Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress.

Protein homeostasis in cells, proteostasis, is maintained through several integrated processes and pathways and its dysregulation may mediate pathology in many diseases including Duchenne muscular dystrophy (DMD). Oxidative stress, heat shock proteins, endoplasmic reticulum (ER) stress and its response, i.e.

Reliability of urine lactate as a novel biomarker of lactate production capacity in maximal swimming.

Context: Postexercise urine lactate may be a novel biomarker of lactate production capacity during exercise.

Objective: To evaluate the reliability and utility of the urine lactate concentration after maximal swimming trials between different training protocols (6 × 50 m and 3 × 100 m) and training states (active and nonactive swimmers).

Materials And Methods: Lactate and creatinine were determined by spectrophotometry in blood and urine.

Monitoring the Response of the Human Urinary Metabolome to Brief Maximal Exercise by a Combination of RP-UPLC-MS and (1)H NMR Spectroscopy.

The delineation of exercise biochemistry by utilizing metabolic fingerprinting has become an established strategy. We present a combined RP-UPLC-MS and (1)H NMR strategy, supplemented by photometric assays, to monitor the response of the human urinary metabolome to short maximal exercise. Seventeen male volunteers performed two identical sprint sessions on separate days, consisting of three 80 m maximal runs.

Myostatin/activin blocking combined with exercise reconditions skeletal muscle expression profile of mdx mice.

Duchenne muscular dystrophy is characterized by muscle wasting and decreased aerobic metabolism. Exercise and blocking of myostatin/activin signaling may independently or combined counteract muscle wasting and dystrophies. The effects of myostatin/activin blocking using soluble activin receptor-Fc (sActRIIB-Fc) administration and wheel running were tested alone or in combination for 7 weeks in dystrophic mdx mice.