No abstract

SUMMARYThe present study was undertaken to investigate the relationship between the extent of impaired chronotropic response and cardiac output during exercise, and exercise tolerance in patients with chronic heart failure. The subjects consisted of 24 patients (mean 60.1 ± 14.0 years) who had mild chronotropic incompetence. Cardiopulmonary exercise testing was performed in all patients, and heart rate (HR), anaerobic threshold (AT), maximum oxygen uptake (peak VO 2 ), slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO 2 slope), and exercise time were measured. Cardiac output (CO) was measured by a thoracic bioimpedance method and cardiac index (CI) was calculated. Plasma norepinephrine (NE) was measured at rest and immediately after the exercise test. The changes in HR, NE, and CI from the resting state to immediately after exercise were calculated as ∆HR, ∆NE, and ∆CI, respectively. The ∆NE was converted to a logarithmic scale and ∆HR/log∆NE was used as a parameter of HR response to sympathetic nerve stimulation. The results were as follows: HR and NE in the resting state had no correlation with AT and with peak VO 2 . ∆HR/log∆NE correlated positively with both AT and peak VO 2 , and negatively with the VE/VCO 2 slope. ∆HR/ log∆NE correlated positively with peak CI, %∆CI, and ∆CI/exercise time. The data suggest that one of the mechanisms of low exercise tolerance in chronic heart failure patients was due to an inadequate increase in CO response against exercise caused by an impaired HR response to increased NE. (Jpn Heart J 2003; 44: 515-525)

In general practice, BNP levels predicted the risk of cardiovascular events other than coronary heart disease events and of death.

SUMMARYThis study was undertaken in acute myocardial infarction (AMI) patients with noninsulin-dependent diabetes mellitus (type 2 DM) to investigate their impaired chronotropic response to exercise. Seventy-one AMI subjects entered the study, 30 with type 2 DM and 41 age-and body mass index-matched non-DM (control) patients. One month after the onset of AMI, these patients underwent cardiopulmonary exercise testing on a treadmill under a ramp protocol. Anaerobic threshold (AT) and peak oxygen uptake (peak VO 2 ) were determined as indicators of exercise capacity. Plasma norepinephrine (NE) concentration was measured in blood samples obtained at 2 time points: during pre-exercise rest and immediately after peak exercise. The change in NE concentration during exercise, as an index of sympathetic nervous activity, was calculated as a percentage: ∆NE = [(NE during exercise)-(resting value)]/(resting value) × 100. The change in heart rate (HR) during exercise was calculated as a simple difference: ∆HR = [(peak HR) -(rest HR)]. Index of chronotropic response to exercise was then quantified as the ∆HR/∆NE during exercise. No significant intergroup differences in ejection fraction at rest or HR at peak exercise were observed. However, VO 2 at AT, peak VO 2 , ∆HR, and ∆HR/∆NE were significantly lower in the type 2 DM group than in the non-DM group. ∆HR correlated with VO 2 at AT (r = 0.49, P < 0.001) and with peak VO 2 (r = 0.53, P < 0.001) in all subjects. Also, ∆HR/∆NE correlated with VO 2 at AT (r = 0.42, P < 0.001) and with peak VO 2 (r = 0.44, P < 0.001) in all subjects. AMI patients with type 2 DM had impaired cardiopulmonary responses to maximal and submaximal exercise testing and impaired chronotropic response to exercise, even though their cardiac function at rest was similar to that of non-DM AMI patients. The data suggest that one mechanism of impaired cardiopulmo-

The aim of this study was to clarify the mechanism of impaired exercise tolerance in chronic sleep-restricted conditions by investigating variables related to heart-rate (HR) response to sympathetic nervous stimulation. Sixteen healthy men (mean age 21.5 years) were tested in a control state, acute sleep-loss state, and chronic sleep-restricted state. Participants underwent cardiopulmonary exercise testing in each state. Their norepinephrine (NE) concentration was measured before and immediately after exercise. Intracellular magnesium (Mg) concentration was measured in a resting state. Exercise duration was shorter and the ratio of HR response to the percentage increase in NE was higher in the chronic sleep-restricted state than in the control state. Intracellular Mg gradually decreased from control to chronic sleep restriction. There was a negative correlation between peak exercise duration and the ratios of HR response to the rate of increase in NE. Intracellular Mg was positively correlated with the ratios of HR response to the increase in NE both in control and in acute sleep loss. The authors conclude that the impaired exercise tolerance in a chronic sleep-restricted state is caused by hypersensitivity of the HR response to sympathetic nervous stimulation, which showed a compensation for decreased intracellular Mg concentration.