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High Potassium Intake Improves Baroreceptor Sensitivity.


beggiatoa
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Came across this study I found interesting. There is a link between exercise intolerance and potassium intake. I have been supplementing with a little potassium along with pantothenic acid and I found this improved exercise capacity, stregth and surprisingly, my OI. I tend to get very lightheaded when I workout, specially with doing squats and this has improved some with the use of potassium. There's also an association between hypothyroidism and weakness, fatigue exercise intolerance and using extra iodine also seems to help.

From another study, it also seems that patients with OI and exercise intolerance have lower levels of potassium in their blood. When they exercise, the serum levels increase rapidly and drop just as rapidly during rest. This could partly explain why we feel so lousy after any kind of exercise. You would think that since potassium is used to lower pressure in the hypertensive, it would have the same effect on us. Well, that hasn't been my experience at least. I'm getting benefits from just using a little extra everyday so there's no need to megadose (that's dangerous). Improving baroreceptor sensitivy also helps OI since they will respond more quickly to drops on BP.

This follows my old post on pantothenic acid.

Full text study I read this from:

http://eurheartj.oxfordjournals.org/content/29/12/1531.full.pdf

This is the original study they cited:

Effect of moderate salt restriction and high potassium intake on pressor hormones, response to noradrenaline and baroreceptor function in man.

Skrabal F, Auböck J, Hörtnagl H, Braunsteiner H.

Abstract

1. Twenty-one normotensive subjects were studied to assess any possible benefits of moderate salt restriction and of high potassium intake in the prevention of hypertension in man. 2. The effects of salt reduction from 200 to 50 mmol/day and/or of an increase of potassium intake from 80 to 200 mmol/day over a 2 week period, on blood pressure, plasma noradrenaline, adrenaline, vasopressin, renin and aldosterone, were measured both at rest and after mental stress. The effects of graded infusion of noradrenaline on blood pressure and heart rate were also studied. 3. Salt restriction lessened the increase of blood pressure during noradrenaline infusion; the combination with high potassium intake also reduced the pressure rise after mental stress. There were no major changes in plasma levels of vasopressin and adrenaline. Plasma noradrenaline increased during the low sodium diet. 4. High potassium intake improved baroreceptor function as revealed by the greater decrease in heart rate for a given rise in pressure after noradrenaline infusion. 5. The results of this study are compatible with a protective effect of a practicable low sodium/high potassium diet on the development of human hypertension.

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Some ideas from the study I want to point out.

In addition, subjects with OI showed an inappropri-ate activation of sinus node parasympathetic modulation before the onset of syncope. Another potentially important finding is the significant positive correlation between serum potassium before the race and the maximally achievable sympathetic drive to resistance vessels, as well as the significantly lower serum pot-assium in OI compared with Non-OI before the marathon.

We also found significantly lower serum potassium in OI compared with Non-OI before the marathon. None of our sub-jects experienced vomiting or diarrhea prior to the race which could have explained this difference. We do not know whether the lower serum potassium concentrations in OI were caused by differences in potassium intake or intra – extra cellular potassium distribution induced by endogenous catecholamines or other mediators. We were not able to obtain reliable dietary information in these subjects. Thus, we can only speculate whether the lower serum potassium levels in association with a limited sympathetic response were due to differences in potassium intake or to an intra– extracellular potassium distribution effect.

This latter possi-bility is not unlikely since cell membrane potential and electrical discharges are involved in sympathetic responses and both are a matter of intra– extracellular potassium gradient and thus also of extracellular potassium levels. The epinephrine-mediated potass-ium shifts in relation to sympathetic responses should be investi-gated in further studies. A high potassium intake may protect from OI, even in the face of minor, if any, effects on serum potass-ium concentration.

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Something else I've noticed since using potassium; less thirst. Found this study to support my personal observations. Potassium supplentation increased aldosterone production and water retention by the body. An inability to retain water is another problem we face. In the study, they used a dose of 3.9 g in supplements but you should in no way use such a high dose. I suggest anyone interested in using potassium start with the lowest dose possible (99 mg) and let your body ajust slowly. Too much, too soon can be very dangerious with potassium.

PMID: 22149452

Conclusions. Potassium supplementation changed renal tubular function and increased water absorption in the distal part of the nephron. In spite of an increase in aldosterone in plasma, blood pressure remained unchanged after potassium supplementation.
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