pattismith
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scientists used to think not so long ago that muscle pain/fatigue after exercise was du to lactic acid building up under anaerobic circumstancies.
It seems that it is not so simple, and that lactic acid may be even protective for the muscle.
Here some lights about it coming from wikipedia:
"Metabolites
Metabolites are the substances (generally waste products) produced as a result of muscular contraction. They include chloride, potassium, lactic acid, ADP, magnesium (Mg2+), reactive oxygen species, and inorganic phosphate.
Accumulation of metabolites can directly or indirectly produce metabolic fatigue within muscle fibers through interference with the release of calcium (Ca2+) from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium.
Chloride
Intracellular chloride partially inhibits the contraction of muscles. Namely, it prevents muscles from contracting due to "false alarms", small stimuli which may cause them to contract (akin to myoclonus). This natural brake helps muscles respond solely to the conscious control or spinal reflexes[citation needed] but also has the effect of reducing the force of conscious contractions.
Potassium
High concentrations of potassium (K+) also causes the muscle cells to decrease in efficiency, causing cramping and fatigue. Potassium builds up in the t-tubule system and around the muscle fiber as a result of action potentials. The shift in K+ changes the membrane potential around the muscle fiber. The change in membrane potential causes a decrease in the release of calcium (Ca2+) from the sarcoplasmic reticulum.[1]
Lactic acid
It was once believed that lactic acid build-up was the cause of muscle fatigue.[2] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.
Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles.
This can lower the sensitivity of contractile apparatus to Ca2+ but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell.
This counters inhibiting effects of potassium on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving potassium ions as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.
Lactic acid is now used as a measure of endurance training effectiveness and VO2 max.[3]
Molecular mechanisms
Muscle fatigue may be due to precise molecular changes that occur in vivo with sustained exercise.
It has been found that the ryanodine receptor present in skeletal muscle undergoes a conformational change during exercise, resulting in "leaky" channels that are deficient in calcium release. These "leaky" channels may be a contributor to muscle fatigue and decreased exercise capacity.[4]"
Interestingly many ME patients could have a "chloride brake" dysfunction that would explain the myoclonus in their symptoms.
About Ryanodine Receptors:
"Ryanodine receptors (RyRs) are high conductance intracellular cation channels that release calcium ions from stores such as the endoplasmic reticulum and sarcoplasmic reticulum.
Although RyRs are expressed in many cell types, their roles have only been extensively characterised in tissues in which they are abundant: RyR1 is essential for excitation–contraction coupling in skeletal muscle; whereas RyR2 is required for the analogous signal transduction pathway in heart. Defects in RyR1 cause malignant hyperthermia and a spectrum of myopathies in skeletal muscle; whereas RyR2 dysregulation can result in fatal cardiac arrhythmias and is involved in heart failure. Altered RyR gating has been implicated in a range of other diseases, including epilepsy, neurodegeneration, pain and cancer."
It seems that it is not so simple, and that lactic acid may be even protective for the muscle.
Here some lights about it coming from wikipedia:
"Metabolites
Metabolites are the substances (generally waste products) produced as a result of muscular contraction. They include chloride, potassium, lactic acid, ADP, magnesium (Mg2+), reactive oxygen species, and inorganic phosphate.
Accumulation of metabolites can directly or indirectly produce metabolic fatigue within muscle fibers through interference with the release of calcium (Ca2+) from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium.
Chloride
Intracellular chloride partially inhibits the contraction of muscles. Namely, it prevents muscles from contracting due to "false alarms", small stimuli which may cause them to contract (akin to myoclonus). This natural brake helps muscles respond solely to the conscious control or spinal reflexes[citation needed] but also has the effect of reducing the force of conscious contractions.
Potassium
High concentrations of potassium (K+) also causes the muscle cells to decrease in efficiency, causing cramping and fatigue. Potassium builds up in the t-tubule system and around the muscle fiber as a result of action potentials. The shift in K+ changes the membrane potential around the muscle fiber. The change in membrane potential causes a decrease in the release of calcium (Ca2+) from the sarcoplasmic reticulum.[1]
Lactic acid
It was once believed that lactic acid build-up was the cause of muscle fatigue.[2] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue.
Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles.
This can lower the sensitivity of contractile apparatus to Ca2+ but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell.
This counters inhibiting effects of potassium on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving potassium ions as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.
Lactic acid is now used as a measure of endurance training effectiveness and VO2 max.[3]
Molecular mechanisms
Muscle fatigue may be due to precise molecular changes that occur in vivo with sustained exercise.
It has been found that the ryanodine receptor present in skeletal muscle undergoes a conformational change during exercise, resulting in "leaky" channels that are deficient in calcium release. These "leaky" channels may be a contributor to muscle fatigue and decreased exercise capacity.[4]"
Interestingly many ME patients could have a "chloride brake" dysfunction that would explain the myoclonus in their symptoms.
About Ryanodine Receptors:
"Ryanodine receptors (RyRs) are high conductance intracellular cation channels that release calcium ions from stores such as the endoplasmic reticulum and sarcoplasmic reticulum.
Although RyRs are expressed in many cell types, their roles have only been extensively characterised in tissues in which they are abundant: RyR1 is essential for excitation–contraction coupling in skeletal muscle; whereas RyR2 is required for the analogous signal transduction pathway in heart. Defects in RyR1 cause malignant hyperthermia and a spectrum of myopathies in skeletal muscle; whereas RyR2 dysregulation can result in fatal cardiac arrhythmias and is involved in heart failure. Altered RyR gating has been implicated in a range of other diseases, including epilepsy, neurodegeneration, pain and cancer."
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