Abstract
BackgroundIntense exercise is a systemic stressor associated with the release of “danger” molecules – alarmins, by damaged or dying cells into systemic circulation to evoke a sterile inflammatory response. Compared with research in clinical diseases, physiological responses of alarmins to exercise and training are not well studied. Short-term responses to exercise and training using a panel of alarmins – HMGB1, S100A8/A9, HSP70 and sRAGE may reveal unique aspects of stress responses to strenuous exercise, with important ramifications when prescribing exercise to generally healthy adults.MethodsA 3-week, high-intensity training program was performed by healthy young men (N = 7). Concurrent aerobic and resistance exercises were performed on 3 consecutive days each week. Blood and saliva were collected before (Pre), immediately after (Post), and 30 min (30 min) after exercise each week, and 24 h after the final exercise session in week 3 (24 h).ResultsPlasma HMGB1, S100A8/A9 and HSP70 increased from Pre to Post (P < 0.05), although at different timepoints during the study, and displayed different kinetics from IL-10, IL-8 and IFN-γ, suggesting unique mechanisms involved in modulating their release and clearance. CD14+CD16− monocytes increased from Pre to Post across 3 weeks; CD14+CD16+ monocytes increased from Pre to Post in week 2 and 3 (P < 0.05). ΔHMGB1 and ΔHSP70 correlated positively with ΔMCP-1 during 3 weeks of training. As well, ΔHMGB1 correlated positively with CD14+CD16− monocytes, suggesting higher alarmin release after strenuous exercise may involve increase in circulating monocytes.ConclusionsPerturbations in systemic alarmins are novel biological signatures for assessing the inflammatory milieu of healthy adults during high-intensity exercise.
Highlights
Intense exercise is a systemic stressor associated with the release of “danger” molecules – alarmins, by damaged or dying cells into systemic circulation to evoke a sterile inflammatory response
The immune system plays a role in modulating physiological adaptation to exercise stimuli - in essence, its response entails the recruitment of specific leukocytes for the mitigation of cellular damage, especially in skeletal muscle
It is plausible that alarmins, as “danger” signals, may play a role in the adaptation to exercise training
Summary
Intense exercise is a systemic stressor associated with the release of “danger” molecules – alarmins, by damaged or dying cells into systemic circulation to evoke a sterile inflammatory response. Compared with research in clinical diseases, physiological responses of alarmins to exercise and training are not well studied. Taking reference from Matzinger’s “danger” model [2], such disturbances in systemic homeostasis can be sensed by the immune system and result in the activation of the sterile inflammatory response. Alarmins are endogenous molecules that activate the immune system when encountering “danger” to the host, such as in the case of infection or cellular stress/damage [2,3,4]. Stressed or damaged cells can quickly release alarmins into systemic circulation, where they bind pattern recognition receptors (PRRs) on antigen presenting cells to activate the immune system [6]. Since the first study on alarmins was published, the list of putative alarmins has grown and currently include high mobility group box protein-1 (HMGB1), high-mobility group nucleosome-binding protein 1 (HMGN1), S100 proteins, heat shock proteins (HSPs), cathelicidin, eosinophil-derived neurotoxin (EDN), defensins, granulysin and mitochondrial DNA, mitochondrial peptides and ATP [3]
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