Acute exercise increases resistance to oxidative stress in young but not older adults

A single bout of acute exercise increases oxidative stress and stimulates a transient increase in antioxidant enzymes. We asked whether this response would induce protection from a subsequent oxidative challenge, different from that of exercise, and whether the effects were affected by aging. We compared young (20 ± 1 years, n = 8) and older (58 ± 6 years, n = 9) healthy men and women. Resistance to oxidative stress was measured by the F₂-isoprostane response to forearm ischemia/reperfusion (I/R) trial. Each participant underwent the I/R trial twice, in random order; once after performing 45 min of cycling on the preceding day (IRX) and a control trial without any physical activity (IRC). Baseline F₂-isoprostane levels were significantly lower at IRX compared to IRC (P < 0.05) and not different between groups. F₂-isoprostane response to IRX was significantly lower compared to IRC in young (P < 0.05) but not different in the older group. Superoxide dismutase activity in response to acute exercise was significantly higher in young compared to older adults (P < 0.05). These data suggest that signal transduction of acute exercise may be impaired with aging. Repeated bouts of transient reactive oxygen species production as seen with regular exercise may be needed to increase resistance to oxidative stress in older individuals.     

Reduced muscle oxidative capacity is independent of O2 availability in elderly people

Impaired O₂ transport to skeletal muscle potentially contributes to the decline in aerobic capacity with aging. Thus, we examined whether (1) skeletal muscle oxidative capacity decreases with age and (2) O₂ availability or mitochondrial capacity limits the maximal rate of mitochondrial ATP synthesis in vivo in sedentary elderly individuals. We used ³¹P-magnetic resonance spectroscopy (³¹P-MRS) to examine the PCr recovery kinetics in six young (26 ± 10 years) and six older (69 ± 3 years) sedentary subjects following 4 min of dynamic plantar flexion exercise under different fractions of inspired O₂ (FiO₂, normoxia 0.2; hyperoxia 1.0). End-exercise pH was not significantly different between old (7.04 ± 0.10) and young (7.05 ± 0.04) and was not affected by breathing hyperoxia (old 7.08 ± 0.08, P > 0.05 and young 7.05 ± 0.03). Likewise, end-exercise PCr was not significantly different between old (19 ± 4 mM) and young (24 ± 5 mM) and was not changed in hyperoxia. The PCr recovery time constant was significantly longer in the old (36 ± 9 s) compared to the young in normoxia (23 ± 8 s, P < 0.05) and was not significantly altered by breathing hyperoxia in both the old (35 ± 9 s) and young (29 ± 10 s) groups. Therefore, this study reveals that the muscle oxidative capacity of both sedentary young and old individuals is independent of O₂ availability and that the decline in oxidative capacity with age is most likely due to limited mitochondrial content and/or mitochondrial dysfunction and not O₂ availability.     

Chronic training increases blood oxidative damage but promotes health in elderly men

The objective of the present study was to investigate a large panel of oxidative stress biomarkers in long-term trained elderly men to analyse the effects of chronic training on an aged population. We collected blood samples from two groups of male volunteers older than 65 years who maintain a measure of functional independence: one group of sedentary subjects without a history of regular physical activity and the other of subjects who have sustained training, starting during middle age (mean training time = 49 ± 8 years). We studied morbidity and polypharmacy, as well as haematological parameters including red cell count, haemoglobin concentration, haematocrit, mean corpuscular volume, red cell distribution width and several oxidative biomarkers including protein carbonyl content and lipid peroxidation in plasma and erythrocytes, red blood cell H₂O₂-induced haemolysis test, plasma total antioxidant activity and the main antioxidant enzymes of erythrocytes: superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase. After adjusting for confounding factors, we observed an increase in all oxidative damage biomarkers in the plasma and erythrocytes of the long-term exercise group. However, we reported a decrease in the number of diseases per subject with statistical differences nearly significant (p = 0.061), reduced intake of medications per subject and lower levels of red cell distribution width in the chronic exercise group. These results indicate that chronic exercise from middle age to old age increases oxidative damage; however, chronic exercise appears to be an effective strategy to attenuate the age-related decline in the elderly.     

Decreased oxidant profile and increased antioxidant capacity in naturally postmenopausal women

Recent works have shown a dual side of estrogens, and research on the relationship between oxidative stress and menopausal status remains unclear and has produced controversial results. In this work, we aimed to evaluate by sensitive methods the oxidant and antioxidant changes that develop after natural menopause. Thirty premenopausal and 28 naturally postmenopausal women volunteered for this study. Blood was collected and plasma used. 17-OH estradiol levels in plasma were estimated. Plasma levels of advanced oxidation protein products (AOPP), lipid peroxidation products (such as hydroperoxides and malondialdehyde (MDA)), and nitrites were measured, and total radical antioxidant parameter testing was performed to determine the oxidant and antioxidant profiles, respectively. Estrogen levels were significantly increased (p < 0.02) in premenopausal women (54.28 ± 9.34 pg/mL) as compared with postmenopausal women (18.10 ± 1.49 pg/mL). Postmenopausal women had lower levels of lipid hydroperoxide oxidation (p < 0.0001), lipid hydroperoxide levels evaluated by the area under the curve (AUC; 1,366,000 ± 179,400 AUC; p < 0.01), and hydroperoxides as measured by the ferrous oxidation-xylenol orange method (31.48 ± 2.7 μM; p < 0.0001). The MDA levels did not differ between pre- and postmenopausal women whether measured by thiobarbituric acid-reactive substances or high-performance liquid chromatography assays. No differences in AOPP and nitrite levels were observed between pre- and postmenopausal women. Postmenopausal women also exhibited a higher total radical antioxidant level (0.89 ± 0.08 μM Trolox; p < 0.0001). Postmenopausal women demonstrated lower levels of oxidative damage and a higher antioxidant capacity than premenopausal women.     

Effects of melatonin and dexpanthenol on antioxidant parameters when combined with estrogen treatment in ovariectomized rats

The purpose of the study was to assess whether it is possible to reduce the oxidative damage using antioxidant agents combined with hormone replacement therapy after menopause. In this prospective experimental study, 50 mature female Wistar albino rats weighing 270–310 g were used. Rats were divided into the following six groups: (1) Ovx group (n = 7): the animals underwent bilateral ovariectomy. No drug was administered following bilateral ovariectomy. (2) Ovx + E₂group (n = 7): bilateral ovariectomy + 17β-estradiol (100 μg/kg/day); (3) Ovx + E₂ + MT5 group (n = 7): bilateral ovariectomy + 17β-estradiol (100 μg/kg/day) + melatonin (5 mg/kg/day); (4) Ovx + E₂ + MT20 group (n = 7): bilateral ovariectomy + 17β-estradiol (100 μg/kg/day) + melatonin (20 mg/kg/day); (5) Ovx + E₂ + Dxp250 group (n = 7): bilateral ovariectomy + 17β-estradiol (100 μg/kg/day) + dexpanthenol (250 mg/kg/day); (6) Ovx + E₂ + Dxp500 group (n = 7): bilateral ovariectomy + 17β-estradiol (100 μg/kg/day) + dexpanthenol (500 mg/kg/day), and the activity of these antioxidative enzymes and oxidative stress products were measured. Enzymatic activity levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase(GSH-Px), and glutathione reductase and levels of free radicals (malondialdehyde (MDA) and nitric oxide) were both analyzed. We observed an increase in the level of GSH activity, but no significant differences in levels of CAT, SOD, and GSH-Px enzymatic activity and in levels of free radical MDA following 17β-estradiol or additional antioxidant treatment (melatonin or dexpanthenol). Despite the present study indicating that the addition of melatonin and dexpanthenol into the hormone replacement therapy regimen may contribute to the antioxidant effect of estrogen, the existence of limited data in this field indicates that further studies are warranted.     

Effects of acute bouts of endurance exercise on retinal vessel diameters are age and intensity dependent

Alterations of retinal vessel diameters are associated with increased cardiovascular risk. We aimed to investigate changes in retinal vessel diameters in response to acute dynamic exercise of different intensities and whether these changes are age dependent. Seventeen healthy seniors (median (IQR) age 68 (65, 69) years) and 15 healthy young adults (median (IQR) age 26 (25, 28) years) first performed a maximal treadmill test (MTT) followed by a submaximal treadmill test (SMTT) and a resting control condition in randomised order. Central retinal arteriolar (CRAE) and central retinal venular (CRVE) diameter equivalents were measured before as well as 5 (t₅) and 40 (t₄₀) minutes after exercise cessation using a static retinal vessel analyser. Both exercise intensities induced a significant dilatation in CRAE and CRVE at t₅ compared to the control condition (P < 0.001). At t₄₀, the mean increase in CRAE and CRVE was greater for MTT compared to that for SMTT (CRAE 1.7 μm (95 % confidence interval (CI) −0.1, 3.6; P = 0.061); CRVE 2.2 μm (95 % CI 0.4, 4.1; P = 0.019)). However, the estimated difference at t₅ between seniors and young adults in their response to MTT compared to SMTT was 5.3 μm (95 % CI 2.0, 8.5; P = 0.002) for CRAE and 4.1 μm (95 % CI −0.4, 8.6; P = 0.076) for CRVE. Wider arteries and veins after maximal versus submaximal exercise for seniors compared to young adults suggest that myogenic vasoconstriction in response to exhaustive exercise may be reduced in seniors. Age-related loss of vascular reactivity has clinical implications since the arteriolar vasoconstriction protects the retinal capillary bed from intraluminal pressure peaks.

Electronic supplementary material

The online version of this article (doi:10.1007/s11357-014-9650-3) contains supplementary material, which is available to authorized users.     

Effect of tumor necrosis factor-α antagonists on oxidative stress in patients with Crohn's disease

AIM: To investigate changes in oxidative stress in Crohn's disease(CD) before and after anti-tumor necrosis factor(TNF)-α treatment.METHODS: A total of 42 patients with active CD, who were scheduled to be treated by anti-TNF-α antibodies, were enrolled. Serum levels of diacron-reactive oxygen metabolites(d-ROM), biological antioxidant potential(BAP), and modified ratio of oxidative stress and antioxidant capacity(m-OA) were measured using the Free Radical Analytical System before and 8 wk after induction of therapy with infliximab or adalimumab. The values for oxidative stress were correlated with disease activity and clinical response as determined by the CD activity index(CDAI) at 8 and 54 wk after the therapy.RESULTS: Prior to treatment, d-ROM showed significant correlations with CDAI(r = 0.42, P 0.01). There was a significant negative correlation between m-OA and CDAI before and after treatment(r =-0.48 vs r =-0.42, P 0.01). CDAI and d-ROM had decreased significantly by 8 wk after treatment(CDAI; 223.3 ± 113.2 vs 158.3 ± 73.4, P 0.01, d-ROM; 373 ± 133 vs 312 ± 101, P 0.05). However, neither BAP nor m-OA had changed significantly. In patients who had responded to the treatment at 8 wk, d-ROM, BAP, and m-OA levels before treatment did not differ significantly between patients with and without loss of response.CONCLUSION: Anti-TNF-α therapy decreases oxi-dative stress in patients with CD, but does not alter the production of antioxidants. Dysregulation of antioxidants may be associated with the disease.     

Postprandial antioxidant gene expression is modified by Mediterranean diet supplemented with coenzyme Q10 in elderly men and women

Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. We have investigated whether the quality of dietary fat alters postprandial gene expression and protein levels involved in oxidative stress and whether the supplementation with coenzyme Q₁₀ (CoQ) improves this situation in an elderly population. Twenty participants were randomized to receive three isocaloric diets each for 4 weeks: Mediterranean diet supplemented with CoQ (Med + CoQ diet), Mediterranean diet (Med diet), saturated fatty acid-rich diet (SFA diet). After 12-h fast, volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. Nrf2, p22^phox and p47^phox, superoxide dismutase 1 and 2 (SOD1 and SOD2), glutathione peroxidase 1 (GPx1), thiorredoxin reductase (TrxR) gene expression and Kelch-like ECH associating protein 1 (Keap-1) and citoplasmic and nuclear Nrf2 protein levels were determined. Med and Med + CoQ diets induced lower Nrf2, p22^phox, p47^phox, SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet. Moreover, Med + CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet. Our results support the antioxidant effect of a Med diet and that exogenous CoQ supplementation has a protective effects against free radical overgeneration through the lowering of postprandial oxidative stress modifying the postprandial antioxidant protein levels and reducing the postprandial expression of antioxidant genes in peripheral blood mononuclear cells.

Electronic supplementary material

The online version of this article (doi:10.1007/s11357-011-9331-4) contains supplementary material, which is available to authorized users.     

Distinguishing exercise intolerance in early‐stage pulmonary hypertension with invasive exercise hemodynamics: Rest V E/VCO2 and ETCO2 identify pulmonary vascular disease

BackgroundAmong subjects with exercise intolerance and suspected early‐stage pulmonary hypertension (PH), early identification of pulmonary vascular disease (PVD) with noninvasive methods is essential for prompt PH management.HypothesisRest gas exchange parameters (minute ventilation to carbon dioxide production ratio: V _E/VCO₂ and end‐tidal carbon dioxide: ETCO₂) can identify PVD in early‐stage PH.MethodsWe conducted a retrospective review of 55 subjects with early‐stage PH (per echocardiogram), undergoing invasive exercise hemodynamics with cardiopulmonary exercise test to distinguish exercise intolerance mechanisms. Based on the rest and exercise hemodynamics, three distinct phenotypes were defined: (1) PVD, (2) pulmonary venous hypertension, and (3) noncardiac dyspnea (no rest or exercise PH). For all tests, *p < .05 was considered statistically significant.ResultsThe mean age was 63.3 ± 13.4 years (53% female). In the overall cohort, higher rest V _E/VCO₂ and lower rest ETCO₂ (mm Hg) correlated with high rest and exercise pulmonary vascular resistance (PVR) (r ~ 0.5–0.6*). On receiver‐operating characteristic analysis to predict PVD (vs. non‐PVD) subjects with noninvasive metrics, area under the curve for pulmonary artery systolic pressure (echocardiogram) = 0.53, rest V _E/VCO₂ = 0.70* and ETCO₂ = 0.73*. Based on this, optimal thresholds of rest V _E/VCO₂ > 40 mm Hg and rest ETCO₂ < 30 mm Hg were applied to the overall cohort. Subjects with both abnormal gas exchange parameters (n = 12, vs. both normal parameters, n = 19) had an exercise PVR 5.2 ± 2.6* (vs. 1.9 ± 1.2), mPAP/CO slope with exercise 10.2 ± 6.0* (vs. 2.9 ± 2.0), and none included subjects from the noncardiac dyspnea group.ConclusionsIn a broad cohort of subjects with suspected early‐stage PH, referred for invasive exercise testing to distinguish mechanisms of exercise intolerance, rest gas exchange parameters (V _E/VCO₂ > 40 mm Hg and ETCO₂ < 30 mm Hg) identify PVD.     

Circulating Lp-PLA2 activity correlates with oxidative stress and cytokines in overweight/obese postmenopausal women not using hormone replacement therapy

Controversy remains regarding whether there is an association between circulating lipoprotein-associated phospholipase A₂ (Lp-PLA₂), cytokines, and oxidative stress in healthy postmenopausal women. We investigated the influence of age on Lp-PLA₂ activity in postmenopausal women not using hormone therapy and the relationship of Lp-PLA₂ enzyme activity to serum cytokine levels and oxidative stress indices. Normal weight (n = 1284) and overweight/obese (n = 707) postmenopausal women not using hormone therapy were categorized into five age groups: 50–54, 55–59, 60–64, 65–69, and 70–89 years. Overweight-obese women showed higher plasma Lp-PLA₂ activity, urinary 8-epi-prostaglandin F_2α (8-epi-PGF_2α), serum interleukin (IL)-6, and smaller LDL particles than normal-weight women after adjusting for age, years postmenopause, smoking, drinking, blood pressure, glucose, insulin, lipid profiles, BMI, and waist circumference. Overweight/obese women 70–89 years old showed higher Lp-PLA₂ activity than those aged 50–54 years, whereas no significant difference in Lp-PLA₂ activity existed across normal-weight female age groups. Overweight/obese women aged ≥65 years showed higher Lp-PLA₂, oxidized LDL (ox-LDL), IL-6, and 8-epi-PGF_2α than age-matched normal-weight controls. Overweight/obese women aged ≥70 years had higher ox-LDL levels than those aged 50–59, and overweight/obese women aged 65–89 showed higher IL-6 and 8-epi-PGF_2α. There were strong positive correlations between Lp-PLA₂ and ox-LDL (r = 0.385, P < 0.001), Lp-PLA₂ and IL-6 (r = 0.293, P < 0.001), and ox-LDL and IL-6 (r = 0.303, P < 0.001) in overweight/obese women; however, these relationships were weak in normal-weight women. These results suggest that aging and obesity-related oxidative and inflammatory mediators are associated with Lp-PLA₂ activity in overweight/obese postmenopausal women not using hormone therapy.     

The skeletal muscle satellite cell response to a single bout of resistance-type exercise is delayed with aging in men

Skeletal muscle satellite cells (SCs) have been shown to be instrumental in the muscle adaptive response to exercise. The present study determines age-related differences in SC content and activation status following a single bout of exercise. Ten young (22 ± 1 years) and 10 elderly (73 ± 1 years) men performed a single bout of resistance-type exercise. Muscle biopsies were collected before and 12, 24, 48, and 72 h after exercise. SC content and activation status were assessed in type I and type II muscle fibers by immunohistochemistry. Myostatin and MyoD protein and messenger RNA (mRNA) expression were determined by Western blotting and rtPCR, respectively. In response to exercise, it took 48 h (young) and 72 h (elderly) for type II muscle fiber SC content to exceed baseline values (P < 0.01). The number of myostatin + SC in type I and II muscle fibers was significantly reduced after 12, 24, and 48 h of post-exercise recovery in both groups (P < 0.01), with a greater reduction observed at 24 and 48 h in the young compared with that in the elderly men (P < 0.01). In conclusion, the increase in type II muscle fiber SC content during post-exercise recovery is delayed with aging and is accompanied by a blunted SC activation response.     

Mediterranean diet supplemented with coenzyme Q10 induces postprandial changes in p53 in response to oxidative DNA damage in elderly subjects

Coenzyme Q10 (CoQ) is a powerful antioxidant that reduces oxidative stress. We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects. In this crossover study, 20 subjects were randomly assigned to receive three isocaloric diets during 4 weeks each: (1) Mediterranean diet (Med diet), (2) Mediterranean diet supplemented with CoQ (Med+CoQ diet), and (3) saturated fatty acid-rich diet (SFA diet). Levels of mRNAs were determined for p53, p21, p53R2, and mdm2. Protein levels of p53, phosphorylated p53 (Ser20), and monoubiquitinated p53 were also measured, both in cytoplasm and nucleus. The extent of DNA damage was measured as plasma 8-OHdG. SFA diet displayed higher postprandial 8-OHdG concentrations, p53 mRNA and monoubiquitinated p53, and lower postprandial Mdm2 mRNA levels compared with Med and Med+CoQ diets (p < 0.05). Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p < 0.05). In conclusion, Med+CoQ diet improves oxidative DNA damage in elderly subjects and reduces processes of cellular oxidation. Our results suggest a starting point for the prevention of oxidative processes associated with aging.     

Thermoregulation and fluid balance during a 30-km march in 60- versus 80-year-old subjects

The presence of impaired thermoregulatory and fluid balance responses to exercise in older individuals is well established. To improve our understanding on thermoregulation and fluid balance during exercise in older individuals, we compared thermoregulatory and fluid balance responses between sexagenarians and octogenarians during prolonged exercise. Forty sexagenarians (60 ± 1 year) and 36 octogenarians (81 ± 2 year) volunteered to participate in a 30-km march at a self-selected pace. Intestinal temperature (T_in) and heart rate were recorded every 5 km. Subjects reported fluid intake, while urine output was measured and sweat rate was calculated. Octogenarians demonstrated a lower baseline T_in and a larger exercise-induced increase in T_in compared to sexagenarians (1.2 ± 0.5 °C versus 0.7 ± 0.4 °C, p < 0.01), while maximum T_in tended to be higher in octogenarians (38.4 ± 0.4 °C versus 38.2 ± 0.3 °C, p = 0.09). Exercise intensity (70 ± 11 % versus 70 ± 9 %) and exercise duration (7 h 45 min ± 0 h 57 min versus 7 h 24 min ± 0 h 58 min) were not different between octogenarians and sexagenarians. Octogenarians demonstrated lower fluid intake (251 ± 97 mL/h versus 325 ± 125 mL/h, p = 0.01) and urine output (28 ± 22 mL/h versus 52 ± 40 mL/h, p < 0.01) compared to sexagenarians. Furthermore, the sweat rate tended to be lower (294 ± 150 mL/h versus 364 ± 148 mL/h, p = 0.07) in the octogenarian group. Sodium levels and plasma volume changes were not different between sexagenarians and octogenarians (all p > 0.05). These results suggest that thermoregulatory responses deteriorate with advancing age, while fluid balance is regulated appropriately during a 30-km walking march under moderate ambient conditions.     

DHEA, DHEA-S and cortisol responses to acute exercise in older adults in relation to exercise training status and sex

The aim of the present study was to investigate resting measures of dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEA-S) and cortisol, and the response and recovery of these hormones to acute exercise, in male and female older adults of different exercise training status. Participants were 49 community-dwelling older adults (23 females) aged between 60 and 77 years who were either sedentary (n = 14), moderately active (n = 14) or endurance trained (n = 21). Participants undertook an acute bout of exercise in the form of an incremental submaximal treadmill test. The exercise lasted on average 23 min 49 s (SD = 2 min 8 s) and participants reached 76.5% (SD = 5.44) of the predicted maximal heart rate. Blood samples were collected prior to exercise, immediately, and 1 h post-exercise. DHEA levels significantly increased immediately post-exercise; however, DHEA-S levels only significantly increased in females. Cortisol significantly decreased immediately post-exercise and 1 h post-exercise compared to pre-exercise. There were no significant differences in resting hormone levels or hormonal responses to exercise between training status groups. The findings suggest that exercise can stimulate DHEA production in older adults and that hormonal responses to exercise differ between male and female older adults.     

Differential effects of late-life initiation of low-dose enalapril and losartan on diastolic function in senescent Fischer 344?×?Brown Norway male rats

No proven pharmacological therapies to delay or reverse age-related diastolic dysfunction exist. We hypothesized that late-life low-dose (non-blood-pressure-lowering) angiotensin-converting enzyme inhibition vs. angiotensin II receptor blockade would be equally efficacious at mitigating diastolic dysfunction in the senescent Fischer 344 × Brown Norway rat. Enalapril (10 mg/kg/day; n = 9) initiated at 24 months of age and continued for 6 months, increased myocardial relaxation (e''), reduced Doppler-derived indices of filling pressure (E/e''), favorably lowered the ratio of phospholamban–SERCA2 and reduced oxidative stress markers, Rac1 and nitrotyrosine, in aged hearts. Treatment with losartan (15 mg/kg/day; n = 9) similarly mitigated signs of cardiac oxidative stress, but impairments in diastolic function persisted when compared with untreated rats (n = 7). Our findings favor the idea that the lusitropic benefit of low-dose angiotensin-converting enzyme inhibitor initiated late in life may be related to an antioxidant-mediated modulation of SERCA2, resulting in improved relaxation rather than via overt effects on cardiac structure or blood pressure.     

Low Dose Iron Therapy in Children with Iron Deficiency: DNA Damage and Oxidant Stress Markers

Conflicting data are available regarding oral iron therapy in iron deficiency (ID), iron deficiency anemia (IDA) and its relation to DNA damage, oxidative stress and antioxidant markers. Our aim was assessment of DNA damage, oxidative stress and anti-oxidant markers in children with ID and IDA before and after low dose iron therapy. The study was conducted in two stages, first stage was assessment of DNA damage using comet assay, malondialdehyde (MDA) and anti-oxidant enzymes levels (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) & total antioxidant capacity (TAC) in thirty-nine children with IDA, forty-five children with ID without anemia and sixty healthy controls. Second stage was assessment of previous markers together with hematological response following oral therapy with 10 mg/day ferric ammonium citrate for 8 weeks. Before treatment, there was no significant difference between the three groups regarding MDA, GPx, SOD, CAT and TAC. A significant increase was detected in the DNA damage in the 2 groups compared to control (p < 0.005). Following iron therapy, hematological parameters was improved together with a significant increase in GPx (P = 0.04), SOD (p = 0.002), TAC (P = 0.001) and non-significant reduction in DNA damage in IDA group. There was a significant increase in SOD (p = 0.001) & TAC (p = 0.001) and significant decrease in DNA damage (p = 0.001) in ID group. Low dose iron therapy could be sufficient to improve antioxidant status and DNA damage together with correction of hematologic indices.     

Influence of exercise intensity on training-induced tendon mechanical properties changes in older individuals

This study compared the effects of low vs. high intensity training on tendon properties in an elderly population. Participants were pair-matched (gender, habitual physical activity, anthropometrics, and baseline knee extension strength) and then randomly assigned to low (LowR, i.e., ~40 % 1RM) or high (High R, i.e., ~80 % 1RM) intensity resistance training programmes for 12 weeks, 3× per week (LowR, n = 9, age 74 ± 5 years; HighR, n = 8, age 68 ± 6 years). Patellar tendon properties (stiffness [K], Young’s modulus [YM], cross-sectional area [T_CSA], and tendon length [T_L]) were measured pre and post training using a combination of magnetic resonance imaging (MRI), B-mode ultrasonography, dynamometry, electromyography and ramped isometric knee extensions. With training K showed no significant change in the LowR group while it incremented by 57.7 % in the HighR group (p < 0.05). The 51.1 % group difference was significant (p < 0.05). These differences were still apparent when the data was normalized for T_CSA and T_L, i.e., significant increase in YM post-intervention in HighR (p < 0.05), but no change in LowR. These findings suggest that when prescribing exercise for a mixed genders elderly population, exercise intensities of ≤40 % 1RM may not be sufficient to affect tendon properties.     

Association of age-related changes in circulating intermediary lipid metabolites, inflammatory and oxidative stress markers, and arterial stiffness in middle-aged men

The relationships between age-related changes in circulating endogenous metabolites, inflammatory and oxidative stress markers, and arterial stiffness in 57 middle-aged (34–55 years), nonobese men were studied over the course of 3 years. Arterial stiffness was measured using brachial-ankle pulse wave velocities (ba-PWV). Plasma metabolomic profiling was performed using ultra-performance liquid chromatography and quadrupole time-of-flight mass spectrometry. After 3 years, decreased HDL cholesterol and increased malondialdehyde (MDA) and ox-LDL levels were observed. Among 15 identified lipids, lysoPCs (C16:0, C18:0, C18:2, C20:4, and C20:5) and linoleyl carnitine were the major plasma metabolites that contributed to the age-related differences. LysoPC16:0 (variable importance in the projection value, 6.2029) was found as the most important plasma metabolite for evaluating these changes. Changes in lysoPC16:0 levels positively correlated with the changes in 8-epi-PGF_2α (r = 0.608), MDA (r = 0.413), high-sensitivity C-reactive protein (r = 0.509), IL-6 (r = 0.497), and ba-PWV (r = 0.283) levels. ba-PWV levels positively correlated with the changes in waist-to-hip ratios (WHR), inflammatory and oxidative stress markers. In a subgroup analysis of subjects with decreased ba-PWVs vs. increased ba-PWVs, changes in WHR and levels of lysoPC16:0, ba-PWV, IL-6, 8-epi-PGF_2α, MDA, and P-selectin were significantly different. Our results suggest that age-related increases in lysoPC16:0 may contribute to lipid peroxidation, thereby activating proinflammatory phenotypes and arterial stiffness.     

Effect of age on in vivo oxidative capacity in two locomotory muscles of the leg

To determine the effects of age and sex on in vivo mitochondrial function of distinct locomotory muscles, the tibialis anterior (TA) and medial gastrocnemius (MG), of young (Y; 24 ± 3 years) and older (O; 69 ± 4) men (M) and women (W) of similar overall physical activity (PA) was compared. In vivo mitochondrial function was measured using phosphorus magnetic resonance spectroscopy, and PA and physical function were measured in all subjects. Overall PA was similar among the groups, although O (n = 17) had fewer daily minutes of moderate-to-vigorous PA (p = 0.001), and slowed physical function (p < 0.05 for all variables), compared with Y (n = 17). In TA, oxidative capacity (V_max; mM s⁻¹) was higher in O than Y (p < 0.001; Y = 0.90 ± 0.12; O = 1.12 ± 0.18). There was no effect of age in MG (p = 0.5; Y = 0.91 ± 0.17; O = 0.96 ± 0.24), but women had higher oxidative capacity than men (p = 0.007; M = 0.84 ± 0.18; W = 1.03 ± 0.18). In vivo mitochondrial function was preserved in healthy O men and women, despite lower intensity PA and physical function in this group. The extent to which compensatory changes in gait may be responsible for this preservation warrants further investigation. Furthermore, women had higher oxidative capacity in the MG, but not the TA.