Bioenergetics of contracting skeletal muscle after partial reduction of blood flow |
| |
Authors: | Hogan Michael C; Gladden L Bruce; Grassi Bruno; Stary Creed M; Samaja Michele |
| |
Abstract: | The purpose ofthis study was to examine the bioenergetics and regulation ofO2 uptake( O2) and force productionin contracting muscle when blood flow was moderately reduced during asteady-state contractile period. Canine gastrocnemius muscle(n = 5) was isolated, and 3-minstimulation periods of isometric, tetanic contractions were elicitedsequentially 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 O2 of thecontracting muscle was significantly (P < 0.05) reduced during the Icondition 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 O2 to tension-time indexremained constant throughout all contraction periods. Musclephosphocreatine concentration, ATP concentration, and lactate effluxwere not significantly different during the I condition compared withthe 0.5-Hz condition with normal blood flow. However, at comparable rates of O2 andtension-time index, muscle phosphocreatine concentration and ATPconcentration were significantly less during the I condition comparedwith normal-flow conditions. These results demonstrate that, in thishighly oxidative muscle, the normal balance ofO2 supply to force output wasmaintained during moderate ischemia by downregulation of forceproduction. In addition,1) the minimal disruption inintracellular homeostasis after the initiation of ischemia waslikely a result of steady-state metabolic conditions having alreadybeen activated, and 2) thedifference in intracellular conditions at comparable rates of O2 and tension-time index between the normal flow and I condition may have been due to altered intracellular O2 tension. |
| |
Keywords: | |
|
| 点击此处可从《Journal of applied physiology (Bethesda, Md. : 1985)》浏览原始摘要信息 |
| 点击此处可从《Journal of applied physiology (Bethesda, Md. : 1985)》下载免费的PDF全文 |
|