T Kreutz

Training alters the skeletal muscle antioxidative capacity in non‐insulin‐dependent type 2 diabetic men

The present study analyzes the oxidative stress situation in the skeletal muscle of overweight/obese men suffering from non‐insulin‐dependent type 2 diabetes mellitus [T2DM, n=16, years=61±7, body mass index (BMI)=31±4 kg/m2] and BMI‐matched non‐diabetic male control subjects (CON, n=7, years=53±6, BMI=30±4 kg/m2). Furthermore, it investigates whether physical training can alter the skeletal muscle antioxidative capacity of T2DM patients at rest. Molecule content analyses (immunohistochemical stainings) of 8‐iso‐prostaglandin‐F2α (8‐Iso‐PGF), superoxide dismutase‐2 (SOD2), glutathione peroxidase‐1 (GPX1), peroxiredoxin isoforms (PRDX 1–6) and heat‐shock‐protein‐70 (HSP70) were performed in biopsies taken from the vastus lateralis muscle. Under basal conditions, 8‐Iso‐PGF was significantly decreased in T2DM patients (−35.7%), whereas PRDX2 and PRDX6 were significantly increased relative to CON (+82.6%; +82.3%). Differences were neither observed in SOD2 nor in GPX1 or PRDX1, 3, 4, 5 density. Regular physical activity (moderate endurance or resistance training twice a week for 3 months) did not alter PRDX1, 2, 3, 4, 6 in the skeletal muscle of T2DM patients, but significantly increased SOD2 (+65.9%), GPX1 (+62.4%), PRDX5 (+37.5%), and HSP70 (+48.5%). Overweight/obese men with non‐insulin‐dependent T2DM exhibit up‐regulated cytosolic peroxiredoxin contents relative to BMI‐matched controls. Regular training further up‐regulates cytosolic and mitochondrial antioxidative enzymes in T2DM patients and improves their cellular protection systems. This may contribute to a retardation of the diseases progression.

Endurance exercise alters cellular immune status and resistin concentrations in men suffering from non-insulin-dependent type 2 diabetes.

It has been demonstrated that alterations of adipocytokines can alter immune status in type 2 diabetes. The present study investigated changes of adipocytokine plasma concentrations and cellular immune status in overweight men, suffering from non-insulin dependent type 2 diabetes (n=14, age 61.0±8.7 years, BMI 31.1±3.5 kg/cm2). Subjects underwent a 3 months endurance exercise intervention (twice per week for up to 45 min) cycling at a heart rate corresponding to a 2 mmol/l lactate threshold. Before and after the intervention testing for adipocytokines (leptin, adiponectin, resistin) and cellular immune status (including T memory-cells and regulative T-cells) was performed by RIA and FACS accordingly.The exercise intervention improved anthropometric and metabolic parameters of all subjects. We observed a significant decline for resistin and for the CD19+ B-cells. The CD4+CD25+CD127low Treg-cells decreased, however not statistically significant. All other parameters remained unchanged.In conclusion, even though only training twice a week, the exercise affected parts of the cellular immune system as well as resistin levels in men suffering from non-insulin dependent type 2 diabetes.

The influence of resistance training on patients with metabolic syndrome--significance of changes in muscle fiber size and muscle fiber distribution.

Geisler, S, Brinkmann, C, Schiffer, T, Kreutz, T, Bloch, W, and Brixius, K. The influence of resistance training on patients with metabolic syndrome-Significance of changes in muscle fiber size and muscle fiber distribution. J Strength Cond Res 25(9): 2598-2604, 2011—People who are afflicted with “metabolic syndrome” exhibit multiple coronary disease risk factors such as insulin resistance, hypertension, hyperlipidemia, or obesity. Twenty-six volunteers (13 women and 13 men) with such disease risk factors (56 ± 5 years) participated in a 14-week resistance training program. Given the fact that resistance training may improve cardiometabolic parameters, the fasting total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides, insulin, glucose value, homeostatic model assessment (HOMA) index, and blood pressure and body mass index (BMI) were measured before and after the training intervention. In addition, muscle biopsies from the vastus lateralis muscle of 11 of the men and 5 of the women were analyzed to determine whether changes in the muscle morphology influence the cardiometabolic parameters. Resistance training resulted in a significant increase in fasting HDL for the entire group (from 44.35 ± 9.43 to 48.57 ± 10.96 mg·dl−1, p = 0.016). No other blood parameter changed significantly. No change was observed in the HOMA index, blood pressure, or BMI. The muscle fiber type distribution did not change, but a significant hypertrophy of muscle fibers was evident (an increase of the ellipse minor axis of 67.3 ± 16.6 to 72.1 ± 12.3 μm, p = 0.004). Moderate intensity resistance training, as was performed in our study, induces hypertrophic impulses but does not seem to have a clear positive influence on cardiometabolic risk factors. However, 2 sessions of moderate intensity resistance training per week can enhance the fasting HDL cholesterol in middle-aged subjects.

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

ZusammenfassungTyp-2-Diabetes mellitus (T2DM) ist mit einem erhöhten Aufkommen freier Radikale assoziiert, die eine entscheidende Rolle in der Manifestation des Diabetes und in der Progression diabetischer Komplikationen spielen. Peroxiredoxine sind bedeutsame Komponenten der erythrozytären antioxidativen Abwehr. Daher verglichen wir die Gehalte an Peroxiredoxin-Isoformen (PRDX1-6 immunohistochemische Färbungen) in den Erythrozyten von übergewichtigen/adipösen T2DM-Männern (n = 6) und von BMI-ähnlichen nicht-diabetischen männlichen Kontrollpersonen (n = 6). Nur die erythrozytären Proteine PRDX1 und PRDX2 konnten immunohistochemisch detektiert werden. PRDX1 war signifikant erhöht bei T2DM-Männern im Vergleich zu den Kontrollpersonen (+95,9 %, P ≤ 0,05). Desweiteren haben wir den Einfluss eines 3-monatigen Ausdauer-Trainingsprogrammes (3mal wöchentlich, Fahrradfahren bei 75 % der maximalen Herzfrequenz) auf die Gehalte an PRDX1 und PRDX2 in den Erythrozyten übergewichtiger/adipöser T2DM-Männer (n = 11) untersucht. Das Training erhöhte basales PRDX2 signifikant (+96 %, P ≤ 0,05). Die Hochregulierung des Peroxiredoxin-Systems könnte dabei helfen, freie Radikale in den Erythrozyten von T2DM-Patienten zu puffern.SummaryType 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 immunohistochemial stainings) in the erythrocytes of overweight/obese T2DM men (n = 6) and of BMI-matched non-diabetic male control subjects (n = 6). Only erythrocyte PRDX1 and PRDX2 proteins were detectable using immunohistochemical methods. PRDX1 was significantly increased in T2DM men relative to control subjects (+95.9%, P ≤ 0.05). Furthermore, we studied the influence of a 3-month endurance training program (3 times a week, cycling at 75% maximal heart rate) on erythrocyte PRDX1 and PRDX2 contents in overweight/obese T2DM men (n = 11). Training significantly increased PRDX2 at rest (+96%, P ≤ 0.05). The up-regulation of the peroxiredoxin system may help counteract free radicals in the erythrocytes of T2DM patients.

Corrigendum: Training-induced alterations of skeletal muscle mitochondrial biogenesis proteins in non-insulin-dependent type 2 diabetic men.

This study investigates whether regular physical activity (moderate endurance or resistance training twice a week for 3 months) influences the key regulatory molecules of mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α), nuclear respiratory factor-1 (NRF1), and mitochondrial transcription factor A (TFAM)) in patients suffering from non-insulin-dependent type 2 diabetes mellitus (T2DM) (n = 16, years = 62 ± 7, body mass index (BMI) = 30 ± 4 kg/m(2)). Seven T2DM men took part in endurance training, and 9 men participated in resistance training. BMI-matched non-diabetic male control subjects (CON) (n = 7, years = 53 ± 6, BMI = 30 ± 4 kg/m(2)) were studied for comparison. The protein contents of PGC1α, NRF1, and TFAM were determined using immunohistochemical staining methods on biopsies taken from the musculus vastus lateralis. At baseline, no differences were observed in NRF1-density between the T2DM men and the CON, while the contents of PGC1α and TFAM were decreased in the T2DM men. PGC1α and TFAM contents were not changed in the T2DM patients after the training period, but NRF1 was decreased. The down-regulation of mitochondrial signaling molecules might explain the patho-physiological reduction in mitochondrial biogenesis found in T2DM. Physical training, as performed in our study, did not reverse the down-regulation of mitochondrial signaling molecules--at least not after 3 months. [corrected].

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. MCT1 localisation was shifted from the centre to the cellular membrane. This resulted in a decrease in the immunohistochemically measured cytosolic MCT1-density. We conclude that strength training alters the acute exercise reaction of MCT1 but not that of CD147 in erythrocytes in patients with NIDDM. This reaction may contribute to long-term normalisation and stabilisation of the regulation of lactate plasma concentration in NIDDM.