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Exercise damages cell membranes with metabolic stress, not mechanical

PainSci » bibliography » Fredsted et al 2007
Tags: biology, random, strain, muscle pain, injury, pain problems, muscle

Two articles on PainSci cite Fredsted 2007: 1. Does Epsom Salt Work?2. Why Drink Water After Massage?

PainSci commentary on Fredsted 2007: ?This page is one of thousands in the bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.

Intense and unfamiliar exercise damages muscle cell membranes and correlates with a flood of calcium into the cells, causing fatigue. But what causes the damage and starts the flood? Mechanical damage has never been ruled out. This experiment chemically blocked 90% of contraction strength in rats, effectively eliminating physical strain from the contraction equation. The rats’ muscles were then electrically stimulated to simulate exercise without mechanical stress. Unfortunately for the rats — actually, everything about this was unfortunate for the rats — their muscle cell membranes were damaged just exactly as they would have been in a normal, intense rat workout. The implication is clear: cell membranes are damaged in exercise by metabolic stress not mechanical stress. The authors concluded that “cell membrane damage depends on Ca2+ influx and energy status and not on mechanical stress.”

~ Paul Ingraham

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Prolonged or unaccustomed exercise leads to muscle cell membrane damage, detectable as release of the intracellular enzyme lactic acid dehydrogenase (LDH). This is correlated to excitation-induced influx of Ca2+, but it cannot be excluded that mechanical stress contributes to the damage. We here explore this question using N-benzyl-p-toluene sulfonamide (BTS), which specifically blocks muscle contraction. Extensor digitorum longus muscles were prepared from 4-wk-old rats and mounted on holders for isometric contractions. Muscles were stimulated intermittently at 40 Hz for 15-60 min or exposed to the Ca2+ ionophore A23187. Electrical stimulation increased 45Ca influx 3-5 fold. This was followed by a progressive release of LDH, which was correlated to the influx of Ca2+. BTS (50 microM) caused a 90% inhibition of contractile force but had no effect on the excitation-induced 45Ca influx. After stimulation, ATP and creatine phosphate levels were higher in BTS-treated muscles, most likely due to the cessation of ATP-utilization for cross-bridge cycling, indicating a better energy status of these muscles. No release of LDH was observed in BTS-treated muscles. However, when exposed to anoxia, electrical stimulation caused a marked increase in LDH release that was not suppressed by BTS but associated with a decrease in the content of ATP. Dynamic passive stretching caused no increase in muscle Ca2+ content and only a minor release of LDH, whereas treatment with A23187 markedly increased LDH release both in control and BTS-treated muscles. In conclusion, after isometric contractions, muscle cell membrane damage depends on Ca2+ influx and energy status and not on mechanical stress.

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