Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.

Background: The aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO₂) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats. Methods: Male Wistar rats were divided into two groups: control (CG, n = 10) and diabetic (DG, n = 8). The animals were submitted to ET on treadmill with simultaneous gas analysis through open respirometry system. ET and VO₂ were assessed 60 days after diabetes induction (STZ, 50 mg/Kg). Results: VO₂ maximum was reduced in STZ-diabetic rats (72.5 ± 1 mL/Kg/min^-1) compared to CG rats (81.1 ± 1 mL/Kg/min^-1). There were positive correlations between ET speed and VO₂ (r = 0.87 for CG and r = 0.8 for DG), as well as between ET speed and VO₂ reserve (r = 0.77 for CG and r = 0.7 for DG). Positive correlations were also obtained between measured VO₂ and VO₂ predicted values (r = 0.81 for CG and r = 0.75 for DG) by linear regression equations to CG (VO₂ = 1.54 * ET speed + 52.34) and DG (VO₂ = 1.16 * ET speed + 51.99). Moreover, we observed that 60% of ET speed corresponded to 72 and 75% of VO₂ reserve for CG and DG, respectively. The maximum ET speed was also correlated with VO₂ maximum for both groups (CG: r = 0.7 and DG: r = 0.7). Conclusion: These results suggest that: a) VO₂ and VO₂ reserve can be estimated using linear regression equations obtained from correlations with ET speed for each studied group; b) exercise training can be prescribed based on ET in control and diabetic-STZ rats; c) physical capacity can be determined by ET. Therefore, ET, which involves a relatively simple methodology and low cost, can be used as an indicator of cardio-respiratory capacity in future studies that investigate the physiological effect of acute or chronic exercise in control and STZ-diabetic male rats.

To evaluate the effect of inspiratory muscle training (IMT) on cardiac autonomic modulation and on peripheral nerve sympathetic activity in patients with chronic heart failure (CHF). Functional capacity, low-frequency (LF) and high-frequency (HF) components of heart rate variability, muscle sympathetic nerve activity inferred by microneurography, and quality of life were determined in 27 patients with CHF who had been sequentially allocated to 1 of 2 groups: (1) control group (with no intervention) and (2) IMT group. Inspiratory muscle training consisted of respiratory exercises, with inspiratory threshold loading of seven 30-minute sessions per week for a period of 12 weeks, with a monthly increase of 30% in maximal inspiratory pressure (PI(max)) at rest. Multivariate analysis was applied to detect differences between baseline and followup period. Inspiratory muscle training significantly increased PI(max) (59.2 ± 4.9 vs 87.5 ± 6.5 cmH(2)O, P = .001) and peak oxygen uptake (14.4 ± 0.7 vs 18.9 ± 0.8 mL·kg(-1)·min(-1), P = .002); decreased the peak ventilation (VE)/carbon dioxide production (VCO(2)) ratio (35.8 ± 0.8 vs 32.5 ± 0.4, P = .001) and the VE/VCO(2) slope (37.3 ± 1.1 vs 31.3 ± 1.1, P = .004); increased the HF component (49.3 ± 4.1 vs 58.4 ± 4.2 normalized units, P = .004) and decreased the LF component (50.7 ± 4.1 vs 41.6 ± 4.2 normalized units, P = .001) of heart rate variability; decreased muscle sympathetic nerve activity (37.1 ± 3 vs 29.5 ± 2.3 bursts per minute, P = .001); and improved quality of life. No significant changes were observed in the control group. Home-based IMT represents an important strategy to improve cardiac and peripheral autonomic controls, functional capacity, and quality of life in patients with CHF.

Background: Because cardiomyopathy is the leading cause of death in diabetic patients, the determination of myocardial function in diabetes mellitus is essential. In the present study, we provide an integrated approach, using noninvasive echocardiography and invasive hemodynamics to assess early changes in myocardial function of diabetic rats. Methods: Diabetes was induced by streptozotocin injection (STZ, 50 mg/kg). After 30 days, echocardiography (noninvasive) at rest and invasive left ventricular (LV) cannulation at rest, during and after volume overload, were performed in diabetic (D, N = 7) and control rats (C, N = 7). The Student t test was performed to compare metabolic and echocardiographic differences between groups at 30 days. ANOVA was used to compare LV invasive measurements, followed by the Student-Newman-Keuls test. Differences were considered significant at P < 0.05 for all tests. Results: Diabetes impaired LV systolic function expressed by reduced fractional shortening, ejection fraction, and velocity of circumferential fiber shortening compared with that in the control group. The diabetic LV diastolic dysfunction was evidenced by diminished E-waves and increased A-waves and isovolumic relaxation time. The myocardial performance index was greater in diabetic compared with control rats, indicating impairment in diastolic and systolic function. The LV systolic pressure was reduced and the LV end-diastolic pressure was increased at rest in diabetic rats. The volume overload increased LVEDP in both groups, while LVEDP remained increased after volume overload only in diabetic rats. Conclusion: These results suggest that STZ-diabetes induces systolic and diastolic dysfunction at rest, and reduces the capacity for cardiac adjustment to volume overload. In addition, it was also demonstrated that rodent echocardiography can be a useful, clinically relevant tool for the study of initial diabetic cardiomyopathy manifestations in asymptomatic patients.

Diabetes and menopause markedly increase the risk of cardiovascular disease in women. The objective of the present study was to investigate the effects of exercise training on cardiovascular autonomic dysfunction and on total mortality in diabetic female rats undergoing ovarian hormone deprivation. Female Wistar rats were divided into ovariectomized groups: sedentary and trained controls and sedentary and trained diabetic rats (streptozotocin, 50 mg/kg IV). Trained groups were submitted to an exercise training protocol on a treadmill (8 weeks). The baroreflex sensitivity was evaluated by heart rate responses to arterial pressure changes. Heart rate variability was determined using the SD of the basal heart rate. Vagal and sympathetic tonus were evaluated by pharmacological blockade. Diabetes impaired baroreflex sensitivity (≈55%), vagal tonus (≈68%), and heart rate variability (≈38%). Exercise training improved baroreflex sensitivity and heart rate variability in control and diabetic groups in relation to their sedentary groups. Trained control rats presented increased vagal tonus compared with that of sedentary ones. The sympathetic tonus was reduced in the trained diabetic group as compared with that of other studied groups. Significant correlations were obtained between heart rate variability and vagal tonus with baroreflex sensitivity. Mortality, assessed during the training period, was reduced in trained diabetic (25%) rats compared with mortality in sedentary diabetic rats (60%). Together, these findings suggest that decreases in baroreflex sensitivity and heart rate variability may be related to increased mortality in female diabetic subjects and that improved autonomic regulation induced by exercise training may contribute to decreased mortality in this population.

Background. Spontaneously hypertensive rats (SHRs) show increased cardiac sympathetic activity, which could stimulate cardiomyocyte hypertrophy, cardia