1. Exercise seems to change the extracellular potassium concentration far beyond the narrow limits seen in resting subjects. To examine alterations in plasma potassium concentration during exercise, twenty healthy, well-trained men ran on the treadmill at 6 deg inclination with catheters inserted in the femoral vein and artery. 2. During 1 min exhausting exercise plasma potassium concentration rose in parallel in the vein and artery, reaching peak post-exercise values of 8.34 +/- 0.23 mmol l-1 and 8.17 +/- 0.29 mmol l-1. After 3 min recovery the potassium concentration was 0.50 +/- 0.05 mmol l-1 below pre-exercise values. Both the rise of plasma potassium concentration during exercise and the decline during recovery followed exponential time courses with a half-time of 25 s. 3. Exercise at reduced intensity showed that the peak post-exercise potassium concentration was linearly related to the exercise intensity. Individual resting, peak and nadir values were proportionally related. 4. The increased potassium concentration during exercise can be explained in full by the electrical activity in the exercising muscles. Repeated 1 min exhausting exercise bouts revealed no relationship between potassium concentration and plasma pH nor glycogen break-down. 5. All of the observations fit a simple model of potassium efflux from active muscle and elimination from blood with the following characteristics: the efflux increases (decreases) stepwise at the onset (end) of exercise, and the efflux rate during exercise increases with exercise intensity. Potassium is eliminated from blood by a proportional regulator which may be the Na(+)-K+ pump of the exercising muscle. Extracellular potassium is indirectly linked to the pump stimulus, and the rate of reuptake is proportional to the extracellular accumulation. Thus no limited maximal power for potassium uptake was found. The post-exercise undershoot of 0.5 mmol l-1 can be explained by a higher gain of the pump after exercise. 6. The large, rapid changes in the plasma potassium concentration during and after exercise is due to the first order kinetics of the reuptake mechanism rather than to a limited power to take up potassium.

Plasma potassium changes with high intensity exercise.

Studies performed at the beginning of the last century revealed the importance of carbohydrate as a fuel during exercise, and the importance of muscle glycogen on performance has subsequently been confirmed in numerous studies. However, the link between glycogen depletion and impaired muscle function during fatigue is not well understood and a direct cause-and-effect relationship between glycogen and muscle function remains to be established. The use of electron microscopy has revealed that glycogen is not homogeneously distributed in skeletal muscle fibres, but rather localized in distinct pools. Furthermore, each glycogen granule has its own metabolic machinery with glycolytic enzymes and regulating proteins. One pool of such glycogenolytic complexes is localized within the myofibrils in close contact with key proteins involved in the excitation-contraction coupling and Ca2+ release from the sarcoplasmic reticulum (SR). We and others have provided experimental evidence in favour of a direct role of decreased glycogen, localized within the myofibrils, for the reduction in SR Ca2+ release during fatigue. This is consistent with compartmentalized energy turnover and distinctly localized glycogen pools being of key importance for SR Ca2+ release and thereby affecting muscle contractility and fatigability.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2013.251629

Muscle glycogen stores and fatigue

The Na-K-ATPase, which maintains the Na+ and K+ gradients across the plasma membrane, can play a major role in modulation of skeletal muscle contractility. Although both α1- and α2-isoforms of the ...

The α1- and α2-isoforms of Na-K-ATPase play different roles in skeletal muscle contractility

K contractures and asymmetrical charge movement were recorded in extensor digitorum longus (e.d.l.) and soleus muscles that had been denervated for 2-68 days. The relationship between maximum tension during a K contracture and membrane potential shifted to more negative potentials in denervated e.d.l. muscles (by -25 mV on average) and to a lesser extent in soleus (by -8 mV on average), and became steeper, more so in e.d.l. than soleus. Apart from an early negative shift of -11 mV in the voltage dependence of tension in e.d.l. muscles during the first week, the other changes in K contractures following denervation occurred progressively during the first 3 weeks and then stabilized. There was a clear difference in charge movement in denervated e.d.l. fibres but little change in denervated soleus fibres, so that the characteristics of charge movement in e.d.l. and soleus became very similar. The maximum amount of charge movement fell from an average normal value of 23 nC/microF to 6 nC/microF in e.d.l. within the first 2 weeks. The voltage sensitivity shifted to more negative potentials (by about -12 mV on average) within the first week. There was no significant change in the slope of the relationship between charge and membrane potential. The effects of denervation on charge movement could only partly explain the changes in K contractures. The only obvious parallels were the early negative shift in the voltage dependence of charge movement and tension in denervated e.d.l. fibres. The other changes in K contractures in denervated fibres could be due to a change in the relationship between charge movement and Ca concentration in the myoplasm or an increase in the Ca affinity of the myofilaments. Although charge movement fell to about a quarter of normal in denervated e.d.l. fibres, membrane capacity increased approximately 3-fold. A similar increase in capacity in soleus fibres was not associated with a change in charge movement. Fewer indentations were seen in denervated than in normal e.d.l. fibres. The decrease paralleled the fall in charge movement.

Excitation‐contraction coupling and charge movement in denervated rat extensor digitorum longus and soleus muscles.

The voltage-activation of contraction in skeletal muscle.

Membrane capacity was measured as a function of fibre diameter in mammalian skeletal muscle fibres under normal conditions and under conditions designed to reduce the membrane chloride conductance, i.e. in solutions in which choride ions were replaced by sulphate or methylsulphate ions, or in normal Krebs solutions containing 2,4-dichlorophenoxyacetic acid (2.5mm). The experiments were done on rat sternomastoid, extensor digitorum longus and soleus muscle fibres. The average membrane capacity of fibres in each muscle was greater than normal when chloride conductance was reduced and the slope of the relationship between membrane capacity and fibre diameter increased. The results were consistent with the hypothesis that the space constant of the transverse tubule system in mammalian fibres is normally short because the transverse tubule membrane has a high chloride conductance. The experimental results imply that the space constant of the transverse tubule system was less than 40 µm for fibres in normal Krebs solution and greater than 100 µm for fibres with low membrane chloride conductance. The space constant was calculated using measured geometrical parameters of the transverse tubule, and measured membrane conductance, and the values were close to 20 µm for fibres in normal Krebs solution and between 50 and 120 µm for fibres with low chloride conductance.

Grant Carter

Papers

The membrane capacity of mammalian skeletal muscle fibres