Neutrophil Death Induced by a Triathlon Competition in Elite Athletes

Levada‐Pires, Adriana Cristina; Cury-Boaventura, Maria Fernanda; Gorjão, Renata; Hirabara, Sandro Massao; Puggina, Enrico Fuini; Peres, Cleto Kaveski; Lambertucci, Rafael Herling; Curi, Rui; Pithon-Curi, Tânia Cristina

doi:10.1249/mss.0b013e31816dc89e

Cited by 19 publications

(35 citation statements)

References 38 publications

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“…Intense exercise was also able to decrease the glutathione concentration (GSH) of lymphocytes, inducing oxidative stress, while the 8, 9 and 3 active caspases content and the DNA fragmentation appeared to increase 75 . Some authors tend to associate intense exercise to apoptosis due to the activity of the high levels of catecholamine produced 72 , while others associate it to the increase of oxidative stress 75,76 . Kruger et al 77 showed that the leukocytes redistribution, a crucial mechanism for hematopoiesis regulation, was active during the alteration in the lymphocytes concentration promoted by the exercise.…”

Section: Subpopulations Of Lymphocytesmentioning

confidence: 99%

Efeito do exercício no sistema imune: resposta, adaptação e sinalização celular

Terra

Da-Silva

Salerno

et al. 2012

Rev Bras Med Esporte

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Introduction: Over the last century, people have become less active, adopting more sedentary habits. This scenario has increased the incidence of chronic diseases such as cardiovascular diseases, type 2 diabetes and metabolic syndrome. The practice of physical activities can influence healthiness by altering the metabolic state and also the immune system. Objective: To review the literature for studies that address the effects promoted by physical exercise on the development of immune responses and the possible signal transduction pathways. Methods: The SciELO and PubMed data bases were consulted. Results: The available literature shows that during the practice of exercise, various subpopulations of leukocytes are altered in accordance with the intensity and duration of the activity performed. Exercise of moderate intensity stimulates a pro-inflammatory response, while those of high intensity tend to promote antiinflammatory responses that could decrease damage to skeletal muscle. Such alterations are observed in cells that present antigens (such as macrophages and dendritic cells), neutrophils, natural killer cells (NK) and in surface molecules like Toll-like receptors (TLR) and major histocompatibility complex class II, as well as the entire repertoire of cytokines. Conclusion: The current state of knowledge suggests that the alterations in the immune system are dependent on parameters inherent to exercise and that in order to have all these alterations occurring, some cell signaling cascades are activated, giving rise to a complex process of phosphorylation/dephosphorylation that culminates in the activation of transcription factors, translation of mRNA's, protein synthesis and cell proliferation.

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Section: Subpopulations Of Lymphocytesmentioning

confidence: 99%

Efeito do exercício no sistema imune: resposta, adaptação e sinalização celular

Terra

Da-Silva

Salerno

et al. 2012

Rev Bras Med Esporte

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“…Initially, RNOS were thought to be detrimental to athlete recovery, but it is now clear that RNOS are important for adaptation to endurance training (Finaud et al 2006, Ristow et al 2009, Powers et al 2010a, skeletal muscle hypertrophy and protein signaling (Makanae et al 2013, Paulsen et al 2014). Nonetheless, a critical balance (captured in the theory of hormesis; Radak et al, (2008) exists between the sufficient or "optimal" dose of RNOS to drive adaptation, and the overproduction of RNOS that could lead to apoptosis, immunosuppression, excessive fatigue and reduced performance (Levada-Pires et al 2008, Lewis et al 2015 The monitoring of elite athletes is widespread with considerable resources devoted to improving performance (Davison et al 2009). Longitudinal monitoring of ARH in elite athletes may allowe the identification of fatigued states, maladaptation, and under-performance in athletes (Lewis et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Effects of exercise on alterations in redox homeostasis in elite male and female endurance athletes using a clinical point-of-care test

Lewis

Towey

Bruinvels

et al. 2016

Appl. Physiol. Nutr. Metab.

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Exercise causes alterations in redox homeostasis (ARH). Measuring ARH in elite athletes may aid in the identification of training tolerance, fatigued states and underperformance. To our knowledge no studies have examined ARH in elite male and female distance runners at sea level. The monitoring of ARH in athletes is hindered by a lack of reliable and repeatable in-the-field testing tools and by the rapid turnaround of results. We examined the effects of various exercise intensities on ARH in healthy (non-overreached) elite male and female endurance athletes using clinical point of care (POC) redox tests, referred to as the free-oxygen-radical-test (FORT; pro-oxidant) and the free-oxygen-radical-defence (FORD; anti-oxidant). Elite male and female endurance athletes (n=22) completed a discontinuous incremental treadmill protocol at submaximal running speeds and a test to exhaustion. Redox measures were analyzed via blood sampling at rest; warm-up; sub-maximal exercise; exhaustion and recovery. FORD was elevated above rest after sub-maximal, and

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“…High-intensity exercise has been shown to cause apoptosis of leukocytes as indicated by various measurements: mitochondrial membrane depolarization Hsu et al 2002;Levada-Pires et al 2008), phosphatidylserine externalization (Lagranha et al 2004;Levada-Pires et al 2008;Mooren et al 2004), DNA fragmentation (Wang and Huang 2005), increased levels of cytochrome c and caspase 3 protein levels in the cytosol, increased expression of proapoptotic Bax and Bcl-Xs gene (Lagranha et al 2004;Levada-Pires et al 2008;Quadrilatero and HoVman-Goetz 2005b), decreased antiapoptotic Bcl-2 protein levels and Bcl-Xl gene expression (Lagranha et al 2004;Levada-Pires et al 2008;Quadrilatero and HoVman-Goetz 2005b); and chromatin condensation (Lagranha et al 2004). After the adventure race, an increase in mitochondrial membrane depolarization was observed.…”

Section: Discussionmentioning

confidence: 99%

The effect of an adventure race on lymphocyte and neutrophil death

et al. 2010

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The effect of an adventure race (Ecomotion Pró), which lasted for 4-5 days, on neutrophil and lymphocyte death from elite athletes was investigated. Blood was collected from 11 athletes at rest and after the adventure race. The following parameters of cell death were measured in neutrophils and lymphocytes: cell membrane integrity, DNA fragmentation, mitochondrial transmembrane depolarization and reactive oxygen species (ROS) production. Phagocytosis capacity was also evaluated in neutrophils. The adventure race raised the proportion of cells with the loss of membrane integrity; lymphocytes by 14% and neutrophils by 16.4%. The proportion of lymphocytes with DNA fragmentation (2.9-fold) and mitochondrial transmembrane depolarization (1.5-fold) increased. However, these parameters did not change in neutrophils. ROS production remained unchanged in lymphocytes, whereas an increase by 2.2-fold was found in neutrophils due to the race. Despite these changes, the phagocytosis capacity did not change in neutrophils after the race. In conclusion, the Ecomotion Pró race-induced neutrophil death by necrosis (as indicated by the loss of membrane integrity) and led to lymphocyte death by apoptosis (as indicated by increase DNA fragmentation and depolarization of mitochondrial membrane).

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Neutrophil Death Induced by a Triathlon Competition in Elite Athletes

Cited by 19 publications

References 38 publications

Efeito do exercício no sistema imune: resposta, adaptação e sinalização celular

Efeito do exercício no sistema imune: resposta, adaptação e sinalização celular

Effects of exercise on alterations in redox homeostasis in elite male and female endurance athletes using a clinical point-of-care test

The effect of an adventure race on lymphocyte and neutrophil death

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