Regular physical activity attenuates the blood pressure response to public speaking and delays the development of hypertension

Objective: The objective of this study was to investigate the effect of regular physical activity on the haemodynamic response to public speaking and to evaluate the long-term effect of exercise on development of hypertension. Participants: We assessed 75 sedentary and 44 active participants screened for stage 1 hypertension with consistent activity habits and 63 normotensive individuals as control. Methods: The blood pressure (BP) response to public speaking was assessed with beat-to-beat noninvasive recording. Definition of incident hypertension was based either on clinic or 24-h BP measurement. Results: The BP response to public speaking was greater in the hypertensive than the normotensive participants (P = 0.018/0.009). Among the former, sedentary participants showed increased BP reactivity to the speech test (45.2 +/- 22.6/22.2 +/- 11.5 mmHg, P < 0.01/<0.001 versus controls), whereas physically active participants had a response similar to that of controls (35.4 +/- 18.5/18.5 +/- 11.5 mmHg, P = not significant). During a median follow-up of 71 months, ambulatory BP did not virtually change in the active participants (-0.9 +/- 7.8/-0.0 +/- 4.7 mmHg) and increased in their sedentary peers (2.8 +/- 9.8/3.2 +/- 7.4 mmHg, P = 0.08/0.003 versus active). Active participants were less likely to develop incident hypertension than sedentary ones. After controlling for several confounders including baseline heart rate, the hazard ratio was 0.53 [95% confidence interval (CI) 0.31-0.94] for clinic hypertension and 0.60 (95% CI 0.37-0.99) for ambulatory hypertension. Inclusion of BP response to public speaking into the Cox model influenced the strength of the association only marginally [hazard ratio = 0.55 (95% CI 0.30-0.97) and hazard ratio = 0.59 (95% CI 0.36-0.99), respectively]. Conclusion: Regular physical activity attenuates the BP reaction to psychosocial stressors. However, this mechanism seems to be only partially responsible for the long-term effect of exercise on BP.