Histamine, mast cell tryptase and post-exercise hypotension in healthy and collapsed marathon runners, Parsons et al, 2021

[Andy]

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 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.

Paywall, https://link.springer.com/article/10.1007/s00421-021-04645-0

 

[Hoopoe]

A possible connection to the horrible heat-induced orthostatic intolerance I get for a few weeks in the beginning of the hot summer.

 

[Ryan31337]

Mast cell "issues" are often considered as overlapping in Dysautonomia/POTS clinics. There's a sensible reluctance to call it MCAS and read into it too much as proponents of that can do, but there's definitely an awareness there can be an impact on cardiovascular symptoms at least.

In my experience this lead to some empirical treatment with H1 and H2 anti-histamines, anti-leukotrienes & sodium cromoglicate.

 

[Mithriel]

A possible connection to the horrible heat-induced orthostatic intolerance I get for a few weeks in the beginning of the hot summer.

I had really bad POTS and dysautonimia a few years back when the weather was really hot. I was surprised when it eased up as the weather became cooler.

The next year's hot weather made it worse again but I went to great lengths to keep cool and that has kept it from being so bad again.

 

[Binkie4]

Mast cell "issues" are often considered as overlapping in Dysautonomia/POTS clinics. There's a sensible reluctance to call it MCAS and read into it too much as proponents of that can do, but there's definitely an awareness there can be an impact on cardiovascular symptoms at least.

In my experience this lead to some empirical treatment with H1 and H2 anti-histamines, anti-leukotrienes & sodium cromoglicate.

I am awaiting an appointment at a dysautonomia clinic for severe OI after also developing mast cell issues ( variously called mast cell irritability and MCAS), and it has just been recommended that I take sodium cromoglicate to add to antihistamines in order to better stabilise the mast cells.
Am pretty new to all this but is there a suggestion that unstabilised mast cells can contribute to dysautonomia?