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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.


Expression of Proteins Involved the Maintenance of Normal Cardiac Ca2+ Homeostasis.(A) Representative blot of RyR and their normalization for total protein and the demonstrative graph of statistical analysis. (B) Representative blot of SERCA2a and their normalization for GAPDH and the demonstrative graph of statistical analysis. (C) Representative blot of phospho-Ser16-Thr17-PLN (p.PLN) and their normalization for total PLN and the demonstrative graph of statistical analysis. (D) Representative blot of NCX and their normalization for GAPDH and the demonstrative graph of statistical analysis. For analysis, we utilized one way ANOVA followed by Duncan’s post hoc. The data are shown as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the C group; †—Different from the RT group.
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pone.0167029.g004: Expression of Proteins Involved the Maintenance of Normal Cardiac Ca2+ Homeostasis.(A) Representative blot of RyR and their normalization for total protein and the demonstrative graph of statistical analysis. (B) Representative blot of SERCA2a and their normalization for GAPDH and the demonstrative graph of statistical analysis. (C) Representative blot of phospho-Ser16-Thr17-PLN (p.PLN) and their normalization for total PLN and the demonstrative graph of statistical analysis. (D) Representative blot of NCX and their normalization for GAPDH and the demonstrative graph of statistical analysis. For analysis, we utilized one way ANOVA followed by Duncan’s post hoc. The data are shown as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the C group; †—Different from the RT group.

Mentions: In Fig 4A, 4B and 4D, we observed that RyR (F(3,16) = 0.263, p = 0.80); SERCA2a (F(3,20) = 0.917, p = 0.40) and NCX (F(3,20) = 0.37, p = 0.70) did not change among the groups. However, the ratio of phospho-PLN to total PLN (Fig 4C) was decreased in both groups submitted the PSD when compared to C and RT groups (F(3,16) = 11.57, p = 0.001), suggesting a reduction of the active form of this protein and consequently diastolic dysfunction.


Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training
Expression of Proteins Involved the Maintenance of Normal Cardiac Ca2+ Homeostasis.(A) Representative blot of RyR and their normalization for total protein and the demonstrative graph of statistical analysis. (B) Representative blot of SERCA2a and their normalization for GAPDH and the demonstrative graph of statistical analysis. (C) Representative blot of phospho-Ser16-Thr17-PLN (p.PLN) and their normalization for total PLN and the demonstrative graph of statistical analysis. (D) Representative blot of NCX and their normalization for GAPDH and the demonstrative graph of statistical analysis. For analysis, we utilized one way ANOVA followed by Duncan’s post hoc. The data are shown as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the C group; †—Different from the RT group.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0167029.g004: Expression of Proteins Involved the Maintenance of Normal Cardiac Ca2+ Homeostasis.(A) Representative blot of RyR and their normalization for total protein and the demonstrative graph of statistical analysis. (B) Representative blot of SERCA2a and their normalization for GAPDH and the demonstrative graph of statistical analysis. (C) Representative blot of phospho-Ser16-Thr17-PLN (p.PLN) and their normalization for total PLN and the demonstrative graph of statistical analysis. (D) Representative blot of NCX and their normalization for GAPDH and the demonstrative graph of statistical analysis. For analysis, we utilized one way ANOVA followed by Duncan’s post hoc. The data are shown as the mean ± standard deviation, significance accepted: p ≤ 0.05. *—Different from the C group; †—Different from the RT group.
Mentions: In Fig 4A, 4B and 4D, we observed that RyR (F(3,16) = 0.263, p = 0.80); SERCA2a (F(3,20) = 0.917, p = 0.40) and NCX (F(3,20) = 0.37, p = 0.70) did not change among the groups. However, the ratio of phospho-PLN to total PLN (Fig 4C) was decreased in both groups submitted the PSD when compared to C and RT groups (F(3,16) = 11.57, p = 0.001), suggesting a reduction of the active form of this protein and consequently diastolic dysfunction.

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.