes in HR and RPE during the Buffalo Concussion Treadmill Test (BCTT) were compared on two test visits: When patients were symptomatic (acute) and after recovery. Results were compared with the test-retest results obtained from a control group consisting of healthy, non-concussed individuals.ResultsPatients had a significantly lower HR at onset of exercise when acutely concussed as compared to when recovered and reported greater perceived exertion at every exercise intensity level when symptomatic, despite exercising at lower workloads, than when recovered. Sympathetic response to increased exertion was not affected by concussion - HR increased in response to exercise at a comparable rate in both tests. These differences observed in response to exercise between the first BCTT and follow-up evaluation in initially concussed patients were not present in non-concussed individuals.ConclusionOur results suggest that during the acute phase after concussion, acutely concussed patients demonstrated an impaired ability to shift from parasympathetic to sympathetic control over heart rate at the onset of exercise. Changes in the autonomic nervous system after concussion may be more complex than previously reported. Continued evaluation of autonomic regulatory effects in the acute phase after concussion is warranted.

Highlights

  • There is increasing interest about the effects of acute concussive injury on the capacity of the central nervous system to appropriately regulate peripheral functions such as cardiovascular rhythm, metabolism and temperature regulation and how this may relate to prolonged recovery from concussion [1,2,3,4]

  • Sympathetic response to increased exertion was not affected by concussion - heart rate (HR) increased in response to exercise at a comparable rate in both tests

  • Elevated HR in response to stress or exercise would be indicative of an uncoupling of the autonomic and cardiovascular systems and an inability of the parasympathetic system to sufficiently contribute to beat-to-beat variability [5]

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Summary

Introduction

There is increasing interest about the effects of acute concussive injury on the capacity of the central nervous system to appropriately regulate peripheral functions such as cardiovascular rhythm, metabolism and temperature regulation and how this may relate to prolonged recovery from concussion [1,2,3,4]. Studies that have addressed disruption in regulatory function after mild or severe traumatic brain injury have generally focused on abnormalities in autonomic control over the sympathetic and parasympathetic nervous system, including control of heart rate (HR) and heart rate variability (HRV) [3,5,6,7]. Studies examining HRV have focused on difficulties in HR recovery (the ability to re-engage the parasympathetic system after termination of cardiovascular exertion) and changes in the relative contribution of the parasympathetic nervous system to the cardiac rhythm following injury [8,9,10]. While research directly examining autonomic regulatory changes following concussion is limited, some support comes from the literature on severe traumatic brain injury (TBI). Significant changes in cardiac autonomic control after TBI have been reported, including parasympathetic withdrawal from the cardiac rhythm (resulting in severe cardiac abnormalities), orthostatic intolerance, and tachycardia [11,12]

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