If you were to fall out of a plane...

Jumping out of a jet won’t kill you- I’ve jumped out of a 727 (a la DB Cooper) three times and I’m still alive. In the 90s the organizers of the World Freefall Convention, an annual skydiving festival, used to bring in a 727 for skydivers to jump from. It carried 180 jumpers at a time. They slowed it down to about 150 mph for us and I got flipped head over heels the first time I dove out of the rear exit, but I survived. The second and third times I knew what to expect and didn’t get tossed around.

You wouldn’t want to jump out if it was going 500 mph but I don’t think even that would kill you.

A friend who is a Ph.D in physics once published this regarding perception and time delays:

***Let’s assume you are reading this on a computer monitor. To read this, light must be emitted or reflected from your screen. The light that is being emitted from the page travels toward your eyes at a speed of something like 2,99792 X 1010cm/sec. This means that light can travel 29.979.200.000 centimeters in one second. To travel the few feet from the page to your eye will require only three nanoseconds

The three nanoseconds that it takes for the light to reach your eye from this page is not a very long time. But, it is not now. Even before you have any possibility to perceive the events happening on this page, they are already in the past. Again, in order for this page to be perceived, it is necessary that the light traveling from the page to your eye actually be absorbed by the eye.

The light impinges on the optical lens of the cornea where it is focused onto the back of the eye. During this process it is slowed ever so slightly. Light does not travel quite as fast through the lens; that is how the lens can focus the light. By slowing the center part of the image a little bit more than the outer part of the image, it is possible to cause the image to bend around the lens, focusing itself.

After being focused by the lens, the light travels through a viscous fluid filling the interior of the eyeball to fall on the retina at the back of the eye. On the retina is a bunch of cells called rods and cones. The rods and cones are spread one layer thick on the retina behind the nerve cells, they receive the light.

The substances in the rods and cones that make the detection of light possible are the photosensitive (or visual) pigments. The major pigment in these cells is rhodopsin, When light strikes rhodopsin, the retinene portion twists and turns, splitting away from the opsin portion. This process requires only a few pico-seconds. It may be one of the fastest biological processes known, but, it still takes us that much more away from now. The splitting of rhodopsin acts as a switch triggering a nerve impulse to the brain. Each rod and cone is a light-sensitive switch with its own wire into the brain.

Visual resolution is limited to the number or rods and cones. When light strikes each cell, the chemical switch in it is turned on, sending a signal along the optic nerve to the visual cortex in the brain.

If the signal to the brain traveled at the speed of light, which is the fastest that any information is supposed to be able to travel, it would still take the signal about one nano-second to reach the brain.

The transmission along the optic nerve is governed by a mixture of electrical transmission and chemical transmission. Consequently, it takes a bit longer than that. The velocity of propagation of the signal along the optic nerve is roughly 10.000 centimeters per second. To travel the few inches from the eyes to the brain could take one millisecond. This is a conservative estimate, since the impulse appears to jump resulting in a higher velocity than if the impulse traveled continuously along the axon. In any case, this is a lot slower than instantaneous. Pushing us still further into the past.

The optic nerve is composed of neurons. Neurons contain a nucleus, cytoplasm with a variety of cell stuff (cytoplasmic structures such as endoplasmic reticulum and Golgi bodies) and a lipid-protein membrane that separates the inside of the cell from the outside.

All cells, including neurons, have a steady electrical voltage difference across their cellular membranes. This is caused by differences in chemical concentrations on the two sides of the cell membrane. The three major ionic chemical components that cause this electrical potential across the cellular membrane are: potassium, sodium, and chloride. All three exist on both sides of the cell membrane, but the amounts are not evenly distributed. Little teeny-tiny pumps continually transport the ions across the cell membrane. But the little pumps aren’t fair. They will transport more of one ion across the membrane than another. In addition, the membrane isn’t fair about which ions it will let diffuse across the membrane.

Diffusion is the process whereby a chemical or ion will drift about, moving itself from one place to another. When a bottle of perfume is opened at one end of a room, it is the process of diffusion that lets the smell travel throughout the room. That could be good or that could be bad, it depends on the brand of perfume. The process of diffusion doesn’t care what the perfume smells like; it will move the molecules of perfume about with total egalitarian disinterest. But the cell membrane is not so indiscriminate.

During the resting state, the membrane allows mainly positive potassium ions to passively diffuse into the cell. The result is lots of positive potassium ions and not very many positive sodium or negative chlorine ions inside the neuron. The outside of the neuron has a lot of positive sodium ions, a bunch of negative chlorine ions, but not very many positive potassium ions. This may not be fair, but it does allow nerve cells to work. The resulting difference in ion concentration across the membrane generates the electrical potential that produces the membrane voltage.

As mentioned earlier, a resting membrane potential based on ionic asymmetry (that means more on one side than the other) and selective permeability (that means little holes like the ones in a spaghetti strainer) is a common feature of almost all living cells. The nerve cells make use of a phenomenon called depolarization to transmit information to the brain — and visa-versa.

Depolarization of the membrane occurs when the membrane rapidly becomes permeable to sodium ion, causing an influx of sodium into the cell from the outside the membrane where the sodium levels have been kept low. The rapid inflow of positive charge drives the membrane voltage from negative 60 mV (resting potential) to positive 40 to 50 mV (action potential).

These local changes in ion concentration activate neighboring sections of the nerve membrane and result in a nerve impulse propagating along the nerve fiber much like dominos, one stimulating the other. In this manner, the information is transmitted from the retina of the eye to the visual cortex of the brain.

During this transmission from the rods and cones to the visual cortex, not only does the signal travel along the individual nerve cells, it must also jump the synaptic gaps between nerve cells.

The synapse is the teeny-tiny gap between neurons. The information is transmitted across this synapse by chemical transmitters migrating from one neuron to the other. These transmitters migrate across the gap much like carrier pigeons. Once the message reaches the other side the next neuron fires and the message is on its way again. Interestingly enough, it is possible to speed up or slow down the transmission rate across this gap by the presence or absence of certain chemicals. Yep, we’re slipping even further into the past.

Late or not, the final destination of this message is the visual cortex. It is here that the nerve impulses coming all the way from the rods and cones of the eyes produce a chemical and electrical distribution. This we call vision.

The data that the brain works with is chemical and electrical distributions found within the brain; not the experience itself. The electrical activity traveling along the optic nerve influence the chemistry of the brain to transmit information received by the nerve cells of the retina; still not the experience itself. The nerve cells of the retina are caused to trigger by changes in the chemical structure of molecules found in the rods and cones of the retina; still not the experience. The structure of the chemicals in the rods and cones of the retina are altered by the absorption of light. Nope, not the experience yet. The light is transmitted from the page to the retina through the mediums of atmosphere, cornea and eyeball fluid; but the light is obviously not the experience. The light is that which is left over after the ambient light of the room is reflected from the page. We will never experience the print on a page. At best we can see the differential absorption of light reflected from the page. Even then we don’t actually see the light; we experience chemical and electrical distributions brought about by the impingement of this light on a whole set of physiological systems.

Not only are we living in the past, we are living in a filtered version of the past with incomplete data and data that has been altered to correspond to previous experience.


Fantastic, thanks. Deserves a bibliographic citation, if you don’t mind!

I had the same experience, and it’s pretty common in accidents. But it’s a memory issue. It doesn’t mean that you didn’t feel anything on the moment. You just don’t remember it.

As Bumbershoot said above, *could *be killed is possible. *Would *be killed is far from a sure thing.

Jets designed for deploying paratroopers put some effort into ensuring the airflow at the exit doors is not too strong. For side exit doors there are often deployable wind deflectors which produce a pocket of relatively still air just outside the door. This helps ensure the trooper gets all the way out before being slammed forcefully rearward by the wind blast & broken on the aft doorway edge.

They also have design features like raised tails that reduce the odds on somebody exiting and crashing into the tail as they’re left behind.

Airliners lack all these things as deliberately designed features, although the tail stairs on a 727 coincidentally come close. Hence its use by both DB Cooper and modern parachuting groups. Which is also why 727s were retrofitted after Cooper to make it mechanically impossible to deploy the stairs inflight.

And, jets used for deploying parachutists are flown straight, level, as slowly as possible and at low altitudes by jet standards. Jumping out under other circumstances is a different animal.

Jumping out at typical jetliner cruise altitudes will result in severe hypoxia & probable unconsciousness unless you have supplemental oxygen. Revival from a hypoxia event usually leaves the person confused & listless for 30-60 seconds. Odds are that exceeds the available time of fall to lowest safe parachute opening altitude. Certainly bottled oxygen & suitable mask and an automatic parachute opening device could resolve this problem. Depending on the altitude you’d also need supplemental oxygen while still on board & preparing to jump even if you didn’t / couldn’t take any with you.

Jumping out at typical jetliner cruise speed would be hard on a person even if they cleared the aircraft cleanly. Not immediately fatally hard in and of itself, but if flail injuries break both arms, you might be unable to deploy your parachute. Or you’d be spinning like mad and suffer eye damage or a g-induced stroke before you regained control over your attitude. Any time you spent unconscious or ineffective due to hypoxia would only exacerbate the odds on injury from out of control tumbling.

Given enough time of fall you’d certainly slow to terminal velocity. But even at that much lower speed, uncontrolled tumbling is hazardous. You certainly can’t safely deploy a parachute in that state; it’d get hopelessly tangled around you.
Bottom line: lots *could *go wrong and the higher & faster the jet’s going the more likely & more severe the injury potential.

This line of thought/phenomenon/stunned realization is discussed in I am not I: The fastest biochemical event and the speed of light, or, The Bathroom Mirror phenomenon. njtt has a daisy-cutter bib cite there.

In the thread I cited above, I think someone suggested enzymatic reactions as the fastest. Is this an enzymatic reaction?

What…?

Don’t heart attacks, at the minimum, take several minutes to kill, by starvation of blood flow and oxygen?

There seems to be a common meme dating back from even when I was a kid in the 60s. And probably from decades before then.

The meme is that whenever a person is truly screwed, trapped in a soon-to-be-fatal situation, they’ll die of a heart attack first, typically almost immediately.

IMO, the whole thing is a *whistling past the graveyard *response to the fear of being trapped for minutes, hours, or days in a no-way-out situation. The idea of being trapped & awaiting certain death is so scary, that positing that people’s body’s have catastrophic malfunctions & drop dead on their own seems like a good idea.

The fact it’s utterly maladaptive & hence very unlikely to be to true never seems to enter into the thinking. But boy do folks like repeating it as if it was fact.
ETA: As to the physiology of heart attacks. …

Once the heart starts either fibrillating or ceases beating, unconsciousness is rapid, at most 10 seconds and usually more like 3-5. Full-up death is minutes later, but for the purpose of avoiding actively experiencing the rest of the unpleasant scenario, the onset of unconsciousness is the point that matters. And it’s pretty close to immediate.