Confused about rigor mortis

[CuriousGeorge2]

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I thought I understood why rigor mortis develops before, but after reviewing how muscle contraction works, I am confused. I get that ATP is not synthesized anymore when you're dead and as a result, if you have the myosin head bound to actin, it can let go, BUT what about the role of calcium in all this?

For normal muscle contraction, before actin and myosin can even interact with each other there has to be release of calcium from the sarcoplasmic reticulum. This calcium release is triggered by activation of motor neuron innervating the muscle.

I know intracellular calcium levels increase when cells die, but I took a look in Robbins and it seems that is secondary to the fact that ATP is no longer synthesized. So, if the ATP runs out before calcium levels in the cell go up, how can we even enter a final cross bridge cycle in the first place?

 

[PiBond]

I thought I understood why rigor mortis develops before, but after reviewing how muscle contraction works, I am confused. I get that ATP is not synthesized anymore when you're dead and as a result, if you have the myosin head bound to actin, it can let go, BUT what about the role of calcium in all this?

For normal muscle contraction, before actin and myosin can even interact with each other there has to be release of calcium from the sarcoplasmic reticulum. This calcium release is triggered by activation of motor neuron innervating the muscle.

I know intracellular calcium levels increase when cells die, but I took a look in Robbins and it seems that is secondary to the fact that ATP is no longer synthesized. So, if the ATP runs out before calcium levels in the cell go up, how can we even enter a cross bridge cycle in the first place?

Just a guess...

Since the Na+/K+ ATPase no longer functions without ATP our resting membrane potential runs down and thus causes the final Ca2+ release.

 

[gravitywave]

binding of ATP isn't necessary for myosin flexion, it's necessary for myosin release.

 

[CuriousGeorge2]

but isn't an intracellular calcium influx required for myosin to bind? And in order for one to get the "chance" to enter a rigor state (i.e. inability for myosin to release), myosin first needs to bind?

 

[gravitywave]

i don't think rigor is so much constitutive contraction as the rigidity conferred by the locked-up crossbridges - the way i understand it is that the myosin gets stuck mid cycle. the crossbridges can't release without bound ATP. no more ATP, no cycling. I think you've put the cart before the horse here: ATP doesn't have to show up for cycling to happen, it's already bound. that way when tropomyosin opens up the binding sites, ATP gets hydrolyzed and cross-bridges form.

So, when ATP gets depleted post-mortem and intracellular calcium levels rise, the ATP for cross-bridging is already in place. crossbridges form, but can't release because there is no more ATP available to bind to myosin and allow the release to occur.

 

[pandamed]

You need ATP to keep Ca2+ ATPase functional. With no ATP, calcium diffuses from the SR (and binds to troponin C)

 

[redsquareblack]

You need ATP to keep Ca2+ ATPase functional. With no ATP, calcium diffuses from the SR (and binds to troponin C)

This.

 

[mddoc1]

You need ATP to keep Ca2+ ATPase functional. With no ATP, calcium diffuses from the SR (and binds to troponin C)

Agree.