Title: Interactions between physical activity, sedentary behaviour and immune reactivity to acute psychological stress - implications for Cardiovascular Disease (CVD)
Funder: The Academy of Medical Sciences

Abstract: Stress is a recognised cardiovascular Disease (CVD) risk factor, and increasingly prevalent within the UK. Short-term stress exposure induces cardiovascular responses, which can predict future CVD risk. It also increases immune and inflammatory markers, such as Interleukin (IL-)6. In people with elevated inflammation at rest, there is a further elevation of inflammation under stress, which could increase CVD risk separately and via interactions with the cardiovascular system. There is substantive evidence of relationships between physical activity (PA), sedentary behaviour (SB) and CVD risk. Importantly PA and SB are different constructs; someone can be active but highly sedentary. Inflammatory markers (including IL-6) link these factors as basal levels of inflammation are elevated in people with low levels of PA, high levels of SB, and existing CVD under resting conditions. These behaviours could further augment our CVD risk via stress-induced inflammation increases, but it is not known the pathways through which this may occur. The challenge of stress stimulus allows us to view and examine negative effects of poor behaviours (low activity, smoking, diet) that may not be seen under resting conditions. I will investigate how PA and SB affect stress reactivity, specifically investigating the immune and inflammatory systems and identifying how PA and SB – and interactions between the two– affect these responses. To recreate real-life stress exposure, both an active stressor (participants engage in a task) and passive stress (with no participant task engagement) will be investigated, providing detail regarding potential mechanisms of disease risk, and a target for intervention.

Lay abstract: We know that people frequently feel stressed by daily life, especially now because of COVID-19. This stress affects our bodies, and over time can contribute to long-term health problems including developing heart disease. When people are stressed for short periods, such as being late or having an important job interview, they experience physical changes such as a fast beating heart and higher blood pressure. We also see changes in some of our immune cells (which fight off infection when we are ill). Short-term these responses can be good but depending on where these cells then move to and how much stress we experience, long-term this could be bad for our health. In people who don't take regular exercise and spend lots of time sitting, we see high levels of these cells when people aren't stressed, and so we want to see if even more of these cells appear when people are stressed (and how they get there) compared to more active people . We will examine this. Linked to this, we do not know how improving our daily behaviours can help our immune responses to stress. Examples of changes we might make are increasing how much physical activity we do or reducing how much time we spend sitting. We will measure these things to see if we can do things to improve how we cope with stress. This is exciting as we can design a programme which works for different people based on their levels of activity and sitting.

Research activity codes: 2.1 BIOLOGICAL AND ENDOGENOUS FACTORS;2.3 PSYCHOLOGICAL, SOCIAL AND ECONOMIC FACTORS
Health categories: CARDIOVASCULAR