Disorders in Magnesium Balance Decrease Erythrocyte Deformability in Athletes

Abstract

Intense sports activity, especially in a warm climate, can cause Mg deficiency because of an imbalance between Mg consumption and its loss with urine and sweat [1,2]. Moreover, strenuous exercises can result in stress and overtraining [3], which disturb the Mg balance of the body [4]. A disturbance in the Mg balance influences various structures and functions of the body and leads to a decrease in physical working capacity [1]. However, the association between the Mg status and blood rheology in athletes is not clear.We have associated an increase in serum Mg with a decrease in the erythrocyte deformability (ED) in athletes [5]. This finding contradicts literature data on the favorable effect of Mg on ED [6,7]. It has been reported that Mg has a direct antioxidant effect on blood cells [8] and promotes accumulation of energyrich compounds in erythrocytes by affecting glycolysis (the phosphofructokinase activity and glucose phosphorylation) and glucose utilization [9]. Moreover, Mg is involved in maintaining a high level of cell hydration through inhibition of the K/Cl cotransport and activation of Na/K/Cl cotransport and Na/K ATPase [10,11]. Magnesium is also an antagonist of Ca and an activator of Ca ATPase [12]. The above effects of Mg can markedly influence the erythrocyte microrheology.Therefore, the present work was designed to study the relationship between Mg balance and erythrocyte rheology in athletes. METHODSThe study was performed with the participation of 45 highly qualified male athletes (masters and candidates of sport) training in different sports: track and field athletics, ski racing, wrestling, and weight lifting.Blood samples were taken in the morning (between 7:30 and 8:30 a.m.) on an empty stomach 24-36 h after a training session. Blood viscosity (BV), plasma viscosity (PV), and erythrocyte suspension viscosity at a hematocrit of 45% (ESV 45 ) were determined at τ = 0.5 Pa with a capillary viscometer ( t = 37 ± 0.5° C). The erythrocyte aggregation index was determined as described in [13]. Erythrocytes were washed twice, and a suspension of them with a hematocrit of 45% was combined with autologous plasma in the proportion 1 : 202. Nonaggregated erythrocytes were counted in a Goryaev chamber. Knowing the total erythrocyte concentration in the suspension, we calculated the percent of aggregated erythrocytes.Serum total protein was determined by the biuret reaction, serum protein fractions were assayed by paper electrophoresis, and fibrinogen was quantitated by Rutberg's technique. Serum total cholesterol (Ch), high density lipoprotein (HDL) Ch, and triglycerides (TG) were determined enzymatically. Reagent kits (Cormay, Poland) and a Shimadzu CL-770 spectrophotometer (Japan) were used. The acid resistance of erythrocytes to 0.002 N HCl was determined as described in [14]. The total working capacity was inferred from PWC 170 (a Ritm-5 bicycle ergometer).Serum Mg was determined spectrophotometrically with standard Lachema kits (Czech Republic), and Na was determined using ion-selective electrodes...