Exercise-induced symptom exacerbation in postconcussive patients is inversely associated with percentage of maximum heart rate at fraction of arterial carbon dioxide (FETCO2) break point, researchers found in a study published in Neurology. Postconcussive changes in cerebrovascular function during exercise may be a protective mechanism.

Progressive exercise aids recovery from concussions, but the intensity of exercise that is beneficial is difficult to determine since exercise could also exacerbate symptoms. Identifying the aspects of exercise that can increase the risk of exacerbating symptoms would aid neurologists in advising patients how to best exercise during their recovery.

Alterations in vascular responses to exercise, particularly the impact of change in arterial CO2, is a likely factor.


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The objective of the study was to determine whether cardiopulmonary and cerebrovascular responses during acute bouts of exercise in youths exacerbated symptoms.

Forty patients (17.6±2.2 years old; 55% females) who had suffered sport-related concussions within the past 3 weeks and were symptomatic at rest and 37 control individuals (18.3±2.4 years old; 62% females) with no past-year history of concussion enrolled in the study between September 2018 and February 2020. They completed modified YMCA branching exercise protocol exercises on a stationary bike.

Postconcussive patients completed exercise testing sessions 12.5±4.7 days and 12.5±4.7 days after concussion. Completion of tests was either after symptom exacerbation (n=7 ≥30 visual-analog scale (VAS) mm) or reaching 85% of age-predicted maximum heart rate (HR). Postconcussive participants had significantly higher Post-Concussion Symptom Inventory (PCSI) scores compared with the control group.

Fraction of end-tidal CO2 (FETCO2), surrogate for arterial CO2, and heart rate increased throughout the exercise, plateaued, and dropped. Exercise intensity and heart rate were associated (R2 > 0.75), except in 7 tests that did not have sufficient signal quality in recording heart rate.

Higher heart rate at FETCO2 break point was linked with less change in symptom burden at both visits.

FETCO2 break point impacted symptom exacerbation regardless of baseline symptom burden.

Among individuals with concussions, resting VAS and FETCO2 break point prompted 68% of variation in exercise-induced symptom exacerbation (R2 = 0.65 [adjusted for number of variables]; FETCO2 β= -1.210±0.517 [S.E.], P <.05).

Change in FETCO2 was linked with cerebral blood flow velocity during exercise. In 73% of individuals, CO2 explained more than 25% of changes in CBF during exercise.

Among postconcussive individuals, researchers identified a moderate, statistically significant relationship between cerebrovascular responses to CO2 at rest and cerebrovascular responses to exercise-induced changes in FETCO2 (R2 = 0.13 P =.01).

Study limitations include generalization to other age groups, exclusion of other concussion symptoms, inability to directly account for impact of pressure changes on flow responses to exercise, and no assessment of hyperemia to the brain.

“While it may not always be beneficial or feasible to increase exercise intensity, intensity may be personalized based on baseline presentation (resting cerebral vasoreactivity and symptom burden),” the researchers stated. “Consequently, increasing exercise frequency along with personalized levels of exercise intensity may provide the optimal level of exercise volume to improve postconcussion outcomes. This is particularly important to note because exercise and exertion can exacerbate concussion symptoms even when symptoms are not apparent at rest, and concussion-like symptoms are present in a large proportion of healthy individuals at rest.”

Reference

Howell DR, Hunt DL, Aaron SE, et al. Association of hemodynamic and cerebrovascular responses to exercise with symptom severity in adolescents and young adults with concussion. Neurol. Published online October 11, 2021. doi: 10.1212/WNL.0000000000012929