General Outlines of Adaptation Processes and the Biological Nature of Exercise Training
Atko Viru in Adaptation in Sports Training, 2017
The adaptive protein synthesis needs: (1) creation of inductors acting on the cellular genetic apparatus and calling forth the specifically related synthesis of the concerned proteins, (2) supply of synthesis processes by building materials’ (amino acids and precursors for synthesis of ribonuclear acids), (3) destruction of the old, physiologically exhausted cellular elements, and (4) supply of synthesis processes by energy. The first task will be fulfilled by the metabolic changes during exercise as well as by hormonal changes during and after exercise (see Chapter 8). An essential role here belongs to protein catabolism.16 All other tasks are deeply related to activation of the mechanism of general adaptation. Therefore, the load of training sessions has to be sufficiently high to activate the mechanism of general adaptation including the pronounced alterations in endocrine functions.
ß-hydroxy-ß-methylbutyrate
Jay R Hoffman in Dietary Supplementation in Sport and Exercise, 2019
The ubiquitin-proteasome pathway (UPP) is considered the primary avenue for protein catabolism in mammals. HMB has been shown to reduce muscle protein degradation by diminishing the UPP partially by inhibition of a protein called proteolysis-inducing factor (PIF) (67). PIF has been noted as a cachectic (body weakening or wasting) indicator as it is elevated in cancer patients and people experiencing losses in lean body mass (34). Ubiquitin-proteasome signalling is regulated by an intricate array of processes and has profound cellular effects ranging from apoptosis (programmed cell death) to cell differentiation and regeneration. In fact, when human myoblasts were treated with HMB in vitro, the number of apoptotic cells were reduced, there were higher levels of anti-apoptotic proteins Bcl-2 and lower levels of the pro-apoptotic protein BAX (38). This is supported in animal models showing that HMB is an inhibitor of myonuclear apoptosis by regulating mitochondrial-associated caspase signalling, a prominent component of the apoptotic pathway (26). Considering the addition of new myonuclei is presumed to be necessary to promote muscle hypertrophy and the maintenance of these nuclei are vital to preserving muscle mass in catabolic conditions, this is likely the principal mechanism underpinning reductions of muscle protein breakdown observed in humans via HMB supplementation.
Acute Malnutrition
Crystal D. Karakochuk, Kyly C. Whitfield, Tim J. Green, Klaus Kraemer in The Biology of the First 1,000 Days, 2017
Muscle is the main storage site of amino acids in the body and, when protein intake is insufficient to sustain metabolism, these amino acids are released, leading to a decrease in muscle mass. The release of amino acids is the result of the activation of ubiquitin-proteasome pathway, which are also activated in numerous conditions leading to muscle mass depletion, including trauma, diabetes, uremia, hyperadrenocortisolism, hyperthyroidism, immobilization, and sepsis [13]. In the event of infection, muscle breakdown can be accelerated by the need to synthesize acute phase proteins, which have a high content of aromatic amino acids. The synthesis of these acute phase proteins, which can account for up to 30% of total protein synthesis, requires a high level of protein catabolism, mainly from muscle [14].
Novel pharmacotherapy for burn wounds: what are the advancements
Published in Expert Opinion on Pharmacotherapy, 2019
Michael R. Hamblin
Inflammatory cytokine levels, serum hormones, protein production, and protein secretion are altered in severe burn injuries. Muscle protein is degraded much faster than it is synthesized, and protein catabolism is directly related to increases in the metabolic rate [42]. Elevated circulating levels of catecholamines, glucagon, cortisol, and gluconeogenic hormones lead to inefficient production of glucose in the liver [46]. Glycolytic-gluconeogenic cycling leads to hyperglycemia and impaired insulin sensitivity [47]. Lactate is recycled to the liver to produce more glucose via the gluconeogenic pathway. While in classical starvation, fat provides the major source of calories, in severe burns the body fails to utilize fat as an energy source, leading instead to protein catabolism to provide an energy source. Treatment of these metabolic disturbances occurring in severe burn patients, involves both nutritional support and pharmacological intervention.
The Relationship Between Nutritional Status, Performance Status, and Survival Among Pancreatic Cancer Patients
Published in Nutrition and Cancer, 2020
Derya Hopanci Bicakli, Ruchan Uslu, Sedat Can Güney, Ahmet Coker
Pancreatic cancer (PanCa) ranks fourth among all cancer-related deaths globally. Many PanCa patients, with aggressive tumor biology of the disease, are caught in the metastatic stage and often progress with poor prognosis (1). One out of three PanCa patients loose >10% of their pre-diagnosis body weight (2,3). Majority of the patients experience symptoms such as abdominal pain, premature satiety, nausea, vomiting, diarrhea, or constipation (4). Surgical resection, one of the major components of PanCa treatment, can induce or worsen these symptoms (5). Protein catabolism also takes place in addition to the tumor-led hyper-metabolism, and energy consumption increases (6). Steatorrhea, one of the symptoms caused by pancreatic endocrine and exocrine insufficiency, leads to bloating, fat absorption failure, diabetes mellitus, weight loss, and malnutrition (5,7). Cachexia is known to be an important cause of reduced quality-of-life (QoL), shortened survival time, and treatment failure among PanCa patients (6,8). Similarly, the stabilization of body weight in nonresectable PanCa cases is associated with patient survival and QoL. Malnutrition has been demonstrated by various studies to cause skeletal muscle wasting and fat deterioration; prolonged hospital stay; increased risk of complications and reduced response to treatment; and increased morbidity and mortality (3,6). The purpose of this study is to evaluate the nutritional status and performance status of PanCa patients and to determine whether these parameters and survival time are related.
The antioxidant system in the soleus muscle of growing rats is stimulated by the administration of a low-protein/high-carbohydrate diet
Published in Archives of Physiology and Biochemistry, 2019
Flavia Hosaki Silvino da Silva, Maisa Pavani dos Santos, Mayara Peron Pereira, Samyra Lopes Buzelle, Edgar Wilibaldo Allebrandt Neto, Bibiana Mozzaquatro Gai, Francyele dos Santos Correia, Cristina Helena Alves, Suelem Aparecida de França, Nair Honda Kawashita
Batistela et al. (2014) investigated the proteolytic pathways and showed inhibition of Caspase-3 activity and the ubiquitin-proteasome system in the soleus muscles of LPHC rats as an adaptive response that contributes to spare protein in a condition of diminished availability of dietary amino acids. We attributed the reduction in the proteolysis to the increase in the carbonylated protein content in soleus muscle, with no increase in TBARS. Studies have shown the association between the reduction in proteasome activity and the increase in ROS production (Shringarpure et al.2003, Davies and Shringarpure 2006, Tromm et al.2012). Some authors have shown that elevated levels of oxidative stress can decrease protein catabolism rates (Squier 2001, Power et al.2014). Proteasome activity in 20S and 26S subunits can be inhibited by the accumulation of protein aggregates due to oxidative stress (Bader and Grune 2006) such as caspase-3 the activity of which can also be inactivated in severe oxidative stress (Borutaite and Brown 2001).