Respiratory ratio

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The respiratory ratio (RR or respiratory coefficient) is a ratio used in calculations of basal metabolic rate (BMR) when estimated from carbon dioxide production. It is calculated from the ratio of carbon dioxide produced by the body to oxygen consumed by the body. Such measurements, like measurements of oxygen uptake, are forms of indirect calorimetry. It is measured using a respirometer. The respiratory ratio value indicates which macronutrients are being metabolized, as different energy pathways are used for fats, carbohydrates, and proteins. [1] If metabolism consists solely of lipids, the respiratory ratio is approximately 0.7, for proteins it is approximately 0.8, and for carbohydrates it is 1.0. Most of the time, however, energy consumption is composed of both fats and carbohydrates. The approximate respiratory ratio of a mixed diet is 0.8. [1] Some of the other factors that may affect the respiratory ratio are energy balance, circulating insulin, and insulin sensitivity. [2]

Contents

It can be used in the alveolar gas equation.

Calculation

The respiratory ratio (RR) is the ratio:

where the term "evolved" refers to carbon dioxide (CO2) removed from the body.

In this calculation, the CO2 and O2 must be given in the same units, and in quantities proportional to the number of molecules. Acceptable inputs would be either moles, or else volumes of gas at standard temperature and pressure.

Many metabolized substances are compounds containing only the elements carbon, hydrogen, and oxygen. Examples include fatty acids, glycerol, carbohydrates, deamination products, and ethanol. For complete oxidation of such compounds, the chemical equation is

and thus metabolism of this compound gives an RR of x/(x + y/4 - z/2).

For glucose, the complete oxidation equation is

Thus, the RR = 6 CO2/ 6 O2 = 1.

For fats, the RR depends on the specific fatty acids present. Amongst the commonly stored fatty acids in vertebrates, RR varies from 0.692 (stearic acid) to as high as 0.759 (docosahexaenoic acid). Historically, it was assumed that 'average fat' had an RR of about 0.71, and this holds true for most mammals including humans. However, a recent survey showed that aquatic animals, especially fish, have fat that should yield higher RRs on oxidation, reaching as high as 0.73 due to high amounts of docosahexaenoic acid. [3]

The range of respiratory ratios for organisms in metabolic balance usually ranges from 1.0 (representing the value expected for pure carbohydrate oxidation) to ~0.7 (the value expected for pure fat oxidation). In general, molecules that are more oxidized (e.g., glucose) require less oxygen to be fully metabolized and, therefore, have higher respiratory ratios. Conversely, molecules that are less oxidized (e.g., fatty acids) require more oxygen for their complete metabolism and have lower respiratory ratios. See BMR for a discussion of how these numbers are derived. A mixed diet of fat and carbohydrate results in an average value between these numbers.

RR value corresponds to a caloric value for each liter (L) of CO2 produced. If O2 consumption numbers are available, they are usually used directly, since they are more direct and reliable estimates of energy production.

RR as measured includes a contribution from the energy produced from protein. However, due to the complexity of the various ways in which different amino acids can be metabolized, no single RR can be assigned to the oxidation of protein in the diet.

Insulin, which increases lipid storage and decreases fat oxidation, is positively associated with increases in the respiratory ratio. [2] A positive energy balance will also lead to an increased respiratory ratio. [2]

Applications

Practical applications of the respiratory ratio can be found in severe cases of chronic obstructive pulmonary disease, in which patients spend a significant amount of energy on respiratory effort. By increasing the proportion of fats in the diet, the respiratory ratio is driven down, causing a relative decrease in the amount of CO2 produced. This reduces the respiratory burden to eliminate CO2, thereby reducing the amount of energy spent on respirations. [4]

Respiratory ratio can be used as an indicator of over or underfeeding. Underfeeding, which forces the body to utilize fat stores, will lower the respiratory ratio, while overfeeding, which causes lipogenesis, will increase it. [5] Underfeeding is marked by a respiratory ratio below 0.85, while a respiratory ratio greater than 1.0 indicates overfeeding. This is particularly important in patients with compromised respiratory systems, as an increased respiratory ratio significantly corresponds to increased respiratory rate and decreased tidal volume, placing compromised patients at a significant risk. [5]

Because of its role in metabolism, respiratory ratio can be used in analysis of liver function and diagnosis of liver disease. In patients with liver cirrhosis, non-protein respiratory ratio (npRR) values act as good indicators in the prediction of overall survival rate. Patients having a npRR < 0.85 show considerably lower survival rates as compared to patients with a npRR > 0.85. [6] A decrease in npRR corresponds to a decrease in glycogen storage by the liver. [6] Similar research indicates that non-alcoholic fatty liver diseases are also accompanied by a low respiratory ratio value, and the non protein respiratory ratio value was a good indication of disease severity. [6]

Recently the respiratory ratio is also used from aquatic scientists to illuminate its environmental applications. Experimental studies with natural bacterioplankton using different single substrates suggested that RR is linked to the elemental composition of the respired compounds. [7] By this way, it is demonstrated that bacterioplankton RR is not only a practical aspect of Bacterioplankton Respiration determination, but also a major ecosystem state variable that provides unique information about aquatic ecosystem functioning. [7] Based on the stoichiometry of the different metabolized substrates, the scientists can predict that dissolved oxygen (O2) and carbon dioxide (CO2) in aquatic ecosystems should covary inversely due to the processing of photosynthesis and respiration. [8] Using this ratio could shed light on the metabolic behavior and the simultaneous roles of chemical and physical forcing that shape the biogeochemistry of aquatic ecosystems. [8]

List of respiratory ratios

Name of the substanceRespiratory ratio
Carbohydrates 1
Proteins 0.8 - 0.9 [1]
Ketones (eucaloric)0.73 [9]
Ketones (hypocaloric)0.66 [10] [11] [12]
Triolein (Fat)0.71
Oleic acid (Fat)0.71
Tripalmitin (Fat)0.7
Malic acid 1.33
Tartaric acid 1.6
Oxalic acid 4.0

[13]

See also

Related Research Articles

<span class="mw-page-title-main">Carbohydrate</span> Organic compound that consists only of carbon, hydrogen, and oxygen

A carbohydrate is a biomolecule consisting of carbon (C), hydrogen (H) and oxygen (O) atoms, usually with a hydrogen–oxygen atom ratio of 2:1 and thus with the empirical formula Cm(H2O)n, which does not mean the H has covalent bonds with O. However, not all carbohydrates conform to this precise stoichiometric definition, nor are all chemicals that do conform to this definition automatically classified as carbohydrates.

<span class="mw-page-title-main">Ketone bodies</span> Chemicals produced during fat metabolism

Ketone bodies are water-soluble molecules or compounds that contain the ketone groups produced from fatty acids by the liver (ketogenesis). Ketone bodies are readily transported into tissues outside the liver, where they are converted into acetyl-CoA —which then enters the citric acid cycle and is oxidized for energy. These liver-derived ketone groups include acetoacetic acid (acetoacetate), beta-hydroxybutyrate, and acetone, a spontaneous breakdown product of acetoacetate.

<span class="mw-page-title-main">Ketosis</span> Using body fats as fuel instead of carbohydrates

Ketosis is a metabolic state characterized by elevated levels of ketone bodies in the blood or urine. Physiological ketosis is a normal response to low glucose availability, such as low-carbohydrate diets or fasting, that provides an additional energy source for the brain in the form of ketones. In physiological ketosis, ketones in the blood are elevated above baseline levels, but the body's acid–base homeostasis is maintained. This contrasts with ketoacidosis, an uncontrolled production of ketones that occurs in pathologic states and causes a metabolic acidosis, which is a medical emergency. Ketoacidosis is most commonly the result of complete insulin deficiency in type 1 diabetes or late-stage type 2 diabetes. Ketone levels can be measured in blood, urine or breath and are generally between 0.5 and 3.0 millimolar (mM) in physiological ketosis, while ketoacidosis may cause blood concentrations greater than 10 mM.

<span class="mw-page-title-main">Cellular respiration</span> Process to convert glucose to ATP in cells

Cellular respiration is the process by which biological fuels are oxidized in the presence of an inorganic electron acceptor, such as oxygen, to drive the bulk production of adenosine triphosphate (ATP), which contains energy. Cellular respiration may be described as a set of metabolic reactions and processes that take place in the cells of organisms to convert chemical energy from nutrients into ATP, and then release waste products.

<span class="mw-page-title-main">Ketogenesis</span> Chemical synthesis of ketone bodies

Ketogenesis is the biochemical process through which organisms produce ketone bodies by breaking down fatty acids and ketogenic amino acids. The process supplies energy to certain organs, particularly the brain, heart and skeletal muscle, under specific scenarios including fasting, caloric restriction, sleep, or others.

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<span class="mw-page-title-main">Ketogenic diet</span> High-fat dietary therapy for epilepsy

The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate dietary therapy that in conventional medicine is used mainly to treat hard-to-control (refractory) epilepsy in children. The diet forces the body to burn fats rather than carbohydrates.

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In biochemistry and metabolism, beta oxidation (also β-oxidation) is the catabolic process by which fatty acid molecules are broken down in the cytosol in prokaryotes and in the mitochondria in eukaryotes to generate acetyl-CoA. Acetyl-CoA enters the citric acid cycle, generating NADH and FADH2, which are electron carriers used in the electron transport chain. It is named as such because the beta carbon of the fatty acid chain undergoes oxidation and is converted to a carbonyl group to start the cycle all over again. Beta-oxidation is primarily facilitated by the mitochondrial trifunctional protein, an enzyme complex associated with the inner mitochondrial membrane, although very long chain fatty acids are oxidized in peroxisomes.

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<span class="mw-page-title-main">Stearoyl-CoA 9-desaturase</span> Class of enzymes

Stearoyl-CoA desaturase (Δ-9-desaturase) is an endoplasmic reticulum enzyme that catalyzes the rate-limiting step in the formation of monounsaturated fatty acids (MUFAs), specifically oleate and palmitoleate from stearoyl-CoA and palmitoyl-CoA. Oleate and palmitoleate are major components of membrane phospholipids, cholesterol esters and alkyl-diacylglycerol. In humans, the enzyme is encoded by the SCD gene.

<span class="mw-page-title-main">Fibroblast growth factor 21</span>

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References

  1. 1 2 3 Widmaier, Eric P.; Raff, Hershel; Strang, Kevin T. (2016). Vander's Human Physiology: The Mechanisms of Body Function (14th ed.). New York: McGraw Hill. ISBN   9781259294099.
  2. 1 2 3 Ellis, Amy C; Hyatt, Tanya C; Gower, Barbara A; Hunter, Gary R (2017-05-02). "Respiratory Quotient Predicts Fat Mass Gain in Premenopausal Women". Obesity. 18 (12): 2255–2259. doi:10.1038/oby.2010.96. ISSN   1930-7381. PMC   3075532 . PMID   20448540.
  3. ↑ Price, E. R.; Mager, E. M. (2020). "Respiratory quotient: Effects of fatty acid composition". Journal of Experimental Zoology. 333 (9): 613–618. doi:10.1002/jez.2422. PMID   33063463. S2CID   222833275.
  4. ↑ Kuo, C. D.; Shiao, G. M.; Lee, J. D. (1993-07-01). "The effects of high-fat and high-carbohydrate diet loads on gas exchange and ventilation in COPD patients and normal subjects". Chest. 104 (1): 189–196. doi:10.1378/chest.104.1.189. ISSN   0012-3692. PMID   8325067.
  5. 1 2 McClave, Stephen A.; Lowen, Cynthia C.; Kleber, Melissa J.; McConnell, J. Wesley; Jung, Laura Y.; Goldsmith, Linda J. (2003-01-01). "Clinical use of the respiratory quotient obtained from indirect calorimetry". Journal of Parenteral and Enteral Nutrition. 27 (1): 21–26. doi:10.1177/014860710302700121. ISSN   0148-6071. PMID   12549594.
  6. 1 2 3 Nishikawa, Hiroki; Enomoto, Hirayuki; Iwata, Yoshinori; Kishino, Kyohei; Shimono, Yoshihiro; Hasegawa, Kunihiro; Nakano, Chikage; Takata, Ryo; Ishii, Akio (2017-01-01). "Prognostic significance of nonprotein respiratory quotient in patients with liver cirrhosis". Medicine. 96 (3): e5800. doi:10.1097/MD.0000000000005800. ISSN   1536-5964. PMC   5279081 . PMID   28099336.
  7. 1 2 Berggren, Martin; Lapierre, Jean-François; del Giorgio, Paul A (May 2012). "Magnitude and regulation of bacterioplankton respiratory quotient across freshwater environmental gradients". The ISME Journal. 6 (5): 984–993. doi:10.1038/ismej.2011.157. ISSN   1751-7362. PMC   3329109 . PMID   22094347.
  8. 1 2 Vachon, Dominic; Sadro, Steven; Bogard, Matthew J.; Lapierre, Jean‐François; Baulch, Helen M.; Rusak, James A.; Denfeld, Blaize A.; Laas, Alo; Klaus, Marcus; Karlsson, Jan; Weyhenmeyer, Gesa A. (August 2020). "Paired O 2 –CO 2 measurements provide emergent insights into aquatic ecosystem function". Limnology and Oceanography Letters. 5 (4): 287–294. doi: 10.1002/lol2.10135 . ISSN   2378-2242.
  9. ↑ Mosek, Amnon; Natour, Haitham; Neufeld, Miri Y.; Shiff, Yaffa; Vaisman, Nachum (2009). "Ketogenic diet treatment in adults with refractory epilepsy: A prospective pilot study". Seizure. 18 (1): 30–3. doi: 10.1016/j.seizure.2008.06.001 . PMID   18675556. S2CID   2393385.
  10. ↑ Johnston, Carol S; Tjonn, Sherrie L; Swan, Pamela D; White, Andrea; Hutchins, Heather; Sears, Barry (2006). "Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets". The American Journal of Clinical Nutrition. 83 (5): 1055–61. doi: 10.1093/ajcn/83.5.1055 . PMID   16685046.
  11. ↑ Phinney, Stephen D.; Horton, Edward S.; Sims, Ethan A. H.; Hanson, John S.; Danforth, Elliot; Lagrange, Betty M. (1980). "Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet". Journal of Clinical Investigation. 66 (5): 1152–61. doi:10.1172/JCI109945. PMC   371554 . PMID   7000826.
  12. ↑ Owen, O. E.; Morgan, A. P.; Kemp, H. G.; Sullivan, J. M.; Herrera, M. G.; Cahill, G. F. (1967). "Brain Metabolism during Fasting*". Journal of Clinical Investigation. 46 (10): 1589–95. doi:10.1172/JCI105650. PMC   292907 . PMID   6061736.
  13. ↑ Telugu Academi, Botany text book, 2007 Version[ verification needed ]
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