Il-kelma "Mulej"

F’dan l-artiklu l-awtur jagħti tifsira tal-kelma “Mulej” u n-nisel tagħha.N/

Impact of short-term dietary modification on postprandial oxidative stress

<p>Abstract</p> <p>Background</p> <p>We have recently reported that short-term (21-day) dietary modification in accordance with a stringent vegan diet (i.e., a Daniel Fast) lowers blood lipids as well as biomarkers of oxidative stress. However, this work only involved measurements obtained in a fasted state. In the present study, we determined the postprandial response to a high-fat milkshake with regards to blood triglycerides (TAG), biomarkers of oxidative stress, and hemodynamic variables before and following a 21-day Daniel Fast.</p> <p>Methods</p> <p>Twenty-two subjects (10 men and 12 women; aged 35 ± 3 years) completed a 21-day Daniel Fast. To induce oxidative stress, a milkshake (fat = 0.8 g·kg^-1; carbohydrate = 1.0 g·kg^-1; protein = 0.25 g·kg^-1) was consumed by subjects on day one and day 22 in a rested and 12-hour fasted state. Before and at 2 and 4 h after consumption of the milkshake, heart rate (HR) and blood pressure were measured. Blood samples were also collected at these times and analyzed for TAG, malondialdehyde (MDA), hydrogen peroxide (H₂O₂), advanced oxidation protein products (AOPP), nitrate/nitrite (NOx), and Trolox Equivalent Antioxidant Capacity (TEAC).</p> <p>Results</p> <p>A time effect was noted for HR (<it>p </it>= 0.006), with values higher at 2 hr post intake of the milkshake as compared to pre intake (<it>p </it>< 0.05). Diastolic blood pressure was lower post fast as compared to pre fast (<it>p </it>= 0.02), and a trend for lower systolic blood pressure was noted (<it>p </it>= 0.07). Time effects were noted for TAG (<it>p </it>= 0.001), MDA (<it>p </it>< 0.0001), H₂O₂(<it>p </it>< 0.0001), AOPP (<it>p </it>< 0.0001), and TEAC (<it>p </it>< 0.0001); all concentrations were higher at 2 h and 4 h post intake compared to pre intake, except for TEAC, which was lower at these times (<it>p </it>< 0.05). A condition effect was noted for NOx (<it>p </it>= 0.02), which was higher post fast as compared to pre fast. No pre/post fast × time interactions were noted (<it>p </it>> 0.05), with the area under the curve from pre to post fast reduced only slightly for TAG (11%), MDA (11%), H₂O₂(8%), and AOPP (12%), with a 37% increase noted for NOx.</p> <p>Conclusion</p> <p>Partaking in a 21-day Daniel Fast does not result in a statistically significant reduction in postprandial oxidative stress. It is possible that a longer time course of adherence to the Daniel Fast eating plan may be needed to observe significant findings.</p

Oxidative stress and exercise training: Effects of exercise intensity, training status, sex, hydration and heat stress

Exercise-induced oxidative stress has been studied extensively; it can mediate fatigue as well as important adaptations to exercise. Little is known, however, on the modulating influences of exercise parameters (e.g. exercise pattern and intensity) or individual factors (sex, hydration status, or heat acclimation status) and their interactions on exercise-induced oxidative stress, acutely or chronically, despite all of these factors having the potential to affect such stress. Therefore, the purpose of this study was to examine within- and between-person factors that are likely to influence exercise-induced oxidative stress, particularly those mentioned above. Samples were collected from participants of four research projects encompassing diverse exercise and environmental conditions and physiological states, and for which the ethical approvals already provided for, or were amended to allow, analysis of additional indices of oxidative stress. Methods: Training status and exercise pattern: Previously sedentary individuals (n=11) were endurance (END) trained for eight weeks by cycling for either 50 min at 65% V ̇O2max, 5 d.wk-1 or six 30-s maximal efforts at 5-min intervals, 3 d.wk-1 (repeat high intensity exercise or RHIE) and were tested before and after training with standardised exercise (50-min steady state and a 10-min work trial). Hydration: Seven trained male runners completed a 6-d fluid-controlled training protocol (hypohydration or euhydration) before an exercise test comprising 70-min of running at 85% of anaerobic threshold and a 3-km time trial. In another hydration study, six trained and six untrained males completed 80-min cycling (40 min at 70% V ̇O2peak then a 40-min work trial) either hypohydrated or euhydrated. Heat acclimation: Six trained rowers completed a 6-d, exercising heat acclimation protocol in 45 °C and 60% relative humidity, increasing from 30 to 45 min.d 1. In all protocols, blood samples were taken before and after exercise and analysed for concentrations of oxidised proteins (advanced oxidation protein products, AOPP) and lipids (malondialdehyde, MDA), and for antioxidant capacity (oxygen radical absorbance capacity, ORAC). Post-exercise samples were collected 30 min after exercise for the study on training status and exercise pattern, and immediately after exercise for the studies on heat acclimation and hydration effects, as well as during exercise in the hydration protocols. Linear mixed models were used to analyse oxidative indices within each study. Results: MDA concentrations had decreased at 30 min after standardised exercise (P=0.028) when untrained (Mean ↓ 0.14 μmol.L-1) and after 8 weeks of both END and RHIE training (Mean ↓ 0.10 μmol.L-1). AOPP concentrations were decreased after standardised exercise when untrained and after 8 weeks of RHIE training (Mean ↓ 5.74 μmol.L-1), but were increased when END trained (↑ 3.87 μmol.L-1; training • exercise • training type interaction: P=0.038). The ORAC was increased 30 min after exercise when untrained (Mean ↑ 1251 μmol.L-1) but decreased when trained (Mean ↓ 925 μmol.L-1), irrespective of training type (training status • exercise interaction: P=0.033). Both acute and chronic hypohydration led to significantly lower oxidative stress concentrations at all times. Both AOPP (Mean 32 vs. 40 μmol.L-1; P=0.046) and MDA (Mean 2.87 vs. 3.13 μmol.L-1; P=0.028) were lower following chronic hypohydration, as was AOPP (Mean 39 vs. 42 μmol.L-1; P=0.035) with acute hypohydration. However, ORAC was not affected consistently. Heat acclimation did not reliably affect oxidative or measures at rest or after exercise. Conclusions: Measuring oxidative stress markers at 30 min after exercise did not reveal the expected increase in oxidative stress, instead a decline below baseline was observed in most cases. Indeed the response to exercise before and after training may have been similar for these polarised forms of exercise. With heat acclimation, oxidative stress was not significantly changed despite the sustained thermal load, potentially indicating an increased ability to neutralise oxidative-stress. It was already known that hypohydration can upregulate antioxidant capacity, and is speculated to have occurred in the present hydration studies, which ultimately eliminated increased oxidative stress. This potentially explains the lack of statistical difference in ORAC. Thus, continued hypohydration then may have caused an over compensation, and oxidative stress markers to fall below euhydrated levels. Manipulation of hydration and up-regulation of antioxidant capacity may potentially be useful in training for sporting performance as a means of increasing antioxidant capacity to delay fatigue; however this requires further evidence and would also require balance with other more negative aspects of hypohydration