Sodium is the major cation of the extracellular fluid. A reduction in the extracellular sodium concentration will result in a fluid shift into intracellular space, which can lead to cellular swelling and its associated complication (12). It is overall eight to 10 times more concentrated in the extracellular than in the intracellular space. The sodium concentration gradient across the cellular membrance and the transmembrance sodium fluxes are regulated by the sodium-potassium pump, which plays an important role in cellular processes (2). Several hyponatremia (sodium
Alteration in total sodium content and in transmembrance sodium flux rates occurs in numerous normal and disease conditions, including exercise muscle (2).
Hyponatremia develops when both sodium and fluid are lose in sweat, the loss of 120 mmol of sodium and 1 L of fluid from the Extracellular Fluid (ECF), corresponding to a fluid loss of 3 L from the total body water, will cause the serum sodium concentration to ruse to 141 mmol [L.sup.-1] (10). If the ECF volume decreases by 1.5 L rather than 1 L, the serum concentration will raise to 146 m mol [l.sup.-1] (10). The historic data prove that dehydration and unreplaced sodium losses during prolonged exercise cause hyponatremia (10).
On the other hand, potassium, the major cation of the intracellular fluid, is released from muscle cells during exercise in direct relation to exercise intensity (3), (12). A rise in potassium (hyperkalaemia) is rapidly reversed after rest from exercise and many even associated with a lowering of potassium levels to below control levels (hyperkalaemia) (12). The resultant of hyperkalaemia may also be due to increased blood flow to the skeletal muscles and/or increased intracellular acidos (12). Barlow et al., showed that the exercise-induced rise in potassium and ventilation are greater at matched sub maximal work rate in subjects with normal left ventricular function (1). Another study showed that the exercise-induced rise in potassium at matched sub maximal work rate tended to be greater in severe chronic heart failure, but it did not reach statistical significance (13). The [DELTA][k.sup.+] from rest to peak exercise was correlated with peak [vo.sub.2]. The amount of potassium related into the circulation from the muscle is dependent on the magnitude of muscle contraction, as reflected by absolute workload (11).
The observation suggested that accumulation of extracellular potassium might be important for the development of fatigue in human muscle (5), (11).
Mc kenna et al. found that the femoral arterial venous potassium difference. During intense cycle exercise was the same before and after training, suggesting that release of potassium to the blood stream was not changed by the training (7).
In another research, observed that 8 weeks of one-legged endurance training (2h) reduced potassium release during exercise. Furthermore, the rise in plasma potassium in dogs induced by exercise was lower in dogs that...