There's been alot of talk lately about triathlon deaths and injuries. I discovered something else that may account for some of this.
SIPE is Swimming Induced Pulmonary Edema. It seems to only happen in open water. It starts as shortness of breath or the onset of a panic attack. It can then proceed to spitting up a pink frothy foam. That's blood from your lungs. But this is not a cardiac event.
The reason I'm bringing it up is because last summer I think I experienced it. Originally I thought it might have been an asthma attack, but now I'm not completely sure. Since it often involves open water swimming, I thought it might have happened to someone else from the forums. Whether it has or not, I thought it should be brought up so people are aware.
There is also a website that has explanations and some links. SIPE
JIM
Armchair SIPE theory of the "you read it first here" variety
The other sports related pulmonary edema I have heard about is HAPE, or high altitude pulmonary edema. What happens in thin air is that the blood pressure to the lungs gets higher, and in essence causes the capillaries to leak a little, almost like a soaker hose.
In cold water, blood is shunted to the core and away from the periphery in order to keep the vital organs warm as long as possible. The capillaries in the periphery, meantime, constrict, plus the external water pressure aids this constriction, almost as if your body were wrapped in a large blood pressure cuff.
Thus the original total volume of a cold water swimmer's blood is thus confined to a smaller space, increasing blood pressure. One of the ways the body deals with this is increased urination to reduce the fluid content.
I wonder if there is any correlation between SIPE occurrence and water temperature. My hypothesis is that SIPE would become more common as water temperature decreases because this would increase the internal blood preessure, which, in turn, might cause the pulmonary arterioles to start acting like soak hoses, a la HAPE.
Note: my armchair theory is probably wrong, but if you are an exercise physiologist looking for a new topic to research, I gladly bequeathe my amateur ruminations for you to either kibosh or validate!
Armchair SIPE theory of the "you read it first here" variety
The other sports related pulmonary edema I have heard about is HAPE, or high altitude pulmonary edema. What happens in thin air is that the blood pressure to the lungs gets higher, and in essence causes the capillaries to leak a little, almost like a soaker hose.
In cold water, blood is shunted to the core and away from the periphery in order to keep the vital organs warm as long as possible. The capillaries in the periphery, meantime, constrict, plus the external water pressure aids this constriction, almost as if your body were wrapped in a large blood pressure cuff.
Thus the original total volume of a cold water swimmer's blood is thus confined to a smaller space, increasing blood pressure. One of the ways the body deals with this is increased urination to reduce the fluid content.
I wonder if there is any correlation between SIPE occurrence and water temperature. My hypothesis is that SIPE would become more common as water temperature decreases because this would increase the internal blood preessure, which, in turn, might cause the pulmonary arterioles to start acting like soak hoses, a la HAPE.
Note: my armchair theory is probably wrong, but if you are an exercise physiologist looking for a new topic to research, I gladly bequeathe my amateur ruminations for you to either kibosh or validate!
