Sprint training enhances ionic regulation during intense exercise in men
Authors: McKenna Michael J. , Heigenhauser George J. F. , McKelvie Robert S. , MacDougall J. Duncan , Jones Norman L. 
Published: September 2004

This study investigated the effects of 7 weeks of sprint training on changes in electrolyte concentrations and acid‐base status in arterial and femoral venous blood, during and following maximal exercise for 30 s on an isokinetic cycle ergometer.

Six healthy males performed maximal exercise, before and after training. Blood samples were drawn simultaneously from brachial arterial and femoral venous catheters, at rest, during the final 10 s of exercise and during 10 min of recovery, and analysed for whole blood and plasma ions and acid‐base variables.

Maximal exercise performance was enhanced after training, with a 13% increase in total work output and a 14% less decline in power output during maximal cycling.

The acute changes in plasma volume, ions and acid‐base variables during maximal exercise were similar to previous observations. Sprint training did not influence the decline in plasma volume during or following maximal exercise. After training, maximal exercise was accompanied by lower arterial and femoral venous plasma [K+] and [Na+] across all measurement times (P < 0.05). Arterial plasma lactate concentration ([Lac−]) was greater (P < 0.05), but femoral venous plasma [Lac−] was unchanged by training.

Net release into, or uptake of ions from plasma passing through the exercising muscle was assessed by arteriovenous concentration differences, corrected for fluid movements. K+ release into plasma during exercise, and a small net K+ uptake from plasma 1 min post‐exercise (P < 0.05), were unchanged by training. A net Na+ loss from plasma during exercise (P < 0.05) tended to be reduced after training (P < 0.06). Release of Lac− into plasma during and after exercise (P < 0.05) was unchanged by training.

Arterial and venous plasma strong ion difference ([SID]; [SID] =[Na+]+[K+]–[Lac−]–[Cl−]) were lower after training (mean differences) by 2.7 and 1.8 mmol l−1, respectively (P < 0.05). Arterial and femoral venous C02 tensions and arterial plasma [HCO3−] were lower after training (mean differences) by 1.7mmHg, 4.5mmHg and 1.2mmol l−1, respectively (P < 0.05), with arterial plasma [H+] being greater after training by 2.2 nmol 1−1 (P < 0.05).

The acute changes in whole blood volume and ion concentrations during maximal exercise were similar to previous observations. Arterial and femoral whole blood [K+] and [Cl−] were increased, whilst [Na+] was lower, across all observation times after training (P < 0.05).

Net uptake or release of ions by exercising muscle was assessed by arteriovenous whole blood concentration differences, corrected for fluid movements. A net K+ uptake by muscle occurred at all times, including exercise, but this was not significantly different after training. An increased net Na+uptake by muscle occurred during exercise (P < 0.05) with greater Na+ uptake after training (P < 0.05). Net muscle Lac− release and Cl− uptake occurred at all times (P < 0.05) and were unchanged by training.

Sprint training improved muscle ion regulation, associated with increased intense exercise performance, at the expense of a greater systemic acidosis. Increased muscle Na+ and K+ uptake by muscle during the final seconds of exercise after training are consistent with a greater activation of the muscle Na+‐K+ pump, reduced cellular K+ loss and the observed lesser rate of fatigue. The greater plasma acidosis found after sprint training was caused by a lower arterial plasma [SID] due to lower plasma [K+] and [Na+], and higher plasma [Lac−].