Why the study?
Cardiovascular risk increases with progression of atherogenesis, motivating evaluation of the cardiovascular and autonomic effects of aerobic exercise training in an experimental model of atherosclerosis.
Does aerobic exercise training improve hemodynamic and autonomic parameters in an ApoE-knockout mouse model of atherosclerosis?
Does aerobic exercise training improve hemodynamic and autonomic parameters in an ApoE-knockout mouse model of atherosclerosis?
Aerobic exercise training improves running capacity, diastolic function, hemodynamic status, and autonomic modulation in an ApoE-knockout mouse model of atherosclerosis.
Aerobic training effects in atherosclerotic models remain hypothesis-generating; human trials needed before any clinical consideration.
Considering the increase of cardiovascular risk with the progression of the atherogenic process and the effectiveness of physical training as a strategy to control/manage the cardiac dysfunction in populations exposed to elevated risks, the aim of this study was to evaluate the cardiovascular and autonomic effects of an aerobic exercise training protocol in an experimental model of atherosclerosis. Considering the cardioprotective effects already known about physical training the hypothesis of this study is that the aerobic exercise training will promote systemic benefits on hemodynamics and autonomic in a model of atherosclerosis. For this, sixteen ApoE‐knockout mice, 15 months old, were divided in 2 groups (n=8, each): sedentary group (APOE 15) and moderate intensity exercise training group (APOE 15T). The exercise training lasted for 6 weeks (5 days/week, 1 hour/day, intensity 60–75% of the maximum treadmill test). At the end of the protocol, the animals were submitted to echocardiography analysis and cannulation for a direct recording of the arterial blood pressure (AP), and then, baroreflex sensitivity and cardiovascular autonomic modulation were evaluated. The aerobic exercise training improved running capacity (APOE 15: 594.90±46.95; APOE 15T: 878.6±68.54 s) and cardiac diastolic function (E/A: APOE 15: 1.10±0.05; APOE 15T: 1.70±0.24), as well as decreased diastolic blood pressure (DAP: APOE 15: 107.0±5.202; APOE 15T: 95.12±0.79 mmHg) and induced resting bradycardia (HR: APOE 15: 704±21; APOE 15T: 613±20 bpm) associated with heart rate variability increase (Var‐PI: APOE 15:1.25±0.09; APOE 15T: 8.81±1.98 ms 2 ; SD‐Pl: APOE 15: 1.09±0.06; APOE 15T: 2.77±0.37 ms). In addition, greater cardiac parasympathetic modulation (RMSSD: APOE 15: 0.99±0.06; APOE 15T: 1.41±0.10 ms) and baroreflex sensitivity improvement (Alpha Index: APOE 15: 0.31±0.044; APOE 15T: 0.66±0.10 ms/mmHg) were also observed. In conclusion, aerobic exercise training may be considered an important non‐pharmacological strategy for the management of cardiovascular risk induced by atherosclerosis, improving running capacity, diastolic function as well as the hemodynamic status and autonomic modulation.
No takes yet. Share an insight, caveat, or question.
Nascimento‐Carvalho et al. (2021) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: