Nutrition
Potential effect of nutrients on mitochondrial performance
Bioenergetic failure of skeletal muscle is associated with acquired weakness in the ICU.
ATP production decreases significantly during critical illness. This decrease is even greater in patients who ultimately do not survive. Proper mitochondrial function is essential for survival.
Hyperglycemia, hypertriglyceridemia, elevated lactate, and free fatty acids are important indicators of metabolism in critically ill patients. This balance between energy substrates is not only disrupted during the critical stages of illness but may continue into the recovery phase.
For example, a recent study found that patients who survived severe burns were unable to use fat for energy in their muscles months after discharge from the ICU.
In this review, the researchers focused on finding evidence for the supplementation of nutrients and other compounds to improve bioenergetic balance both in the acute phase, when patients are in the ICU, and in the recovery phase.
Several vitamins are necessary for mitochondrial function, either as cofactors in energy metabolism and/or acting as antioxidants. This study focuses in particular on the B group, vitamins C and E.
Other compounds have also been analyzed: selenium, zinc, coenzyme Q10, caffeine, melatonin, carnitine, nitrate (improves recovery but is not recommended during the acute phase), and lipoic acid.
The results of this review indicate that all these components form a complex network, which makes it necessary to emphasize that mitochondrial bioenergetic function will be optimal when the substrates and cofactors in this network are available in optimal combinations.
Combined deficiencies are probably more common than single nutrient deficiencies, and therefore research into combined deficiencies and the role of combined supplementation will be of great interest. Consequently, it is difficult to draw conclusions about the effects of a single nutrient on the oxidative phosphorylation process, as many nutrients cooperate in metabolic pathways. Supplementation with one nutrient is unlikely to enhance the subsequent effects when there is a deficiency of another micronutrient.
The researchers conclude that, taken together, the evidence that impaired mitochondrial bioenergetic function in muscle plays a crucial role in determining recovery from critical illness is compelling.
However, plasma nutrient levels may be low during critical illness due to increased losses through body fluids and increased endothelial permeability, redistribution, altered protein binding, and inadequate intake. As a result, plasma levels are unlikely to reflect tissue stores of micronutrients during critical illness. This makes it even more difficult to interpret the associations found.
ATP production decreases significantly during critical illness. This decrease is even greater in patients who ultimately do not survive. Proper mitochondrial function is essential for survival.
Hyperglycemia, hypertriglyceridemia, elevated lactate, and free fatty acids are important indicators of metabolism in critically ill patients. This balance between energy substrates is not only disrupted during the critical stages of illness but may continue into the recovery phase.
For example, a recent study found that patients who survived severe burns were unable to use fat for energy in their muscles months after discharge from the ICU.
In this review, the researchers focused on finding evidence for the supplementation of nutrients and other compounds to improve bioenergetic balance both in the acute phase, when patients are in the ICU, and in the recovery phase.
Several vitamins are necessary for mitochondrial function, either as cofactors in energy metabolism and/or acting as antioxidants. This study focuses in particular on the B group, vitamins C and E.
Other compounds have also been analyzed: selenium, zinc, coenzyme Q10, caffeine, melatonin, carnitine, nitrate (improves recovery but is not recommended during the acute phase), and lipoic acid.
The results of this review indicate that all these components form a complex network, which makes it necessary to emphasize that mitochondrial bioenergetic function will be optimal when the substrates and cofactors in this network are available in optimal combinations.
Combined deficiencies are probably more common than single nutrient deficiencies, and therefore research into combined deficiencies and the role of combined supplementation will be of great interest. Consequently, it is difficult to draw conclusions about the effects of a single nutrient on the oxidative phosphorylation process, as many nutrients cooperate in metabolic pathways. Supplementation with one nutrient is unlikely to enhance the subsequent effects when there is a deficiency of another micronutrient.
The researchers conclude that, taken together, the evidence that impaired mitochondrial bioenergetic function in muscle plays a crucial role in determining recovery from critical illness is compelling.
However, plasma nutrient levels may be low during critical illness due to increased losses through body fluids and increased endothelial permeability, redistribution, altered protein binding, and inadequate intake. As a result, plasma levels are unlikely to reflect tissue stores of micronutrients during critical illness. This makes it even more difficult to interpret the associations found.
* The news published on studies do not represent an official position of ICNS, nor a clinical recommendation.


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