Dose Response of Acute ATP Supplementation on Strength Training Performance

Background: Chronic oral ATP supplementation benefits cardiovascular health, muscular performance, body composition, and recovery while attenuating muscle breakdown and fatigue. A single 400 mg dose of oral ATP supplementation improved lower body resistance training performance and energy expenditure in recreational resistance trained males, however, the minimal effective dose is currently unknown.Materials and Methods: Twenty recreationally trained men (age 28.6 ± 1.0 years, body mass 81.2 ± 2.0 kg, height 175.2 ± 1.4 cm, 1RM 141.5 ± 5.0 kg) consumed a single dose of either 400 mg, 200 mg, or 100 mg ATP (PEAK ATP®, TSI USA LLC, Missoula, MT, USA) or a placebo in a randomized, placebo-controlled crossover design, separated by a one week wash out between treatments. After warm-up, participants performed 4 sets of half-squats using free-weights until movement failure separated by 2 mins of rest between sets.Results: In comparison to placebo, 400 mg ATP significantly increased the number of set 1 repetitions (+13%, p = 0.04), and numerically increased total repetitions (+7%, p = 0.19) and total weight lifted (+6%, p = 0.22). 200 mg ATP numerically increased set 1 repetitions (+4% p = 0.47), while 100 mg ATP showed no improvements over placebo. 100 mg ATP (−4%, p < 0.05) and 400 mg ATP (−4%, p = 0.11) decreased the perceived rate of exertion compared to placebo.Conclusions: In this study, the effective minimal dose of acute oral ATP supplementation during resistance exercise to increase performance was determined to be 400 mg, while as little as 100 mg showed improvements in perceived exertion.

Clinical assessment of muscle condition in cats

Loss of muscle occurs in feline patients as a result of multiple chronic conditions, and muscle atrophy may worsen the prognosis for cats that are living with these diseases. In states of health, a balance exists between cellular processes that build muscle and processes that break it down. Disease states such as kidney disease, cancers, cardiac disease, and metabolic conditions promote chronic systemic inflammation which shifts this balance in favour of muscle breakdown. If noted, muscle loss should prompt a thorough medical investigation including nutritional and clinical history, laboratory work, and imaging studies, as well as the creation of an in-depth nutritional management plan. Veterinary nurses are the first line in recognising muscle loss, identifying historical clues as to its cause, and educating clients about diagnostic and therapeutic plans for associated disease management.

Elevated Cardiac Troponin T in Patients with Lupus Myositis Presenting with Noncardiac Chest Pain

Patients with systemic lupus erythematosus (SLE) presenting with chest pain pose a unique diagnostic challenge, with causes ranging from cardiopulmonary disease to esophageal disorders and musculoskeletal chest wall pain. The most common biomarkers for myocardial injury are cardiac troponin T and I (cTnT and cTnI) due to their high sensitivity for the early detection of myocardial infarction. In the idiopathic inflammatory myopathies, cTnT is commonly elevated, and this reflects skeletal muscle breakdown rather than myocardial damage. Similar observations have not been reported in SLE myositis to date. We present two cases of patients with SLE and associated myositis who presented with chest pain and elevated cTnT. Both patients had a normal cTnI, transthoracic echocardiogram, and cardiac magnetic resonance imaging, likely indicating noncardiac chest pain. Clinicians should be aware that the specificity of cTnT might be lower in SLE myositis and that cTnI elevation may be more specific in detecting myocardial insult.

Rehabilitation Nutrition for Injury Recovery of Athletes: The Role of Macronutrient Intake

An adequate and balanced diet is of utmost importance in recovery and rehabilitation. “Rehabilitation nutrition” for injury recovery of athletes is similar to sports nutrition, except for the differences that concern the prevention of the risk or presence of sarcopenia, malnutrition, or dysphagia. Rehabilitation nutrition also aims, combined with training, to an adequate long-term nutritional status of the athlete and also in physical condition improvement, in terms of endurance and resistance. The aim of this paper is to define the proper nutrition for athletes in order to hasten their return to the sports after surgery or injury. Energy intake should be higher than the energy target in order to fight sarcopenia—that is 25–30 kcal/kg of body weight. Macro- and micro-nutrients play an important role in metabolism, energy production, hemoglobin synthesis, lean mass and bone mass maintenance, immunity, health, and protection against oxidative damage. Nutritional strategies, such as supplementation of suboptimal protein intake with leucine are feasible and effective in offsetting anabolic resistance. Thus, maintaining muscle mass, without gaining fat, becomes challenging for the injured athlete. A dietary strategy should be tailored to the athlete’s needs, considering amounts, frequency, type and, most of all, protein quality. During rehabilitation, simultaneous carbohydrates and protein intake can inhibit muscle breakdown and muscle atrophy. The long-term intake of omega-3 fatty acids enhances anabolic sensitivity to amino acids; thus, it may be beneficial to the injured athlete. Adequate intakes of macronutrients can play a major role supporting athletes’ anabolism.

Metabolic Signatures of Life Span Regulated by Mating, Sex Peptide, and Mifepristone/RU486 in Female Drosophila melanogaster

Mating and transfer of male sex peptide (SP), or transgenic expression of SP, causes inflammation and decreased life span in female Drosophila. Mifepristone rescues these effects, yielding dramatic increases in life span. Here targeted metabolomics data were integrated with further analysis of extant transcriptomic data. Each of 7 genes positively correlated with life span were expressed in the brain or eye and involved regulation of gene expression and signaling. Genes negatively correlated with life span were preferentially expressed in midgut and involved protein degradation, amino acid metabolism, and immune response. Across all conditions, life span was positively correlated with muscle breakdown product 1/3-methylhistidine and purine breakdown product urate, and negatively correlated with tryptophan breakdown product kynurenic acid, suggesting a SP-induced shift from somatic maintenance/turnover pathways to the costly production of energy and lipids from dietary amino acids. Some limited overlap was observed between genes regulated by mifepristone and genes known to be regulated by ecdysone; however, mifepristone was unable to compete with ecdysone for activation of an ecdysone-responsive transgenic reporter. In contrast, genes regulated by mifepristone were highly enriched for genes regulated by juvenile hormone (JH), and mifepristone rescued the negative effect of JH analog methoprene on life span in adult virgin females. The data indicate that mifepristone increases life span and decreases inflammation in mated females by antagonizing JH signaling downstream of male SP. Finally, mifepristone increased life span of mated, but not unmated, Caenorhabditis elegans, in 2 of 3 trials, suggesting possible evolutionary conservation of mifepristone mechanisms.

Update Review about Metabolic Myopathies

The aim of this review is to summarize and discuss recent findings and new insights in the etiology and phenotype of metabolic myopathies. The review relies on a systematic literature review of recent publications. Metabolic myopathies are a heterogeneous group of disorders characterized by mostly inherited defects of enzymatic pathways involved in muscle cell metabolism. Metabolic myopathies present with either permanent (fixed) or episodic abnormalities, such as weakness, wasting, exercise-intolerance, myalgia, or an increase of muscle breakdown products (creatine-kinase, myoglobin) during exercise. Though limb and respiratory muscles are most frequently affected, facial, extra-ocular, and axial muscles may be occasionally also involved. Age at onset and prognosis vary considerably. There are multiple disease mechanisms and the pathophysiology is complex. Genes most recently related to metabolic myopathy include PGM1, GYG1, RBCK1, VMA21, MTO1, KARS, and ISCA2. The number of metabolic myopathies is steadily increasing. There is limited evidence from the literature that could guide diagnosis and treatment of metabolic myopathies. Treatment is limited to mainly non-invasive or invasive symptomatic measures. In conclusion, the field of metabolic myopathies is evolving with the more widespread availability and application of next generation sequencing technologies worldwide. This will broaden the knowledge about pathophysiology and putative therapeutic strategies for this group of neuromuscular disorders.

Muscle wasting in the critically ill patient: how to minimise subsequent disability

Muscle wasting in critically ill patients is the most common complication associated with critical care. It has significant effects on physical and psychological health, mortality and quality of life. It is most severe in the first few days of illness and in the most critically unwell patients, with muscle loss estimated to occur at 2–3% per day. This muscle loss is likely a result of a reduction in protein synthesis relative to muscle breakdown, resulting in altered protein homeostasis. The associated weakness is associated with in an increase in both short- and long-term mortality and morbidity, with these detrimental effects demonstrated up to 5 years post discharge. This article highlights the significant impact that muscle wasting has on critically ill patients' outcomes, how this can be reduced, and how this might change in the future.

Acute Toxin-mediated Rhabdomyolysis During Treatment With Trimethoprim-sulfamethoxazole

Rhabdomyolysis is a condition in which skeletal muscle breakdown causes the release of intracellular components into the bloodstream – defined as elevations in serum creatine kinase levels. The etiology of rhabdomyolysis is varied and may be the result of toxin-mediated mechanisms or metabolic derangements, or they may develop secondary to other conditions such as seizures, trauma and prolonged immobilization. In this case, we present a patient with suspected acute toxin-mediated rhabdomyolysis in the setting of trimethoprim-sulfamethoxazole (TMP-SMX) therapy for urinary tract infection. To our knowledge, this marks the fifth case report of an otherwise healthy patient diagnosed with rhabdomyolysis thought to be secondary to TMP-SMX.