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Vascular and central hemodynamic changes following exercise-induced heat stress
Wesley K Lefferts1, Kevin S Heffernan2, Eric M Hultquist3
1Skidmore College, Saratoga Springs, NY, USA Syracuse University, Syracuse, NY, USA.
Exercise-induced heat stress increases myocardial workload and reduces coronary blood flow, potentially raising cardiac vulnerability during strenuous activity in the heat. This study investigated heat stress effects on vascular function and coronary perfusion.
Area of Science:
- Cardiovascular Physiology
- Environmental Extremes
- Exercise Science
Background:
- Occupational heat stress poses risks to cardiovascular health.
- Firefighters face significant exercise-induced heat stress (EIHS) due to protective gear.
- Understanding EIHS effects on hemodynamics and coronary perfusion is crucial for safety.
Purpose of the Study:
- To investigate the impact of EIHS on vascular function and central hemodynamic load.
- To assess changes in coronary perfusion indices under heat stress conditions.
- To determine if EIHS affects aortic stiffness and myocardial work.
Main Methods:
- 12 healthy men underwent 100 minutes of intermittent exercise in two conditions: heat stress (HS) with firefighter PPE and no heat stress (NHS) with cooling.
- Vascular-hemodynamic measures, including aortic blood pressure, reflected wave pressure (Pb), systolic (SPTI) and diastolic pressure time-integral (DPTI), and aortic stiffness, were recorded pre- and post-exercise.
- Pulse wave velocity was also assessed.
Main Results:
- SPTI was significantly greater, while DPTI and Pb were significantly lower post-exercise in the HS condition compared to NHS.
- No significant differences in pulse wave velocity or aortic stiffness were observed between conditions.
- EIHS led to increased indices of myocardial work and reduced indices of coronary perfusion.
Conclusions:
- EIHS does not alter aortic stiffness but increases myocardial workload.
- Reduced coronary perfusion indices under EIHS may be linked to heart rate responses.
- A potential mismatch between myocardial oxygen demand and supply during EIHS could increase cardiac vulnerability to ischemia.
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