Extreme anaerobic exercise causes reduced cytotoxicity and increased cytokine production by peripheral blood lymphocytes.

Exercise has many beneficial effects for our body, but can become detrimental at high intensity, especially for our immune system. Little is known about the underlying mechanism of impaired immune functionality under conditions of intense physical strain. Freedivers, people who dive to high depths on a single breath, perform extreme exercise under anaerobic conditions. In this study, we investigated the impact of freediving on the cytotoxic arm of the immune system. At rest, elite freedivers did not display changes in their immunological profile compared to non-diving controls. In contrast, after a freedive, granzyme B and IL-2 production were reduced, whereas IFNγ and TNF secretion were increased by cytotoxic immune cells. Using in vitro models mimicking freedive conditions, we could show that hypoxia in combination with stress hyperglycemia had a negative impact on Granzyme B secretion, whereas IL-2 production was inhibited by stress hormones. Our findings suggest that in response to extreme exercise, cytotoxic immune cells transiently change their functional profile to limit tissue damage.

Correlation between immunological-inflammatory markers and endothelial disfunction in the early stage of coronary heart disease.

Classical risk factors for endothelial dysfunction (ED), such as age, gender, total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and smoking history are utilised for the Framingham score and Systemic Coronary Risk Estimation (SCORE) for evaluation of the 10-year cardiovascular risk in routine practice. Nonetheless, pro-inflammatory mediators are deeply involved in the initiation and the progression of ED and coronary artery disease (CAD), and act additionally or independently of metabolic factors before clinical manifestations of the disease appear. C-reactive protein, a marker of intimal thickening of the myeloid-related protein 8/14 heterodimer, monocyte chemotactic protein 1, interleukin-15, the cytotoxic mediator, granulysin, and the matrix metalloproteinase 9 could be valuable, single, fast, and non-invasive laboratory tools for ED deterioration degree assessment. We propose to investigate the impact of pro-inflammatory biomarkers on ED, measured by previously established clinical methods in patients with yet undiagnosed CAD and at medium risk for an acute coronary event. It could be useful to measure and correlate the concentration of particular inflammatory markers in peripheral blood samples and the results of the Framingham and SCORE charts, multi-slice computed tomography coronary angiography, echocardiography, brachial artery flow-mediated dilatation, carotid-femoral pulse wave velocity, ankle-brachial index, carotid wall thickening, myocardial perfusion scintigraphy, and particularly, cardiac magnetic resonance imaging. The goal would be that the degree of correlation between particular inflammatory markers and the results of some methods for the assessment of ED or cardiac ischaemic imaging could be emphasised and pro-inflammatory markers positioned in the pathogenetic algorithm of CAD.