A multi-centre study of potassium deficiency in the elderly

Fletcher, Andrew J; Standen, S.

doi:10.1185/03007997309111725

Cited by 3 publications

(4 citation statements)

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“…These observations indicate that when the capacity of the Na + ,K + -pumps is reduced, the ability to maintain contractility is impaired, probably reflecting an impaired ability to clear K + from the interstitial water space. These observations offer an explanation of the fatigue often experienced by patients suffering from K + deficiency (Fletcher & Standen 1973) or digitalis intoxication. Decreased K + intake is associated with a decline in muscle grip strength (Judge & Cowan 1971), and in rats maintained on K + -deficient fodder, swimming led to exhaustion within only 44 min, whereas the pair-fed controls kept on fodder with normal K + content continued swimming for 175 min (Bollaert et al 1993).…”

Section: Effects Of Reducing Na + K + -Pump Activity or Capacity On mentioning

confidence: 76%

“…These observations offer an explanation of the fatigue often experienced by patients suffering from K + deficiency (Fletcher & Standen 1973) or digitalis intoxication. Decreased K + intake is associated with a decline in muscle grip strength (Judge & Cowan 1971), and in rats maintained on K + ‐deficient fodder, swimming led to exhaustion within only 44 min, whereas the pair‐fed controls kept on fodder with normal K + content continued swimming for 175 min (Bollaert et al.…”

Section: Effects Of Reducing Na+k+‐pump Activity or Capacity On Contmentioning

confidence: 83%

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Role of Na⁺,K⁺‐pumps and transmembrane Na⁺,K⁺‐distribution in muscle function

Clausen

2007

Acta Physiologica

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Na(+),K(+)-ATPase situated in the plasma membrane mediates active extrusion of Na(+) and intracellular accumulation of K(+). This transport system the Na(+),K(+)-pump is the major regulator of the transmembrane distribution of Na(+) and K(+), and is itself subject to regulation by a wide variety of factors in skeletal muscles. The excitation of skeletal muscles is elicited by a rapid influx of Na(+), followed by an equivalent efflux of K(+) across sarcolemmal and t-tubular membranes. Due to their size and sudden onset, these events constitute the major transport challenge for the Na(+),K(+)-pumps. Skeletal muscles contain the largest single pool of K(+) in the organism. During intense exercise, the Na(+),K(+)-pumps cannot readily reaccumulate K(+) into the muscle cells. Therefore, the working muscles undergo a net loss of K(+), causing up to a doubling of the K(+) concentration in the arterial blood plasma in less than 1 min and even larger increases in interstitial K(+). This may induce depolarization, loss of excitability and force, in particular in muscles, where the excitation-induced passive Na(+),K(+)-fluxes are large. During continuous stimulation of isolated rat muscles, there is a highly significant correlation between the rise in extracellular K(+) and the rate of force decline. Fortunately, excitation increases the Na(+),K(+)-pumping rate within seconds. Thus, maximum activation of up to 20-fold above the resting transport rate may be reached in 10 s, with utilization of all available Na(+),K(+)-pumps. In muscles, where excitability is reduced by pre-exposure to high [K(+)]o, acute activation of the Na(+),K(+)-pumps by hormones or intermittent electrical stimulation restores excitability and contractility. In working muscles, the Na(+),K(+)-pumps, due to rapid activation of their large transport capacity, play a dynamic regulatory role in the from second to second ongoing restoration and maintenance of excitability and force. Excitation is a self-limiting process that depends on the leak/pump ratio for Na(+) and K(+). Acute inhibition of the Na(+),K(+)-pumps with ouabain or downregulation of the Na(+),K(+)-pump capacity clearly reduces contractile endurance in isolated muscles. The Na(+),K(+)-pumps are a limiting factor for contractile force and endurance. This is in particular noted if their capacity is reduced because of inactivity or disease. For these reasons, tight regulation of the Na(+),K(+)-pumps is crucial for the maintenance of plasma K(+), membrane potential and excitability in skeletal muscle. This is achieved by: (1) acute activation of the Na(+),K(+)-pumps elicited by excitation, catecholamines, insulin, insulin-like growth factor I, calcitonins and amylin; and (2) long-term regulation of the content of Na(+),K(+)-pumps exerted by thyroid hormones, adrenal steroids, insulin, training, inactivity, fasting, K(+)-deficiency or K(+)-overload. In conclusion, the Na(+),K(+)-pump is a central target for regulation of Na(+),K(+)-distribution, important for the contractile performance of skeletal ...

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Section: Effects Of Reducing Na + K + -Pump Activity or Capacity On mentioning

confidence: 76%

Section: Effects Of Reducing Na+k+‐pump Activity or Capacity On Contmentioning

confidence: 83%

Role of Na⁺,K⁺‐pumps and transmembrane Na⁺,K⁺‐distribution in muscle function

Clausen

2007

Acta Physiologica

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“…It is possible that particular behavioral and cardiovascular changes induced by sodium depletion may be a result of an electrolyte imbalance. For example, depression has been reported in humans as a symptom of hypokalemia and other electrolyte disturbances (Fletcher & Standen, 1973; Malinow & Lion, 1979). Therefore, to evaluate changes in electrolyte balance, we measured plasma sodium and potassium levels in a separate group of sodium depleted rats and two control groups (Experiment 3).…”

Section: Discussionmentioning

confidence: 99%

Reduced hedonic behavior and altered cardiovascular function induced by mild sodium depletion in rats.

Grippo¹,

Moffitt²,

Beltz³

et al. 2006

Behavioral Neuroscience

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Interactions among sodium homeostasis, fatigue, mood, and cardiovascular regulation have been described previously. The present study investigates the effects of sodium deficiency on an index of mood (hypohedonia; Experiment 1), cardiovascular function (Experiment 2), and plasma electrolytes (Experiment 3) in rats. Following 48 hr of sodium depletion with a diuretic (furosemide) and a sodium deficient diet, rats displayed hypohedonia evidenced by reduced responding for rewarding electrical brain stimulation into the hypothalamus. Also, sodium depletion produced increased heart rate and reduced heart rate variability. Plasma sodium levels were lower in sodium-depleted rats versus control rats, whereas potassium levels were unchanged. Thus, mild sodium depletion produces hypohedonia and cardiovascular alterations, which has implications for understanding behavioral and cardiovascular consequences of sodium deficiency.

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“…Thus, in rats maintained on K ϩ -deficient fodder (plasma K ϩ 1.9 mM), swimming led to exhaustion in only 44 min, whereas the pairfed controls continued swimming for 175 min (31). K ϩ deficiency is associated with fatigue, which is a returning complaint of patients losing K ϩ due to, e.g., the commonly occurring chronic treatment with diuretics (145). Moreover, decreased K ϩ intake is associated with a decline in muscle grip strength in elderly subjects (231).…”

Section: Effects Of Na ؉ -K ؉ Pump Inhibition or Downregulationmentioning

confidence: 99%

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Clausen

2003

Physiological Reviews

505

673

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In skeletal muscle, excitation may cause loss of K+, increased extracellular K+ ([K+]o), intracellular Na+ ([Na+]i), and depolarization. Since these events interfere with excitability, the processes of excitation can be self-limiting. During work, therefore, the impending loss of excitability has to be counterbalanced by prompt restoration of Na+-K+ gradients. Since this is the major function of the Na+-K+ pumps, it is crucial that their activity and capacity are adequate. This is achieved in two ways: 1) by acute activation of the Na+-K+ pumps and 2) by long-term regulation of Na+-K+ pump content or capacity. 1) Depending on frequency of stimulation, excitation may activate up to all of the Na+-K+ pumps available within 10 s, causing up to 22-fold increase in Na+ efflux. Activation of the Na+-K+ pumps by hormones is slower and less pronounced. When muscles are inhibited by high [K+]o or low [Na+]o, acute hormone- or excitation-induced activation of the Na+-K+ pumps can restore excitability and contractile force in 10-20 min. Conversely, inhibition of the Na+-K+ pumps by ouabain leads to progressive loss of contractility and endurance. 2) Na+-K+ pump content is upregulated by training, thyroid hormones, insulin, glucocorticoids, and K+ overload. Downregulation is seen during immobilization, K+ deficiency, hypoxia, heart failure, hypothyroidism, starvation, diabetes, alcoholism, myotonic dystrophy, and McArdle disease. Reduced Na+-K+ pump content leads to loss of contractility and endurance, possibly contributing to the fatigue associated with several of these conditions. Increasing excitation-induced Na+ influx by augmenting the open-time or the content of Na+ channels reduces contractile endurance. Excitability and contractility depend on the ratio between passive Na+-K+ leaks and Na+-K+ pump activity, the passive leaks often playing a dominant role. The Na+-K+ pump is a central target for regulation of Na+-K+ distribution and excitability, essential for second-to-second ongoing maintenance of excitability during work.

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A multi-centre study of potassium deficiency in the elderly

Cited by 3 publications

References 4 publications

Role of Na⁺,K⁺‐pumps and transmembrane Na⁺,K⁺‐distribution in muscle function

Role of Na⁺,K⁺‐pumps and transmembrane Na⁺,K⁺‐distribution in muscle function

Reduced hedonic behavior and altered cardiovascular function induced by mild sodium depletion in rats.

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

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A multi-centre study of potassium deficiency in the elderly

Cited by 3 publications

References 4 publications

Role of Na+,K+‐pumps and transmembrane Na+,K+‐distribution in muscle function

Role of Na+,K+‐pumps and transmembrane Na+,K+‐distribution in muscle function

Reduced hedonic behavior and altered cardiovascular function induced by mild sodium depletion in rats.

Na+-K+Pump Regulation and Skeletal Muscle Contractility

Contact Info

Product

Resources

About

Role of Na⁺,K⁺‐pumps and transmembrane Na⁺,K⁺‐distribution in muscle function

Role of Na⁺,K⁺‐pumps and transmembrane Na⁺,K⁺‐distribution in muscle function

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility