Abstract
BackgroundParadoxical 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.MethodsMale 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.ResultsCompared 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.ConclusionsResistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.
Highlights
In plurality, sleep is defined as a vital state of homeostatic regulation with specific behavioral and electrophysiological characteristics
The left ventricle systolic area and the left ventricle cavity diameter were reduced in the paradoxical sleep deprivation for 96 hours (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 nuclear factor of activated T-cells 3 (NFATc3) and GATA binding protein 4 (GATA-4), proteins involved in the pathologic cardiac hypertrophy pathway
Summary
Sleep is defined as a vital state of homeostatic regulation with specific behavioral and electrophysiological characteristics. Sleep is divided into two phases, non- rapid eye movements (NREM) and rapid eye movements (REM) The former is associated with progressive reduced neuronal activity with three defined phases: N1, N2, N3 (slow wave sleep) [3]. The latter, is characterized by vivid dreaming and a high level of brain activity despite the muscular atony that suggests a deep sleep. This phase is known as paradoxical sleep in rats [4,5]. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation
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