Antioxidant Activity of NADH and Its Analogue - An In Vitro Study

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Effects of Diet and Exercise on Endocrine Function of Skeletal Muscle

Skeletal muscle has been recognized as an endocrine tissue that releases appreciable amounts of circulating proteins, called myokines. Currently, we know that the skeletal muscles synthesize several hundreds of peptides classified as myokines, and muscle contraction stimulates their release [1,2]. Myokines can act in autocrine, paracrine or endocrine mode and there is an increasing number of data showing that they can affect different organs and tissues, e.g., the brain, bones, adipocyte tissue, heart artery, and many others [3]. For instance, the interleukins IL-6 and IL-10, released by the muscles during exercise, exert powerful local and systemic anti-inflammatory effects. Furthermore, IL-10 has been shown to provide cardio-and neuroprotection, which is mediated by the activation of anti-apoptotic protein kinase B (PKB or Akt) [4,5]. In addition, myokines like SPARC and oncostatin M show inhibitory activity against colon and breast cancer cells, respectively. Skeletal muscles represent the largest organ of the human body (the muscles constitute approximately 40% of total body mass), thus their role in the regulation of metabolic processes via myokines appears to be very important. Unfortunately, there is a limited amount of data demonstrating the effects of nutraceuticals on exercise-induced release of myokines. It has been shown that release of IL-6 from skeletal muscle was inhibited in persons supplemented with vitamin C and E. We hypothesize that natural compounds may exert their protective activity against some human diseases by modulating myokine synthesis

The Effect of Vitamin D3 Supplementation on Physical Capacity among Active College-Aged Males

Vitamin D3 supplementation can affect strength and power; however, the effect on both aerobic and anaerobic performance remains unclear. Here, we investigate the effects of eight weeks of a high dose of vitamin D3 supplementation and its impact on circulating 25-hydroxyvitamin D (25-OH-D3) concentrations and selected indicators of physical capacity. Subjects (n = 28, age 21.1 ± 1.6) were divided into two groups: supplemented (SUP), which was given 6000 IU of vitamin D3 daily for eight weeks; and placebo group (PLA). Serum 25-OH-D3 concentrations were determined in pre- and post-intervention. Aerobic ( V . O2max test) and anaerobic (Wingate Anaerobic Test) capacity were determined before and after the supplementation. The mean baseline concentration of 25-OH-D3 was recognized as deficient (20 ng/mL) and significantly increased over time in the supplemented group (p < 0.01, η2 = 0.86), whilst it remained unchanged in the placebo group. Moreover, the supplementation caused a significant improvement in maximal aerobic (p < 0.05, η2 = 0.27) and anaerobic power (p < 0.01, η2 = 0.51) whereas no changes were observed in PLA group. The V . O2max differences were also significant in the supplemented group (p < 0.05). In summary, the changes in aerobic and anaerobic capacity observed in this study were associated with a serum concentration of 25-OH-D3. Our data imply that vitamin D3 supplementation with a dose of 6000 IU daily for eight weeks is sufficient to improve physical capacity and vitamin D3 status

Iron Status in Elderly Women Impacts Myostatin, Adiponectin and Osteocalcin Levels Induced by Nordic Walking Training

Impaired iron metabolism is associated with increased risk of many morbidities. Exercise was shown to have a beneficial role; however, the mechanism is not well understood. The purpose of this study was to assess the relationship between exerkines and iron metabolism in elderly women before and after 12 weeks of Nordic Walking (NW) training. Exerkines like myostatin, adiponectin, and osteocalcin have been shown to have several positive effects on metabolism. Thirty-six post-menopausal women (66 ± 5 years old, mean ± SD) were randomly assigned to a NW intervention group (n = 18; body mass, 68.8 ± 11.37 kg; fat, 23.43 ± 7.5 kg; free fat mass, 45.37 ± 5.92 kg) or a control group (n = 18; body mass, 68.34 ± 11.81 kg; fat, 23.61 ± 10.03 kg; free fat mass, 44.73 ± 3.9 kg). The training was performed three times a week for 12 weeks, with the intensity adjusted to 70% of the individual maximum ability. Before and one day after the 12-weeks intervention, performance indices were assessed using a senior fitness test. Blood samples (5 mL) were obtained from the participants between 7 and 8 AM, following an overnight fast, at baseline and one day immediately after the 12-week training program. A significant and large time × group interaction was observed for iron (NW: 98.6 ± 26.68 to 76.1 ± 15.31; CON: 100.6 ± 25.37 to 99.1 ± 27.2; p = 0.01; η p 2 = 0.21), myostatin (NW: 4.42 ± 1.97 to 3.83 ± 1.52; CON: 4.11 ± 0.95 to 4.84 ± 1.19; p = 0.00; η p 2 = 0.62), adiponectin (NW: 12.0 ± 9.46 to 14.6 ± 10.64; CON: 12.8 ± 8.99 to 11.9 ± 8.53; p = 0.00; η p 2 = 0.58), and osteocalcin (NW: 38.9 ± 26.04 to 41.6 ± 25.09; CON: 37.1 ± 33.2 to 37.2 ± 32.29; p = 0.03; η p 2 = 0.13). Furthermore, we have observed the correlations: basal ferritin levels were inversely correlated with changes in myostatin (r = −0.51, p = 0.05), change in adiponectin, and change in serum iron (r = −0.45, p = 0.05), basal iron, and osteocalcin after training (r = -0.55, p = 0.04). These findings indicate that iron modulates NW training-induced changes in exerkine levels

Swim Training Affects on Muscle Lactate Metabolism, Nicotinamide Adenine Dinucleotides Concentration, and the Activity of NADH Shuttle Enzymes in a Mouse Model of Amyotrophic Lateral Sclerosis

In this study, we aim to verify whether swim training can improve lactate metabolism, NAD+ and NADH levels, as well as modify the activity of glycolytic and NADH shuttle enzymes and monocarboxylate transporters (MCTs) in skeletal muscle of amyotrophic lateral sclerosis (ALS) mice. ALS mice (SOD1G93A) (n = 7 per group) were analyzed before the onset of ALS, at first disease symptoms (trained and untrained), and the last stage of disease (trained and untrained), and then compared with a wild-type (WT) group of mice. The blood lactate and the skeletal muscle concentration of lactate, NAD+ and NADH, MCT1 and MCT4 protein levels, as well as lactate dehydrogenase (LDH) and malate dehydrogenase (MDH) activities in skeletal muscle were determined by fluorometric, Western blotting, liquid chromatography-MS3 spectrometry, and spectrometric methods. In the untrained terminal ALS group, there were decreased blood lactate levels (p < 0.001) and increased skeletal muscle lactate levels (p < 0.05) as compared with a WT group of mice. The amount of nicotinamide adenine dinucleotides in the ALS groups were also significantly reduced as well as LDH activity and the level of MCT1. Swim training increased lactate levels in the blood (p < 0.05 vs. ALS TERMINAL untrained). In addition, cytosolic MDH activity and the cMDH/LDH 2.1 ratio were significantly higher in trained vs. untrained mice (p < 0.05). The data indicate significant dysfunction of lactate metabolism in ALS mice, associated with a reduction in muscle anaerobic metabolism and NADH transporting enzymes, as well as swim-induced compensation of energy demands in the ALS mice