Why the study?
Acute sympathetic stress can cause cardiac fibrosis and may also lead to mental dysfunction, prompting investigation into the effects of exercise training on cardiac damage, neuroinflammation, brain function, and behavior.
Does exercise training improve behavior, brain function, and cardiac damage in rats after high-dose isoproterenol-induced cardiac damage?
Does exercise training improve behavior, brain function, and cardiac damage in rats after high-dose isoproterenol-induced cardiac damage?
In a rat model of isoproterenol-induced cardiac damage, subsequent exercise training improved brain function and normalized anxiety but did not reverse cardiac fibrosis.
Answers are grounded in this paper and cite their sources.
May normalize anxiety via BDNF in rodent cardiac-injury models without reversing damage; leaves open translation to human HF.
Acute sympathetic stress can result in cardiac fibrosis, but may also lead to mental dysfunction. Exercise training after isoproterenol (ISO)-induced acute sympathetic stress was investigated regarding cardiac damage, neuroinflammation, brain function and behavior. Male Wistar rats (12 months) received ISO or saline. One week later, treadmill running or control handling (sedentary) started. After 4 weeks, cognitive- and exploratory behavior were evaluated, and heart and brain tissues were analyzed regarding cardiac damage, hippocampal neuroinflammation and neuronal function. ISO did not affect cognitive performance nor hippocampal function. However, ISO reduced anxiety, coinciding with locally reduced microglia (processes) size in the hippocampus. Exercise in ISO rats reversed anxiety, did not affect microglia morphology, but increased brain function. Thus, exercise after ISO did not affect cardiac damage, cognition or hippocampal neuroinflammation, but normalized anxiety. Increased localized BDNF expression may indicate improved brain function.
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Tóth et al. (2021) studied this question.
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