Attenuated Heart Rate Recovery in Mercury-Exposed Individuals
minute after exercise for protocols that stop exercise abruptly [2– 4] . Since the authors did not use a post-exercise cool down protocol, HRR1 ≤ 18 beats/min should have been assumed to be abnormal in this case. Thus, their definition of abnormal HRR1 as <12 beats/min is not correct. It would be informative to know how many subjects had abnormal HRR1 in each group in this regard. Finally, the authors defined heart rate reserve as the change in heart rate from rest to peak exercise during exercise. However, heart rate reserve is actually the difference between the attainable heart rate at peak exercise (220 – age in years) and resting heart rate [2, 5] . Meanwhile, the heart rate reserve is calculated as a percentage as: (peak heart rate – resting heart rate in beats per min)/ ([220 – age in years] – [resting heart rate in beats per min]) × 100 [2, 5] . Heart rate reserve as a percentage is also considered to indicate the chronotropic response. A heart rate reserve below 80% is considered to be evidence of an impaired chronotropic response, which is a powerful indicator of mortality [3] . Therefore, it would be interesting to know if there was any difference between the mercury-exposed group and control subjects in terms of heart rate reserve in percentages. Dear Editor, We read with great enthusiasm the article by Yilmaz et al. [1] that investigated the heart rate recovery (HRR) of mercury-exposed individuals. They reported that HRR at the first (HRR1), second, and third minute were attenuated in mercury-exposed patients when compared to normal subjects. Interestingly, there were no significant correlations between blood, urine, or hair mercury levels and heart rate recovery at these time points. Furthermore, the duration of mercury exposure was not associated with HRR. Collectively, these findings suggest that, when toxic enough, mercury might lead to long-lasting or even permanent damage to the autonomic nervous system. HRR1 was purely vagal, meanwhile HRR at 2 and 3 min were under the control of both parasympathetic and sympathetic systems [2, 3] . Thus, mercury-induced damage is likely to be a double-edged sword to the autonomic nervous system. Is there any explanation to this in the authors’ perspectives? Are there any cut-off values for mercury to be considered toxic? The authors further reported that exercise testing was terminated (cessation of exercise) abruptly with the patient in the standing or sitting positon (with no ‘cool down’ period) or the patient kept walking at a predetermined speed and incline (cool down period). Abnormal HRR1 is usually defined as a heart rate that declines ≤ 12 beats/min in the first minute after exercise for protocols that use a cool down after exercise, or ≤ 18 beats/min in the first Published online: October 5, 2016