给你找了篇论文。有比较完整的描述。

https://www.ncbi.nlm.nih.gov/books/NBK576425/

特别拷贝了“病理生理学”那一段，提到了我说的内容。

概要是心脏把血液打到下肢，下肢的肌肉强烈收缩，又把血液通过静脉打回心脏。所以，下肢肌肉成了“第二心脏”。

突然停止，第二心脏功能没了，造成下肢静脉淤积（我文中说的，小腿要爆炸的感觉）。

（论文后面没说下去。就是我接下来讲的低血压，大脑缺氧，休克。。。。）

Pathophysiology

While the exact mechanism of exercise-associated collapse remains to be determined, it was previously believed to be caused by dehydration and/or hyperthermia. More recent evidence indicates that transient postural hypotension resulting from an interaction of athletic bradycardia, lower extremity pooling post endurance workout, and impaired cardiac baroreflexes are the principal causes.[6]

Trained endurance athletes tend to have mild left ventricular dilation and hypertrophy that allows for a more efficient cardiac output and a subsequent lower resting heart rate. During endurance exercise, heart rate increases to account for subsequent increases in metabolic demand. Increased metabolic demand requires increased vasodilation for the high-demand muscle groups, usually the lower extremities. This vasodilation is offset by the lower extremity muscles functioning as a ‘second heart’ by moving the increased lower body blood volume back to the heart to support the high cardiac output needed during vigorous exercise. However, this ‘second heart’ effect is lost with the cessation of exercise. When done abruptly, such as upon crossing the finish line of a marathon, venous pooling in the lower extremities results due to impaired baroreflex control.

When coupled with a quick return towards a resting heart rate as seen in trained athletes, insufficient blood supply results, creating a hypotensive setting. This exercise-associated postural hypotension (EAPH) may result in symptoms caused by a decline in systolic blood pressure below supine values leading to an exertional-related collapse when standing.

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