Effect of diet versus diet and exercise on weight loss and body composition in class II and III obesity: A systematic review

Class II and III obesity (BMI >35 kg·m2) have increased dramatically in recent years. Current clinical guidelines suggest diet and exercise as first line treatment for adults throughout the spectrum of overweight and obesity. However, to date there is no systematic review that examines the effects of diet and exercise on this high risk population. This systematic review will examine the combined effects of diet versus diet and exercise on body composition in severe obesity. Medline and Cinahl were searched for randomised controlled trials comparing diet and exercise to diet alone. Studies published until July 2013 were included if they used reliable methods for analysing body composition in adults with BMI ≥ 35 kg·m2. Five of 459 studies met the inclusion criteria. Two studies, both in older adults, reported that exercise reduced lean mass loss during weight loss. Two studies showed that exercise facilitated (greater) fat mass loss. The remaining study reported no differences in body composition when exercise is added to energy restriction. Exercise training during energy restriction for individuals with BMI ≥35 kg.m2 may influence body composition outcomes but the evidence is limited. Further studies should focus on the efficacy of different exercise protocols during energy restriction for this population in order to better inform decision making for the treatment of severe obesity in respect to favourable body composition outcomes

Comparing methods for prescribing exercise for individuals with chronic heart failure

This study examined the accuracy of current recommended guidelines for prescribing exercise intensity using the methods of percentage of heart rate reserve (%HRR), percentage of VO2 peak (%VO2peak) and percentage of VO2 reserve (%VO2R) in a clinical population of chronic heart failure (CHF) patients. The precision of prescription of exercise intensity for 45 patients with stable CHF (39:6 M:F, 65&plusmn;9 yrs (mean&plusmn;SD)) was investigated. VO2peak testing is relatively common among patients with cardiac disease, but the assessment of VO2rest is not common practice and the accepted standard value of 3.5 mL/kg/min is assumed in the application of %VO2R (%VO2R3.5). In this study, VO2rest was recorded for 3 min prior to the start of a symptom-limited exercise test on a cycle ergometer. Target exercise intensities were calculated using the VO2 corresponding to 50 or 80 %HRR, VO2peak and VO2R. The VO2 values were then converted into prescribed speeds on a treadmill in km/hr at 1 %grade using ACSM&rsquo;s metabolic equation for walking. Target intensities and prescribed treadmill speeds were also calculated with the %VO2R method using the mean VO2rest value of participants (3.9 mL/kg/min) (%VO2R3.9). This was then compared to the exercise intensities and prescribed treadmill speeds using patient&rsquo;s measured VO2rest. Error in prescription correlates the difference between %VO2R3.5 and %VO2R3.9 compared to %VO2R with measured VO2rest. Prescription of exercise intensity through the %HRR method is imprecise for patients on medications that blunt the HR response to exercise. %VO2R method offers a significant improvement in exercise prescription compared to %VO2peak. However, a disparity of 10 % still exists in the %VO2R method using the standard 3.5 mL/kg/min for VO2rest in the %VO2R equation. The mean measured VO2rest in the 45 CHF patients was 11 % higher (3.9&plusmn;0.8 mL/kg/min) than the standard value provided by ACSM. Applying the mean measured VO2rest value of 3.9 mL/kg/min rather than the standard assumed value of 3.5 mL/kg/min proved to be closer to the prescribed intensity determined by the actual measured resting VO2. These results suggest that the %HRR method should not be used to prescribe exercise intensity for CHF patients. Instead, VO2 should be used to prescribe exercise intensity and be expressed as %VO2R with measured variables (VO2rest and VO2peak).<br /

Patterns of Coral Disease across the Hawaiian Archipelago: Relating Disease to Environment

In Hawaii, coral reefs occur across a gradient of biological (host abundance), climatic (sea surface temperature anomalies) and anthropogenic conditions from the human-impacted reefs of the main Hawaiian Islands (MHI) to the pristine reefs of the northwestern Hawaiian Islands (NWHI). Coral disease surveys were conducted at 142 sites from across the Archipelago and disease patterns examined. Twelve diseases were recorded from three coral genera (Porites, Montipora, Acropora) with Porites having the highest prevalence. Porites growth anomalies (PorGAs) were significantly more prevalent within and indicative of reefs in the MHI and Porites trematodiasis (PorTrm) was significantly more prevalent within and indicative of reefs in the NWHI. Porites tissue loss syndrome (PorTLS) was also important in driving regional differences but that relationship was less clear. These results highlight the importance of understanding disease ecology when interpreting patterns of disease occurrence. PorTrm is caused by a parasitic flatworm that utilizes multiple hosts during its life cycle (fish, mollusk and coral). All three hosts must be present for the disease to occur and higher host abundance leads to higher disease prevalence. Thus, a high prevalence of PorTrm on Hawaiian reefs would be an indicator of a healthy coral reef ecosystem. In contrast, the high occurrence of PorGAs within the MHI suggests that PorGAs are related, directly or indirectly, to some environmental co-factor associated with increased human population sizes. Focusing on the three indicator diseases (PorGAs, PorTrm, PorTLS) we used statistical modeling to examine the underlying associations between disease prevalence and 14 different predictor variables (biotic and abiotic). All three diseases showed positive associations with host abundance and negative associations with thermal stress. The association with human population density differed among disease states with PorGAs showing a positive and PorTrm showing a negative association, but no significant explanatory power was offered for PorTLS

The Complete Genome Sequence of Thermoproteus tenax: A Physiologically Versatile Member of the Crenarchaeota

Here, we report on the complete genome sequence of the hyperthermophilic Crenarchaeum Thermoproteus tenax (strain Kra 1, DSM 2078(T)) a type strain of the crenarchaeotal order Thermoproteales. Its circular 1.84-megabase genome harbors no extrachromosomal elements and 2,051 open reading frames are identified, covering 90.6% of the complete sequence, which represents a high coding density. Derived from the gene content, T. tenax is a representative member of the Crenarchaeota. The organism is strictly anaerobic and sulfur-dependent with optimal growth at 86 degrees C and pH 5.6. One particular feature is the great metabolic versatility, which is not accompanied by a distinct increase of genome size or information density as compared to other Crenarchaeota. T. tenax is able to grow chemolithoautotrophically (CO2/H-2) as well as chemoorganoheterotrophically in presence of various organic substrates. All pathways for synthesizing the 20 proteinogenic amino acids are present. In addition, two presumably complete gene sets for NADH:quinone oxidoreductase (complex I) were identified in the genome and there is evidence that either NADH or reduced ferredoxin might serve as electron donor. Beside the typical archaeal A(0)A(1)-ATP synthase, a membrane-bound pyrophosphatase is found, which might contribute to energy conservation. Surprisingly, all genes required for dissimilatory sulfate reduction are present, which is confirmed by growth experiments. Mentionable is furthermore, the presence of two proteins (ParA family ATPase, actin-like protein) that might be involved in cell division in Thermoproteales, where the ESCRT system is absent, and of genes involved in genetic competence (DprA, ComF) that is so far unique within Archaea

Accreditation Downunder

Exercise is now accepted as highleffective in reducing the risk of many chronic diseases by both the scientific and medical communities (Unites States Department of Helath and Human Services, 1996), as well as preventing their progression, relapse and recurrence. It has also long been recognised as an effective treatment for a diverse range of injuries, diseases and conditions. Clinical exercise services have three main outcome goals: to improve function; clinical status; and quality of life, and these are supported by a growing body of evidence demonstrating the efficacy of exercise across a wide array of chronic medical conditions

Evidence‐based approach to exercise prescription in chronic heart failure

The benefits of moderate exercise appear to outweigh the risk

Circuit resistance training in chronic heart failure improves skeletal muscle mitochondrial ATP production rate - a randomised controlled trial

Background. We aimed to determine the role of skeletal muscle mitochondrial ATP production rate (MAPR) in relation to exercise tolerance following resistance training in CHF. Methods and Results. Thirteen CHF patients (NYHA functional class 2.3 ± 0.5; LVEF 26 ± 8%; age 70 ± 8 years) underwent testing for VO2peak, and resting vastus lateralis muscle biopsy. Patients were then randomly allocated to 11 weeks of RT, (n = 7) or continuance of usual care (C, n = 6) following which testing was repeated. Muscle samples were analysed for MAPR, metabolic enzyme activity and capillary density. VO2peak and MAPR in the presence of the pyruvate and malate (P+M) substrate combination, representing carbohydrate metabolism, increased in RT (p<0.05) and decreased in C (p<0.05) with a significant difference between groups (VO2peak p = 0.005; MAPR p = 0.03). There was a strong correlation between the change in MAPR and the change in VO2peak over the study (r = 0.875; p < 0.0001), the change in MAPR accounting for 70% of the change in VO2peak. Conclusions. These findings suggest that mitochondrial ATP production is a major determinant of aerobic capacity in CHF patients and can be favourably altered by muscle trengthening exercise

Respiratory muscle dysfunction and training in chronic heart failure

Patients with chronic heart failure exhibit significantly reduced respiratory muscle strength and endurance. These impairments are associated with numerous alterations in respiratory muscle structure and function, including a shift in muscle fibre phenotype, reduced oxidative capacity, and altered intracellular calcium regulation. There is now substantial evidence that selective respiratory muscle training in patients withCHFincreases respiratory muscle strength and overall aerobic capacity. The majority of studies have used a regimen of inspiratory muscle training against either a fixed or incremental inspiratory load, expressed as a percentage of MIP. The benefit of whole body aerobic and strength exercise in CHF patients has been well documented and is now implemented in many rehabilitation programes for these patients.The recent trial ofWinkelmann et al. [46], demonstrating that inspiratory muscle training in combination with whole-body aerobic training was more beneficial than aerobic training alone, should be repeated in a separate CHF cohort. If the results are concordant, inspiratory muscle training should be incorporated into existing rehabilitation programes for patients with CHF