We have recently demonstrated that the overnight profiles of cardiac interbeat autocorrelation coefficient of R-R intervals ( r RR) calculated at 1-min intervals are related to the changes in sleep electroencephalographic (EEG) mean frequency, which reflect depth of sleep. Other quantitative measures of the Poincaré plots, i.e., the standard deviation of normal R-R intervals (SDNN) and the root mean square difference among successive R-R normal intervals (RMSSD), are commonly used to evaluate heart rate variability. The present study was designed to compare the nocturnal profiles of r RR, SDNN, and RMSSD with the R-R spectral power components: high-frequency (HF) power, reflecting parasympathetic activity; low-frequency (LF) power, reflecting a predominance of sympathetic activity with a parasympathetic component; and the LF-to-HF ratio (LF/HF), regarded as an index of sympathovagal balance. r RR, SDNN, RMSSD, and the spectral power components were calculated every 5 min during sleep in 15 healthy subjects. The overnight profiles of r RR and LF/HF showed coordinate variations with highly significant correlation coefficients ( P < 0.001 in all subjects). SDNN correlated with LF power ( P < 0.001), and RMSSD correlated with HF power ( P < 0.001). The overnight profiles of r RR and EEG mean frequency were found to be closely related with highly cross-correlated coefficients ( P < 0.001). SDNN and EEG mean frequency were also highly cross correlated ( P < 0.001 in all subjects but 1). No systematic relationship was found between RMSSD and EEG mean frequency. In conclusion, r RR appears to be a new tool for evaluating the dynamic beat-to-beat interval behavior and the sympathovagal balance continuously during sleep. This nonlinear method may provide new insight into autonomic disorders.

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There is little doubt that moderate training improves cardiac vagal activity and thus has a cardioprotective effect against lethal arrhythmias. Our purpose was to learn whether a higher training load would further increase this beneficial effect. Cardiac autonomic control was inferred from heart rate variability (HRV) and analyzed in three groups of young subjects (24.5 +/- 3.0 yr) with different training states in a period free of stressful stimuli or overload. HRV was analyzed in 5-min segments during slow-wave sleep (SWS, a parasympathetic state that offers high electrocardiographic stationarity) and compared with data collected during quiet waking periods in the morning. Sleep parameters, fatigue, and stress levels checked by questionnaire were identical for all three groups with no signs of overtraining in the highly trained (HT) participants. During SWS, a significant (P <0.05) increase in absolute and normalized vagal-related HRV indexes was observed in moderately trained (MT) individuals compared with sedentary (Sed) subjects; this increase did not persist in HT athletes. During waking periods, most of the absolute HRV indexes indistinctly increased in MT individuals compared with controls (P < 0.05) but did not increase in HT athletes. Normalized spectral HRV indexes did not change significantly among the three groups. Heart rate was similar for MT and Sed subjects but was significantly (P <0.05) lower in HT athletes under both recording conditions. These results indicate that SWS discriminates the state of sympathovagal balance better than waking periods. A moderate training load is sufficient to increase vagal-related HRV indexes. However, in HT individuals, despite lower heart rate, vagal-related HRV indexes return to Sed values even in the absence of competition, fatigue, or overload.

The atrial natriuretic peptide (ANP) plays an important role in chronic heart failure (CHF), delaying the progression of the disease. However, despite high ANP levels, natriuresis falls when CHF progresses from a compensated to a decompensated state, suggesting emergence of renal resistance to ANP. Several mechanisms have been proposed to explain renal hyporesponsiveness, including decreased renal ANP availability, down-regulation of natriuretic peptide receptors and altered ANP intracellular transduction signal. It has been demonstrated that the activity of neutral endopeptidase (NEP) is increased in CHF, and that its inhibition enhances renal cGMP production and renal sodium excretion. In vitro as well as in vivo studies have provided strong evidence of an increased degradation of intracellular cGMP by phosphodiesterase in CHF. In experimental models, ANP-dependent natriuresis is improved by phosphodiesterase inhibitors, which may arise as new therapeutic agents in CHF. Sodium-retaining systems likely contribute to renal hyporesponsiveness to ANP through different mechanisms. Among these systems, the renin-angiotensin-aldosterone system has received particular attention, as angiotensin II and ANP have renal actions at the same sites and inhibition of angiotensinconverting enzyme and angiotensin-receptor blockade improve ANP hyporesponsiveness. Less is known about the interactions between the sympathetic nervous system, endothelin or vasopressin and ANP, which may also blunt ANP-induced natriuresis.To summarize, renal hyporesponsiveness to ANP is probably multifactorial. New treatments designed to restore renal ANP efficiency should limit sodium retention in CHF patients and thus delay the progression to overt heart failure.

The profiles of plasma glucose, insulin, and C-peptide were studied in normal men receiving continuous enteral nutrition. Large oscillations occurred with periods of 53-113 min. Their mean amplitudes, expressed as a percentage of the 24-h mean, were as high as 20% for glucose, 54% for insulin, and 56% for C-peptide. The oscillations of plasma insulin levels throughout the 24 h were concomitant with those of C-peptide. Rapid 8- to 14-min plasma insulin and glucose oscillations were smaller in magnitude and could only be detected in some segments of the longer period oscillations. These results indicate that in addition to the previously described 8- to 14-min oscillations, plasma glucose, insulin, and C-peptide oscillate at a mean 80-min periodicity in man during continuous enteral nutrition. These oscillations may reflect a pancreatic oscillatory mechanism and/or cyclic variations in gastrointestinal motility or peripheral glucose uptake.