Jacek Wilczak

Creatine and β-hydroxy-β-methylbutyrate (HMB) additively increase lean body mass and muscle strength during a weight-training program

We investigated whether creatine (CR) and beta-hydroxy-beta-methylbutyrate (HMB) act by similar or different mechanisms to increase lean body mass (LBM) and strength in humans undergoing progressive resistance-exercise training. In this double-blind, 3-wk study, subjects (n = 40) were randomized to placebo (PL; n = 10), CR (20.0 g of CR/d for 7 d followed by 10.0 g of CR/d for 14 d; n = 11), HMB (3.0 g of HMB/d; n = 9), or CR-and-HMB (CR/HMB; n = 10) treatment groups. Over 3 wk, all subjects gained LBM, which was assessed by bioelectrical impedance analysis. The CR, HMB and CR/HMB groups gained 0.92, 0.39, and 1.54 kg of LBM, respectively, over the placebo group, with a significant effect with CR supplementation (main effect P = 0.05) and a trend with HMB supplementation (main effect P = 0.08). These effects were additive because there was no interaction between CR and HMB (CR x HMB main effect P = 0.73). Across all exercises, HMB, CR, and CR/HMB supplementation caused accumulative strength increases of 37.5, 39.1, and 51.9 kg, respectively, above the placebo group. The exercise-induced rise in serum creatine phosphokinase was markedly suppressed with HMB supplementation (main effect P = 0.01). However, CR supplementation antagonized the HMB effects on serum creatine phosphokinase (CR x HMB interactive effect P = 0.04). Urine urea nitrogen and plasma urea were not affected by CR supplementation, but both decreased with HMB supplementation (HMB effect P < 0.05), suggesting a nitrogen-sparing effect. In summary, CR and HMB can increase LBM and strength, and the effects are additive. Although not definitive, these results suggest that CR and HMB act by different mechanisms.

Antioxidant activity and chemical difference in fruit of different Actinidia sp.

Abstract The present research aimed at evaluating the vitamin C, total phenolic content (TPC), phenolic compounds, carotenoids, and chlorophyll contents, as well as antioxidant activity (AAC) of six Actinidia species fruit. Vitamin C, phenolic compounds, carotenoids and chlorophylls were measured using high-performance liquid chromatography. TPC was determined using the Folin–Ciocalteau reagent, and AAC using 2,2-diphenyl-1-picryl hydrazyl (DPPH) assay. The highest concentrations of vitamin C and TPC were found for Actinidia kolomikta fruit (1008.3 and 634.1 mg/100 g fresh weight [FW], respectively). Among phenolic compounds, seven phenolic acids and three flavonoids were identified. The 2,5-dihydroxybenzoic acid prevailed in A. kolomikta (425.54 mg/100 g FW), while tannic acid dominated in other species (4.63–100.43 mg/100 g FW). The largest amounts of chlorophylls and carotenoids were identified as Actinidia macrosperma (4.02 and 2.09 mg/100 g FW, respectively). The AAC of fruit extracts decreased in the order of A. kolomikta > Actinidia purpurea > Actinidia melanandra > A. macrosperma > Actinidia arguta > Actinidia deliciosa according to the DPPH assay.

Hepato- and gastro- protective activity of purified oat 1-3, 1-4-β-d-glucans of different molecular weight.

Protective and antioxidant properties of highly purified oat β-glucans of high and low molecular weight in liver and stomach were evaluated. The novelty in approach was to determine whether dietary β-glucans affect the parameters of oxidative stress directly in the stomach and indirectly in the liver, especially in inflammation states. Physicochemical properties e.g. viscoelastic was found as strictly dependent from molecular weight of oat β-glucans hence its metabolic activity could also show dependence. Three groups of rats were fed control diet and diet supplemented with low and high molecular weights oat β-glucans. Animals were divided into controls and individuals with experimentally induced intestinal inflammation. Most active in increasing of total antioxidant status was low molecular weight β-glucan. High molecular weight β-glucan supplementation inhibits lipid oxidation the most in LPS treated animals. The results obtained from experiment encourage for dietary intervention with oat β-glucans for stomach and liver protection during existing enteritis.

No adverse lung effects of 7- and 28-day inhalation exposure of rats to emissions from petrodiesel fuel containing 20% rapeseed methyl esters (B20) with and without particulate filter – the FuelHealth project

Abstract Increased use of biofuels raises concerns about health effects of new emissions. We analyzed relative lung health effects, on Fisher 344 rats, of diesel engine exhausts emissions (DEE) from a Euro 5-classified diesel engine running on petrodiesel fuel containing 20% rapeseed methyl esters (B20) with and without diesel particulate filter (DPF). One group of animals was exposed to DEE for 7 days (6 h/day), and another group for 28 days (6 h/day, 5 days/week), both with and without DPF. The animals (n = 7/treatment) were exposed in whole body exposure chambers. Animals breathing clean air were used as controls. Genotoxic effects of the lungs by the Comet assay, histological examination of lung tissue, bronchoalveolar lavage fluid (BALF) markers of pulmonary injury, and mRNA markers of inflammation and oxidative stress were analyzed. Our results showed that a minor number of genes related to inflammation were slightly differently expressed in the exposed animals compared to control. Histological analysis also revealed only minor effects on inflammatory tissue markers in the lungs, and this was supported by flow cytometry and ELISA analysis of cytokines in BALF. No exposure-related indications of genotoxicity were observed. Overall, exposure to DEE with or without DPF technology produced no adverse effects in the endpoints analyzed in the rat lung tissue or the BALF. Overall, exposure to DEE from a modern Euro 5 light vehicle engine run on B20 fuel with or without DPF technology produced no adverse effects in the endpoints analyzed in the rat lung tissue or the BALF.

The effects of 1st and 2nd generation biodiesel exhaust exposure on hematological and biochemical blood indices of Fisher344 male rats – The FuelHealth project

Diesel exhaust emissions (DEE), being one of the main causes of ambient air pollution, exert a detrimental effect on human health and increase morbidity and mortality related to cardiovascular and pulmonary diseases. Therefore, the objective of the present study was to investigate potential adverse effects of exhausts emissions from B7 fuel, the first-generation biofuel containing 7% of fatty acid methyl esters (FAME), and SHB20 fuel, the second-generation biofuel containing 20% FAME/hydrotreated vegetable oil (HVO), after a whole-body exposure with and without diesel particle filter (DPF). The experiment was performed on 95 male Fischer 344 rats, divided into 10 groups (8 experimental, 2 control). Animals were exposed to DEE (diluted with charcoal-filtered room air to 2.1-2.2% (v/v)) for 7 or 28 days (6 h/day, 5 days/week) in an inhalation chamber. DEE originated from Euro 5 engine with or without DPF treatment, run on B7 or SHB20 fuel. Animals in the control groups were exposed to clean air. Our results showed that the majority of haematological and biochemical parameters examined in blood were at a similar level in the exposed and control animals. However, exposure to DEE from the SHB20 fuel caused an increase in the number of red blood cells (RBC) and haemoglobin concentration. Moreover, 7 days exposure to DEE from SHB20 fuel induced genotoxic effects manifested by increased levels of DNA single-strand breaks in peripheral blood lymphocytes. Furthermore, inhalation of both types of DEE induced oxidative stress and caused imbalance of anti-oxidant defence enzymes. In conclusion, exposure to DEE from B7, which was associated with higher exposure to polycyclic aromatic hydrocarbons, resulted in decreased number of T and NK lymphocytes, while DEE from SHB20 induced a higher level of DNA single-strand breaks, oxidative stress and increased red blood cells parameters. Additionally, DPF technology generated increased number of smaller PM and made the DEE more reactive and more harmful, manifested as deregulation of redox balance.