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4 Histamine, mast cell tryptase and post-exercise hypotension in healthy and collapsed marathon runners
  1. Iain Parsons1,2,
  2. Michael Stacey3 and
  3. David Woods3
  1. 1Cardiology and General Internal Medicine, South London
  2. 2Academic Department of Military Medicine
  3. 3Academic Department of Military Medicine

Abstract

Introduction Heat stress exacerbates post-exercise hypotension and cardiovascular disturbances from elevated body temperature and may contribute to exertion-related incapacity. Mast cell degranulation and muscle mass are considered likely modifiers, though this hypothesis lacks practical evidence. This study had three aims: 1) to characterise pre-post responses in histamine and mast cell tryptase (MCT); 2) to investigate relationships between whole body muscle mass (WBMM) and changes in blood pressure post marathon; 3) to identify any differences in runners incapacitated from marathon running.

Methods 24 recreational runners were recruited and successfully completed the 2019 Brighton Marathon (COMPLETION). WBMM was measured by bioimpedance at rested baseline. A further eight participants were recruited from incapacitated runners diagnosed with heat illness (COLLAPSE). Histamine, MCT, blood pressure, heart rate, body temperature and echocardiographic measures were taken before and after exercise (COMPLETION) and upon hyperthermic incapacitation (COLLAPSE).

Results In COMPLETION, MCT increased by nearly 50% from baseline (p=0.001), whereas histamine and body temperature did not vary (P>0.9462). Systolic (sBP), diastolic (dBP) and mean (MAP) arterial blood pressures and systemic vascular resistance (SVR) declined (p<0.019). WBMM negatively correlated with ΔsBP (r=-0.43, p=0.046). For COLLAPSE versus COMPLETION there were significant elevations in MCT (1769±244 ng/L vs 1179±431, p=0.001) and body temperature (39.8±1.3 vs 36.2±0.8°C, p<0.0001) with a non-significant rise in histamine (9.6±17.9μg/L vs 13.7±33.9, p=0.1074) and significantly lower MAP, dBP and SVR (p<0.0327).

Conclusions These data support the hypothesis that mast cell degranulation is a vasodilatory mechanism underlying PEH and exercise associated collapse. The magnitude of PEH is inversely proportional to the muscle mass and enhanced by concomitant body heating.

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