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A reflex is an unconscious action in response to some specific stimulus, e.g., blinking an eye, or pulling the hand away from a hot pin

I know from school biology, and reading online that withdrawal reflexes are quick because

  • CNS is involved
  • Danger receptors send impulses to prevent inhibition of flexion

When a person is extremely obese, do these flexion impulses take longer?

Is a withdrawal reflex in an obese person noticeably slower than in case of a reasonably fit person?

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Do you have some reason to suspect that it would be slower? –  Richard Smith Jul 23 '12 at 19:14
    
Merely speculating. An obese person probably does not generate extra nerves/muscles to support their extra mass. Rather any existing nerves may be compressed, and pre-obesity muscles might be distended(sp?) by the added mass already/ –  Everyone Jul 23 '12 at 19:24
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2 Answers 2

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No, what would weight have to do it? An obese person has more fat than a person of a normal weight, but fat isn't innervated by nerves (or motor neurons, at least). What about very muscular people? In this case, they actually have more muscles that require innervation, and this comes from increased branching at the nerve terminal.

Since you mentioned muscles, let's focus on motor neurons (or motoneurons). Remember that the cell body of motor neurons is actually in the spinal cord. In the case of alpha motor neurons, which innervate skeletal muscle, the cell body is in the ventral horn. What you think of as a "nerve [bundle]" is really just a collection of cell axons. The axons can regrow if cut in the middle, but you don't grow more axons very easily.

Additionally, a spinal reflex is very quick because it involves the CNS, but not the brain. Look at the example of the patellar (knee-jerk) reflex. The stretch is sensed and transmitted to the spinal cord, causing contraction of the quadriceps while simultaneously inhibiting the antagonist muscle, the hamstrings.

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I went into this with the same assumptions that jello did, but I found two studies that had some interesting results.

Isojärvi (2010) found that in obese and under-exercised adults, physical fitness level predicted, among other things, a significant proportion of the variance of nerve conduction velocity and F-wave latency. So, these individuals may theoretically have a slower response to noxious stimuli.

While Type II diabetes is not always a result of obesity, there is often a high correlation between the two. Oltman (2005) found that, in "Zucker diabetic fatty" rats (an animal model of Type II diabetes), motor nerve conduction velocity in the sciatic was significantly slowed. This effect, too, would affect the rate with which an individual could withdraw a limb from a noxious stimuli.

So, I don't think that anatomical changes in the bodies of individuals who are obese would have any effect, but clearly there are physiological changes in the neurons of these individuals.


References:

Isojärvi H, Keinänen-Kiukaanniemi S, Kallio M, Kaikkonen K, Jämsä T, Korpelainen J, Korpelainen R. (2010). Exercise and fitness are related to peripheral nervous system function in overweight adults. Med Sci Sports Exerc. 42(7):1241-5.

Oltman CL, Coppey LJ, Gellett JS, Davidson EP, Lund DD, Yorek MA. (2005). Progression of vascular and neural dysfunction in sciatic nerves of Zucker diabetic fatty and Zucker rats. Am J Physiol Endocrinol Metab. 289(1):E113-22.

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That's really interesting, thanks. I didn't realize there would be such measurable changes, even in the larger nerves. Diabetic neuropathy causes serious problems for people, initially in the hands and feet, due to their distance from the brain. But apparently excess weight can cause negative physiological changes to nerves. –  jello Jul 30 '12 at 12:35
    
@jello Yes, I learned a few things I didn't know. My mention of you wasn't a critique in any way, it was more saying that you'd already covered 95% of it, so I wouldn't rehash the info. –  jonsca Jul 30 '12 at 15:02
    
I didn't take it that way, no worries :) –  jello Jul 31 '12 at 1:39
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