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Moderate-intensity physical activity reduces systemic inflammation and maintains cardiorespiratory function following
Alannah van Waveren1,2, Mitch J Duncan1,3, Fiona Coulson1,2
1School of Medical and Applied Science, CQ University Rockhampton, Bruce Highway, Queensland, 4702, Australia.
Aims:
The purpose of the current study is to 1) examine the beneficial effects of moderate levels of physical activity (PA) on functional and biochemical markers of the cardiorespiratory system, 2) establish the detrimental effects of a single, daily particulate matter (PM) exposure event on cardiorespiratory function and 3) determine if exercising during daily PM exposure increases the deleterious effects caused by PM exposure due to increased inhalation of particulates on cardiorespiratory function.
Methods:
Four groups of 16 rats were used: control (CON), PA, PM2.5 exposed and PA combined with PM2.5 exposure (PA + PM). Animals were purchased at 4 weeks old. However, both PA and PM exposure was initiated when the animals reached 8 weeks of age, for 8 weeks.
Results:
PA alone did not alter body weight or blood pressure (BP) compared to control animals. However, there was a significant decrease in epididymal fat pad mass in the PA group. The PM exposed rats were hypertensive, showed increased systemic inflammation and oxidative stress, and had decreased spleen mass without pathological changes in the cardiac action potential or impaired vascular function. PA was able to decrease systemic inflammation in PM exposed animals, including a reduction in IL-6 serum levels, however, this did not translate to an improvement in BP or vascular reactivity. Smooth muscle relaxation in the trachea from the combination PA + PM group was not significantly different to CON and PA groups but was significantly higher than the PM group.
Conclusions:
The current study showed that while there is an increased cardiovascular disease (CVD) risk associated with PM exposure, engaging in PA during exposure events imposes no increased risk with exercise providing a protective mechanism against some of the biochemical signaling changes caused by inhaled PM.
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