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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.


Main echocardiographic variables.Results of (A) E wave: maximum protodiastolic mitral flow velocity; (B) A wave: maximum telediastolic mitral flow velocity; (C) EDT: E-wave deceleration time; (D) LA: left atrium diameter; (E) LVAWd: diastolic left ventricle anterior wall thickness; (F) LVPWd: diastolic left ventricle posterior wall thickness. Repeated Measure ANOVA with post hoc Duncan Test. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. N = 10. *—Different from the baseline of the same group; †—Different from the C group at the same time; ‡—Different from the RT at the same time; x—Different from the PSD96 group at same time.
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pone.0167029.g005: Main echocardiographic variables.Results of (A) E wave: maximum protodiastolic mitral flow velocity; (B) A wave: maximum telediastolic mitral flow velocity; (C) EDT: E-wave deceleration time; (D) LA: left atrium diameter; (E) LVAWd: diastolic left ventricle anterior wall thickness; (F) LVPWd: diastolic left ventricle posterior wall thickness. Repeated Measure ANOVA with post hoc Duncan Test. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. N = 10. *—Different from the baseline of the same group; †—Different from the C group at the same time; ‡—Different from the RT at the same time; x—Different from the PSD96 group at same time.

Mentions: LVSA was reduced post protocol in the PSD96 group compared to the C group (F(3,22) = 1854.01, p = 0.03) and increased at the post protocol time point compared to baseline. Similarly, LVDA was higher in the C group post protocol when compared to baseline (F(3,25) = 5.537, p = 0.02). The Fig 5 show the main results of this analysis.


Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training
Main echocardiographic variables.Results of (A) E wave: maximum protodiastolic mitral flow velocity; (B) A wave: maximum telediastolic mitral flow velocity; (C) EDT: E-wave deceleration time; (D) LA: left atrium diameter; (E) LVAWd: diastolic left ventricle anterior wall thickness; (F) LVPWd: diastolic left ventricle posterior wall thickness. Repeated Measure ANOVA with post hoc Duncan Test. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. N = 10. *—Different from the baseline of the same group; †—Different from the C group at the same time; ‡—Different from the RT at the same time; x—Different from the PSD96 group at same time.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5120843&req=5

pone.0167029.g005: Main echocardiographic variables.Results of (A) E wave: maximum protodiastolic mitral flow velocity; (B) A wave: maximum telediastolic mitral flow velocity; (C) EDT: E-wave deceleration time; (D) LA: left atrium diameter; (E) LVAWd: diastolic left ventricle anterior wall thickness; (F) LVPWd: diastolic left ventricle posterior wall thickness. Repeated Measure ANOVA with post hoc Duncan Test. The data are presented as the mean ± standard deviation, significance accepted: p ≤ 0.05. N = 10. *—Different from the baseline of the same group; †—Different from the C group at the same time; ‡—Different from the RT at the same time; x—Different from the PSD96 group at same time.
Mentions: LVSA was reduced post protocol in the PSD96 group compared to the C group (F(3,22) = 1854.01, p = 0.03) and increased at the post protocol time point compared to baseline. Similarly, LVDA was higher in the C group post protocol when compared to baseline (F(3,25) = 5.537, p = 0.02). The Fig 5 show the main results of this analysis.

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.