The Effect of a 100-km Ultra-Marathon under Freezing Conditions on Selected Immunological and Hematological Parameters

Abstract

Although moderate exercise is beneficial for the human body and its immune system, exhaustive ultra-endurance performance in cold conditions might be harmful. The aim of this study was to examine the effect of a 100-km ultra-marathon under cold conditions (temperatures from −1°C to +1°C) on selected immunological, biochemical and hematological parameters. Participants were 15 runners (12 men and three women, age 40.3 ± 9.7 years, body mass 67.3 ± 9.0 kg and body height 1.74 ± 0.10 m, mean ± standard deviation). Leukocytes increased (p < 0.01) and, particularly, the number of leucocytes doubled in seven out of 15 athletes. Immature neutrophils, mature neutrophils and monocytes increased (p < 0.02), whereas lymphocytes and eosinophils did not change. IgG increased (p < 0.02), but IgA and IgM remained unchanged. Platelets increased (p < 0.01), whereas red blood cells, hematocrit and hemoglobin did not change. lactate dehydrogenase (LDH) and creatine kinase (CK) increased (p < 0.01), but alanine aminotransferase (ALT) did not change. There was an association between the markers of the acute inflammation of the organism (i.e., neutrophils, immature neutrophils, platelets, and monocytes) and the markers of muscle damage (i.e., CK, platelets, and LDH). There were no relationships among all the markers in relation to upper respiratory tract infections and liver damage. The highest change was noted in the increase of the number of immature neutrophils (1,019.2%) and CK levels (1,077.6%). In summary, this is the first study investigating immunological, hematological and biochemical parameters and showing that running a 100-km ultra-marathon under cold conditions leads to changes in several immunological, biochemical and hematological parameters indicating a severe stress on the body associated with increasing susceptibility to the development of infections.

Immune and Hormonal Response to High-intensity Exercise During Orienteering

“…During intense physical exercise, an athlete's physiological status is expected to be associated with his or her immune response [5,6] since it produces a stress condition that triggers metabolic, endocrinological, neuropsychological, and immunological changes [4]. Accordingly, in the present study some cytokines were correlated with cortisol levels.…”

“…Activities that involve intense, long-term physical exercise, such as orienteering, are known to be stressors and sources of physio-pathological changes [4]. The mechanisms of adaptation to stress and physical exercise have common elements, involving muscle injury and immune response activation.…”

Elevation of leukocyte counts is associated with an increase in the intensity and duration of exercise

“…We also found that leucocyte counts and that of its subtypes increased more than 200% following continuous exercise for 30 min at all intensities, suggesting that there is a lower risk of heart attack when sedentary subjects in our study exercised for less than 30 min at a moderate intensity. Similarly, a significant increase in leucocytes was also found among endurance and sprint athletes [22][23][24][25][26]. A previous study also reported that the number of leucocytes is increased even 3 h after exercise [7].…”

Physiology and Pathophysiology in Ultra-Marathon Running

“…The stress-related inflammation affects the bone marrow and leads to an increased leukocyte turnover (Spiropoulos et al, 2010 ). Markers of an inflammatory process include leucocytes (Jee et al, 2013 ; Bird et al, 2014 ; Chiu et al, 2015 ; Jastrzebski et al, 2016 ; Zakovska et al, 2017 ), C-reactive protein (Kim et al, 2009 ; Waśkiewicz et al, 2012 ; Kasprowicz et al, 2013 ), ferritin (Chiu et al, 2015 ), TNF-α (Nieman et al, 2000 ; Simons and Kennedy, 2004 ; Jee and Jin, 2012 ; Chiu et al, 2013 , 2015 ), blood sedimentation reaction, iron (Fallon, 2001 ), y-interferon (Simons and Kennedy, 2004 ), Interleukin 1 receptor antagonist (Nieman et al, 2000 ), Interleukin-1b (Simons and Kennedy, 2004 ; Gill et al, 2015b ), Interleukin-8 (Nieman et al, 2000 ; Gill et al, 2015b ), Interleukin-10 (Nieman et al, 2000 ; Simons and Kennedy, 2004 ; Gill et al, 2015b ) and Interleukin-6 (Fallon et al, 1999a ; Waśkiewicz et al, 2012 ; Kasprowicz et al, 2013 ).…”