AbstractExtreme physical exertion is commonly associated with acute physiological changes in immune variables known to disturb host defences. Likely induced by the production of stress hormones (e.g., cortisol), partaking in ultra-endurance events with accompanying physiological stressors ((e.g., environmental extremes, sleep deprivation and compromised hydration and (or) nutritional status)) may amplify stress hormone responses and compromise immune status to a greater extent. To date, research investigating the impact of extreme physical exertion (e.g., ultra-marathon events) on physiological variables is extremely limited. More recently, the potential use of probiotics with known immunomodulatory effects may be considered an appropriate nutritional strategy to improve host defences and minimise and (or) prevent sub-clinical or clinically significant outcomes in active populations.
With this in mind, the purpose of this thesis was to investigate the effects of: 1) a multi-stage ultra-marathon (total distance: 230 km) in hot ambient conditions (32-40°C), and a 24 h continuous ultra-marathon (total distance range: 122-208 km) in temperate ambient
conditions (0-20°C) on salivary anti-microbial protein (S-AMP) and stress hormone response, and self-reported incidence of upper respiratory symptoms (URS); 2) a multi-stage ultra-marathon in hot ambient conditions, and a 24 h continuous ultra-marathon in temperate ambient conditions on circulatory endotoxin concentration, cytokine profile, and self-reported incidence of gastrointestinal (GI) symptoms; and 3), acute high dose supplementation of Lactobacillus casei (L.casei) on S-AMP responses, circulatory endotoxin concentration and cytokine profile in response to exertional-heat stress (EHS).
A multi-stage ultra-marathon in hot ambient conditions (Chapter 4) decreased post-stage salivary IgA (S-IgA) responses. Salivary alpha-amylase (S-α-amylase) and salivary lysozyme (S-lysozyme) responses increased and (or) remained unchanged post-stage throughout. Salivary cortisol (S-cortisol) responses fluctuated throughout the multi-stage ultra-marathon competition. URS were minimally reported (n=1) during and in the one month period
following the ultra-marathon.
A 24 h continuous ultra-marathon in temperate ambient conditions (Chapter 5) decreased S-IgA and S-lysozyme responses post-competition. S-α-amylase and S-cortisol responses increased post-competition. No URS were reported during and in the one month following the ultra-marathon.
The implications of the results in Chapter 4 and Chapter 5 demonstrated perturbations to oral-respiratory mucosal immune responses during extreme physical exertion; however, this did not result in URS. Therefore, it would be prudent to minimise accompanying physiological stressors during periods of extreme physical exertion. The results in Chapter 4and Chapter 5 cannot be generalised to other times of the year. Appropriate education (e.g.,
hydration maintenance, non-infectious episode management, medical management of established respiratory illness) and information (i.e., pollen and pollution counts at the location of the event or competition) may help prevent unwanted URS manifestations and performance decrements. However, limitations of the multi-stage ultra-marathon study (Chapter 4) include the failure to measure other S-AMPs with other anti-bacterial and anti-viral properties and the inability to assess and accurately differentiate between infectious vs. non-infectious episodes. Limitations of the 24 h continuous ultra-marathon study (Chapter 5) include the failure to determine the time-course of recovery of S-AMPs (i.e., the length of time mucosal immune status is depressed). Notably, both studies also took place during the
summer months (Chapter 4: second week of July, Chapter 5: first week of September) when infectious episodes (e.g., verified Epstein-Barr virus reactivation, Rhinovirus and Influenza infections) are fewer compared to winter months. Thus, the prevalence of URSI
reported is in part, likely dependent on the time of year the event or competition takes place.
A multi-stage ultra-marathon in hot ambient conditions (Chapter 6) increased resting and post-stage circulatory gram-negative bacterial endotoxin concentration. Increases in pro-inflammatory cytokines post-stage (i.e., interleukin-1 beta (IL-1β), tumour necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ)) were counteracted by a compensatory anti-inflammatory cytokine response (i.e., interleukin-10 (IL-10) and interleukin-1 receptor
antagonist (IL-1ra)). GI symptoms were commonly reported (58% reported at least one severe GI symptom) during the multi-stage ultra-marathon.
A 24 h continuous ultra-marathon in temperate ambient conditions (Chapter 7) increased post-competition circulatory gram-negative bacterial endotoxin concentration. Increases in pro-inflammatory cytokines (i.e., interleukin-6 (IL-6) IL-1β, TNF-α)) post-competition were counteracted by a compensatory anti-inflammatory cytokine response (i.e., IL-10). GI symptoms were commonly reported (75% reported at least one severe GI symptom) during the ultra-marathon.
The implications of the results in Chapter 6 and Chapter 7 suggest that whilst in well-trained individuals where the exertional-heat stress is well tolerated, clinically significant episodes ((e.g., exertional-heat illness, systemic inflammatory response syndrome (SIRS), sepsis and autoimmune conditions)) may be offset, individuals who are inadequately trained may pose a greater risk for development of clinically significant episodes. Notably,
exertional-heat illness continues to be a military problem during training and operations whereby the hospitalization rate of heat stroke has markedly increased (i.e., a five-fold increase; 1.8 per 100,000 in 1980 to 14.5 per 100,000 in 2001) (Carter et al. 2005).
Additionally, delayed elevation of inflammatory variables ((e.g., C-reactive protein (CRP) and cytokine profile)) after competition may play a role in the aetiology of undefined underperformance and chronic fatigue syndromes. Appropriate education and competition
preparation (e.g., the need to be well-trained to complete the required distance, heat acclimation protocols, hydration maintenance, cooling strategies) may help prevent clinically
significant episodes occurring in ‘high-risk’ and (or) illness prone individuals. However, limitations of the multi-stage ultra-marathon study (Chapter 6) include the failure to measure other variables (e.g., anti-endotoxin antibodies or endotoxin neutralising capacity) and measurements (e.g., core body temperature; Tcore). Limitations of the 24 h continuous ultra-marathon study (Chapter 7) include the failure to determine the time-course of recovery of
CRP and cytokine profile (i.e., the length of time inflammatory variables remain elevated).
These observational studies applied exercise models of an extreme nature (Chapter 4 to Chapter 7) unlike the majority of previous research. Additionally, measuring a number of time-related immune variables and tracking over a five day period (Chapter 4 and Chapter 6) is currently absent. Whilst these studies attempted to identify the key immune variables that may lead to potential sub-clinical and clinically significant outcomes, a lack of adequate
research control did not allow for definitive conclusions to be made about the effects of individual and combined physiological stressors on the immune variables measured. For example, the degree and duration to which an individual is exposed to a single or combination of stressors is dependent on a number of factors (e.g., environmental conditions during the ultra-marathons) Therefore, determining which individual or combination of
stressors is responsible for the perturbations in immune variables observed, whether a cumulative effect of stressor exposure is present or whether a particular stressor (s) exerts a greater influence over others is limited.
Seven consecutive days probiotic supplementation containing L.casei (x 1011 colony forming units (CFU)/day)) did not influence S-IgA, S-α-amylase or S-lysozyme responses at rest after EHS, and during the recovery period compared with a placebo (Chapter 8). Probiotic supplementation did not prevent or attenuate EHS induced endotoxaemia and cytokinaemia; nor is it more positively favourable over a placebo (Chapter 9).
The implications of the results in Chapter 8 and Chapter 9 suggest that whilst in healthy individuals probiotic supplementation is not justified, further investigation into ‘high-risk’ and (or) illness prone individuals (i.e., those who commonly experience URS or GI
symptoms) may be warranted. Limitations of the probiotic-EHS (Chapter 8 and Chapter 9) include the failure for further exploration of the mechanistic responses of probiotics. For
example, additional measurements such as intestinal permeability tests (e.g., urinary excretion ratio of lactulose to rhamnose). Whilst these laboratory-controlled studies (Chapter 8 and Chapter 9) provide insight into the impact of a specific probiotic strategy as observed in athletic populations on key immune variables, a larger sample size including both males and females would be considered more representative of the endurance running population and would have allowed for further sub-group analysis (e.g., hydration status); whilst a longer probiotic supplementation period in accordance with previous clinical models is an area of further research.
|Date of Award||2016|
|Supervisor||Ricardo Da Costa (Supervisor), Doug Thake (Supervisor) & Mike Price (Supervisor)|