PhD Student

Course Start: 10/03/2014
Supervisor: Dr John Hough, PhD

Working thesis title

The design of a short-duration exercise bout suitable to highlight endocrine and immune alterations when in an overreached state - Examining the mechanisms of the HPA and HPG axes and the immune system in response to chronic exercise-induced stress.

Abstract

High-demand occupations push individuals to their limits leading to chronic illness if insufficiently recovered. Resting endocrine and immunological markers of chronic stress and inflammation have been suggested but the information gained from these markers is somewhat limited. Exercise-induced responses of endocrine/immune stress markers may be more reliable to highlight chronic stress compared with resting measures. For example, blunted cortisol and testosterone responses to acute exercise following a period of chronic physiological stress have been reported (Hough et al., 2013 & 2015).

Continuously overloading the body by intensifying the training sessions (for example 6-day period of intensified training) has been shown to suppress the immune system (Lancaster et al., 2003, Nieman, 2000, Pedersen et al., 1996) increasing the risk of common infections, such as URTI (Heath et al., 1992, Nieman, 1994). Although neutrophils and monocytes are considered as the primary intervenients in an inflammatory response, management of these cells are accomplished by a group of soluble hormone-like proteins, known as cytokines (Simpson et al., 1997).

Referring back to cortisol, this hormone also has an influence in the regulation of the exercise-induced, acute inflammatory response by raising neutrophil numbers and suppressing lymphocytes such as natural killer (NK) cells (Malm et al., 2004). Supporting this idea, magnitude and function of circulating cells of the innate immune system, such as neutrophils and NK-cells, and the acquired immune system (e.g. T and B lymphocytes) may be altered by acute and chronic exposure to exercise (Walsh et al., 2011).

Research Questions

• Does a short-term high-intensity running bout elicit an elevation in plasma and salivary cortisol and testosterone concentrations?
• Could this running bout be a useful tool to track individuals at risk of suffering from the Overtraining Syndrome?
• What are the mechanisms behind the dysfunction of steroid and peptide hormones when in an overreached state?
• Do neutrophil oxidative burst and phagocytic activity alter following a period of intensified training and after recovery from that (no exercise)?
• Is an individual immunological response to an in vitro-stimulated bacterial infection [LPS-stimulated pro- (IL-6, IL-1β, TNF-α) and anti-inflammatory (IL-10) cytokine responses] different when in a healthy state compared to an overreached state?

Contact Information

T: +44 (0)1234 793053 
E: diogo.leal@study.beds.ac.uk
Twitter: @Diogo_Luis_Leal
LinkedIn: Diogo Leal