Redox signaling and skeletal muscle adaptation during aerobic exercise.

Redox regulation is a fundamental physiological phenomenon related to oxygen-dependent metabolism, and skeletal muscle is mainly regarded as a primary site for oxidative phosphorylation. Several studies have revealed the importance of reactive oxygen and nitrogen species (RONS) in the signaling process relating to muscle adaptation during exercise. To date, improving knowledge of redox signaling in modulating exercise adaptation has been the subject of comprehensive work and scientific inquiry. The primary aim of this review is to elucidate the molecular and biochemical pathways aligned to RONS as activators of skeletal muscle adaptation and to further identify the interconnecting mechanisms controlling redox balance. We also discuss the RONS-mediated pathways during the muscle adaptive process, including mitochondrial biogenesis, muscle remodeling, vascular angiogenesis, neuron regeneration, and the role of exogenous antioxidants.

Severe hypoxaemic hypercapnia compounds cerebral oxidative-nitrosative stress during extreme apnoea: Implications for cerebral bioenergetic function.

We examined the extent to which apnoea-induced extremes of oxygen demand/carbon dioxide production impact redox regulation of cerebral bioenergetic function. Ten ultra-elite apnoeists (six men and four women) performed two maximal dry apnoeas preceded by normoxic normoventilation, resulting in severe end-apnoea hypoxaemic hypercapnia, and hyperoxic hyperventilation designed to ablate hypoxaemia, resulting in hyperoxaemic hypercapnia. Transcerebral exchange of ascorbate radicals (by electron paramagnetic resonance spectroscopy) and nitric oxide metabolites (by tri-iodide chemiluminescence) were calculated as the product of global cerebral blood flow (by duplex ultrasound) and radial arterial (a) to internal jugular venous (v) concentration gradients. Apnoea duration increased from 306 ± 62 s during hypoxaemic hypercapnia to 959 ± 201 s in hyperoxaemic hypercapnia (P ≤ 0.001). Apnoea generally increased global cerebral blood flow (all P ≤ 0.001) but was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose (P = 0.015-0.044). This was associated with a general net cerebral output (v > a) of ascorbate radicals that was greater in hypoxaemic hypercapnia (P = 0.046 vs. hyperoxaemic hypercapnia) and coincided with a selective suppression in plasma nitrite uptake (a > v) and global cerebral blood flow (P = 0.034 to <0.001 vs. hyperoxaemic hypercapnia), implying reduced consumption and delivery of nitric oxide consistent with elevated cerebral oxidative-nitrosative stress. In contrast, we failed to observe equidirectional gradients consistent with S-nitrosohaemoglobin consumption and plasma S-nitrosothiol delivery during apnoea (all P ≥ 0.05). Collectively, these findings highlight a key catalytic role for hypoxaemic hypercapnia in cerebral oxidative-nitrosative stress. KEY POINTS: Local sampling of blood across the cerebral circulation in ultra-elite apnoeists determined the extent to which severe end-apnoea hypoxaemic hypercapnia (prior normoxic normoventilation) and hyperoxaemic hypercapnia (prior hyperoxic hyperventilation) impact free radical-mediated nitric oxide bioavailability and global cerebral bioenergetic function. Apnoea generally increased the net cerebral output of free radicals and suppressed plasma nitrite consumption, thereby reducing delivery of nitric oxide consistent with elevated oxidative-nitrosative stress. The apnoea-induced elevation in global cerebral blood flow was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose. Cerebral oxidative-nitrosative stress was greater during hypoxaemic hypercapnia compared with hyperoxaemic hypercapnia and coincided with a lower apnoea-induced elevation in global cerebral blood flow, highlighting a key catalytic role for hypoxaemia. This applied model of voluntary human asphyxia might have broader implications for the management and treatment of neurological diseases characterized by extremes of oxygen demand and carbon dioxide production.

A systematic review and meta-analysis of the SIRT1 response to exercise.

Sirtuin 1 (SIRT1) is a key physiological regulator of metabolism and a target of therapeutic interventions for cardiometabolic and ageing-related disorders. Determining the factors and possible mechanisms of acute and adaptive SIRT1 response to exercise is essential for optimising exercise interventions aligned to the prevention and onset of disease. Exercise-induced SIRT1 upregulation has been reported in animals, but, to date, data in humans have been inconsistent. This exploratory systematic review and meta-analysis aims to assess various exercise interventions measuring SIRT1 in healthy participants. A total of 34 studies were included in the meta-analysis (13 single bout exercise, 21 training interventions). Studies were grouped according to tissue sample type (blood, muscle), biomarkers (gene expression, protein content, enzyme level, enzyme activity), and exercise protocols. A single bout of high-intensity or fasted exercise per se increases skeletal muscle SIRT1 gene expression as measured by qPCR or RT-PCR, while repeated resistance training alone increases blood SIRT1 levels measured by ELISA. A limited number of studies also show a propensity for an increase in muscle SIRT1 activity as measured by fluorometric or sirtuin activity assay. In conclusion, exercise acutely upregulates muscle SIRT1 gene expression and chronically increases SIRT1 blood enzyme levels.

Astaxanthin promotes mitochondrial biogenesis and antioxidant capacity in chronic high-intensity interval training.

PURPOSE: Reactive oxygen and nitrogen species are required for exercise-induced molecular adaptations; however, excessive exercise may cause cellular oxidative distress. We postulate that astaxanthin (ASX) can neutralize oxidative distress and stimulate mitochondrial biogenesis in high-intensity exercise-trained mice. METHODS: Six-week-old mice (n = 8/group) were treated with ASX (10 mg/kg BW) or placebo. Training groups participated in 30 min/day high-intensity interval training (HIIT) for 6 weeks. Gastrocnemius muscle was collected and assayed following the exercise training period. RESULTS: Compared to the HIIT control mice, the ASX-treated HIIT mice reduced malonaldehyde levels and upregulated the expression of Nrf2 and FOXO3a. Meanwhile, the genes NQO1 and GCLC, modulated by Nrf2, and SOD2, regulated by FOXO3a, and GPx4, were transcriptionally upregulated in the ASX-treated HIIT group. Meanwhile, the expression of energy sensors, AMPK, SIRT1, and SIRT3, increased in the ASX-treated HIIT group compared to the HIIT control group. Additionally, PGC-1α, regulated by AMPK and SIRT1, was upregulated in the ASX-treated HIIT group. Further, the increased PGC-1α stimulated the transcript of NRF1 and Tfam and mitochondrial proteins IDH2 and ATP50. Finally, the ASX-treated HIIT mice had upregulations in the transcript level of mitochondrial fusion factors, including Mfn1, Mfn2, and OPA1. However, the protein level of AMPK, SIRT1, and FOXO3a, and the transcript level of Nrf2, NQO1, PGC-1α, NRF1, Mfn1, Mfn2, and OPA1 decreased in the HIIT control group compared to the sedentary control group. CONCLUSION: Supplementation with ASX can reduce oxidative stress and promote antioxidant capacity and mitochondrial biogenesis during strenuous HIIT exercise in mice.

Oxidative Stress and Exercise.

It is now well-established that regular moderate-intensity exercise training can activate salient cell adaptive properties, leading to a state of oxidative eustress [...].

Circadian Clocks, Redox Homeostasis, and Exercise: Time to Connect the Dots?

Compelling research has documented how the circadian system is essential for the maintenance of several key biological processes including homeostasis, cardiovascular control, and glucose metabolism. Circadian clock disruptions, or losses of rhythmicity, have been implicated in the development of several diseases, premature ageing, and are regarded as health risks. Redox reactions involving reactive oxygen and nitrogen species (RONS) regulate several physiological functions such as cell signalling and the immune response. However, oxidative stress is associated with the pathological effects of RONS, resulting in a loss of cell signalling and damaging modifications to important molecules such as DNA. Direct connections have been established between circadian rhythms and oxidative stress on the basis that disruptions to circadian rhythms can affect redox biology, and vice versa, in a bi-directional relationship. For instance, the expression and activity of several key antioxidant enzymes (SOD, GPx, and CAT) appear to follow circadian patterns. Consequently, the ability to unravel these interactions has opened an exciting area of redox biology. Exercise exerts numerous benefits to health and, as a potent environmental cue, has the capacity to adjust disrupted circadian systems. In fact, the response to a given exercise stimulus may also exhibit circadian variation. At the same time, the relationship between exercise, RONS, and oxidative stress has also been scrutinised, whereby it is clear that exercise-induced RONS can elicit both helpful and potentially harmful health effects that are dependent on the type, intensity, and duration of exercise. To date, it appears that the emerging interface between circadian rhythmicity and oxidative stress/redox metabolism has not been explored in relation to exercise. This review aims to summarise the evidence supporting the conceptual link between the circadian clock, oxidative stress/redox homeostasis, and exercise stimuli. We believe carefully designed investigations of this nexus are required, which could be harnessed to tackle theories concerned with, for example, the existence of an optimal time to exercise to accrue physiological benefits.

"Why would you not listen? It is like being given the winning lottery numbers and deciding not to take them": semi-structured interviews with post-acute myocardial infarction patients and their significant others exploring factors that influence participation in cardiac rehabilitation and long-term exercise training.

PURPOSE: Despite the clinical benefits, coronary artery disease patient participation rates in cardiac rehabilitation (CR) and long-term exercise are poor. This study explored the factors related to participation in these interventions from the perspectives of post-acute myocardial infarction (AMI) patients and their significant others. METHODS: Semi-structured interviews were performed with post-AMI patients (number (n) = 10) and their significant others (n = 10) following phase-III and phase-IV CR. Reflexive thematic analysis with an inductive orientation was utilised to identify themes within the dataset (ClinicalTrials.gov identifier: NCT03907293). RESULTS: The overarching theme of the data was a perceived need to improve health, with the participants viewing health benefits as the principal motive for participating in CR and long-term exercise training. Three further themes were identified: motivation, extrinsic influences, and CR experience. These themes captured the underlying elements of the participants' decision to take part in CR and long-term exercise training for the purpose of health improvements. CONCLUSION: An AMI collectively impacts the attitudes and beliefs of patients and their significant others in relation to CR participation, long-term exercise, and health. The factors identified in this study may inform strategies to promote patient enrollment in CR and adherence to long-term exercise.IMPLICATIONS FOR REHABILITATIONPost-AMI patients and their significant others reported that health benefits were the primary motive for participating in CR and long-term exercise, with aspects related to motivation, extrinsic influences, and CR experience underpinning the decision.Healthcare professionals should supply information about health benefits during the CR referral process, with insights into the experiences of CR graduates potentially improving the strength of recommendation.CR facilitators may promote long-term exercise adherence by assisting patients with the identification of an enjoyable exercise modality.Healthcare professionals should include significant others in the CR referral process, which may enable these individuals to support the patients' decisions.

Exercise and Cardioprotection in Coronary Artery Disease: A Pilot Quasi-Experimental Study.

Sirtuin-1 is a protein that may orchestrate the cardioprotective effect of exercise by controlling cellular processes. This pilot study assessed the feasibility of performing a quasi-experimental study in this area. Patients with postacute myocardial infarction were recruited across four hospital sites in the United Kingdom. The participants were offered one weekly exercise session at Phase-III and Phase-IV cardiac rehabilitation (CR). Measurements were obtained pre-Phase-III CR (Week 1), post-Phase-III CR (Week 8), and post-Phase-IV CR (Week 22). Twenty-eight patients were recruited (79% male, 100% White, 60.2 ± 10.5 years old). The recruitment rate was not fulfilled (<70% eligible patients recruited; 0.9 participants recruited per week over 30 weeks). The success criteria for dropout rate, adherence rate, and collection of sirtuin-1 measures were satisfied. A large increase in sirtuin-1 (0.14 ± 0.03, d ≥ 0.8) was seen after Phase-III and Phase-IV CR. Collectively, a quasi-experimental study is feasible with a revised recruitment strategy.

The metabolic-epigenetic nexus in type 2 diabetes mellitus.

The prevalence of type 2 diabetes mellitus (T2DM) continues to rise globally. Yet the aetiology and pathophysiology of this noncommunicable, polygenic disease, is poorly understood. Lifestyle factors, such as poor dietary intake, lack of exercise, and abnormal glycaemia, are purported to play a role in disease onset and progression, and these environmental factors may disrupt specific epigenetic mechanisms, leading to a reprogramming of gene transcription. The hyperglycaemic cell per se, alters epigenetics through chemical modifications to DNA and histones via metabolic intermediates such as succinate, α-ketoglutarate and O-GlcNAc. To illustrate, α-ketoglutarate is considered a salient co-factor in the activation of the ten-eleven translocation (TET) dioxygenases, which drives DNA demethylation. On the contrary, succinate and other mitochondrial tricarboxylic acid cycle intermediates, inhibit TET activity predisposing to a state of hypermethylation. Hyperglycaemia depletes intracellular ascorbic acid, and damages DNA by enhancing the production of reactive oxygen species (ROS); this compromised cell milieu exacerbates the oxidation of 5-methylcytosine alongside a destabilisation of TET. These metabolic connections may regulate DNA methylation, affecting gene transcription and pancreatic islet ß-cell function in T2DM. This complex interrelationship between metabolism and epigenetic alterations may provide a conceptual foundation for understanding how pathologic stimuli modify and control the intricacies of T2DM. As such, this narrative review will comprehensively evaluate and detail the interplay between metabolism and epigenetic modifications in T2DM.

Effectiveness of Exercise on Fatigue and Sleep Quality in Fibromyalgia: A Systematic Review and Meta-analysis of Randomized Trials.

OBJECTIVES: To determine the effects of exercise on fatigue and sleep quality in fibromyalgia (primary aim) and to identify which type of exercise is the most effective in achieving these outcomes (secondary aim). DATA SOURCES: PubMed and Web of Science were searched from inception until October 18, 2018. STUDY SELECTION: Eligible studies contained information on population (fibromyalgia), intervention (exercise), and outcomes (fatigue or sleep). Randomized controlled trials (RCT) testing the effectiveness of exercise compared with usual care and randomized trials (RT) comparing the effectiveness of 2 different exercise interventions were included for the primary and secondary aims of the present review, respectively. Two independent researchers performed the search, screening, and final eligibility of the articles. Of 696 studies identified, 17 RCTs (n=1003) were included for fatigue and 12 RCTs (n=731) for sleep. Furthermore, 21 RTs compared the effectiveness of different exercise interventions (n=1254). DATA EXTRACTION: Two independent researchers extracted the key information from each eligible study. DATA SYNTHESIS: Separate random-effect meta-analyses were performed to examine the effects from RCTs and from RTs (primary and secondary aims). Standardized mean differences (SMD) effect sizes were calculated using Hedges' adjusted g. Effect sizes of 0.2, 0.4, and 0.8 were considered small, moderate, and large. Compared with usual care, exercise had moderate effects on fatigue and a small effect on sleep quality (SMD, -0.47; 95% confidence interval [CI], -0.67 to -0.27; P<.001 and SMD, -0.17; 95% CI, -0.32 to -0.01; P=.04). RTs in which fatigue was the primary outcome were the most beneficial for lowering fatigue. Additionally, meditative exercise programs were the most effective for improving sleep quality. CONCLUSIONS: Exercise is moderately effective for lowering fatigue and has small effects on enhancing sleep quality in fibromyalgia. Meditative exercise programs may be considered for improving sleep quality in fibromyalgia.

The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage.

High-intensity exercise damages mitochondrial DNA (mtDNA) in skeletal muscle. Whether MitoQ - a redox active mitochondrial targeted quinone - can reduce exercise-induced mtDNA damage is unknown. In a double-blind, randomized, placebo-controlled design, twenty-four healthy male participants consisting of two groups (placebo; n = 12, MitoQ; n = 12) performed an exercise trial of 4 x 4-min bouts at 90-95% of heart rate max. Participants completed an acute (20 mg MitoQ or placebo 1-h pre-exercise) and chronic (21 days of supplementation) phase. Blood and skeletal muscle were sampled immediately pre- and post-exercise and analysed for nuclear and mtDNA damage, lipid hydroperoxides, lipid soluble antioxidants, and the ascorbyl free radical. Exercise significantly increased nuclear and mtDNA damage across lymphocytes and muscle (P < 0.05), which was accompanied with changes in lipid hydroperoxides, ascorbyl free radical, and α-tocopherol (P < 0.05). Acute MitoQ treatment failed to impact any biomarker likely due to insufficient initial bioavailability. However, chronic MitoQ treatment attenuated nuclear (P < 0.05) and mtDNA damage in lymphocytes and muscle tissue (P < 0.05). Our work is the first to show a protective effect of chronic MitoQ supplementation on the mitochondrial and nuclear genomes in lymphocytes and human muscle tissue following exercise, which is important for genome stability.

A combined γ-H2AX and 53BP1 approach to determine the DNA damage-repair response to exercise in hypoxia.

This study examines the interplay between exercise and hypoxia in relation to the DNA damage-repair response; with specific interest to DNA double strand damage. Following two V̇O2max tests, 14 healthy, male participants completed two exercise trials (hypoxia; 12% FiO2, normoxia; 20.9% FiO2) consisting of cycling for 30-min at 80-85% of V̇O2max relative to the environmental condition. Blood was sampled pre-, immediately post-, 2-, and 4-h post-exercise with additional blood cultured in vitro for 24-, 48-, and 72-h following the experimental trial. Samples were analysed for single- and double-strand DNA damage, FPG-sensitive sites, lipid hydroperoxides, lipid soluble antioxidants, and the ascorbyl free radical quantified by EPR. Exercise increased single strand breaks and FPG-sensitive sites (P < 0.05) which was exacerbated following hypoxia (P = 0.02) and a similar increase in DNA double strand breaks occurred as a result of hypoxia per se (P < 0.000). With respect to the DNA damage-repair response, single strand breaks, FPG-sensitive sites, and double strand lesions were fully repaired by the 4- (in vivo), 24-, and 48-h (in vitro) time-points respectively. Changes in lipid hydroperoxides (P = 0.001), the ascorbyl free radical (P = 0.02), and lipid soluble antioxidants (P > 0.05), were also observed following exercise in hypoxia. These findings highlight significant single- and double strand DNA damage and oxidative stress as a function of high-intensity exercise, which is substantially exacerbated in hypoxia and may be attributed to multiple mechanisms of ROS generation. In addition, full repair of DNA damage (SSB, DSB, and FPG-sensitive sites) was observed within 24- and 48-h of normoxic and hypoxic exercise, respectively.

Exercise and inflammation in coronary artery disease: A systematic review and meta-analysis of randomised trials.

Current evidence suggests that chronic inflammation contributes to the development of coronary artery disease (CAD). Interestingly, exercise may constitute a method of reducing inflammation in this patient population. As such, this systematic review and meta-analysis examined the evidence generated by randomised studies that investigated the effect of exercise on inflammatory biomarkers in CAD. Literature was sought from various sources. Outcomes were pooled in a random-effects model to calculate standardised mean differences (SMD) with 95% confidence intervals (CI). Twenty-five studies were reviewed; post-intervention C-reactive protein (SMD: -0.55 (95% CI: -0.93, -0.16), P = 0.005), fibrinogen (SMD: -0.52 (95% CI: -0.74, -0.29, P = <0.00001)), and von Willebrand factor (SMD: -1.57 (95% CI: -2.23, -0.92), P = <0.00001) values were significantly lower in exercise groups compared to controls. In addition, qualitative analyses identified evidence that supports a beneficial effect of exercise on these acute-phase reactants. However, the impact of exercise on anti-inflammatory cytokines, adhesion molecules, and chemokines is equivocal, which may be attributed to a paucity of research. Nevertheless, the findings of this review suggest that exercise induces an anti-inflammatory effect in CAD patients. Although, the quality of evidence needs to be improved by further randomised studies with high methodological qualities and large sample sizes.

Correction to: DNA Damage Following Acute Aerobic Exercise: A Systematic Review and Meta-analysis.

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DNA Damage Following Acute Aerobic Exercise: A Systematic Review and Meta-analysis.

BACKGROUND: Exercise is widely recognised for its health enhancing benefits. Despite this, an overproduction of reactive oxygen and nitrogen species (RONS), outstripping antioxidant defence mechanisms, can lead to a state of (chronic) oxidative stress. DNA is a vulnerable target of RONS attack and, if left unrepaired, DNA damage may cause genetic instability. OBJECTIVE: This meta-analysis aimed to systematically investigate and assess the overall effect of studies reporting DNA damage following acute aerobic exercise. METHODS: Web of Science, PubMed, MEDLINE, EMBASE, and Scopus were searched until April 2019. Outcomes included (1) multiple time-points (TPs) of measuring DNA damage post-exercise, (2) two different quantification methods (comet assay and 8-oxo-2'-deoxyguanosine; 8-OHdG), and (3) protocols of high intensity (≥ 75% of maximum rate of oxygen consumption; VO2-max) and long distance (≥ 42 km). RESULTS: Literature search identified 4316 non-duplicate records of which 35 studies were included in the meta-analysis. The evidence was strong, showcasing an increase in DNA damage immediately following acute aerobic exercise with a large-effect size at TP 0 (0 h) (SMD = 0.875; 95% CI 0.5, 1.25; p < 0.05). When comparing between comet assay and 8-OHdG at TP 0, a significant difference was observed only when using the comet assay. Finally, when isolating protocols of long-distance and high-intensity exercise, increased DNA damage was only observed in the latter. (SMD = 0.48; 95% CI - 0.16, 1.03; p = 0.15 and SMD = 1.18; 95% CI 0.71, 1.65; p < 0.05 respectively). CONCLUSIONS: A substantial increase in DNA damage occurs immediately following acute aerobic exercise. This increase remains significant between 2 h and 1 day, but not within 5-28 days post-exercise. Such an increase was not observed in protocols of a long-distance. The relationship between exercise and DNA damage may be explained through the hormesis theory, which is somewhat one-dimensional, and thus limited. The hormesis theory describes how exercise modulates any advantageous or harmful effects mediated through RONS, by increasing DNA oxidation between the two end-points of the curve: physical inactivity and overtraining. We propose a more intricate approach to explain this relationship: a multi-dimensional model, to develop a better understanding of the complexity of the relationship between DNA integrity and exercise.

Endothelial Dysfunction in Cystic Fibrosis: Role of Oxidative Stress.

Oxidative stress and vascular endothelial dysfunction are established characteristics of cystic fibrosis (CF). Oxidative stress may contribute to vascular dysfunction via inhibition of nitric oxide (NO) bioavailability. Purpose. To determine if ingestion of a single antioxidant cocktail (AOC) improves vascular endothelial function in patients with CF. Methods. In 18 patients with CF (age 8-39 y), brachial artery flow-mediated dilation (FMD) was assessed using a Doppler ultrasound prior to and two hours following either an AOC (n = 18; 1,000 mg vitamin C, 600 IU vitamin E, and 600 mg α-lipoic acid) or a placebo (n = 9). In a subgroup of patients (n = 9), changes in serum concentrations of α-tocopherol and lipid hydroperoxide (LOOH) were assessed following AOC and placebo. Results. A significant (p = 0.032) increase in FMD was observed following AOC (Δ1.9 ± 3.3%), compared to no change following placebo (Δ - 0.8 ± 1.9%). Moreover, compared with placebo, AOC prevented the decrease in α-tocopherol (Δ0.48 ± 2.91 vs. -1.98 ± 2.32 µM, p = 0.024) and tended to decrease LOOH (Δ - 0.2 ± 0.1 vs. 0.1 ± 0.1 µM, p = 0.063). Conclusions. These data demonstrate that ingestion of an antioxidant cocktail can improve vascular endothelial function and improve oxidative stress in patients with CF, providing evidence that oxidative stress is a key contributor to vascular endothelial dysfunction in CF.

High-Dose Astaxanthin Supplementation Suppresses Antioxidant Enzyme Activity during Moderate-Intensity Swimming Training in Mice.

Exercise-induced reactive oxygen and nitrogen species are increasingly considered as beneficial health promotion. Astaxanthin (ASX) has been recognized as a potent antioxidant suitable for human ingestion. We investigated whether ASX administration suppressed antioxidant enzyme activity in moderate-intensity exercise. Seven-week-old male C57BL/6 mice (n = 8/group) were treated with ASX (5, 15, and 30 mg/kg BW) combined with 45 min/day moderate-intensity swimming training for four weeks. Results showed that the mice administrated with 15 and 30 mg/kg of ASX decreased glutathione peroxidase, catalase, malondialdehyde, and creatine kinase levels in plasma or muscle, compared with the swimming control group. Beyond that, these two (15 and 30 mg/kg BW) dosages of ASX downregulated gastrocnemius muscle erythroid 2p45 (NF-E2)-related factor 2 (Nrf2). Meanwhile, mRNA of Nrf2 and Nrf2-dependent enzymes in mice heart were also downregulated in the ASX-treated groups. However, the mice treated with 15 or 30 mg/kg ASX had increased constitutive nitric oxidase synthase and superoxide dismutase activity, compared with the swimming and sedentary control groups. Our findings indicate that high-dose administration of astaxanthin can blunt antioxidant enzyme activity and downregulate transcription of Nrf2 and Nrf2-dependent enzymes along with attenuating plasma and muscle MDA.

Preceding exercise and postprandial hypertriglyceridemia: effects on lymphocyte cell DNA damage and vascular inflammation.

BACKGROUND: Exercise has proved effective in attenuating the unfavourable response normally associated with postprandial hypertriglyceridemia (PHTG) and accompanying oxidative stress. Yet, the acute effects of prior exercise and PHTG on DNA damage remains unknown. The purpose of this study was to examine if walking alters PHTG-induced oxidative damage and the interrelated inflammatory mechanisms. METHODS: Twelve apparently healthy, recreationally active, male participants (22.4 ± 4.1 years; 179.2 ± 6 cm; 84.2 ± 14.7 kg; 51.3 ± 8.6 ml·kg- 1·min- 1) completed a randomised, crossover study consisting of two trials: (1) a high-fat meal alone (resting control) or (2) a high-fat meal immediately following 1 h of moderate exercise (65% maximal heart rate). Venous blood samples were collected at baseline, immediately post-exercise or rest, as well as at 2, 4 and 6 h post-meal. Biomarkers of oxidative damage (DNA single-strand breaks, lipid peroxidation and free radical metabolism) and inflammation were determined using conventional biochemistry techniques. RESULTS: DNA damage, lipid peroxidation, free radical metabolism and triglycerides increased postprandially (main effect for time, p < 0.05), regardless of completing 1 h of preceding moderate intensity exercise. Plasma antioxidants (α-tocopherol and γ-tocopherol) also mobilised in response to the high-fat meal (main effect for time, p < 0.05), but no changes were detected for retinol-binding protein-4. CONCLUSION: The ingestion of a high fat meal induces postprandial oxidative stress, inflammation and a rise in DNA damage that remains unaltered by one hour of preceding exercise.

Cold water immersion improves recovery of sprint speed following a simulated tournament.

It is a common requirement in tournament scenarios for athletes to compete multiple times in a relatively short time period, with insufficient recovery time not allowing full restoration of physical performance. This study aimed to develop a greater understanding of the physiological stress experienced by athletes in a tournament scenario, and how a commonly used recovery strategy, cold water immersion (CWI), might influence these markers. Twenty-one trained male games players (age 19 ± 2; body mass 78.0 ± 8.8 kg) were randomised into a CWI group (n = 11) or a control group (n = 10). To simulate a tournament, participants completed the Loughborough Intermittent Shuttle Test (LIST) on three occasions in five days. Recovery was assessed at specific time points using markers of sprint performance, muscle function, muscle soreness and biochemical markers of damage (creatine kinase, CK), inflammation (IL-6 and C-Reactive Protein) and oxidative stress (lipid hydroperoxides and activity of 6 lipid-soluble antioxidants). The simulated tournament was associated with perturbations in some, but not all, markers of physiological stress and recovery. Cold water immersion was associated with improved recovery of sprint speed 24 h after the final LIST (ES = 0.83 ± 0.59; p = .034) and attenuated the efflux of CK pre- and post-LIST 3 (p < .01). The tournament scenario resulted in an escalation of physiological stress that, in the main, cold water immersion was ineffective at managing. These data suggest that CWI is not harmful, and provides limited benefits in attenuating the deleterious effects experienced during tournament scenarios.

Assessing the usefulness of acute physiological responses following resistance exercise: sensitivity, magnitude of change, and time course of measures.

A variety of strategies exist to modulate the acute physiological responses following resistance exercise aimed at enhancing recovery and/or adaptation processes. To assess the true impact of these strategies, it is important to know the ability of different measures to detect meaningful change. We investigated the sensitivity of measures used to quantify acute physiological responses to resistance exercise and constructed a physiological profile to characterise the magnitude of change and the time course of these responses. Eight males accustomed to regular resistance exercise performed experimental sessions during a "control week", void of an exercise stimulus. The following week, termed the "exercise week", participants repeated this sequence of experimental sessions, and they also performed a bout of lower-limb resistance exercise following the baseline assessments. Assessments were conducted at baseline and at 2, 6, 24, 48, 72, and 96 h after the intervention. On the basis of the signal-to-noise ratio, the most sensitive measures were maximal voluntary isometric contraction, 20-m sprint, countermovement jump peak force, rate of force development (100-200 ms), muscle soreness, Daily Analysis Of Life Demands For Athletes part B, limb girth, matrix metalloproteinase-9, interleukin-6, creatine kinase, and high-sensitivity C-reactive protein with ratios >1.5. Clear changes in these measures following resistance exercise were determined via magnitude-based inferences. These findings highlight measures that can detect real changes in acute physiological responses following resistance exercise in trained individuals. Researchers investigating strategies to manipulate acute physiological responses for recovery and/or adaptation can use these measures, as well as the recommended sampling points, to be confident that their interventions are making a worthwhile impact.