Starting a new study, together with MD Maria Mathiassen and Dr.Philos Jonny Hisdal. The goal of study is to map which changes in an individual’s blood samples and lung function could be perceived as normal after hard and prolonged physical effort.
The subjects in our study are triathletes competing in Norseman Xtreme Triathlon 2016.
What do we do?
- Blood samples will be collected at three stages: The first sample will be drawn on the day before the competition, the second just after they cross the finish line at Gaustadtoppen or Gaustablikk, and the final sample will be drawn before they depart from Gaustablikk on the day after the competition.
- A spirometry test (breathing test) will be conducted to measure their lung function.
- They will also be asked to complete a survey that aims to map participants’ training loads during the year prior to the competition. We will also ask some questions pertaining to everyday lung symptoms. Their input into the survey is provided anonymously.
Blood samples will be collected by an experienced medical doctor and a bioengineer. The spirometry test will be conducted by physiologists from the Norwegian School of Sport Sciences.
From the Protocol:
Maria Mathiassen – Telemark Hospital
Jørgen Melau –Vestfold Hospital
Jonny Hisdal – Oslo University Hospital, Aker
Trine Stensrud – Norwegian School of Sport Sciences
A triathlon competition comprises swimming, cycling, and running – and always in that order. At a dinner party at the Waikiki Swim Club in Hawaii in 1977, a group of soldiers, among them John Collins, a marine officer, debated which sport was the toughest; swimming, running, or cycling. They decided to set up a competition that included all three sports in consecutive order, and where the winner would be named “Ironman”. On 18 February 1978, 15 athletes convened on Waikiki Beach for the first ever Ironman.
There are several triathlon events, the most common of which are:
- Sprint: 750 m swimming, 20 km cycling, 5 km running
- Olympic: 1500 m swimming, 40 km cycling, 10 km running
- Full distance (“Ironman”): 3800 m swimming, 180 km cycling, 42 km running
Triathlon is experiencing strong growth in Norway. In 2011, Norway had 80 triathlon clubs with a total of 2000 members. In 2015, the numbers had grown to 184 clubs and 3900 members[i]. The Norwegian Triathlon Association expects up to 20 000 individuals to compete in a triathlon event during 2016.
Several previous studies have concluded that long term extreme physical strain may lead to muscle damage, systemic inflammation, immunological changes, and increased oxidative stress[ii]. Muscle damage induced by physical activity is accompanied by an increase in inflammatory mediators, and this increase seems to be connected to the length and intensity of the strain [iii]. Several studies over the past few years have documented that hard physical strain can cause fever, mobilization and increase in the numbers of both neutrophilic leucocytes and monocytes, and impairment of the cellular immune system. This could again lead to increased susceptibility to infections[iv]. In recent year, particular attention has been paid to cytokines, especially interleukines, as mediators for these responses.
Extreme endurance competitions such as full distance triathlons and ultraruns are gaining in popularity. The duration of these events is often very long, sometimes more than 12 hours, and participants push their bodies to the extreme. Some athletes are so exhausted afterwards that they require medical assistance from an emergency room, or hospitalization.
Previous studies1 have shown that prolonged physical strain can increase the level of classic inflammation parameters and metabolites at levels which in ordinary patients would be perceived as highly pathological, but reference values and values for athletes who do not require medical treatment have to date not been determined.
Changes in the kidney function have been described in several different endurance sports, including triathlon and marathon[v]. Impaired kidney function may lead to significant increases in creatinine, carbamide, and uric acid[vi]. Protein in urine may be an indication of kidney damage, but the temporary increase seen after endurance competitions is considered normal[vii].
Former studies have also shown an increase in various cardiovascular markers, such as
pro-BNP, BNP, CK-MB and Troponin I and T following prolonged physical strain[viii]. An increased concentration of these in the plasma is normally associated with heart desease and myocardial damage, and constitutes an important marker that is used on a daily basis in clinical medicine, but prolonged physical activity has also been seen to cause an increase in Troponin among nearly 50 % of healthy athletes[ix] [x].
Acute inflammatory response is an important part of the pathogenesis of myocardial damage caused by acute coronary syndrome[xi] [xii] and endothelial dysfunction is especially related to recruitment of leukocytes in atherosclerosis[xiii]. Inflammation markers have therefore become important parts in the diagnostics of myocardial damage[xiv],
Studies have also shown that prolonged and intensive training can induce bronchial hyperresponsiveness, increased inflammation of the respiratory tract, and a higher frequency of asthma, especially among endurance athletes[xv]. Substantial training over time, with high intensity, and in unfavorable environments, may lead to epithelial damage as a result of mechanical, thermal, and osmotic wear during high minute ventilation, and can over time induce remodeling of the respiratory system[xvi]. Inflammation markers in the induced sputum of winter athletes and swimmers have been reported as correlating with the number of traning hours per week[xvii]. Swimmers have been found to have an elevated share of eosinophil and neutrophil cells, when compared with controls[xviii].
Purpose and topic:
The purpose of this study is therefore to examine among Norseman Xtreme Triathlon finishers, their levels of classic biomarkers, such as CRP, creatinine, pro-BNP, BNP, troponin and electrolytes; endothelium-specific endothelial adhesion molecules, such as ICAM-1, VCAM-1 and E-selectin; and the inflammation markers CD4+, CD8+, CD16+, CD34+, CD56+, IL-4, IL-6, IL-8, IL-12, IL-33, TNF-This will enable us to map which biochemical changes can be perceived as normal in an individual after prolonged physical effort, and furthermore to assess which reference values to use with these individuals in situations where medical evaluation is necessary. We also want to examine which values can be expected 12-24 hours after crossing the finish line, compared to the already defined reference scope.
Triathletes are required to master three different endurance sports. They therefore need to work out in different environments, including in swimming pools, where they inhale organic chlorine compounds that can cause irritation, particularly of the respiratory tract. To date, only a few studies have examined respiratory inflammation in triathletes. This study aims to examine acute effects on BHR and inflammatory markers in induced sputum from triathletes before and after completing the Norseman Xtreme Triathlon.
[i] The Norwegian Triathlon Association; www.triathlon.no
[ii] Comassi M, Vitolo E, Pratali L, Del Turco S, Dellanoce C, Rossi C, et al. Acute effects of different degrees of ultra-endurance exercise on systemic inflammatory responses. Intern Med J. 2015. January;45(1):74–9. doi: 10.1111/imj.12625
[iii] Pedersen BK, Hoffman-Goetz L. Exercise and the immune system: regulation, integration, and adaptation. Physiol Rev. 2000. July;80(3):1055–81. Review.
[iv] Suzuki K, Nakaji S, Yamada M, Totsuka M, Sato K, Sugawara K. Systemic inflammatory response to exhaustive exercise. Cytokine kinetics. Exerc Immunol Rev. 2002;8:6–48
[v] Scotney B, Reid S. Body Weight, Serum Sodium Levels, and Renal Function in an Ultra-Distance Mountain Run. Clin J Sport Med. 2014. July 9.
[vi] Radák Z, Ogonovszky H, Dubecz J, Pavlik G, Sasvari M, Pucsok J, et al. Super-marathon race increases serum and urinary nitrotyrosine and carbonyl levels. Eur J Clin Invest. 2003; 33(8): 726–30.
[vii] Reid RI, Hosking DH, Ramsey EW. Haematuria following a marathon run: source and significance. Br J Urol. 1987; 59(2): 133–6.
[viii] Scharhag J, Herrmann M, Urhausen A, et al. Independent elevations of N-terminal pro-brain natriuretic peptide and cardiac troponins in endurance athletes after prolonged strenuous exercise. Am Heart J 2005;150:1128-34
[ix] Lippi G, Schena F, Salvagno GL, et al. Comparison of conventional and highly-sensitive troponin I measurement in ultra-marathon runners. J Thromb Thrombolysis 2012;33:338-42.
[x] Tjora S, Gjestland H, Mordal S, et al. Troponin rise in healthy subjects during exercise test. Int J Cardiol 2011;151:375-6.
[xi] Entman ML, Ballantyne CM. Inflammation in acute coronary syndromes. Circulation 1993;22:800-3.
[xii] Fuster V, Badimón L. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992;326: 242-50.
[xiii] Gimbrone MA. Vascular endothelium: an integrator of pathophysiologic stimuli in atherosclerosis. Am J Cardiol 1995;75:678-708.
[xiv] Shyu KG, Chang H, Lin CC, Kuan P. Circulating intercellular adhesion molecule-1 and E-selectin in patients with acute coronary syndrome. Chest 1996;77:543-9.
[xv] Carlsen, K. H., Anderson, S. D., Bjermer, L., Bonini, S., Brusasco, V., Canonica, W., . . . Clinical, I. (2008). Exercise-induced asthma, respiratory and allergic disorders in elite athletes: epidemiology, mechanisms and diagnosis: part I of the report from the Joint Task Force of the European Respiratory Society (ERS) and the European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA2LEN. Allergy, 63(4), 387-403
[xvi] Bougault, V., Turmel, J., St-Laurent, J., Bertrand, M., & Boulet, L. P. (2009). Asthma, airway inflammation and epithelial damage in swimmers and cold-air athletes. Eur Respir J, 33(4), 740-746.
[xvii] Bougault, V., Turmel, J., & Boulet, L. P. (2010). Bronchial challenges and respiratory symptoms in elite swimmers and winter sport athletes: Airway hyperresponsiveness in asthma: its measurement and clinical significance. Chest, 138(2 Suppl), 31S-37S.
[xviii] Moreira, A., Palmares, C., Lopes, C., & Delgado, L. (2011). Airway vascular damage in elite swimmers. Respir Med, 105(11), 1761-1765.