Cerebral palsy (CP) is a non-progressive and permanent neurological disorder leading to musculoskeletal dysfunction and immobility. A major clinical problem with CP is early development of cardiovascular diseases with increased rates of mortality. Due to the inevitability of motor dysfunction adults with CP can develop health risk factors, such as obesity and hypertension, at a higher rate compared to the general population. To date, the physiological basis for CP has not been established; how cardiovascular dynamics, such as heart rate (HR), blood pressure (BP), and blood flow (BF), are controlled in individuals with CP has never been identified. PURPOSE: To determine differential cardiovascular responses to acute dynamic exercise in adults with CP. METHODS: Total of eighteen adults with and without CP participated in the study. HR from ECG, beat-to-beat arterial BP from Finapres and brachial BP, and respiration via pneumobelt were continuously measured before, during and after 2 minutes of dynamic handgrip exercise at 35% and 50% of maximal voluntary contraction. In addition, diameter, blood velocity, and flow of the brachial artery were measured using Doppler ultrasound on the contracting arm throughout the experiment.

RESULTS: At rest, both control and CP groups had similar resting HR (60.7±1.9 control and 63.0±7.5 CP, bpm). While resting respiratory rate was lower in CP group compared to the control, resting mean arterial pressure (MAP) and brachial blood flow tended to be higher in CP (p=0.08). MAP and HR were significantly increased to exercise from rest in both groups with no group differences (MAP, ∆ 9.3±2.2 control and ∆11.2±3.3 CP, mmHg; HR, ∆8.4±1.5 control and ∆12.1±4.1 CP, bpm). Respiratory rate was significantly increased to exercise from rest in only the CP group. The delta changes of blood flow from rest to exercise was slightly smaller in the CP group. CONCLUSIONS: While HR and MAP increased to exercise from rest in similar fashion in both groups, increase in BF to exercise was blunted in adults with CP. Our preliminary data suggest that there are differential neural control mechanisms to regulate BP in the CP population. Other mechanisms, possibly vascular contribution from non-contracting limbs or chemoreceptor activity, may contribute to BP response during exercise in the CP population.



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