The role of muscle pH as a determinant of sympathetic nervous system (SNS) activity during exercise is not fully understood. Victor et al. (1988) demonstrated that the amount of SNS activity during physical exercise was proportional to the muscle cell pH. However, Vissing (2000) found that muscular acidosis was not a prerequisite for SNS activity in exercise. The aim of the present study was to study the effect of induced alkalosis on the sympatho-adrenal response to high-intensity exercise.

With local ethics committee approval, eight male subjects (age 19 ± 1 years (mean ± S.D.), body mass 69.2 ± 9.7 kg, body fat 10.2 ± 2.7 % andV_O2,max 43 ± 5 ml kg^-1 min^-1) attended the laboratory on three occasions following preliminary testing. On each occasion subjects were given one of three solutions in a randomised order: placebo (0.3 g (kg body mass)^-1 of CaCO₃ + 1 g NaCl, A) or 0.3 g kg^-1 (B), or 0.5 g (kg body mass)^-1 (C) of tri-sodium citrate (C₆H₅Na₃O₇,) in 500 ml of water. One hour following ingestion subjects performed a test on an electromagnetically braked cycle ergometer at a workload calculated to elicit 110 % ofV_O2,max for 2 min. Blood samples (11 ml) taken from an antecubital vein were first used to determine pH and blood base excess (BBE) then, after the addition of EGTA and glutathione, the remaining blood was centrifuged and analysed for plasma catecholamines by HPLC with electrochemical detection (Davies et al. 1981). Data were analysed using one-way and repeated measures ANOVA with post-hoc testing where appropriate. Significance was established at the P < 0.05 level.

Blood pH and BBE were significantly increased following ingestion of C (P < 0.05) but not B when compared with A (pH 7.39 ± 0.03 A, 7.40 ± 0.03 B, and 7.42 ± 0.02 C; BBE 2.9 ± 2.9 A, 6.4 ± 1.3 B, and 6.5 ± 0.9 mmol l^-1 C). All trials demonstrated a significant decrease in pH and BBE immediately, 5, 10 and 15 min post-exercise. However, the blood pH and BBE at all time points post-exercise in conditions B and C were significantly greater than condition A. There were significant increases in plasma noradrenaline (NA) and adrenaline (AD) concentrations immediately (NA 4.6 ± 2.1 A, 4.2 ± 1.8 B, and 4.6 ± 2.2 nmol l^-1 C; AD 0.6 ± 0.3 A, 0.5 ± 0.2 B, and 0.5 ± 0.3 nmol l^-1 C) and 5 min post-exercise (NA 2.1 ± 0.6 A, 2.1 ± 0.6 B, and 2.2 ± 0.6 nmol l^-1 C; AD 0.2 ± 0.1 A, 0.2 ± 0.1 B, and 0.2 ± 0.1 nmol l^-1 C, P < 0.05) but there was no change in the plasma dopamine (DA) concentration. No significant differences in plasma NA, AD and DA concentrations were found between trials at any time.

The results of this investigation demonstrate that although significant alkalosis was induced following sodium citrate ingestion, no effect was observed on antecubital vein plasma catecholamine responses to high-intensity exercise. This suggests that alterations in alkalosis may not be important for sympatho-adrenal activity in exercise.