Effectiveness of alternative vs traditional exercises on cardiac rehabilitation program utilization in women with or at high risk of cardiovascular disease: a systematic review protocol.

OBJECTIVE: This review will evaluate the effectiveness of alternative vs traditional forms of exercise on cardiac rehabilitation program utilization and other outcomes in women with or at high risk of cardiovascular disease. INTRODUCTION: Exercise-based cardiac rehabilitation programs improve health outcomes in women with or at high risk of cardiovascular disease. However, such programs are underutilized worldwide, particularly among women. Some women perceive traditional gym-based exercise in cardiac rehabilitation programs (eg, typically treadmills, cycle ergometers, traditional resistance training) to be excessively rigorous and unpleasant, resulting in diminished participation and completion. Alternative forms of exercise such as yoga, tai chi, qi gong, or Pilates may be more enjoyable and motivating exercise options for women, enhancing engagement in rehabilitation programs. However, the effectiveness of these alternative exercises in improving program utilization is still inconsistent and needs to be systematically evaluated and synthesized. INCLUSION CRITERIA: This review will focus on randomized controlled trials of studies measuring the effectiveness of alternative vs traditional forms of exercise on cardiac rehabilitation program utilization as well as clinical, physiological, or patient-reported outcomes in women with or at high risk of cardiovascular disease. METHODS: The review will follow the JBI methodology for systematic reviews of effectiveness. Databases including MEDLINE (Ovid), CINAHL (EBSCOhost), Cochrane CENTRAL, Embase (Ovid), Emcare (Ovid), Scopus, Web of Science, LILACS, and PsycINFO (Ovid) will be searched. Two independent reviewers will screen articles and then extract and synthesize data. Methodological quality will be assessed using JBI's standardized instruments. GRADE will be used to determine the certainty of evidence. REVIEW REGISTRATION: PROSPERO CRD42022354996.

Medicare reimbursed telehealth exercise physiology services were underutilised through the coronavirus (COVID-19) pandemic: an ecological study.

Objectives To describe the quantity and cost of in-person and telehealth exercise physiology (EP) reimbursed under the Medicare Benefits Schedule (MBS) in Australia before and during the coronavirus disease 2019 (COVID-19) pandemic. Methods This study uses publicly available MBS data to describe EP services (in-person and telehealth) reimbursed by Medicare between January 2020 and December 2021. Data were extracted at state and national levels. Results Despite a reduction in quantity and cost in quartile (Q) 2 2020 (41% reduction), MBS-reimbursed EP services have remained relatively constant at a national level through the 2-year observation period. Service claims averaged 88 555 per quarter in 2020 and 95 015 in 2021. The proportion of telehealth consultations relative to total quarterly claims for EP was <1% in Q1 2020, 6.0% in Q2 2020, 2.4% in Q3 2020 and 1.7% in Q4 2020. This dropped to an average of 1.4% across 2021 (Q1-Q4). States undergoing lockdown periods reported decreased service rates relative to February 2020 (i.e. pre-lockdown). EP services were associated with a Medicare expenditure of AUD17.9M in 2020 (telehealth = 2.4% of total) and AUD19.7M (telehealth = 1.5% of total) in 2021. Conclusions Quantity and cost of MBS-reimbursed EP services remained relatively constant throughout the height of service disruption due to COVID-19 (2020/21). Telehealth uptake during this time has been minimal for EP.

The effect of heat therapy on blood pressure and peripheral vascular function: A systematic review and meta-analysis.

NEW FINDINGS: What is the topic of this review? We have conducted a systematic review and meta-analysis on the current evidence for the effect of heat therapy on blood pressure and vascular function. What advances does it highlight? We found that heat therapy reduced mean arterial, systolic and diastolic blood pressure. We also observed that heat therapy improved vascular function, as assessed via brachial artery flow-mediated dilatation. Our results suggest that heat therapy is a promising therapeutic tool that should be optimized further, via mode and dose, for the prevention and treatment of cardiovascular disease risk factors. ABSTRACT: Lifelong sauna exposure is associated with reduced cardiovascular disease risk. Recent studies have investigated the effect of heat therapy on markers of cardiovascular health. We aimed to conduct a systematic review with meta-analysis to determine the effects of heat therapy on blood pressure and indices of vascular function in healthy and clinical populations. Four databases were searched up to September 2020 for studies investigating heat therapy on outcomes including blood pressure and vascular function. Grading of Recommendations, Assessment, Development and Evaluations (GRADE) was used to assess the certainty of evidence. A total of 4522 titles were screened, and 15 studies were included. Healthy and clinical populations were included. Heat exposure was for 30-90 min, over 10-36 sessions. Compared with control conditions, heat therapy reduced mean arterial pressure [n = 4 studies; mean difference (MD): -5.86 mmHg, 95% confidence interval (CI): -8.63, -3.10; P < 0.0001], systolic blood pressure (n = 10; MD: -3.94 mmHg, 95% CI: -7.22, -0.67; P = 0.02) and diastolic blood pressure (n = 9; MD: -3.88 mmHg, 95% CI: -6.13, -1.63; P = 0.0007) and improved flow-mediated dilatation (n = 5; MD: 1.95%, 95% CI: 0.14, 3.76; P = 0.03). Resting heart rate was unchanged (n = 10; MD: -1.25 beats/min; 95% CI: -3.20, 0.70; P = 0.21). Early evidence also suggests benefits for arterial stiffness and cutaneous microvascular function. The certainty of evidence was moderate for the effect of heat therapy on systolic and diastolic blood pressure and heart rate and low for the effect of heat therapy on mean arterial pressure and flow-mediated dilatation. Heat therapy is an effective therapeutic tool to reduce blood pressure and improve macrovascular function. Future research should aim to optimize heat therapy, including the mode and dose, for the prevention and management of cardiovascular disease.

Exercise and sport science australia position stand update on exercise and hypertension.

Hypertension is the most common circulatory system condition, accounting for >40% of the cardiovascular disease total burden. One-third of Australians aged over 18 years have hypertension and in 68% of these it is uncontrolled. Australian data show hypertension accounts for 6% of general practitioner (GP) consults. Recent evidence has confirmed exercise is an effective adjunct therapy for hypertension management and the objective of this document is to provide a contemporary, evidence-based guide for optimal delivery of an exercise programme for blood pressure management. This work is an update to the 2009 Exercise and Sport Science Australia (ESSA) position stand. In most cases, the first line treatment to reduce BP is initiation of lifestyle changes, of which regular aerobic exercise is a principal component. Aerobic and resistance activities remain the cornerstone of exercise-based management of blood pressure, but recent work has uncovered variations on traditional delivery of exercise, such as high intensity interval training (HIIT) and a new exercise modality, isometric resistance training (IRT) may offer alternative management regimens. Exercise Physiologists, as well as other health care professionals, play an important role in helping to achieve BP control in patients with hypertension by reinforcing healthy lifestyle habits and prescribing appropriate exercise.

Turning Up the Heat: An Evaluation of the Evidence for Heating to Promote Exercise Recovery, Muscle Rehabilitation and Adaptation.

Historically, heat has been used in various clinical and sports rehabilitation settings to treat soft tissue injuries. More recently, interest has emerged in using heat to pre-condition muscle against injury. The aim of this narrative review was to collate information on different types of heat therapy, explain the physiological rationale for heat therapy, and to summarise and evaluate the effects of heat therapy before, during and after muscle injury, immobilisation and strength training. Studies on skeletal muscle cells demonstrate that heat attenuates cellular damage and protein degradation (following in vitro challenges/insults to the cells). Heat also increases the expression of heat shock proteins (HSPs) and upregulates the expression of genes involved in muscle growth and differentiation. In rats, applying heat before and after muscle injury or immobilisation typically reduces cellular damage and muscle atrophy, and promotes more rapid muscle growth/regeneration. In humans, some research has demonstrated benefits of microwave diathermy (and, to a lesser extent, hot water immersion) before exercise for restricting muscle soreness and restoring muscle function after exercise. By contrast, the benefits of applying heat to muscle after exercise are more variable. Animal studies reveal that applying heat during limb immobilisation attenuates muscle atrophy and oxidative stress. Heating muscle may also enhance the benefits of strength training for improving muscle mass in humans. Further research is needed to identify the most effective forms of heat therapy and to investigate the benefits of heat therapy for restricting muscle wasting in the elderly and those individuals recovering from serious injury or illness.

Sulforaphane and Other Nutrigenomic Nrf2 Activators: Can the Clinician's Expectation Be Matched by the Reality?

The recognition that food-derived nonnutrient molecules can modulate gene expression to influence intracellular molecular mechanisms has seen the emergence of the fields of nutrigenomics and nutrigenetics. The aim of this review is to describe the properties of nutrigenomic activators of transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), comparing the potential for sulforaphane and other phytochemicals to demonstrate clinical efficacy as complementary medicines. Broccoli-derived sulforaphane emerges as a phytochemical with this capability, with oral doses capable of favourably modifying genes associated with chemoprevention. Compared with widely used phytochemical-based supplements like curcumin, silymarin, and resveratrol, sulforaphane more potently activates Nrf2 to induce the expression of a battery of cytoprotective genes. By virtue of its lipophilic nature and low molecular weight, sulforaphane displays significantly higher bioavailability than the polyphenol-based dietary supplements that also activate Nrf2. Nrf2 activation induces cytoprotective genes such as those playing key roles in cellular defense mechanisms including redox status and detoxification. Both its high bioavailability and significant Nrf2 inducer capacity contribute to the therapeutic potential of sulforaphane-yielding supplements.

Effect of tocopherol on atherosclerosis, vascular function, and inflammation in apolipoprotein E knockout mice with subtotal nephrectomy.

BACKGROUND/AIMS: Inflammation and endothelial dysfunction contribute to cardiovascular disease, prevalent in chronic kidney disease (CKD). Antioxidant supplements such as tocopherols may reduce inflammation and atherosclerosis. This study aimed to investigate the effect of tocopherol supplementation on vascular function, aortic plaque formation, and inflammation in apolipoprotein E(-/-) mice with 5/6 nephrectomy as a model of combined cardiovascular and kidney disease. METHODS: Nephrectomized mice were assigned to a normal chow diet group (normal chow), a group receiving 1000 mg/kg diet of α-tocopherol supplementation or a group receiving 1000 mg/kg diet mixed-tocopherol (60% γ-tocopherol). RESULTS: Following 12 weeks, in vitro aortic endothelial-independent relaxation was enhanced with both α-tocopherol and mixed-tocopherol (P < 0.05), while mixed-tocopherol enhanced aortic contraction at noradrenaline concentrations of 3 × 10(-7) M to 3 × 10(-5) M (P < 0.05), when compared to normal chow. Supplementation with α- and mixed-tocopherol reduced systemic concentrations of IL-6 (P < 0.001 and P < 0.001, respectively) and IL-10 (P < 0.05 and P < 0.001, respectively), while α-tocopherol also reduced MCP-1 (P < 0.05) and tumor necrosis factor (TNF)-α (P < 0.05). Aortic sinus plaque area was significantly reduced with α-tocopherol supplementation when compared to normal chow (P < 0.01). CONCLUSION: Tocopherol supplementation favorably influenced vascular function and cytokine profile, while it was also effective in reducing atherosclerosis in the apolipoprotein E(-/-) mouse with CKD.

Central and peripheral adjustments during high-intensity exercise following cold water immersion.

PURPOSE: We investigated the acute effects of cold water immersion (CWI) or passive recovery (PAS) on physiological responses during high-intensity interval training (HIIT). METHODS: In a crossover design, 14 cyclists completed 2 HIIT sessions (HIIT1 and HIIT2) separated by 30 min. Between HIIT sessions, they stood in cold water (10 °C) up to their umbilicus, or at room temperature (27 °C) for 5 min. The natural logarithm of square-root of mean squared differences of successive R-R intervals (ln rMSSD) was assessed pre- and post-HIIT1 and HIIT2. Stroke volume (SV), cardiac output (Q), O2 uptake (VO2), total muscle hemoglobin (t Hb) and oxygenation of the vastus lateralis were recorded (using near infrared spectroscopy); heart rate, Q, and VO2 on-kinetics (i.e., mean response time, MRT), muscle de-oxygenation rate, and anaerobic contribution to exercise were calculated for HIIT1 and HIIT2. RESULTS: ln rMSSD was likely higher [between-trial difference (90% confidence interval) [+13.2% (3.3; 24.0)] after CWI compared with PAS. CWI also likely increased SV [+5.9% (-0.1; 12.1)], possibly increased Q [+4.4% (-1.0; 10.3)], possibly slowed Q MRT [+18.3% (-4.1; 46.0)], very likely slowed VO2 MRT [+16.5% (5.8; 28.4)], and likely increased the anaerobic contribution to exercise [+9.7% (-1.7; 22.5)]. CONCLUSION: CWI between HIIT slowed VO2 on-kinetics, leading to increased anaerobic contribution during HIIT2. This detrimental effect of CWI was likely related to peripheral adjustments, because the slowing of VO2 on-kinetics was twofold greater than that of central delivery of O2 (i.e., Q). CWI has detrimental effects on high-intensity aerobic exercise performance that persist for ≥ 45 min.

Sulforaphane: translational research from laboratory bench to clinic.

Cruciferous vegetables are widely acknowledged to provide chemopreventive benefits in humans, but they are not generally consumed at levels that effect significant change in biomarkers of health. Because consumers have embraced the notion that dietary supplements may prevent disease, this review considers whether an appropriately validated sulforaphane-yielding broccoli sprout supplement may deliver clinical benefit. The crucifer-derived bioactive phytochemical sulforaphane is a significant inducer of nuclear factor erythroid 2-related factor 2 (Nrf2), the transcription factor that activates the cell's endogenous defenses via a battery of cytoprotective genes. For a broccoli sprout supplement to demonstrate bioactivity in vivo, it must retain both the sulforaphane-yielding precursor compound, glucoraphanin, and the activity of glucoraphanin's intrinsic myrosinase enzyme. Many broccoli sprout supplements are myrosinase inactive, but current labeling does not reflect this. For the benefit of clinicians and consumers, this review summarizes the findings of in vitro studies and clinical trials, interpreting them in the context of clinical relevance. Standardization of sulforaphane nomenclature and assay protocols will be necessary to remove inconsistency and ambiguity in the labeling of currently available broccoli sprout products.

Astaxanthin in cardiovascular health and disease.

Oxidative stress and inflammation are established processes contributing to cardiovascular disease caused by atherosclerosis. However, antioxidant therapies tested in cardiovascular disease such as vitamin E, C and ß-carotene have proved unsuccessful at reducing cardiovascular events and mortality. Although these outcomes may reflect limitations in trial design, new, more potent antioxidant therapies are being pursued. Astaxanthin, a carotenoid found in microalgae, fungi, complex plants, seafood, flamingos and quail is one such agent. It has antioxidant and anti-inflammatory effects. Limited, short duration and small sample size studies have assessed the effects of astaxanthin on oxidative stress and inflammation biomarkers and have investigated bioavailability and safety. So far no significant adverse events have been observed and biomarkers of oxidative stress and inflammation are attenuated with astaxanthin supplementation. Experimental investigations in a range of species using a cardiac ischaemia-reperfusion model demonstrated cardiac muscle preservation when astaxanthin is administered either orally or intravenously prior to the induction of ischaemia. Human clinical cardiovascular studies using astaxanthin therapy have not yet been reported. On the basis of the promising results of experimental cardiovascular studies and the physicochemical and antioxidant properties and safety profile of astaxanthin, clinical trials should be undertaken.

Effects of exercise and antioxidant supplementation on endothelial gene expression.

BACKGROUND: The molecular mechanisms of exercise training induced cardiovascular protection are poorly understood. There is growing evidence that reactive oxygen species may be involved in a number of these adaptations and that antioxidants may be used to investigate this effect. OBJECTIVE: To determine the effects of exercise training and/or antioxidant supplementation on myocardial endothelium and vascular endothelium gene expression. METHODS: Male Wistar rats were divided into four groups: i) control; ii) exercise trained (90 min of treadmill running 4d per week, 14 weeks); iii) antioxidant-supplemented (α-tocopherol 1000 IU kg(-1) diet and α-lipoic acid 1.6 g kg(-1) diet, mixed with rat chow) and iv) exercise trained and antioxidant-supplemented. RESULTS: cDNA microarray analysis showed diverse expression changes in both left ventricular and coronary artery endothelial cells. In particular, RT-PCR analysis showed that a gene involved in cardiovascular disease progression, Ras homolog gene family member A, was down-regulated by exercise, and up-regulated by antioxidant supplementation in left ventricular endothelial cells. Furthermore, an important gene involved in inflammation, IL-6, was down-regulated by all treatments. CONCLUSIONS: Exercise training and/or antioxidant supplementation affects cardiac endothelial cell gene expression, and their effects on genes such as ras homolog gene family member A and IL-6 provides insight into the molecular mechanisms of their influences on cardiovascular diseases.

Antioxidant supplementation during exercise training: beneficial or detrimental?

High levels of reactive oxygen species (ROS) produced in skeletal muscle during exercise have been associated with muscle damage and impaired muscle function. Supporting endogenous defence systems with additional oral doses of antioxidants has received much attention as a noninvasive strategy to prevent or reduce oxidative stress, decrease muscle damage and improve exercise performance. Over 150 articles have been published on this topic, with almost all of these being small-scale, low-quality studies. The consistent finding is that antioxidant supplementation attenuates exercise-induced oxidative stress. However, any physiological implications of this have yet to be consistently demonstrated, with most studies reporting no effects on exercise-induced muscle damage and performance. Moreover, a growing body of evidence indicates detrimental effects of antioxidant supplementation on the health and performance benefits of exercise training. Indeed, although ROS are associated with harmful biological events, they are also essential to the development and optimal function of every cell. The aim of this review is to present and discuss 23 studies that have shown that antioxidant supplementation interferes with exercise training-induced adaptations. The main findings of these studies are that, in certain situations, loading the cell with high doses of antioxidants leads to a blunting of the positive effects of exercise training and interferes with important ROS-mediated physiological processes, such as vasodilation and insulin signalling. More research is needed to produce evidence-based guidelines regarding the use of antioxidant supplementation during exercise training. We recommend that an adequate intake of vitamins and minerals through a varied and balanced diet remains the best approach to maintain the optimal antioxidant status in exercising individuals.

The effects of dietary fish oil on inflammation, fibrosis and oxidative stress associated with obstructive renal injury in rats.

SCOPE: We examined whether dietary supplementation with fish oil modulates inflammation, fibrosis and oxidative stress following obstructive renal injury. METHODS AND RESULTS: Three groups of Sprague-Dawley rats (n=16 per group) were fed for 4 wk on normal rat chow (oleic acid), chow containing fish oil (33 g eicosapentaenoic acid and 26 g docosahexaenoic acid per kg diet), or chow containing safflower oil (60 g linoleic acid per kg diet). All diets contained 7% fat. After 4 wk, the rats were further subdivided into four smaller groups (n=4 per group). Unilateral ureteral obstruction was induced in three groups (for 4, 7 and 14 days). The fourth group for each diet did not undergo surgery, and was sacrificed as controls at 14 days. When rats were sacrificed, plasma and portions of the kidneys were removed and frozen; other portions of kidney tissue were fixed and prepared for histology. Compared with normal chow and safflower oil, fish oil attenuated collagen deposition, macrophage infiltration, TGF-ß expression, apoptosis, and tissue levels of arachidonic acid, MIP-1α, IL-1ß, MCP-1 and leukotriene B(4). Compared with normal chow, fish oil increased the expression of HO-1 protein in kidney tissue. CONCLUSIONS: Fish oil intake reduced inflammation, fibrosis and oxidative stress following obstructive renal injury.

Nutritional compounds influence tissue factor expression and inflammation of chronic kidney disease patients in vitro.

OBJECTIVE: Nutritional compounds that potentially limit inflammation and tissue factor expression may decrease the progression of chronic kidney disease (CKD) and associated cardiovascular disease. This project aimed to determine the effect of curcumin, bovine colostrum, and fish oil on inflammatory cytokine and tissue factor procoagulant activity of peripheral blood mononuclear cells (PBMCs) from patients with CKD before dialysis. METHODS: Peripheral blood mononuclear cells from patients with CKD before dialysis (n = 13) and age- and sex-matched healthy controls (n = 12) were cultured alone and with low and high doses of the nutritional compounds for 24 h. Cells were cultured with and without lipopolysaccharide. Supernatants were analyzed for tumor necrosis factor-α, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, IL-1ß, C-reactive protein, and tissue factor procoagulant activity. RESULTS: The production of C-reactive protein, monocyte chemoattractant protein-1, IL-6, and IL-1ß by PBMCs was inhibited by low- and high-dose fish oil in the CKD group (P < 0.05). Curcumin decreased secretion of IL-6 (P = 0.015) and IL-1 ß (P = 0.016). Curcumin was more effective than colostrum at decreasing the procoagulant activity of PBMCs in the CKD and control groups (P < 0.019). CONCLUSION: Fish oil decreased inflammatory cytokine secretion from CKD PBMCs. In addition, the beneficial effects of curcumin were demonstrated in decreasing inflammation in vitro, often to a similar magnitude as fish oil.

Antioxidant supplementation reduces skeletal muscle mitochondrial biogenesis.

PURPOSE: Exercise increases the production of reactive oxygen species (ROS) in skeletal muscle, and athletes often consume antioxidant supplements in the belief they will attenuate ROS-related muscle damage and fatigue during exercise. However, exercise-induced ROS may regulate beneficial skeletal muscle adaptations, such as increased mitochondrial biogenesis. We therefore investigated the effects of long-term antioxidant supplementation with vitamin E and α-lipoic acid on changes in markers of mitochondrial biogenesis in the skeletal muscle of exercise-trained and sedentary rats. METHODS: Male Wistar rats were divided into four groups: 1) sedentary control diet, 2) sedentary antioxidant diet, 3) exercise control diet, and 4) exercise antioxidant diet. Animals ran on a treadmill 4 d · wk at ∼ 70%VO2max for up to 90 min · d for 14 wk. RESULTS: Consistent with the augmentation of skeletal muscle mitochondrial biogenesis and antioxidant defenses, after training there were significant increases in peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) messenger RNA (mRNA) and protein, cytochrome C oxidase subunit IV (COX IV) and cytochrome C protein abundance, citrate synthase activity, Nfe2l2, and SOD2 protein (P < 0.05). Antioxidant supplementation reduced PGC-1α mRNA, PGC-1α and COX IV protein, and citrate synthase enzyme activity (P < 0.05) in both sedentary and exercise-trained rats. CONCLUSIONS: Vitamin E and α-lipoic acid supplementation suppresses skeletal muscle mitochondrial biogenesis, regardless of training status.

Omega-3 polyunsaturated fatty acids in the treatment of kidney disease.

After more than 25 years of published investigation, including randomized controlled trials, the role of omega-3 polyunsaturated fatty acids in the treatment of kidney disease remains unclear. In vitro and in vivo experimental studies support the efficacy of omega-3 polyunsaturated fatty acids on inflammatory pathways involved with the progression of kidney disease. Clinical investigations have focused predominantly on immunoglobulin A (IgA) nephropathy. More recently, lupus nephritis, polycystic kidney disease, and other glomerular diseases have been investigated. Clinical trials have shown conflicting results for the efficacy of omega-3 polyunsaturated fatty acids in IgA nephropathy, which may relate to varying doses, proportions of eicosapentaenoic acid and docosahexaenoic acid, duration of therapy, and sample size of the study populations. Meta-analyses of clinical trials using omega-3 polyunsaturated fatty acids in IgA nephropathy have been limited by the quality of available studies. However, guidelines suggest that omega-3 polyunsaturated fatty acids should be considered in progressive IgA nephropathy. Omega-3 polyunsaturated fatty acids decrease blood pressure, a known accelerant of kidney disease progression. Well-designed, adequately powered, randomized, controlled clinical trials are required to further investigate the potential benefits of omega-3 polyunsaturated fatty acids on the progression of kidney disease and patient survival.

Astaxanthin, oxidative stress, inflammation and cardiovascular disease.

It is accepted that oxidative stress and inflammation play an integral role in the pathophysiology of many chronic diseases including atherosclerotic cardiovascular disease. The xanthophyll carotenoid dietary supplement astaxanthin has demonstrated potential as an antioxidant and anti-inflammatory therapeutic agent in models of cardiovascular disease. There have been at least eight clinical studies conducted in over 180 humans using astaxanthin to assess its safety, bioavailability and clinical aspects relevant to oxidative stress, inflammation or the cardiovascular system. There have been no adverse outcomes reported. Studies have demonstrated reduced markers of oxidative stress and inflammation and improved blood rheology. A larger number of experimental studies have been performed using astaxanthin. In particular, studies in a variety of animals using a model of myocardial ischemia and reperfusion have demonstrated protective effects from prior administration of astaxanthin both intravenously and orally. Future clinical studies and trials will help determine the efficacy of antioxidants such as astaxanthin on vascular structure, function, oxidative stress and inflammation in a variety of patients at risk of, or with, established cardiovascular disease. These may lead to large intervention trials assessing cardiovascular morbidity and mortality.

Bovine colostrum modulates cytokine production in human peripheral blood mononuclear cells stimulated with lipopolysaccharide and phytohemagglutinin.

Bovine colostrum has been shown to influence the cytokine production of bovine leukocytes. However, it remains unknown whether processed bovine colostrum, a supplement popular among athletes to enhance immune function, is able to modulate cytokine secretion of human lymphocytes and monocytes. The aim of this investigation was to determine the influence of a commercially available bovine colostrum protein concentrate (CPC) to stimulate cytokine production by human peripheral blood mononuclear cells (PBMCs). Blood was sampled from four healthy male endurance athletes who had abstained from exercise for 48 h. PBMCs were separated and cultured with bovine CPC concentrations of 0 (control), 1.25, 2.5, and 5% with and without lipopolysaccharide (LPS) (3 microg/mL) and phytohemagglutinin (PHA) (2.5 microg/mL). Cell supernatants were collected at 6 and 24 h of culture for the determination of tumor necrosis factor (TNF), interferon (IFN)-gamma, interleukin (IL)-10, IL-6, IL-4, and IL-2 concentrations. Bovine CPC significantly stimulated the release of IFN-gamma, IL-10, and IL-2 (p < 0.03). The addition of LPS to PBMCs cocultured with bovine CPC significantly stimulated the release of IL-2 and inhibited the early release of TNF, IL-6, and IL-4 (p < 0.02). Phytohemagglutinin stimulation in combination with bovine CPC significantly increased the secretion of IL-10 and IL-2 at 6 h of culture and inhibited IFN-gamma and TNF (p < 0.05). This data show that a commercial bovine CPC is able to modulate in vitro cytokine production of human PBMCs. Alterations in cytokine secretion may be a potential mechanism for reported benefits associated with supplementation.

Astaxanthin vs placebo on arterial stiffness, oxidative stress and inflammation in renal transplant patients (Xanthin): a randomised controlled trial.

BACKGROUND: There is evidence that renal transplant recipients have accelerated atherosclerosis manifest by increased cardiovascular morbidity and mortality. The high incidence of atherosclerosis is, in part, related to increased arterial stiffness, vascular dysfunction, elevated oxidative stress and inflammation associated with immunosuppressive therapy. The dietary supplement astaxanthin has shown promise as an antioxidant and anti-inflammatory therapeutic agent in cardiovascular disease. The aim of this trial is to investigate the effects of astaxanthin supplementation on arterial stiffness, oxidative stress and inflammation in renal transplant patients. METHOD AND DESIGN: This is a randomised, placebo controlled clinical trial. A total of 66 renal transplant recipients will be enrolled and allocated to receive either 12 mg/day of astaxanthin or an identical placebo for one-year. Patients will be stratified into four groups according to the type of immunosuppressant therapy they receive: 1) cyclosporine, 2) sirolimus, 3) tacrolimus or 4) prednisolone+/-azathioprine, mycophenolate mofetil or mycophenolate sodium. Primary outcome measures will be changes in 1) arterial stiffness measured by aortic pulse wave velocity (PWV), 2) oxidative stress assessed by plasma isoprostanes and 3) inflammation by plasma pentraxin 3. Secondary outcomes will include changes in vascular function assessed using the brachial artery reactivity (BAR) technique, carotid artery intimal medial thickness (CIMT), augmentation index (AIx), left ventricular afterload and additional measures of oxidative stress and inflammation. Patients will undergo these measures at baseline, six and 12 months. DISCUSSION: The results of this study will help determine the efficacy of astaxanthin on vascular structure, oxidative stress and inflammation in renal transplant patients. This may lead to a larger intervention trial assessing cardiovascular morbidity and mortality. TRIAL REGISTRATION: ACTRN12608000159358.

Oxidative stress in half and full Ironman triathletes.

INTRODUCTION: Ultraendurance athletes who maintain a very high volume of exercise may, as a result of greater production of reactive oxygen species (ROS), be particularly susceptible to oxidative damage. PURPOSE: This study sought to examine and compare pre- and postrace markers of oxidative stress in ultraendurance athletes training for, and competing in, either a half or a full Ironman triathlon. METHODS: Resting and postexercise blood was sampled from 16 half Ironman triathletes, 29 full Ironman triathletes, and age-matched, relatively inactive controls. Blood was analyzed for markers of oxidative stress (malondialdehyde (MDA) concentration) and antioxidant status (glutathione peroxidase (GPX), catalase (CAT), and superoxide dismutase (SOD) activities). RESULTS: Compared with controls, the half Ironman triathletes had significantly (P < 0.001) higher erythrocyte GPX activity at rest, whereas the Ironman triathletes had significantly (P < 0.05) lower resting plasma MDA and significantly (P < 0.05) greater resting activities of GPX and CAT compared with controls. As a result of the half Ironman triathlon, there was a significant (P < 0.05) increase in MDA and significant (P < 0.05) decreases in erythrocyte GPX, SOD, and CAT activities. These changes also occurred in response to the Ironman triathlon; MDA significantly (P < 0.05) increased, and there were significant (P < 0.001) decreases in GPX, CAT, and SOD activities. Users of antioxidant supplements in both the half and full Ironman races had significantly (P < 0.05) elevated MDA after races compared with nonsupplementers. CONCLUSION: The present investigation indicates that training for and competing in half and full Ironman triathlons has different effects on erythrocyte antioxidant enzyme activities and oxidative stress.