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Acidosis is a condition in which there is an excess of acid in the body, causing an imbalance in the body's pH level, which should be slightly alkaline. It can be caused by a variety of factors, including intense exercise, certain medications, and health conditions. Lactic acidosis, a type of acidosis caused by a buildup of lactic acid in the bloodstream, is particularly relevant to muscle excitation. While lactic acid is normally produced during exercise to fuel muscles, excessive buildup can lead to lactic acidosis, causing symptoms such as muscle soreness, burning, and nausea. Intracellular acidosis, specifically, has been found to enhance the excitability of working muscles, which may be mediated by decreased chloride permeability. This process highlights the protective effects of acidosis during muscle fatigue.
| Characteristics | Values |
|---|---|
| Intracellular acidosis | Enhances muscle excitability by decreasing chloride permeability |
| Lactic acidosis | Caused by intense exercise, alcohol consumption, or health conditions |
| Muscle fatigue | Caused by intracellular acidosis, but not solely due to increased lactate production |
| Metabolic acidosis | Impairs muscle function by hindering mitochondrial function and reducing energy production |
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What You'll Learn
Intracellular acidosis and muscle fatigue
The variability in the size of intracellular acidosis during muscle fatigue reflects the involvement of different metabolic pathways, the presence or absence of blood flow, and the effectiveness of pH-regulating pathways. Intracellular acidosis affects muscle cell function in several ways, including reducing maximal Ca2+-activated force and Ca2+ sensitivity, slowing the maximal shortening velocity, and prolonging relaxation. However, it is important to note that acidosis is not the sole metabolic change causing muscle fatigue, and some aspects, such as the failure of Ca2+ release, do not appear to be caused by acidosis.
The development of acidosis during intense exercise has traditionally been attributed to increased lactic acid production, leading to the release of a proton and the formation of the acid salt sodium lactate. This theory suggests that if lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in decreased cellular pH. However, recent evidence challenges this notion, indicating that lactate production retards rather than causes acidosis and that acidosis is caused by reactions other than lactate production.
During intense exercise, the increased demand for ATP to fuel muscle contraction exceeds the capacity of mitochondrial respiration, resulting in greater reliance on non-mitochondrial sources of ATP, such as glycolysis and the phosphagen system. The breakdown of ATP to ADP and P(i) releases protons, contributing to acidosis. Additionally, lactate production increases to prevent pyruvate accumulation and supply NAD(+) for glycolysis, making it an indirect marker of metabolic conditions leading to acidosis.
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Lactic acidosis and intense exercise
Lactic acidosis is a condition that occurs when there is a build-up of lactic acid in the bloodstream. During intense exercise, the body uses oxygen to break down glucose for energy. However, during periods of intense exercise, there may not be enough oxygen available to complete this process, so a substance called lactate is produced. This lactate can be converted into energy without oxygen, but if it builds up faster than it can be burned off, it leads to lactic acidosis.
Lactic acidosis can also be caused by certain health conditions, such as lung or heart conditions, that deprive the body of oxygen. Additionally, some medications, toxins, or other substances can interfere with the body's ability to break down lactate, leading to a build-up.
The symptoms of lactic acidosis include a burning feeling in the muscles, cramps, nausea, weakness, and exhaustion. It is important to listen to these symptoms and adjust your exercise routine accordingly, as lactic acidosis can damage your organs.
To prevent lactic acidosis during intense exercise, it is recommended to start with a gradual exercise routine and build up intensity and duration over time. Proper fueling and hydration before and after exercise can also help prevent lactic acidosis. Active recovery methods, such as low-intensity movements like yoga or walking, can also help clear lactic acid from the body.
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Acidosis and calcium binding
Intracellular acidosis, which is often accompanied by muscle fatigue, has been shown to enhance the excitability of working muscles. This occurs when muscles become depolarized, which is common in working muscles.
Acidosis affects calcium binding in the body. The effect of metabolic acidosis on calcium is complex and involves bone, the parathyroid gland, and the kidneys. Metabolic acidosis increases urinary calcium excretion, which is caused by the dissociation of sodium reabsorption from calcium reabsorption. Metabolic acidosis also increases ionized calcium in the blood, which is mobilized from bone and due to decreased binding to albumin.
Research has shown that acidosis reduces maximal Ca2+-activated force and Ca2+ sensitivity, slows the maximal shortening velocity, and prolongs relaxation. However, acidosis is not the only cause of muscle fatigue, and there are other important aspects of muscle fatigue (e.g., the failure of Ca2+ release) that do not appear to be caused by acidosis.
The development of acidosis during intense exercise has traditionally been attributed to the increased production of lactic acid, which releases a proton and forms the acid salt sodium lactate. However, recent research has shown that lactic acid does not cause acidosis, but rather, retards it. Acidosis is caused by reactions other than lactate production, such as the breakdown of ATP to ADP and P(i), which releases a proton.
In summary, acidosis increases muscle excitation and affects calcium binding in the body, particularly in the blood, bones, and kidneys.
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Acidosis and chloride conductance
Acidosis is associated with muscle fatigue, which is often accompanied by intracellular acidosis. This process may be mediated by decreased chloride permeability, which enables action potentials to be propagated along the internal network of tubules in a muscle fibre, despite muscle depolarization. This implicates chloride ion channels in muscle function and suggests that intracellular acidosis has protective effects during muscle fatigue.
Niflumic acid inhibits chloride conductance by directly inhibiting the CLC-1 channel and by increasing intracellular calcium. This is supported by research on rat skeletal muscle fibres, which found that intracellular acidosis enhances the excitability of working muscles. This is due to decreased chloride permeability, which allows action potentials to be propagated along the T-system, preserving muscle excitability when muscles become depolarized.
Research on rat soleus muscles has also shown that muscle acidification is associated with reduced chloride conductance, indicating that the recovery of excitability in K+-depressed muscles induced by muscle acidification is related to a reduction in inhibitory Cl− currents. This may be due to the inhibition of ClC-1 channels, which reduces the Na+ current needed to generate an action potential.
Furthermore, acidification reduced the rheobase current by 26% at 4 mM K+ and increased the number of excitable fibres at elevated [K+]o. At 11 mM K+ and normal pH, a recovery of excitability and force similar to the observations with muscle acidification could be induced by reducing extracellular Cl− or by blocking the major muscle Cl− channel, ClC-1, with 30 μM 9-AC.
In summary, acidosis is associated with muscle fatigue and intracellular acidosis, which can be mitigated by decreased chloride permeability. Niflumic acid inhibits chloride conductance, and research on rat skeletal muscle fibres and soleus muscles has shown that intracellular acidosis enhances muscle excitability and reduces chloride conductance, respectively. These findings suggest that the recovery of excitability in K+-depressed muscles is related to reduced inhibitory Cl− currents and the inhibition of ClC-1 channels.
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Acidosis and protein degradation
Acidosis is a clinical condition with both acute and chronic forms. Chronic metabolic acidosis increases protein degradation, while its effects on protein synthesis are less clear. Metabolic acidosis increases whole-body proteolysis due to a large increase in protein degradation and a moderate increase in protein synthesis.
Most studies on the relationship between acidosis and protein metabolism have focused on patients with chronic renal failure and metabolic acidosis. However, because chronic renal failure is associated with other abnormal metabolic conditions such as malnutrition, it is challenging to isolate the effects of acidosis on protein metabolism.
Acidosis is frequently associated with protein wasting and disruptions in amino acid metabolism. The influence of acidosis on protein metabolism is significantly influenced by other abnormal metabolic conditions caused by specific illnesses, making it difficult to attribute the effects solely to acidosis.
Studies have shown that acidosis increases protein degradation and amino acid oxidation, particularly leucine, in skeletal muscle. This results in muscle wasting and a negative nitrogen balance. The correction of metabolic acidosis may have beneficial effects on protein wasting and could potentially reduce morbidity and mortality.
Intracellular acidosis in skeletal muscles is commonly associated with muscle fatigue. However, it also plays a role in preserving muscle excitability when muscles become depolarized due to increased activity. This protective effect during muscle fatigue is mediated by decreased chloride permeability, which allows action potentials to propagate along the T system, a network of tubules within a muscle fiber.
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Frequently asked questions
Acidosis is a condition where there is a buildup of acid in the body, causing an imbalance in the body's pH level, which should be slightly alkaline.
Acidosis can be caused by a variety of factors, including intense exercise, certain medications, and health conditions such as liver disease, kidney disease, or heart failure.
Acidosis increases muscle excitation by affecting the concentration of H+ ions, which compete with Ca2+ ions involved in muscle contraction. It also slows the rates of myosin attachment and detachment, impacting the myosin cross-bridge cycle.
Symptoms of acidosis include muscle ache, burning, rapid breathing, nausea, stomach pain, weakness, and exhaustion.
Treatment for acidosis depends on the underlying cause. In the case of exercise-induced acidosis, slowing down or stopping the exercise can help. For acidosis caused by medications or health conditions, medical advice should be sought.
