SLC41A1, a Na+/Mg2+ exchanger, is downregulated during exercise.

Serum magnesium (Mg) levels are closely controlled through a variety of Mg transporters and ionic channels during physiological conditions. These levels have been shown to increase during exercise. However, the effect of Mg transporter expression during exercise remains to be determined. The purpose of this study was to examine the gene expression of SLC41A1, a Na+/Mg2+ exchanger, during exercise. In the present study, male C57BL/6JNarl mice (n=16, 8 weeks old) were subjected to 3 h forced exercise on a treadmill. The mice in the control and Mg groups were injected with saline and Mg (MgSO4, 90 mg/kg, intraperitoneal), respectively. Blood samples were obtained at three time points: prior to, following and 24 h after exercise. The gene expression levels of SLC41A1 were significantly downregulated to 23.6±4.6 and 12.6±10.2% following exercise in the control and Mg groups, respectively. The expression levels returned to the basal levels 24 h after exercise in the two groups and there was no significant difference found between the two groups. The downregulated role of SLC41A1 expression and its interaction with the Mg status in exercise requires further investigation.

Effects of magnesium sulfate on dynamic changes of brain glucose and its metabolites during a short-term forced swimming in gerbils.

This investigation examined the acute effects of magnesium on the dynamic changes of brain glucose, lactate, pyruvate and magnesium levels in conscious gerbils during forced swimming. Gerbils were pretreated with saline (control group) and magnesium sulfate (90 mg kg(-1), intraperitoneal injection) before a 15 min forced swimming period. The basal levels of glucose, pyruvate, lactate, and magnesium in brain dialysates were 338 +/- 18, 21 +/- 2, 450 +/- 39, and 2.1 +/- 0.1 microM, respectively, with no significant difference between groups. Magnesium levels were found slightly higher (but not significant) in the magnesium-treated group. However, brain glucose and pyruvate levels in the control group decreased to about 50 and 60% of the basal level (P = 0.01) after swimming, respectively. Pretreatment with magnesium sulfate immediately increased glucose levels to about 140% of the basal level, and increased pyruvate levels to about 150% of the basal level during forced swimming (P = 0.01). Both glucose and pyruvate levels returned to the basal level after 30 min of the recovery. The lactate levels of the control group increased to about 160% of the basal level (P = 0.01) during swimming, whereas pretreatment with magnesium sulfate attenuated lactate levels to 130% of the basal level (P = 0.01). Magnesium supplementation may be beneficial because it provides an additional glucose source and may also promote the recovery of energy substrates in the brain during and after forced exercise. In order to achieve optimal physical performance, further investigation as to dosage of magnesium supplementation is needed.