Abstract

We aimed to test whether moderate physical training can induce long-lasting protection against cardiovascular risk factors induced by high fat diet (HFD) intake, even after cessation of training. 90-days-old Wistar rats were submitted to a sedentary lifestyle or moderate physical training, three times a week, for 30 days. Following this, at 120 days-of age, sedentary and trained rats received a hypercaloric diet (HFD) or a commercial diet normal fat diet (NFD) for 30 days. Body weight (BW) and food intake were evaluated weekly. At 150 days-of age, hemodynamic measures (systolic, diastolic, mean blood pressure, pulse pressure, pulse interval and heart rate) were made via an indwelling femoral artery catheter. Beat-to-beat data were analyzed to calculate power spectra of systolic blood pressure (SBP) and pulse interval. After euthanasia, mesenteric fat pads were removed and weighted and total blood was stored for later analysis of lipid profile. Consumption of a HFD increased blood pressure (BP), pulse pressure, low frequency BP variability, BW gain, fat pad stores and induced dyslipidemia. Interestingly, prior physical training was able to partially protect against this rise in BP and body fat stores. Prior physical training did not totally protect against the effects of HFD consumption but previously trained animals did demonstrate resistance to the development of cardiometabolic alterations, which illustrate that the benefits of physical training may be partially maintained even after 30 days of detraining period.

Highlights

  • According to the World Health Organization (2018) noncommunicable diseases such as cardiovascular disease, cancer, diabetes and chronic lung disease cause nearly two thirds of all deaths across the globe (Donaldson, 2017)

  • The current study shows, for the first time, that moderate physical training performed three times a week in adulthood protects against Blood pressure (BP) increase induced by HFD consumption even when the HFD occurs during a detraining period

  • It is well known that HFD consumption is strongly associated with increased cardiovascular risks, including hypertension, sympathetic over activity, tachycardia and dyslipidemia among other parameters (Barnes et al, 2003; Prior et al, 2010; Armitage et al, 2012; Tofolo et al, 2014; Xue et al, 2016)

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Summary

Introduction

According to the World Health Organization (2018) noncommunicable diseases such as cardiovascular disease, cancer, diabetes and chronic lung disease cause nearly two thirds of all deaths across the globe (Donaldson, 2017). Cardiovascular disease is responsible for three quarters of the deaths in low and middle income countries, placing a burden on public health systems and emerging economies (World Health Organization, 2015). Cardiovascular dysfunction in response to a HFD is thought to be dependent on sympathetic nervous system arousal that results in increased plasma norepinephrine turnover in the heart, increases renal sympathetic nerve activity, and increased BP variability (in the LF domain) contributing to the deregulation of BP (Prior et al, 2010; Armitage et al, 2012)

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