Endurance training alters basal erythrocyte MCT-1 contents and affects the lactate distribution between plasma and red blood cells in T2DM men following maximal exercise.

Chronic elevated lactate levels are associated with insulin resistance in patients with type 2 diabetes mellitus (T2DM). Furthermore, lactacidosis plays a role in limiting physical performance. Erythrocytes, which take up lactate via monocarboxylate transporter (MCT) proteins, may help transport lactate within the blood from lactate-producing to lactate-consuming organs.

Strength training alters MCT1-protein expression and exercise-induced translocation in erythrocytes of men with non-insulin-dependent type-2 diabetes.

We investigated the cellular distribution of lactate transporter (MCT1) and its chaperone CD147 (using immunohistochemistry and fluorescence-activated cell sorting) in the erythrocytes of men with non-insulin-dependent type-2 diabetes (NIDDM, n = 11, 61 ± 8 years of age) under acute exercise (ergometer cycling test, World Health Organisation scheme) performed before and after a 3-month strength training program. Cytosolic MCT1 distribution and membraneous CD147 density did not change after acute exercise (ergometer). After the 3-month strength training, MCT1-density was increased and the reaction of MCT1 (but not that of CD147) towards acute exercise (ergometer) was altered.

Training increases peroxiredoxin 2 contents in the erythrocytes of overweight/obese men suffering from type 2 diabetes.

Type 2 diabetes mellitus (T2DM) is associated with an increased release of free radicals which play an important role in the manifestation of diabetes and in the progression of diabetic complications. Peroxiredoxins are thought to be essential components of the erythrocyte antioxidative defense. Therefore, we compared peroxiredoxin isoform contents (PRDX1-6 immuno-histochemial stainings) in the erythrocytes of overweight/obese T2DM men (n = 6) and of BMI-matched non-diabetic male control subjects (n = 6).