Clarke MS, Bamman MM, Feeback DL.

FASEB J. 1999 Mar 12; 13: A415.

USRA, NASA/JSC, Houston, TX 77058, USA.

We previously reported that unloading of skeletal muscle results in alteration of the biophysical properties of the sarcolemma leading to increased susceptibility to mechanically-induced sarcolemma disruption. As we had previously demonstrated that increased membrane cholesterol results in increased endothelial susceptibility to mechanically-induced membrane damage we tested the hypothesis that the unloading-induced increase in sarcolemma susceptibility to mechanical damage was also correlated to elevated sarcolemma cholesterol. Utilizing muscle obtained from both human bedrest (BDR) subjects and hindlimb suspended (HLS) rats we detected a significant increase in muscle membrane cholesterol after unloading. This increase was not observed in the triceps muscle of the intermittently loaded front limb of HLS animals or in muscle obtained from BDR subjects who performed atrophy-preventing resistive exercise. As elevated membrane cholesterol has previously been showed to increase sarcolemma DHP-sensitive channel activity and inhibit Ca/Mg ATPase activity, we also tested the hypothesis that increased sarcolemma or sarcoplasmic reticulum cholesterol content may lead to elevated intra-myofiber calcium. Utilizing perfusion fixed rat muscle stained for free calcium we have demonstrated a significant increase in the amount of free intra-myofiber calcium after unloading. We hypothesize that such an increase in myofiber calcium due to modulation of calcium channel activity by elevated membrane cholesterol may lead to the activation of a number of catabolic pathways in unloaded muscle.

Publication Types:

• Meeting Abstracts

Keywords:

• Animals
• Calcium
• Cholesterol
• Hindlimb
• Hindlimb Suspension
• Humans
• Intracellular Membranes
• Membranes
• Muscle, Skeletal
• Muscles
• Rats
• Ryanodine Receptor Calcium Release Channel
• Sarcolemma
• Sarcoplasmic Reticulum
• NASA Discipline Developmental Biology
• Non-NASA Center

Other ID:

• 20603511

UI: 102194947

From Meeting Abstracts