Question

Why would elevated extracellular K+ decrease force output from a muscle?

Answer 1

Extracellular [K] is regulated closely to maintain normal membrane excitability by the concerted regulatory responses of muscle and kidney. Although kidney is responsible for ultimately matching K output to K intake each day, muscle contains more than 90% of the body’s K and can buffer changes in extracellular fluid [K] by either acutely taking up extracellular fluid K or releasing intracellular fluid K from muscle.

It long has been assumed that the changes in muscle K transport are a function of sodium pump (Na,K-adenosine triphosphatase [Na, K-ATPasel]) abundance, especially that of the 2 isoform, which predominates in skeletal muscle. Potassium transport between the ECF and ICF is mediated by an array of transporters including P-type ATPases, cotransporters, and channels.  Plasma membrane sodium pumps (Na,K-ATPase) actively transport K from ECF into the cell and the renal hydrogen potassium pumps (H,K-ATPase) expressed during K-deficient states actively reabsorb K from the renal tubular fluid back into the ECF.

Depending on the intensity of muscle contraction, the net flux of water from the plasma compartment into contracting muscles can account for up to 50% of the increase in plasma [K]. This water flux is very rapid at the onset of exercise and is nearly complete within the first 5 min of cycling exercise at 85% of peak VO2. The water flux is due to the rapid accumulation of osmotically active metabolites such as inorganic phosphate, creatine and lactate resulting from phosphocreatine hydrolysis and activation of glycolysis at the onset of exercise. As exercise continues and osmolytes accumulate in the interstitium there is an increase in muscle extracellular fluid volume that persists until after exercise has stopped . A potential beneficial effect of K ÷ efflux may be to counteract the osmotic flux of water into the cells at the onset of contraction.

The phase, characterized by a slowly decreasing plasma [K +] during exercise of low to moderate intensity, indicates that the net rate of K + uptake by all tissues in the body exceeds the net rate of K + release from contracting muscle. There is evidence, obtained during submaximal cycling exercise, that the increase in Na+,K+-AT - Pase activity in contracting skeletal muscle may be sufficient to cause a net uptake of K + by contracting muscle during the period of exercise. This may account for at least some of the early observations that muscles sampled at the end of prolonged submaximal exercise have shown little or no decrease in K + content.

The phase which is characterized by a slowing rate of rise and peaking of plasma [K+]: This is primarily due to the very rapid activation of Na,K ATPase and active transport of interstitial K + back into contracting muscle. There is also an increased rate of K + uptake by non-contracting tissues and a slowing of the net flux of water from the plasma compartment. Thus the inward rate of K + transport approaches that of net K + release. The rationale for a primary role by contracting skeletal muscle for attenuating the increase in plasma [K +] is that these tissues have a markedly elevated Na+,K+-ATPase activity and the capacity for restoring K + lost through repeated contraction and relaxation cycles. Substantial activation of Na+,K+-ATPase may occur within 10 s following stimulation of the muscle and that maximal in vivo rates in humans may be achieved within 30s after the onset of supramaximal intensity exercise.

The K + uptake during exercise can be estimated from the ateriovenous plasma [K +] difference and plasma flow in the initial seconds after cessation of exercise.