What is respiratory exchange ratio (RER)? What is respiratory quotient (RQ)?
Prepared by Dr Ma Hon Ming, SMO TPH (M&EC) and Dr Lo Ho Yin, MO AHNH (Med)
RER is the ratio of carbon dioxide output to oxygen uptake (VCO2 / VO2) measured at the mouth ie external respiration whereas RQ is the ratio of CO2 production to O2 consumption through tissue metabolism (mCO2 / mO2) ie cellular respiration. RER approximates RQ only at steady state conditions when VO2 = m02 and VC02= mCO2 (eg at rest or after 3-4 min steady state exercise at constant workload). In clinical practice, RER is more readily obtained by measuring VCO2 and VO2. In steady states, RQ = RER. In non-steady states, dynamic RER values reflects active coupling of external respiration to cellular respiration.
In metabolic assessments by indirect calorimetry (either open circuit using canopy or close circuit for patients on ventilator), VCO2, VO2 and RER are obtained. RQ = RER in steady state. Based on known values of RQ (carbohydrate 1.0, protein 0.82, fat 0.71, mixed diet 0.85, ketosis 0.67 to 0.7, lipogenesis 1.0-1.2) and urinary nitrogen excretion of patients, we can assess their caloric and metabolic status. The goals are to ensure adequate caloric intake, to optimise nutritional formula and avoid overfeeding to prevent excessive CO2 production that escalates ventilatory demands. Dietary manipulation may change RQ. Physical fitness & endurance training can also change RQ through increased energy utilisation from fatty acid metabolism at a given workload.
In cardiopulmonary exercise testing, RER is derived from breath by breath O2 and CO2 flow measurements at the mouth. RER at rest stays ~ 0.8 (Westernised food). However, subjects who are anxious or hyperventilating for various reasons often have RER> I. Thus, VE and EtCO2 should be taken into consideration when interpreting RER values. During exercise, changes in cellular respiration needed to increase energy output are closely linked to external respiration through the circulation.
Studies on VCO2- VO2 relationship (V-slope) gave us valuable insights into our body wisdom. During exercise with cycle ergometer at increasing work rates (ramp), a steady state for VCO2 & VO2 is achieved at 3 to 4 min at work rates not causing increase in arterial lactate. This is the lower 'aerobic' component slope SI (RER ~ 0.95 corresponding to increase carbohydrate utilization during exercise). With glycogen depletion study (fasting and vigorous exercise on preceding day), SI falls to 0.79-0.81, showing that SI in V-slope plot below anaerobic threshold (AT) represented muscle substrate RQ.
With progressive increase in work rates, capillary PO2 reaches a 'critical' level below which mitochondria cannot consume oxygen (N~ l4mmHg, chronic stable heart failure~ 22mmHg) and lactate rises significantly. VO2 continues to increase at a rate proportional to the rise in lactate but VCO2 further diverges from VO2 increase due to extra CO2 release from cells as HCO3- buffered lactic acid. This is the steeper, upper 'anaerobic' component slope S2. This CO2 rise and HCO3- consumption shifts the O2 dissociation to the right (Bohr effect). Thus lactic acidosis serves to facilitate O2 dissociation and O2 transport to muscle cells without further reduction in end-capillary PO2. From this stage onward, RER is > 1.
AT occurs around a normal subject's mid-work capacity, not at V02 max. RER continues to increase as exercise progresses, up to > 1.6 in short duration, high work rate testing. During cool down, RER returns rapidly to baseline levels with occasional shoot-ups from hyperventilation. RER at peak exercise> 1 (eg RER >1.15 in some computerised ramp protocol) is often taken as indicator that a subject has made good effort. This contrasts with those with 'functional' impairment whose RER always stays < 1 with very high breathing and heart rate reserve even at 'peak' exercise.
(Food for thoughts or exams! - 1) RQ differences: male vs female, obese vs lean, hyperthyroid vs euthyroid, changes with age and pregnancy. 2) RER changes during exercise in COPD. Answers can befound in the references below)
References
1. Pulmonary Function Testing and Cardiopulmonary Stress Testing/Vincent C. Madama. Delmar Publishers lnc 1993.
2. Clinical Exercise Testing I Norman L. Jones- 4thed. WB Saunders Co. 1997.
3. Manual of Pulmonary Function Testing I Gregg L. Ruppel- ih ed. Mosby 1998.
4. Nutritional Aspects of Lung Disease. Michael Donahoe, Robert M. Rogers. Ch 11, vol. 16. Current Pulmonologyl Donald F. Tierney. Mosby 1995.
5. Critical Care Handbook of the Massachusettes General Hospital I editors, William E. Hurford,DeanHess- 3rded. LW&W 2000.
6. Manual of Clinical Problems in Pulmonary Medicine I Richard A. Bordow, Andrew L. Ries, Timothy A. Morris- 5thed. 2001.
7. Role of Cardiopulmonary Exercise Testing in Rehabilitation Medicine. Ma HM. Rehabilitation Medicine Dissertation HKCP Jan 2000.
8. Substrate utilisation during endurance exercise in men and women after endurance training. Carter SL et al. Am L Physiol Endocrinol Metab 2001 Jun ; 280(6) : E898-907
9. Carbohydrate metabolism during exercise in females: effect of reduced fat availability. Howlett KF et al. Metabolism 2001 Apr; 50(4):481-487.
10. The effect of an increased free fatty acid concentration on thermogenesis and substrate oxidation in obese and lean men. Schiffelers SL et al. lnt J Obes Relat Metab Disord 2001 Jan; 25(1):33-38.
11. Critical capillary PO2 and the role of lactate production in oxyhemoglobin dissociation during exercise. Wasserman K. Adv Exp Med BioI 1999; 471:321-323.
12. Diagnosing cardiovascular and lung pathophysiology from exercise gas exchange Wasserman K. Chest 1997 Oct; 112(4):1091-1101.
13. Ventilation during exercise in chronic heart failure. Wasserman K. et al. Basic Res Cardioll996; 91 Suppll:l-l1.
14. Lactic acidosis as a facilitator of oxyhemoglobin dissociation during exercise. StringerW et al. J Appl Physiol1994 Apr; 76(4):1462-1467.
15. The bioenergetic and gas exchange basis of exercise testing. Whipp BJ. Clin Chest Med 1994 Jun; 15(2):173-192.
16. Coupling of external to cellular respiration during exercise: the wisdom of the body revisited. Wassserman K. Am J Physiol1994 Apr; 266 :E519-539.
17. Comparison of gas exchange, lactate and lactic acidosis thresholds in patients with chronic obstructive pulmonary disease. Patessio A et al. Am Rev Respir Dis 1993 Sep; 148(3):622-626.
18. Factors affecting the components of the alveolar CO2 output-O2 uptake relationship during incremental exercise in man. Cooper CB et al. Exp Physiol1992 Jan; 77 (I): 51-64.
19. Gas exchange theory and the lactic acidosis (anaerobic) threshold. Wasserman K. etal. Circulation 1990Jan; 81( 1 Suppl ):114-30.
20. A new perspective in pulmonary rehabilitation: anaerobic threshold as a discriminant in training. Cassaburi R et al. Eur Respir J Suppl 1989 Jul; 618s-623s.
21. Effect of altering the proportion of dietary fat and carbohydrate on exercise gas exchange in normal subjects. Sue CY et al. Am Rev Respir Dis 1989 Jun; 139(6):1430-4.
22. Metabolic acidosis during exercise in patients with chronic obstructive pulmonary disease. Use of the V-slope method for anaerobic threshold determination. Sue DY et al. Chest 1988Nov; 94(5);931-938.
23. The anaerobic threshold: definition, physiological significance and identification. Wasserman K. Adv Cardiol1986; 351-23.
24. A new method for detecting anaerobic threshold by gas exchange. Beaver WL et al. J Appl Physiol1986 Jun; 60(6):2020-2027.
25. The anaerobic threshold measurement to evaluate exercise performance. Wasserman K. Am Rev Respir Dis 1984 Feb; 129:S35-40.
26. The anaerobic threshold measurement in exercise testing. Wasserman K. Clin Chest Med 1984 Mar; 5(1) :77-88.
27. Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction. Nery LE et al. J Appl Physiol1982 Dec; 53(6):1594-1602.
28. Anaerobic threshold alterations caused by endurance training in middle-aged men Davis JA et al. J Appl Physiol1979 Jun; 46(6): 1039-1046.
RER is the ratio of carbon dioxide output to oxygen uptake (VCO2 / VO2) measured at the mouth ie external respiration whereas RQ is the ratio of CO2 production to O2 consumption through tissue metabolism (mCO2 / mO2) ie cellular respiration. RER approximates RQ only at steady state conditions when VO2 = m02 and VC02= mCO2 (eg at rest or after 3-4 min steady state exercise at constant workload). In clinical practice, RER is more readily obtained by measuring VCO2 and VO2. In steady states, RQ = RER. In non-steady states, dynamic RER values reflects active coupling of external respiration to cellular respiration.
In metabolic assessments by indirect calorimetry (either open circuit using canopy or close circuit for patients on ventilator), VCO2, VO2 and RER are obtained. RQ = RER in steady state. Based on known values of RQ (carbohydrate 1.0, protein 0.82, fat 0.71, mixed diet 0.85, ketosis 0.67 to 0.7, lipogenesis 1.0-1.2) and urinary nitrogen excretion of patients, we can assess their caloric and metabolic status. The goals are to ensure adequate caloric intake, to optimise nutritional formula and avoid overfeeding to prevent excessive CO2 production that escalates ventilatory demands. Dietary manipulation may change RQ. Physical fitness & endurance training can also change RQ through increased energy utilisation from fatty acid metabolism at a given workload.
In cardiopulmonary exercise testing, RER is derived from breath by breath O2 and CO2 flow measurements at the mouth. RER at rest stays ~ 0.8 (Westernised food). However, subjects who are anxious or hyperventilating for various reasons often have RER> I. Thus, VE and EtCO2 should be taken into consideration when interpreting RER values. During exercise, changes in cellular respiration needed to increase energy output are closely linked to external respiration through the circulation.
Studies on VCO2- VO2 relationship (V-slope) gave us valuable insights into our body wisdom. During exercise with cycle ergometer at increasing work rates (ramp), a steady state for VCO2 & VO2 is achieved at 3 to 4 min at work rates not causing increase in arterial lactate. This is the lower 'aerobic' component slope SI (RER ~ 0.95 corresponding to increase carbohydrate utilization during exercise). With glycogen depletion study (fasting and vigorous exercise on preceding day), SI falls to 0.79-0.81, showing that SI in V-slope plot below anaerobic threshold (AT) represented muscle substrate RQ.
With progressive increase in work rates, capillary PO2 reaches a 'critical' level below which mitochondria cannot consume oxygen (N~ l4mmHg, chronic stable heart failure~ 22mmHg) and lactate rises significantly. VO2 continues to increase at a rate proportional to the rise in lactate but VCO2 further diverges from VO2 increase due to extra CO2 release from cells as HCO3- buffered lactic acid. This is the steeper, upper 'anaerobic' component slope S2. This CO2 rise and HCO3- consumption shifts the O2 dissociation to the right (Bohr effect). Thus lactic acidosis serves to facilitate O2 dissociation and O2 transport to muscle cells without further reduction in end-capillary PO2. From this stage onward, RER is > 1.
AT occurs around a normal subject's mid-work capacity, not at V02 max. RER continues to increase as exercise progresses, up to > 1.6 in short duration, high work rate testing. During cool down, RER returns rapidly to baseline levels with occasional shoot-ups from hyperventilation. RER at peak exercise> 1 (eg RER >1.15 in some computerised ramp protocol) is often taken as indicator that a subject has made good effort. This contrasts with those with 'functional' impairment whose RER always stays < 1 with very high breathing and heart rate reserve even at 'peak' exercise.
(Food for thoughts or exams! - 1) RQ differences: male vs female, obese vs lean, hyperthyroid vs euthyroid, changes with age and pregnancy. 2) RER changes during exercise in COPD. Answers can befound in the references below)
References
1. Pulmonary Function Testing and Cardiopulmonary Stress Testing/Vincent C. Madama. Delmar Publishers lnc 1993.
2. Clinical Exercise Testing I Norman L. Jones- 4thed. WB Saunders Co. 1997.
3. Manual of Pulmonary Function Testing I Gregg L. Ruppel- ih ed. Mosby 1998.
4. Nutritional Aspects of Lung Disease. Michael Donahoe, Robert M. Rogers. Ch 11, vol. 16. Current Pulmonologyl Donald F. Tierney. Mosby 1995.
5. Critical Care Handbook of the Massachusettes General Hospital I editors, William E. Hurford,DeanHess- 3rded. LW&W 2000.
6. Manual of Clinical Problems in Pulmonary Medicine I Richard A. Bordow, Andrew L. Ries, Timothy A. Morris- 5thed. 2001.
7. Role of Cardiopulmonary Exercise Testing in Rehabilitation Medicine. Ma HM. Rehabilitation Medicine Dissertation HKCP Jan 2000.
8. Substrate utilisation during endurance exercise in men and women after endurance training. Carter SL et al. Am L Physiol Endocrinol Metab 2001 Jun ; 280(6) : E898-907
9. Carbohydrate metabolism during exercise in females: effect of reduced fat availability. Howlett KF et al. Metabolism 2001 Apr; 50(4):481-487.
10. The effect of an increased free fatty acid concentration on thermogenesis and substrate oxidation in obese and lean men. Schiffelers SL et al. lnt J Obes Relat Metab Disord 2001 Jan; 25(1):33-38.
11. Critical capillary PO2 and the role of lactate production in oxyhemoglobin dissociation during exercise. Wasserman K. Adv Exp Med BioI 1999; 471:321-323.
12. Diagnosing cardiovascular and lung pathophysiology from exercise gas exchange Wasserman K. Chest 1997 Oct; 112(4):1091-1101.
13. Ventilation during exercise in chronic heart failure. Wasserman K. et al. Basic Res Cardioll996; 91 Suppll:l-l1.
14. Lactic acidosis as a facilitator of oxyhemoglobin dissociation during exercise. StringerW et al. J Appl Physiol1994 Apr; 76(4):1462-1467.
15. The bioenergetic and gas exchange basis of exercise testing. Whipp BJ. Clin Chest Med 1994 Jun; 15(2):173-192.
16. Coupling of external to cellular respiration during exercise: the wisdom of the body revisited. Wassserman K. Am J Physiol1994 Apr; 266 :E519-539.
17. Comparison of gas exchange, lactate and lactic acidosis thresholds in patients with chronic obstructive pulmonary disease. Patessio A et al. Am Rev Respir Dis 1993 Sep; 148(3):622-626.
18. Factors affecting the components of the alveolar CO2 output-O2 uptake relationship during incremental exercise in man. Cooper CB et al. Exp Physiol1992 Jan; 77 (I): 51-64.
19. Gas exchange theory and the lactic acidosis (anaerobic) threshold. Wasserman K. etal. Circulation 1990Jan; 81( 1 Suppl ):114-30.
20. A new perspective in pulmonary rehabilitation: anaerobic threshold as a discriminant in training. Cassaburi R et al. Eur Respir J Suppl 1989 Jul; 618s-623s.
21. Effect of altering the proportion of dietary fat and carbohydrate on exercise gas exchange in normal subjects. Sue CY et al. Am Rev Respir Dis 1989 Jun; 139(6):1430-4.
22. Metabolic acidosis during exercise in patients with chronic obstructive pulmonary disease. Use of the V-slope method for anaerobic threshold determination. Sue DY et al. Chest 1988Nov; 94(5);931-938.
23. The anaerobic threshold: definition, physiological significance and identification. Wasserman K. Adv Cardiol1986; 351-23.
24. A new method for detecting anaerobic threshold by gas exchange. Beaver WL et al. J Appl Physiol1986 Jun; 60(6):2020-2027.
25. The anaerobic threshold measurement to evaluate exercise performance. Wasserman K. Am Rev Respir Dis 1984 Feb; 129:S35-40.
26. The anaerobic threshold measurement in exercise testing. Wasserman K. Clin Chest Med 1984 Mar; 5(1) :77-88.
27. Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction. Nery LE et al. J Appl Physiol1982 Dec; 53(6):1594-1602.
28. Anaerobic threshold alterations caused by endurance training in middle-aged men Davis JA et al. J Appl Physiol1979 Jun; 46(6): 1039-1046.
