Blunted heart rate recovery is associated with exaggerated blood pressure response during exercise testing.

Increased sympathetic activity and endothelial dysfunction are the proposed mechanisms underlying exaggerated blood pressure response to exercise (EBPR). However, data regarding heart rate behavior in patients with EBPR are lacking. We hypothesized that heart rate recovery (HRR) could be impaired in patients with EBPR. A total of 75 normotensive subjects who were referred for exercise treadmill test examination and experienced EBPR were included to this cross-sectional case-control study. The control group consisted of 75 age- and gender-matched normotensive subjects without EBPR. EBPR was defined as a peak exercise systolic blood pressure (BP) ≥210 mmHg in men and ≥190 mmHg in women. HRR was defined as the difference in HR from peak exercise to 1 min in recovery; abnormal HRR was defined as ≤12 beats/min. These parameters were compared with respect to occurrence of EBPR. Mean values of systolic and diastolic BP at baseline, peak exercise, and the first minute of the recovery were significantly higher in the subjects with EBPR. Mean HRR values were significantly lower (P < 0.001) in subjects with EBPR when compared with those without. Pearson's correlation analysis revealed a significant positive correlation between the decrease in systolic BP during the recovery and degree of HRR in individuals without EBPR (r = 0.42, P < 0.001). Such a correlation was not observed in subjects with EBPR (r = 0.11, P = 0.34). The percentage of abnormal HRR indicating impaired parasympathetic reactivation was higher in subjects with EBPR (29 % vs 13 %, P = 0.02). In logistic regression analyses, HRR and resting systolic BP were the only determinants associated with the occurrence of EBPR (P = 0.001 and P < 0.001, respectively). Decreased HRR was observed in normotensive individuals with EBPR. In subjects with normal BP response to exercise, a linear correlation existed between the degree of HRR and decrease in systolic BP during the recovery period. However, such a correlation was not found in subjects with EBPR. Our data suggest that mechanisms underlying the blunting of the HRR might be associated with the genesis of EBPR. The association between the extent of HRR and adverse cardiovascular outcomes in patients with EBPR needs to be investigated in detail in future research.