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.
三个星期前的今天，b姐早晨起来跑步。她吃了个香蕉，预热跑两英里，然后加速到正常速度。在不到四英里的时候，她觉得想方便一下，就往回家跑。刚进卫生间，突然发生眩晕，两眼发黑，浑身盗汗，恶心，差点儿晕倒。然后躺了十分钟，才继续晨跑。测了血糖正常，血氧正常，也没有空腹，可为什么会发生休克现象？其实，这个现象几乎每个人都发生过。一般很轻微，你不一定注意到。不管你是不是跑步。如果晕倒，大多认为是低血糖。其实有些是和重力性休克混淆了。不少人知道，我也多次提及，但也许还有人不太清楚。这里再说一下。
日常生活中，人体的血液向全身供养，大脑躯干内脏四肢。其中大脑约20%，其他看你的活动方式分布，如果在电脑前，下肢大约分到8%，然后需要经常走动则加倍到16%。在吃东西时，肠胃消化系统消耗大量血养。而在跑步时，这个比例就打破了，血液重新分流，Blood shunt到肌肉系统。而肠胃系统靠边站，得不到供给。这就是为什么跑步的时候吃东西几乎完全不能消化。这个时候，大腿的供血循环占据了接近一半。高速的奔跑，肌肉又把血液通过静脉打回心脏，以获得更多的带氧能源。马拉松比赛一般要三到五个小时，人体按惯性一直依照这个分布泵送血液。
比赛途中，你可能会要上厕所，忍得很难受，好不容易路边有个Porta Potty, 你快速抢到一个。你一秒钟都不想浪费。为了几分甚至几秒的时间，你已经艰苦训练了多少个月甚至多年。你不能想象在比赛途中排队上厕所，你这个比赛等于毁了。冲进厕所，关门，扭了门扣，也不管马桶是不是干净，一屁股坐下去，。。。。这个时候，你的心跳还在剧烈跳动，突然你两眼一黑，浑身猛然冒出大量汗水，恶心，头晕目眩，几乎昏倒。这就是休克了。因为你急刹车了。火车急刹车后还要冲出去2公里，你突然停在了狭小闷热的厕所里。你的大腿突然停止了运动，肌肉不再压缩泵回血液，血压瞬间下降，大脑得不到供给。l
这是非常危险的。上厕所有三次危险，第一进门时。第二是出门时，路边厕所排放在不同的地方，出来时你想快速恢复速度，没看脚下，一脚踏空。我自己有两次，一次摔倒，也见过别人出来时跌倒。第三次重新加速时，又一次难受的时刻。我自己的方法，是进去时看清，扶稳，坐下去前，保持两脚继续原地踏步，动作尽量缓慢减速。
另外一个危险的时刻，就是终点线。这时你已经耗尽所有的能量，而且到终点的时候，观众欢呼，照相机摄像机对着你，大部分赛手都在作最后400米冲刺。你冲线了，精疲力尽地保持着微笑。然后你就两眼发黑，喜悦，难受。在一些大型马拉松比赛中，比如纽约，芝加哥，洛杉矶，海军陆战队，因为都是几万人的大赛，志愿者会让你赛后继续往前走。你很想停下来，拍几张照片。所以不想走。这个时候，其实是不能突然停的。我每次跑完都坚持走十分钟左右。而一些小型马拉松，没人催你，你就要自觉了，不能立即停。
我曾经停过，小腿突然发涨，好像要爆炸掉。这时可能有几种情况，可能是重力性休克，也可能是抽筋，或者心脏问题，乳酸堆积等。不同原因要对症下药。我保持快速走动，逐步减慢速度，不急刹车，等心率降到90才停下慢慢走。有时我不比赛但作志愿者，我特别在终点线注意每个赛手的状况，看谁需要特殊照顾。
现在知道该如何应对，还有你上次说过红绿灯停下来等，让心跳不要那么快，也是很好的建议
节奏跑的干呕还是运动过量，Overexertion. 虽然也可能是EAPH。
父母大惊小怪，再也不让自己孩子参加运动了。我爸妈说那些人“没文化”，哈哈
我们几个伙伴却私下一致认为这是最彻底的了断方式，因为是自己在做最喜欢的运动。
不好意思，鞋有点土
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。。。。）
PathophysiologyWhile 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.