Although the acute physiological responses to continuous exercise have been well documented in CHD patients, no previous study has examined the responses to high-intensity intermittent exercise in these patients. The purpose of this study was to compare the physiological responses to a high-intensity interval exercise (HIIE) protocol versus a moderate-intensity continuous exercise (MICE) protocol of similar energy expenditure in CHD patients. twenty patients with stable CHD (19 males and 1 female, 62 ± 11 yr) were assigned in random order to a single session of HIIE corresponding to 15-s intervals at 100% of peak power output (PPO) and 15-s passive recovery intervals and, 2 wk later, to an isocaloric MICE corresponding to 70% of PPO. both protocols were equivalent in terms of energy expenditure. The HIIE protocol resulted in lower mean ventilation (P < 0.001) for a small difference in metabolic demand. All participants preferred the HIIE mainly because the perceived exertion measured by the Borg scale was lower (P < 0.05). No elevation of serum concentration of troponin T was found in all participants at baseline and at 20 min and 24 h after the exercise sessions, thus excluding the presence of any exercise-induced myocardial injury in our patients. when considering physiological responses, safety, and perceived exertion, the HIIE protocol seemed to be well tolerated and more efficient in this group of stable CHD patients.

The exact pathophysiology of Tako-Tsubo cardiomyopathy (TTC) remains unknown but a role for sympathetic hyperactivity has been suggested. Up to now, no direct evidence of sympathetic nerve hyperactivity has been established nor involvement of sympathetic baroreflex identified. The aim of our study was to determine, by direct sympathetic nerve activity (SNS) recording if sympathetic nervous system activity is increased and spontaneous baroreflex control of sympathetic activity reduced in patients with TTC. We included 13 patients who presented with TTC and compared their SNS activity and spontaneous baroreflex control of sympathetic activity with that of 13 control patients with acutely decompensated chronic heart failure. SNS activity was evaluated by microneurography, a technique assessing muscle sympathetic nerve activity (MSNA). Spontaneous baroreflex control of sympathetic activity was evaluated as the absolute value of the slope of the regression line representing the relationship between spontaneous diastolic blood pressure values and concomitant SNS activity. Control patients were matched for age, sex, left ventricular ejection fraction and creatinine clearance. The mean age of the patients with TTC was 80 years, all patients were women. There were no significant differences between the two groups of patients for blood pressure, heart rate or oxygen saturation level. TTC patients presented a significant increase in sympathetic nerve activity (MSNA median 63.3 bursts/min [interquartile range 61.3 to 66.0] vs median 55.7 bursts/min [interquartile range 51.0 to 61.7]; p = 0.0089) and a decrease in spontaneous baroreflex control of sympathetic activity compared to matched control patients (spontaneous baroreflex control of sympathetic activity median 0.7%burst/mmHg [interquartile range 0.4 to 1.9] vs median 2.4%burst/mmHg [interquartile range 1.8 to 2.9]; p = 0.005). We report for the first time, through direct measurement of sympathetic nerve activity, that patients with TTC exhibit elevated SNS activity associated with a decrease in spontaneous baroreflex control of sympathetic activity. These data may explain the pathophysiology and clinical presentation of patient with TTC.