Journal Article
Histamine, mast cell tryptase and post-exercise hypotension in healthy and collapsed marathon runners
I. T. Parsons; M. J. Stacey; L. Faconti; N. Hill; J. O’Hara; E. Walter; B. Farukh; R. McNally; H. Sharp; A. Patten; R. Grimaldi; N. Gall; P. Chowienczyk; D. R. Woods
European Journal of Applied Physiology · Vol. 121, Issue 5 · pp. 1451-1459 · 2021
Abstract
Purpose Heat stress exacerbates post-exercise hypotension (PEH) and cardiovascular disturbances from elevated body temperature may contribute to exertion-related incapacity. Mast cell degranulation and muscle mass are possible modifiers, though these hypotheses lack 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 incapacitated runners. Methods 24 recreational runners were recruited and successfully completed the 2019 Brighton Marathon (COMPLETION). WBMM was measured at baseline. A further eight participants were recruited from incapacitated runners (COLLAPSE). Histamine, MCT, blood pressure, heart rate, body temperature and echocardiographic measures were taken before and after exercise (COMPLETION) and upon incapacitation (COLLAPSE). Results In completion, MCT increased by nearly 50% from baseline ( p = 0.0049), whereas histamine and body temperature did not vary ( p > 0.946). Systolic (SBP), diastolic (DBP) and mean (MAP) arterial blood pressures and systemic vascular resistance (SVR) declined ( p < 0.019). WBMM negatively correlated with $$\Delta $$ Δ SBP ( r = − 0.43, p = 0.046). For collapse versus completion, there were significant elevations in MCT (1.77 ± 0.25 μg/L vs 1.18 ± 0.43 μg/L, p = 0.001) and body temperature (39.8 ± 1.3 °C vs 36.2 ± 0.8 °C, p < 0.0001) with a non-significant rise in histamine (9.6 ± 17.9 μg/L vs 13.7 ± 33.9 μg/L, p = 0.107) and significantly lower MAP, DBP and SVR ( p < 0.033). Conclusion 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.