title: Effect of extracellular osmolality on metabolism in contracting mammalian skeletal muscle in vitro.
abstract: Extensive research has been conducted on hepatocyte metabolism perturbed under the influence of anisosmotic stress. However, much less is known about the behaviour of skeletal muscle metabolism under similar conditions. After establishing a working model to study anisosmotic stress in resting mammalian skeletal muscle, the current study tested the hypothesis that hyperosmotic (HYPER) stress would lead to increased creatine, lactate, and measured enzyme activity, whereas hypo-osmotic (HYPO) stress would lead to decreased metabolites and enzyme activity vs. iso-osmotic (ISO) stress post contraction. Rat soleus (SOL) and extensor digitorum longus (EDL) were isolated and incubated in an organ bath (95% O2, 5% CO2, pH 7.4, 25 degrees C) altered to targeted osmotic conditions (ISO, 290 osmol.L(-1); HYPO, 180 osmol.L(-1); HYPER, 400 osmol.L(-1)). Muscle samples were flash frozen after 10 min of contraction. Post contraction, muscle water content in the SOL HYPO condition was 18% greater than ISO, and HYPER had approximately 14% less water content than ISO (p < 0.05). In the HYPO condition, EDL had 21% greater water content than ISO, and HYPER had 17% less water content than ISO (p < 0.05). SOL HYPO resulted in higher phosphocreatine and lower lactate and creatine vs. HYPER (p < 0.05) but there were no differences in EDL between HYPO and HYPER. Pyruvate dehydrogenase activity increased in SOL HYPER vs. HYPO, whereas glycogen phosphorylase a increased in EDL HYPER vs. HYPO. In conclusion, fibre-type-specific responses exist after contraction such that when SOL muscle is perturbed in HYPER, as compared with HYPO, media, metabolic activity increases. Future work should focus on glucose uptake-regulation during anisosmotic conditions.
authors.affiliation: Centre for Muscle Metabolism and Biophysics, Department of Physical Education and Kinesiology, Faculty of Applied Health Sciences, Brock University, St. Catharines, ON L2S 3A1, Canada.
authors.forename: Naomi M
authors.initials: NM
authors.lastname: Cermak
authors.forename: Paul J
authors.initials: PJ
authors.lastname: LeBlanc
authors.forename: Sandra J
authors.initials: SJ
authors.lastname: Peters
authors.forename: Rene
authors.initials: R
authors.lastname: Vandenboom
authors.forename: Brian D
authors.initials: BD
authors.lastname: Roy
mesh_terms: D000818:Animals; D003401:Creatine / Q000032:analysis; D045604:Extracellular Fluid / Q000737:chemistry*; D024982:Glycogen Phosphorylase, Muscle Form; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000032:analysis; D008297:Male; D008954:Models, Biological; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000737:chemistry / Q000201:enzymology / Q000378:metabolism*; D009928:Organ Specificity; D009994:Osmolar Concentration; D010725:Phosphocreatine / Q000032:analysis; D030481:Pyruvate Dehydrogenase (Lipoamide) / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D020318:Rats, Long-Evans; D013312:Stress, Physiological; D013997:Time Factors; D014867:Water / Q000032:analysis
chemical_list: D010725:Phosphocreatine; D014867:Water; D019344:Lactic Acid; D030481:Pyruvate Dehydrogenase (Lipoamide); D024982:Glycogen Phosphorylase, Muscle Form; D003401:Creatine