Background: 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. 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. Methods: A 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). Results: Plasma 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, while ΔHMGB1 correlated positively with CD14+CD16- monocytes, suggesting higher alarmin release after strenuous exercise may involve increase in circulating monocytes. Conclusions: Perturbations in systemic alarmins are novel biological signatures for assessing the inflammatory milieu of healthy adults during high-intensity exercise.
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Posted 14 Feb, 2020
On 12 Feb, 2020
On 12 Feb, 2020
On 11 Feb, 2020
On 11 Feb, 2020
On 11 Feb, 2020
Posted 14 Feb, 2020
On 12 Feb, 2020
On 12 Feb, 2020
On 11 Feb, 2020
On 11 Feb, 2020
On 11 Feb, 2020
Background: 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. 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. Methods: A 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). Results: Plasma 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, while ΔHMGB1 correlated positively with CD14+CD16- monocytes, suggesting higher alarmin release after strenuous exercise may involve increase in circulating monocytes. Conclusions: Perturbations in systemic alarmins are novel biological signatures for assessing the inflammatory milieu of healthy adults during high-intensity exercise.
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