title: Bioenergetics of contracting skeletal muscle after partial reduction of blood flow.
abstract: The purpose of this study was to examine the bioenergetics and regulation of O2 uptake (VO2) and force production in contracting muscle when blood flow was moderately reduced during a steady-state contractile period. Canine gastrocnemius muscle (n = 5) was isolated, and 3-min stimulation periods of isometric, tetanic contractions were elicited sequentially at rates of 0.25, 0.33, and 0.5 contractions/s (Hz) immediately followed by a reduction of blood flow [ischemic (I) condition] to 46 +/- 3% of the value obtained at 0.5 Hz with normal blood flow. The VO2 of the contracting muscle was significantly (P < 0.05) reduced during the I condition [6.5 +/- 0.8 (SE) ml . 100 g-1 . min-1] compared with the same stimulation frequency with normal flow (11.2 +/- 1.5 ml . 100 g-1 . min-1), as was the tension-time index (79 +/- 12 vs. 123 +/- 22 N . g-1 . min-1, respectively). The ratio of VO2 to tension-time index remained constant throughout all contraction periods. Muscle phosphocreatine concentration, ATP concentration, and lactate efflux were not significantly different during the I condition compared with the 0. 5-Hz condition with normal blood flow. However, at comparable rates of VO2 and tension-time index, muscle phosphocreatine concentration and ATP concentration were significantly less during the I condition compared with normal-flow conditions. These results demonstrate that, in this highly oxidative muscle, the normal balance of O2 supply to force output was maintained during moderate ischemia by downregulation of force production. In addition, 1) the minimal disruption in intracellular homeostasis after the initiation of ischemia was likely a result of steady-state metabolic conditions having already been activated, and 2) the difference in intracellular conditions at comparable rates of VO2 and tension-time index between the normal flow and I condition may have been due to altered intracellular O2 tension.
authors.affiliation: Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623, USA. mchogan@ucsd.edu
authors.forename: M C
authors.initials: MC
authors.lastname: Hogan
authors.forename: L B
authors.initials: LB
authors.lastname: Gladden
authors.forename: B
authors.initials: B
authors.lastname: Grassi
authors.forename: C M
authors.initials: CM
authors.lastname: Stary
authors.forename: M
authors.initials: M
authors.lastname: Samaja
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000332:Aerobiosis / Q000502:physiology; D000818:Animals; D004285:Dogs; D004558:Electric Stimulation; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006019:Glycolysis / Q000502:physiology; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008931:Mitochondria, Muscle / Q000378:metabolism / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D010725:Phosphocreatine / Q000097:blood; D012039:Regional Blood Flow / Q000502:physiology
chemical_list: D010725:Phosphocreatine; D019344:Lactic Acid; D000255:Adenosine Triphosphate