Background: Strenuous exercise is associated with tissue damage. This activates the innate immune system and local inflammation. Interaction between innate and adaptive immunity is essential for maintaining health, suggesting that the adaptive immune system may also be altered by exercise. Objectives: To determine exercise induced changes in the adaptive immune system by measuring the immunoglobulin isotype and subclass response to an ultra-marathon. Methods: Venepuncture was performed on 11 experienced volunteers (six men, five women; mean (SD) age 43 (9.8) years) 24 hours before the projected finishing time and immediately after and 3, 24, and 72 hours after an ultra-marathon (90 km). Serum was stored at 280˚C. IgM, IgD, IgA, IgG, IgG1, 2, 3, and 4, and total IgE were measured. Results: The following immunoglobulins were significantly (p(0.05) altered after the race: IgD, immediately (251%) and 24 hours (241%) after; IgM 24 hours after (223%); total IgG immediately after (+12%). There were no reports of symptoms of upper respiratory tract infections after the ultra-marathon. Conclusions: In experienced ultra-endurance runners, alterations in immunoglobulin concentrations after a race suggest an enhanced immune response, including isotype switching, interactions with the innate immune system, and a secondary antibody response. These alterations may have a role in the maintenance of subject health after an ultra-marathon.

Bakgrund: För att lyckas med att genomföra en Ironman krävs att man som utövare har en strategi gällande hur man ska disponera sin energi för att kunna bli en ”finisher”. Detta kallas pacing eller pacing strategi och är den egenstyrda ansträgningen som kan hjälpa utövaren att lyckas med sitt mål och optimera den egna prestationen. Att paca ”rätt” blir därför viktigt för att optimera den egna prestationen då loppet innehåller tre olika moment: simning, cykling och löpning. Syfte: Syftet med denna studie var att undersöka pulsmätning som ett sätt att studera och förstå pacing inom Ironman triathlon. Finns det ett samband mellan utövarens intensitet och cykeltid och har de deltagare som haft en liten pulsvariation en bättre sluttid? Metod: 22 deltagare genomförde ett test för att fastställa sin maxpuls, HRmax. I samband med Ironman Kalmar 2016 registrerades deltagarnas pulsdata med hjälp av pulsmätare och utifrån insamlad pulsdata beräknades deltagarnas intensitet och pulsvariation under cykelmomentet. Dessa värden korrelerades mot deltagarnas cykeltider. Resultat: Den relativa arbetspulsen för studiegruppen var 140 ±9.2 slag/min. Varken intensitet eller variation i intensitet visade något signifikant samband med sluttid även om en trend mot signifikans fanns för intensitet vs cykeltid, p=0.066. Slutsats: Spridningen i gruppen gällande vald intensitet var för stor för att tydligt kunna studera intensitetens betydelse för prestation under cykeldelen i ett IronMan och fler studier är nödvändiga för att kunna kartlägga detta. / Background: In order to succeed in an Ironman it is necessary to have a strategy on how to dispose your energy during the 8-16 hour race. This is called pacing or pacing strategy and is the self-selected effort that can help the competitor to optimize their performance. Based on heart rate measurement, this is particularly interesting during the 180 km cycle section, where drafting is not allowed.Aim: The aim of this investigation was to study pacing in Ironman thriathlon. Is there a relationship between the competitors intensity and biketime and did those who had smaller variation in intensity achieved a better biketime?Method: 22 competitive triathletes undertook a test to find out their HRmax. In conjunction with Ironman Kalmar 2016 the participants HR-data was registered with heartrate monitors and the data was then analyzed in order to determine the participants mean intensity and variation in intensity. These factors were used to understand pacing based on the participants heartrate and correlated to biketimes for each participant. Results: Average intensity for the participants was 140 ±9.2 bpm and the results show no significanct correlation between biketime and either the intensity chosen by the competitor or the variation in intensity. However, there was  a trend towards significance for the intensity vs biketime, p = 0.066. Conclusion: This study was unable to determine the effect of pacing due to the selected intensity within the group was too large to clearly study the importance of intensity for performance during the cycle part of an IronMan and further studies are required.

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Background - Regular exercise reduces the risk of cardiovascular disease and subsequent sudden cardiac death (SCD). However, a small, but notable proportion of athletes die suddenly due to inherited or congenital disorders of the heart that predispose to malignant ventricular arrhythmias. Such tragedies are highly publicised, particularly when high-profile athletes are involved. To date, limited evidence for the efficacy of cardiovascular pre-participation screening exists outside of the Italian experience. Furthermore, limited data exists examining the impact of ethnicity on cardiac adaptations to physical training. Whilst the cardiovascular benefits of exercise are well known, the impact of life-long endurance exercise is less well understood. Long term high-intensity endurance exercise is associated with changes in cardiac morphology together with electrocardiographic alterations that are believed to be physiologic in nature. Recent data however, has suggested a number of deleterious adaptive changes in cardiac structure, function and electrical activity in response to life-long endurance activity. Aims and Objectives - The aims of this PhD were; 1) To find an effective preparticipation screening method that would successfully identify pre-existing cardiovascular abnormalities, 2) To identify the prevalence of hypertrophic cardiomyopathy and Long QT syndrome in elite UK athletes; 3) To examine the impact and significance of ethnicity upon left ventricular remodelling in elite athletes, and 4) To examine the acute and chronic impact of ultra-endurance exercise across the life-span in male endurance athletes. Major Results and Conclusions – 1) Study 2 sought to confirm the efficacy of resting 12-Lead ECG ‘alongside’ personal/family history questionnaires and physical examinations as collective tools to identify diseases that have the potential of causing sudden death within a cohort of elite junior athletes (n=1074) and physically active school children (n=1646). Nine participants were identified with a positive diagnosis of a disease associated with SCD. None of those diagnosed with a disease associated with SCD were symptomatic or had a family history of note. Thus, personal symptoms and family history questionnaires alone are inadequate in the identification of individuals with diseases associated with SCD. In conclusion, resting 12-Lead ECG is paramount when screening for diseases that have the potential of causing sudden death in the young. 2) Study 3 examined 3,500 asymptomatic elite athletes (75% male) with a mean age of 20.5 ± 5.8 years with 12-lead ECG and 2-dimensional echocardiography. None had a known family history of HCM. Of the 3,500 athletes, 53 (1.5%) had LVH (mean 13.6 ± 0.9mm, range 13 to 16mm), and of these 50 had a dilated LV cavity with normal diastolic function to indicate physiological left ventricular hypertrophy. Three (0.08%) athletes with LVH had a non-dilated LV cavity and associated deep T-wave inversion that could have been consistent with HCM. However, none of the 3 athletes had any other phenotypic features of HCM on further non-invasive testing and none had first-degree relatives with features of HCM. In conclusion, the prevalence of HCM in elite athletes is significantly less than in the general population; with the demands of strenuous exercise on the cardiovascular system selecting out most individuals with HCM. Study 4 examined 2000 elite athletes in order to identify the prevalence of Long QT syndrome. Three athletes had a QTc value of >500 ms and all exhibited one of: paradoxical prolongation of QTc during exercise, a confirmatory genetic mutation, or prolonged QTc in a first-degree relative. In contrast, none of the athletes with a QTc value of <500 ms had any other features to indicate LQTS. Accordingly, the prevalence of a prolonged QTc interval in elite British athletes is 0.4%. 3) Study 6 examined 300 nationally ranked UK black male athletes (mean age 20.5 years) in comparison to 150 black and white sedentary individuals and 300 highly-trained white male athletes. Black athletes exhibited greater LV wall thickness and cavity size compared with sedentary black and white individuals. Black athletes had greater LV wall thickness compared with white athletes. A minority of black athlete’s exhibit LVH ≥15 mm; proposing that in the absence of cardiac symptoms or a family history of HCM, an LV wall thickness ≥15 mm in black athletes may represent physiologic LVH when the LV cavity is enlarged and diastolic indexes are normal. 7 black athletes (12%) with LVH displaying deep T-wave inversions in leads V1 to V4. In conclusion, in the absence of obvious pathology, these electrical anomalies in black athletes likely represent a normal spectrum of ECG changes in response to physical training. 4) Study 8 examined 17 male participants (age 33.5 ± 6.5 years, 26–40 years) using cardiac magnetic resonance (CMR) and echocardiography before and after a marathon to investigate the relationship between systolic function and diastolic function against biomarkers of cardiac damage. Results demonstrates biomarkers of myocardial cell damage following an acute bout of prolonged exercise are not associated with either systolic or diastolic functional measures, and do not seem to be associated with any detectable myocardial inflammation, oedema, or scarring using either gold standard techniques of gadolinium enhanced CMR or echocardiography respectively. The impact of multiple episodes of prolonged exercise, as experienced by highly trained veteran endurance athlete is not fully understood. 5) Study 10 examined the cardiac structure and function of 12 life-long, competitive endurance veteran athletes (> 50 yrs, mean ± SD marathons 178 ± 209 (range 20 – 650)) against 17 young male endurance athletes (<40 yrs) using echocardiography and CMR with late gadolinium enhancement (LGE) to assess myocardial fibrosis. Lifelong veteran athletes had smaller LV and RV end-diastolic and end-systolic volumes (p<0.05) but maintained LV and RV systolic function compared with young athletes. In 6 (50%) of the veteran athletes LGE of CMR indicated the presence of myocardial fibrosis; no LGE in the young athletes. The prevalence of LGE in veteran athletes was not associated with the number of competitive marathons or ultra-endurance marathons (>50 miles) completed, age, LV and RV end-diastolic volumes or LV mass (p>0.05). In conclusion, there is limited evidence at present demonstrating that cardiovascular re-modelling following lifelong endurance exercise leads to long-term disease progression, cardiovascular disability or SCD.

No description available.