This question comes from my video about GOATS! so you should watch that first to get an intro on fainting goats (congenital myotonia) and also just because goat science is awesome.
I just spent half an hour digging through scientific literature trying to find reports of congenital myotonia (“fainting syndrome”) in a wild animal and came up with exactly zilch, zero, and nada. We see it in goats, horses, dogs, cats, people… all of which are domesticated species (except for maybe people), but no reported cases in wild animals. Does that mean it’s impossible?
First let me summarize what should happen in a normal skeletal muscle contraction, then I’ll answer that question.
Muscle cells, like nerve cells, actively maintain different concentrations of ions on either side of their membrane. This resting membrane potential is super-interesting, but also pretty complicated, so instead of me turning this answer into a textbook chapter, all you need to remember right now is that the inside of a muscle cell is slightly negative compared to the outside. The ions we need to keep in mind right now are sodium (Na+, higher conc. outside), potassium (K+, higher concentration inside), and chloride (Cl-, higher concentration outside).
When a nerve impulse reaches a muscle fiber, the neurotransmitter acetylcholine opens a sodium-specific door on the muscle and lets some Na+ ions inside.
Sodium is a positive ion, so it makes the inside of the muscle more positive. Then that initial burst of Na+ leads to an even larger Na+ wave. Positivity breeds positivity, people!
This burst of positive charge into the muscle cell is essentially what makes it contract (although I’m leaving out a bunch of stuff, like how calcium comes into play, to dig into more detail on all this, check out these great illustrations from MDA.org)
Of course, muscles don’t usually stay contracted, unless you’re dead, diseased, or get a cramp. Why not? After a short amount of time, potassium ions flow out of the cell through their own special potassium doors (making the inside more negative again) and chloride ions move in through their special chloride doors (making the inside even more negative).
It’s the return to that original inside-negative state that makes the muscle relax (now maybe you can start to see why loss of salt/electrolytes can lead to cramps?)
Finally we come to the fainting goats. Congenital myotonia leads to a mutation in that chloride channel I mentioned up there (if you’re into gene and protein names, it’s called CLCN1), meaning that those muscle cells take longer to return to their normal negative-on-the-inside charge and stay locked in the “on” state.
That’s what we see in “fainting” goats, or any other creature with congenital myotonia. The muscles just lock up, and the “fainting” is really just “falling over thanks to suddenly obtaining the flexibility of a statue.”
So does this mutation exist in wild animals? Probably. There’s no reason a wild animal could gain a spontaneous mutation in its chloride channel gene and have particularly rigid offspring. Only these statue-creatures would be easy pickings for predators, as in “easiest meal evar,” and that mutation wouldn’t be able spread throughout the population. Since we can’t keep track of every single wild animal and their offspring, we probably never see it (although there might be isolated reports out there). Like, what’s happening with this panda? I don’t even know.
On the other hand, we inbreed the hell out of domesticated animals, and thanks to fences, sharp sticks, and sheepdogs, we tend to keep them fairly safe from predators (not to mention that humans don’t have any predators except each other). So whether or not they have the genetic misfortune of crumpling into a heap of myotonic hilarity every time we sneak up behind them, we’ve artificially (and accidentally) amplified this mutation in domesticated breeds (although breeders are often encouraged to not breed “fainting” animals).
So the answer to your question is almost certainly yes, although the Bad Wolves keep the Weeping Angels from taking over.