Date of Completion


Embargo Period



Elaine C. Lee, Lawrence E. Armstrong, Douglas J. Casa, Craig Denegar

Field of Study



Master of Science

Open Access

Open Access


Given that hyperthermia and other exercise-stress induce cellular release of HSPs into circulation, it is important to consider the contribution of circulating HSP concentrations ([HSPs]) on systemic inflammation associated with exertional heat stroke pathophysiology (EHS). We compared the circulating [HSP90alpha], [HSP60], [HSP70], and [HSP27] in two athletic events with high and low incidences of EHS. The aims were to characterize the changes in circulating [HSPs] from pre- to post-event and to elucidate the potential for HSPs as EHS susceptibility biomarkers. Thirty (age: 44±11year; height: 174.89±9.5cm; mass: 74.2±14.05kg; BMI: 24.11±3.13kg × m-2; %body fat: 19.74±4.03%) and fifty-six participants (age: 51±11year; height: 176.49±6.50cm; mass: 86.89±13.96kg; BMI: 27.85±3.76kg × m-2; %body fat: 13.17±8.03%) were recruited for the Falmouth Road Race (FRR) and the Hotter’N Hell 100 (HHH), respectively. Gastrointestinal temperature (TGI) and blood samples were obtained at pre- and post-event for both events. Blood samples were analyzed for circulating [HSP90alpha], [HSP60], [HSP70], and [HSP27] with ELISAs. Significant increases in TGI, [HSP90alpha], and [HSP27] were observed for both FRR and HHH from pre- to post-event (pGI for either event (p>0.05). A significant age effect on post-race [HSP27] was detected in FRR where participants with higher [HSP27] were significantly older than those with lower [HSP27] (p0.05). In conclusion, the potential contribution of HSPs to immune signaling and inflammation during EHS pathophysiology should not be overlooked, however, they are unreliable biomarkers of EHS risk.

Major Advisor

Elaine C. Lee