Force Output While Peating

Gl;itch.e

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Can you elaborate on that?
Ray's examples show that a lot of what we attempt to do with our diet here is phosphate lowering. Either by avoidance or by active wasting. I think that this extra loss of phosphate may (in active individuals) may reduce the ability to generate ATP sufficiently. I have no solid proof of that. Its just a thought at this stage.

forgetting all that, what does your training and food intake pre-during look like?
 
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Peatit

Peatit

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forgetting all that, what does your training and food intake pre-during look like?
My training is essentially the same since a long time and consists of a 3 days split, one day for each big movement worked in low-medium rep ranges (1-8) for a few sets.
I eat much protein (milk, eggs, gelatin, sometimes red meat or shellfish) and sugar (from fruits or table sugar), coffee, all day long and I don't have any particular pre-workout meal. During training, I only drink water with baking soda.
 
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Peatit

Peatit

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I just found this:
https://en.wikipedia.org/wiki/Thyrotoxic_myopathy

Wikipedia said:
Excess thyroxine is believed to bring about the onset of thyrotoxic myopathy and eventually cause the degradation of muscle tissue. Thyroxine is a hormone produced in the thyroid gland that regulates the growth metabolism of the nervous system and regulates basal metabolic rate of many cell types. Scientists agree thyroxine brings about the degradation of muscle fibers specifically at the motor end plates of neuromuscular junctions. There is debate as to whether thyroxine degrades the motor end plates from the muscular side, from the nervous system side, or a combination.[7]

To understand how high levels of thyroxine can be toxic and lead to thyrotoxic myopathy physiologically, consider basic neuromuscular junction function. Under normal circumstances, muscle contraction occurs when electrical impulses travel down descending axons from the brain or spinal cord towards the neuromuscular junction. The axon terminal depolarizes and releases Acetylcholine (ACh), a neurotransmitter, which in turn stimulates the motor end plate (MEP) of the muscle fiber the nerve is innervating. When the MEP depolarizes the muscle fiber releases calcium initiating the process of muscle contraction.

With the onset of TM due to thyroxine toxicity, there is evidence to suggest that structural changes in MEPs could lead to muscle fiber degradation, weakness, and fatigue. Research indicates that decreased levels of Acetylcholinesterase AChE, an enzyme that breaks down ACh, was observed within the neuromuscular junction.[7] This decrease in AChE blocks degradation of ACh causing ACh to increasingly stimulate the MEP of the muscle fiber. Over stimulation of MEP could cause more muscle contractions which eventually evoke muscle fiber fatigue, weakness, and finally degradation, which are characteristic symptoms of TM.[7] It is believed this decrease in AChE and MEP structural changes could be the result of over stimulation of thyroxin blocking the axoplasmic flow of trophic factors down the axon terminal[8] especially considering thyroxine's role in nervous system growth and metabolism regulation.

Other research indicates muscle fiber fatigue, weakness, and degradation associated with TM is the direct action thyroxine has on the muscle fibers themselves. Research suggests thyroxine directly causes a decrease in protein kinase affinity to cAMP within muscle fibers [9][10] This causes an increase in cAMP within the muscle fibers since protein kinases are not inactivating cAMP. Increased levels of cAMP within the muscle fibers cause increased release of Ca2+ from the muscle fiber's sarcoplasmic reticulum which eventually leads to more muscle contractions. Like the nervous system proposal increased muscle contractions eventually evoke muscle fiber fatigue, weakness, and finally degradation, which are characteristic symptoms of TM. There is evidence to support both theories; it has been suggested that toxic levels of thyroxine may ultimately attack muscle fibers directly and indirectly by the motor neurons that innervate the affected muscle fibers
 

CoolTweetPete

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@Peatit, I've seen water with baking soda mentioned here before, but I have not tried it. What's the reasoning behind using it during a workout? pH related?
 

DrJ

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I have not noticed a drop in strength. My squat, standing press, deadlifts, and rows still slowly progress. I still see the same pattern of plateau and breakthrough that I previously experienced. Should note that I'm in my early thirties so my goals are just modest strength improvements while maintaining low body fat. I'm not exactly a gym rat at 2-3 35min workouts/week. The only thing I've noticed since Peating is that the veins in my arms pop out less when not working out than when I was doing IF, but I've come to believe this is probably a good thing. Oh, and that I feel awesome just about all the time :)
 

CoolTweetPete

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CoolTweetPete, I think it increases CO2 level in blood so the organs oxygenation is better and apparently, endurance, but the latter is pointless for me.

Ah, very interesting. I'll try that out tonight instead of salted water and see how it goes. Merci.
 

chispas

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I can share my experience if anyone is interested: I too experienced low strength for a while, even though I was otherwise feeling great on a Peat-style "diet". What made a positive change for me was the increase consumption of salt to a very large degree - I believe Haidut has posted a study about the value of salt in the diet. I believe the salt helps the cell hold onto water and nutrient - perhaps glycogen as well, I'm not sure. In any case, OJ with salt pumps up my muscles very well before I've even lifted anything - generally only a teaspoon or two is necessary for the effect. The great thing about fruit and fruit juices is that they preserve strength. When I wasn't eating fruits at all (before Peat) I had varying degrees of strength from week to week, sometimes day to day. Nowadays, once I achieve a new PB in strength, the strength doesn't diminish, even if I go a couple of weeks without training. It is also important to mention that I consume many grams of glycine per day, which is anti-catabolic. However, again, in the past this had little effect, until I started eating a lot more fruit and sugar.
 

nbznj

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Are you sure you're eating enough? I've struggled with that mere notion since the day I started lifting. I train following Sheiko principles which are great because A) you don't need to train balls to the walls to make progress B) it's low intensity C) it's only 3 days a week so you have 4 days of active recovery and plenty of time to live life

That being said I'm 6.3, 215-220lbs and hovering 10% fat, most probably too lean, most probably some sort of "orthorexic" eating disorder. I eat 3500kcal a day with 60g of fat from dairy, coconut, cocoa, beef. I believe it's not enough and it's causing issues. Are you eating enough?

More salt helps. More cholesterol, probably. But ultimately it's going to be more food. Lifting takes a huuuuge toll.
 
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Peatit

Peatit

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As a followup, now, two years later, I must say that my strength has markedly increased, maybe the body needs some time to adapt to a euthyroid state, especially the nervous system.
I also had to reduce significantly my training volume, this actually might have been the decisive factor, but it is a little disturbing because one would imagine that the recovery capacity will increase with oxidative metabolism improvement.
Also, I noticed that while I was restoring a normal thyroid condition, my muscles "flattened", I guess that also could explain the loss of strength by the mechanical leverages modifications.
This flattening could be explained by several metabolic improvements and this is maybe why thyroid has a so bad rep in the bodybuilding community but this is certainly discussed on numerous threads here.
 

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