Both acute exercise and excessive training can cause oxidative stress. The resulting increase in free radicals and the inadequate response from antioxidant systems can lead to a framework of cellular damage. An association between affected tissue and the biomarkers of oxidative stress that appear in plasma has not been clearly established. The aim of this study was to evaluate the source of oxidative stress biomarkers found in the plasma of untrained rats after a single bout of swimming exercise at 2 different intensities: low intensity (SBLIE) or high intensity (SBHIE). Immediately after the exercise, aspartate transaminase (AST), alanine transaminase (ALT), γ-glutamyltransferase (GGT), and lactate dehydrogenase (LDH) were measured in plasma to characterize cell damage. Oxidative stress was assessed using protein carbonylation (PC), total antioxidant capacity (TAC), and thiobarbituric acid reactive substances (TBARS) quantified by malondialdehyde concentration. SBHIE raised levels of plasma AST (93%) and ALT (17%), and both exercise regimens produced an increase in GGT (7%) and LDH (∼55%). Plasma levels of PC and TBARS were greater in the SBHIE group; there were no changes in TAC. SBLIE caused only a modest increase in TBARS. In muscle, there were no changes in TAC, PC, or TBARS, regardless of exercise intensity, In the liver, TAC and TBARS increased significantly in both the SBLIE and SBHIE groups. This indicates that the oxidative stress biomarkers measured in the plasma immediately after a single bout of swimming exercise were generated primarily in the liver, not in muscle.

No abstract

Physical exercise is known to activate the sympathetic nervous system, which influences the production of saliva from salivary glands. Our examination of saliva collected from highly trained athletes before and after a number of physical competititions showed an increase in the secretion of S-type cystatins and cystatin C as a subacute response to aerobic and anaerobic exercise. The elevation in salivary cystatins was transient and the recovery time course differed from that of amylase and other salivary proteins. An in vitro assay was developed based on a cell line from a human submandibular gland (HSG) that differentiated into acinus-like structures. Treatments with the β-adrenergic agonist isoproterenol caused a shift in the intracellular distribution of S-type cystatins and cystatin C, promoting their accumulation at the outer regions of the acinus prior to release and suggesting the activation of a directional transport involving co-migration of both molecules. In another treatment using non-differentiated HSG cells, it was evident that both expression and secretion of cystatin C increased upon addition of the β-adrenergic agonist, and these effects were essentially eliminated by the antagonist propranolol. The HSG cell line appears to have potential as a model for exploring the mechanism of cystatin secretion, particularly the S-type cystatins that originate primarily in the submandibular glands.

No abstract

Introdução: A sarcopenia é uma síndrome caracterizada por perda progressiva e generalizada de massa e força muscular esquelética com risco de comprometimento funcional, aumento da probabilidade de quedas e perda de autonomia. Método: Foi realizada uma revisão integrativa da literatura científica, com utilização de artigos publicados nas bases de dados PubMed®, BVS® e Scielo® em português e inglês. Foram utilizados para busca os descritores "sarcopenia", "idoso" or “elderly” e "proteína" or “protein” sendo cruzados para busca com o operador booleano AND. Resultados: Com prevalência que varia entre 3 a 24% em idosos, é um processo resultante de mecanismos fisiopatológicos que incluem envelhecimento, comprometimento neuromuscular, exercício físico, fatores endócrinos, estresse oxidativo e alimentação. No que diz repeito a alimentação, o consumo inadequado de calorias totais e proteínas parece ser os principais fatores contribuintes. Conclusão: a ingestão adequada de calorias e proteínas (0,8/kg/dia) e a suplementação de whey protein (20 a 40g/dia), creatina (0,3g/kg/dia), vitamina D e cálcio (1.200 a 1.500 mg por dia) podem prevenir e tratar o avanço da sarcopenia em idosos.