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Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training

View Article: PubMed Central - PubMed

ABSTRACT

Background: Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation.

Methods: Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated.

Results: Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway.

Conclusions: Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.

No MeSH data available.


Body weight variation throughout 4 days of paradoxical sleep deprivation.Body weight change (g) of the C (n = 10), RT (n = 10), PSD96 (n = 10), RT/PSD96 (n = 10) groups during 4 days of PSD. The variation was calculated by the equation: current weight—previous weight. Repeated measure ANOVA followed by Duncan’s post hoc. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the previous body weight in the same group; †—Different from the C group at the same time; ‡—Different from the RT group at the same time; x—Different from the PSD96 group at the same time.
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pone.0167029.g002: Body weight variation throughout 4 days of paradoxical sleep deprivation.Body weight change (g) of the C (n = 10), RT (n = 10), PSD96 (n = 10), RT/PSD96 (n = 10) groups during 4 days of PSD. The variation was calculated by the equation: current weight—previous weight. Repeated measure ANOVA followed by Duncan’s post hoc. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the previous body weight in the same group; †—Different from the C group at the same time; ‡—Different from the RT group at the same time; x—Different from the PSD96 group at the same time.

Mentions: Forty-eight hours after the last training session, the PSD96 and RT/PSD96 groups were submitted to SD. Every day of this protocol the body weight was evaluated for calculated the variation throughout 4 days, by the equation: current weight–previous weight (Fig 2). While the Δ of the C group did not vary significantly, the PSD96 and RT/PSD96 groups had negative Δ during 96 hours, indicating weight loss. Drastic weight loss occurred during the first 24 hours for both groups submitted to PSD, but the reduction in body mass in the RT/PSD96 group was milder. The ΔBW was reduced at 72 and 96 hours for both groups, which indicates that the animals adapted to the experimental procedure.


Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training
Body weight variation throughout 4 days of paradoxical sleep deprivation.Body weight change (g) of the C (n = 10), RT (n = 10), PSD96 (n = 10), RT/PSD96 (n = 10) groups during 4 days of PSD. The variation was calculated by the equation: current weight—previous weight. Repeated measure ANOVA followed by Duncan’s post hoc. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the previous body weight in the same group; †—Different from the C group at the same time; ‡—Different from the RT group at the same time; x—Different from the PSD96 group at the same time.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5120843&req=5

pone.0167029.g002: Body weight variation throughout 4 days of paradoxical sleep deprivation.Body weight change (g) of the C (n = 10), RT (n = 10), PSD96 (n = 10), RT/PSD96 (n = 10) groups during 4 days of PSD. The variation was calculated by the equation: current weight—previous weight. Repeated measure ANOVA followed by Duncan’s post hoc. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the previous body weight in the same group; †—Different from the C group at the same time; ‡—Different from the RT group at the same time; x—Different from the PSD96 group at the same time.
Mentions: Forty-eight hours after the last training session, the PSD96 and RT/PSD96 groups were submitted to SD. Every day of this protocol the body weight was evaluated for calculated the variation throughout 4 days, by the equation: current weight–previous weight (Fig 2). While the Δ of the C group did not vary significantly, the PSD96 and RT/PSD96 groups had negative Δ during 96 hours, indicating weight loss. Drastic weight loss occurred during the first 24 hours for both groups submitted to PSD, but the reduction in body mass in the RT/PSD96 group was milder. The ΔBW was reduced at 72 and 96 hours for both groups, which indicates that the animals adapted to the experimental procedure.

View Article: PubMed Central - PubMed

ABSTRACT

Background: Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation.

Methods: Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated.

Results: Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway.

Conclusions: Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.

No MeSH data available.