Basal Respiratory Quotient Research Articles

Modelling Accumulation of Respiratory-CO2 in Closed Rooms Leading to Decision-Making on Room Occupancy

A model predicting time required to attain undesired levels of respiratory-CO2 in closed rooms is described. The model works under the following assumptions: (1) room air is well-mixed, (2) indoor CO2 does not exchange with outdoor CO2, (3) there is no effect of individual occupants on CO2 exhalation rate of other occupants, (4) there is no indoor CO2 sink and all exhaled CO2 end up increasing CO2 concentration in the room, (5) apart from respiration, there is no other source of indoor CO2, (6) breathing rates of occupants are constant throughout the period of occupation of room. The model makes use of anthropocentric parameters like body weight, height, du bois surface area, MET levels, etc., to calculate dedicated individual CO2 exhalation rate and uses room volume and number of occupants to predict time required to reach user-earmarked levels of CO2. A model run showed that in a closed room of 12 × 12 × 10 m3, respiration by one person at rest (65 kg body weight, 1.7 m height, basal respiratory quotient of 0.83) would take 4.37 h to reach 2000 ppmV indoor CO2 when background indoor CO2 level was 380 ppmV. This model would help allocating desired number of occupants in closed rooms to help avoid building up of undesirable levels of CO2 in poorly ventilated offices, schools, hospitals or households that might frequently experience high levels of indoor CO2, undermining health and performance of occupants, patients and workers.

1918-P: Carbohydrate and Fat Oxidation Fasting and in Response to a Hyperinsulinemic Clamp is Similar in Obese Youth Regardless of PCOS Status

Whole-body metabolic flexibility (MF), i.e., switching substrate oxidation between fasting and fed states often becomes abnormal with insulin resistance (IR). Data regarding MF in women with PCOS, whom often have IR, are mixed and confounded by varied diets and habitual physical activity. No study has assessed MF in response to a multi-phase hyperinsulinemic-euglycemic clamp in PCOS females relative to non-PCOS with similar habitual physical activity and controlled diet. Adolescent girls with obesity and PCOS (age 14.9 ± 1.5 years; BMI 35 ± 4 kg/m2), 10 obese controls (age 13.5 ± 1.3; BMI 32 ± 2) and 13 normal BMI PCOS (age 16.2 ± 1.5; BMI 22.8 ± 2) were included. All girls were sedentary per questionnaire and 7 day accelerometry. A 4-phase hyperinulinemic-euglycemic clamp (basal, 10, 16 and 80 mU/m2/min of insulin) including glucose and glycerol tracers was performed. Glucose rate of disappearance (Rd), glycerol rate of appearance (Ra) and respiratory quotient (RQ) were assessed during each clamp phase. MF was defined as a change in RQ from baseline to each phase (ΔRQ). Basal RQs were not different between groups. Lean PCOS had higher ΔRQ at phase 10 compared to obese PCOS (p=0.005) and obese controls (p=0.003). All groups had similar ΔRQs at 16 and 80 phases. In multivariable regression models, Δ 10 glycerol Ra (Δ from baseline to 10 phase) was associated with phase 10 ΔRQ, independent of age and BMI (p=0.04); Δ 80 glycerol Ra and Δ 80 glucose Rd were associated with phase 80 ΔRQ, independent of age and BMI (p=0.048). Sedentary obese adolescents regardless of PCOS status have lower MF compared to lean PCOS during the low insulin dose which was associated with whole body lipolysis. However, this difference is not found during the high insulin dose, suggesting obese girls have only subtle defects in MF. Further, PCOS is not associated with lower MF once diet and habitual activity are matched. Disclosure P. Wiromrat: None. C.A. Rynders: None. K.J. Nadeau: None. M. Cree-Green: None. Funding American Diabetes Association (7-11-CD-08 to K.J.N.); American Heart Association (13CRP14120015); Thrasher Research Fund; National Center for Research Resources Colorado (TL1TR002533); Pediatric Endocrinology Society; National Institute of Diabetes and Digestive and Kidney Diseases (T32DK063687, K23DK107871)

Lipid Oxidation Assessed by Indirect Calorimetry Predicts Metabolic Syndrome and Type 2 Diabetes.

Purpose: Diabetes has been linked to an impaired ability to oxidize fatty acids. Fat oxidation can be assessed clinically by a respiratory quotient measurement during fasting. We hypothesized that a respiratory quotient might predict metabolic syndrome and type 2 diabetes onset.Methods: In this longitudinal study we used an existing database of 233 individuals who had complete nutritional and biochemical data at baseline and after 12-month follow-up. All participants underwent an indirect calorimetry to measure the respiratory quotient. We excluded participants with diabetes, metabolic syndrome, chronic diseases, and those who had changed food habits in the previous 3 months. Only 88 subjects met the inclusion criteria.Results: Two individuals developed type 2 diabetes and 10 metabolic syndrome after 1 year. Participants in the high respiratory quotient group (>0.91) had a higher incidence of metabolic syndrome/diabetes than those in the low quotient group (25 vs. 8% p = 0.04). In this group, mean basal respiratory quotient was 0.97 ± 0.04. In the high respiratory quotient group, Kaplan-Meier curves showed a greater probability of having metabolic syndrome/diabetes than those in the low respiratoryquotient group (log Rank χ2-test = 8.44; p = 0.004). A multivariable Cox proportional hazards model demonstrated that energy expenditure and weight increase did not predict metabolic syndrome/diabetes [HR (95% CI) = 1 (0.996–1.005), p = 0.86 and 3.9 (0.407–38.061), p = 0.23, respectively).Conclusions: A greater probability of metabolic syndrome/diabetes was found in individuals with a basal respiratory quotient of >0.91 than in those with a respiratoryquotient of ≤ 0.91 after 1 year. In the short-term anthropometric measurements and their variation overtime were not correlated with metabolic syndrome/diabetes.

Independent effects of diet and exercise training on fat oxidation in non-alcoholic fatty liver disease.

AIMTo investigate the independent effects of 6-mo of dietary energy restriction or exercise training on whole-body and hepatic fat oxidation of patients with non-alcoholic fatty liver disease (NAFLD).METHODSParticipants were randomised into either circuit exercise training (EX; n = 13; 3 h/wk without changes in dietary habits), or dietary energy restriction (ER) without changes in structured physical activity (ER; n = 8). Respiratory quotient (RQ) and whole-body fat oxidation rates (Fatox) were determined by indirect calorimetry under basal, insulin-stimulated and exercise conditions. Severity of disease and steatosis was determined by liver histology; hepatic Fatox was estimated from plasma β-hydroxybutyrate concentrations; cardiorespiratory fitness was expressed as VO2peak. Complete-case analysis was performed (EX: n = 10; ER: n = 6).RESULTSHepatic steatosis and NAFLD activity score decreased with ER but not with EX. β-hydroxybutyrate concentrations increased significantly in response to ER (0.08 ± 0.02 mmol/L vs 0.12 ± 0.04 mmol/L, P = 0.03) but remained unchanged in response to EX (0.10 ± 0.03 mmol/L vs 0.11 ± 0.07 mmol/L, P = 0.39). Basal RQ decreased (P = 0.05) in response to EX, while this change was not significant after ER (P = 0.38). VO2peak (P < 0.001) and maximal Fatox during aerobic exercise (P = 0.03) improved with EX but not with ER (P > 0.05). The increase in β-hydroxybutyrate concentrations was correlated with the reduction in hepatic steatosis (r = -0.56, P = 0.04).CONCLUSIONER and EX lead to specific benefits on fat metabolism of patients with NAFLD. Increased hepatic Fatox in response to ER could be one mechanism through which the ER group achieved reduction in steatosis.

Whole-body substrate metabolism is associated with disease severity in patients with non-alcoholic fatty liver disease

ObjectivesIn non-alcoholic fatty liver disease (NAFLD), hepatic steatosis is intricately linked with a number of metabolic alterations. We studied substrate utilisation in NAFLD during basal, insulin-stimulated and exercise conditions, and...

Inflexibility of energy substrate oxidation in type 1 diabetic patients

Obese, insulin-resistant patients have been shown to have metabolic inflexibility. The goal of this study was to examine the effect of insulin administration on energy metabolism in lean, type 1 diabetic (DM1) patients. Eleven DM1 patients without vascular complications and 11 healthy controls (C) were examined. We performed a 2-step hyperinsulinemic euglycemic clamp (240 minutes; period 1: 1 mU · kg −1 · min −1 and period 2: 10 mU · kg −1 · min −1) combined with indirect calorimetry during basal period B (B, −45 to 0 minutes), period 1, and period 2 of the clamp. The metabolic clearance rates of glucose (MCR) were lower in DM1 compared with C in period 1 (12.54 ± 3.38 v 17.41 ± 6.18 mL · kg −1 · min −1; P < .02), as well as in period 2 (21.63 ± 6.47 v 26.61 ± 4.45 mL · kg −1 · min −1; P < .05). Basal respiratory quotient (RQ) was lower in DM1 compared with C (0.72 ± 0.04 v 0.75 ± 0.04; P < .03). Insulin administration was accompanied by an increase in RQ in both groups, which was lower in DM1 compared with C (period 1: +0.09 ± 0.04 v +0.11 ± 0.07; P < .001; period 2: +0.13 ± 0.04 v +0.16 ± 0.04; P < .001). Glucose oxidation did not differ between the groups in period B; however, it was lower in DM1 compared with C in periods 1 (1.17 ± 0.67 v 3.28 ± 1.11 mg · kg −1 · min −1; P < .003); and 2 (2.10 ± 0.64 v 3.28 ± 0.93 mg · kg −1 · min −1; P < .009). Lipid oxidation was higher in DM1 in all periods compared with C; period B (3.28 ± 0.77 v 1.16 ± 0.55 mg · kg −1 · min −1; P < .001), period 1 (1.10 ± 0.41 v 0.67 ± 0.54 mg · kg −1 · min −1; P < .05), and period 2 (0.99 ± 0.29 v 0.52 ± 0.58 mg · kg −1 · min −1; P < .01). The groups did not differ in protein oxidation. In conclusion, DM1 patients with secondary insulin resistance (IR) are characterized by metabolic inflexibility manifesting itself by smaller increases in RQ and glucose oxidation after insulin administration during the euglycemic clamp.

Altered energy metabolism in anorexia nervosa.

Optimal nutritional rehabilitation of anorexia nervosa requires more information concerning actual energy and substrate requirements. To this end, indirect calorimetry was performed in female patients (n=34, age 20.9+/-1.2 yr, body mass index [BMI] 15.6+/-0.2 kg/m(2); mean+/-SEM) soon after commencement of refeeding and at the time of discharge from hospital (n=18, BMI 19.0+/-0.3 kg/m(2)). Healthy female controls (n=18, age 24.6+/-1.3 yr, BMI 21.6+/-0.6 kg/m(2)) were also tested. Resting energy expenditure (REE) and respiratory quotient (RQ) were measured in the fasting state, followed by diet-induced thermogenesis (DIT) and RQ over a 4 h period following a 100 g oral glucose load. Compared with post-refeeding patients and controls, pre-refeeding patients had a high basal RQ and a low REE, with a paradoxically higher DIT (13.2+/-0.9% of REE vs. 8.3+/-1.2% and 8.6+/-0.9% in post-refeeding patients and controls, respectively). RQ values in pre-refeeding patients exceeded unity following the glucose load, probably reflecting net lipogenesis, whereas in the post-refeeding patients, post-glucose RQ was similar to that of controls, suggesting premature curtailment of lipogenesis. These data demonstrate energy wasting in emaciated patients with anorexia nervosa. Biological repair processes could account for disproportionate energy loss early in refeeding and there may be some later impediment to full restoration of fat stores.

Whole body fat oxidation is related to in situ adipose tissue lipolytic response to isoproterenol in males.

A high 24-h respiratory quotient (RQ), i.e., low fat oxidation, predicts weight gain. To determine whether impaired fat mobilization (lipolysis) may contribute to weight gain, we studied the relation between lipolytic response to nonselective beta-adrenergic stimulation and RQ measured in a respiratory chamber in 21 males (11 Caucasians, 10 Pima Indians; age 32 +/- 5 yr, weight 93 +/- 24 kg, body fat 30 +/- 8%; means +/- SD) and 23 females (10 Caucasians, 13 Pima Indians; age 32 +/- 9 yr, weight 95 +/- 26 kg, body fat 44 +/- 8%). Lipolytic response was assessed as the relative increase in dialysate glycerol concentration (% above baseline) when isoproterenol (1 micromol/l) was added to the perfusate of a microdialysis probe inserted in the abdominal subcutaneous adipose tissue. In males, but not in females, basal RQ measured during sleep from 0500 to 0630 and adjusted for waist circumference was negatively correlated to lipolytic response (r = -0.66, P = 0.001). The results suggest that in males, impaired beta-adrenergic-mediated lipolysis may contribute to low rates of fat oxidation, a condition known to predispose to weight gain.

Correlation between amino acid induced changes in energy expenditure and protein metabolism in humans

The relationship between energy expenditure and protein metabolism during amino acid (AA) administration wasevaluated in normal humans. A balanced AA solution was infused for 180 min at five different rates: 20 (study I), 40 (study II) , 80 (study III) , 160 (study IV), and 240 mg · m 2 −1 · min −1 (study V), on separate days, in seven normal, overnight-fasted subjects (age 25 ± 2 y; height 172 ± 5 cm; weight 68 ± 4 kg). Indirect calorimetry and [I- 14C] leucine infusion techniques were employed. Basal total plasma AA concentration averaged 1827 ± 121 μmol/L and increased to 2192 ± 142, 2576 ± 158, 3677 ± 195, 5638 ± 237, and 7185 ± 261 μmol/L in studies I–V, respectively. Basal energy expenditure averaged 0.60 ± 0.02 kcal· M 2 −1· min −1 and increased slightly in studies I and II (to 0.62 ± 0.03, 0.63 ± 0.02, respectively), and significantly in studies III–V (to 0.65 ± 0.03, 0.70 ± 0.04, and 0.77 ± 0.05 kcal· m 2 −1 · min −1, respectively; all P < 0.01 versus basal; P < 0.05−0.01 for each study versus preceding study). Basal nonoxidative leucine disposal (NOLD), an index of protein synthesis, averaged 73 ± 3 μmol·m 2 −1·min −1 and increased, albeit not significantly, in studies I and II (to 75 ± 5, 76 ± 4, respectively). In contrast, a significant increase in NOLD was observed in studies III–V (to 87 ± 7, 103 ± 7, and 127 ± 9 μmol · ml 2 −1· min −1, respectively; all P < 0.01 versus basal; P < 0.05−0.01 for each study versus preceding study). Basal respiratory quotient averaged 0.81 ± 0.02 and did not change significantly in studies I–V (0.80 ± 0.02, 0.79 ± 0.02, 0.80 ± 0.03, 0.82 ± 0.02 and 0.82 ± 0.03, respectively). The thermic effect of AA administration, calculated as percent of the AA energy infused, was constant and averaged 24 ± 4, 19 ± 3, 17 ± 4, 17 ± 3, and 18 ± 3% in studies I–V, respectively. When AA-induced increase in protein synthesis was plotted with the increment in energy expenditure, a positive correlation was obtained ( r = 0.792, P < 0.001). In summary, during AA administration ( 1) the absolute rise in energy expenditure is dose-dependent and does not show evidence of achieving a plateau; ( 2) it is positively correlated with AA-induced protein synthesis; and ( 3) the thermic effect is not dependent upon the AA dose administered. The data provide a quantitative assessment of AA-induced thermogenesis in normal humans and the energy needs associated with an acute stimulation of protein synthesis.

Correlation between amino acid induced changes in energy expenditure and protein metabolism in humans.

The relationship between energy expenditure and protein metabolism during amino acid (AA) administration was evaluated in normal humans. A balanced AA solution was infused for 180 min at five different rates: 20 (study I), 40 (study II), 80 (study III), 160 (study IV), and 240 mg.m2(-1).min-1 (study V), on separate days, in seven normal, overnight-fasted subjects (age 25 +/- 2 y; height 172 +/- 5 cm; weight 68 +/- 4 kg). Indirect calorimetry and [1-14C] leucine infusion techniques were employed. Basal total plasma AA concentration averaged 1827 +/- 121 mumol/L and increased to 2192 +/- 142, 2576 +/- 158, 3677 +/- 195, 5638 +/- 237, and 7185 +/- 261 mumol/L in studies I-V, respectively. Basal energy expenditure averaged 0.60 +/- 0.02 kcal.m2(-1).min-1 and increased slightly in studies I and II (to 0.62 +/- 0.03, 0.63 +/- 0.02, respectively), and significantly in studies III-V (to 0.65 +/- 0.03, 0.70 +/- 0.04, and 0.77 +/- 0.05 kcal.m2(-1).min-1, respectively, all P < 0.01 versus basal; P < 0.05-0.01 for each study versus preceding study). Basal nonoxidative leucine disposal (NOLD), an index of protein synthesis, averaged 73 +/- 3 mumol.m2(-1).min-1 and increased, albeit not significantly, in studies I and II (to 75 +/- 5, 76 +/- 4, respectively). In contrast, a significant increase in NOLD was observed in studies III-V (to 87 +/- 7, 103 +/- 7, and 127 +/- 9 mumol.m2(-1).min-1, respectively; all P < 0.01 versus basal; P < 0.05-0.01 for each study versus preceding study). Basal respiratory quotient averaged 0.81 +/- 0.02 and did not change significantly in studies I-V (0.80 +/- 0.02, 0.79 +/- 0.02, 0.80 +/- 0.03, 0.82 +/- 0.02 and 0.82 +/- 0.03, respectively). The thermic effect of AA administration, calculated as percent of the AA energy infused, was constant and averaged 24 +/- 4, 19 +/- 3, 17 +/- 4, 17 +/- 3, and 18 +/- 3% in studies I-V, respectively. When AA-induced increase in protein synthesis was plotted with the increment in energy expenditure, a positive correlation was obtained (r = 0.792, P < 0.001). In summary, during AA administration (1) the absolute rise in energy expenditure is dose-dependent and does not show evidence of achieving a plateau; (2) it is positively correlated with AA-induced protein synthesis; and (3) the thermic effect is not dependent upon the AA dose administered. The data provide a quantitative assessment of AA-induced thermogenesis in normal humans and the energy needs associated with an acute stimulation of protein synthesis.

The Effects of Fat Distribution on Resting Energy Expenditure in Premenopausal Morbidly Obese Females.

BACKGROUND: upper body, or abdominal, distribution of body fat is associated with a number of metabolic and hormonal aberrations that could influence resting energy expenditure REE. The purpose of our study was to examine the effects of fat distribution on REE of 96 morbidly obese premenopausal females. METHODS: the study population consisted of three groups of study subjects, 32 with lower body fat distribution (LBD) and waist-to-hip circumference ratios WHR < 0.80, 20 with intermediate (INT) fat distribution and WHR between 0.80 and 0.85 and 34 females with upper body distribution of fat (UBD) and WHR > 0.85. Indices measured included: (1) REE; (2) maximal oxygen consumption during an exercise tolerance test (VO&inf2; max); (3) basal respiratory quotient (RO); (4) fasting blood glucose; and (5) serum cholesterol and triglycerides. RESULTS: we found that morbidly obese women who store fat abdominally (WHR > 0.80) have significantly (p < 0.01) higher REE (kcal per h per BSA) than those with lower body obesity. Levels of triglyceride and glucose of the UBD group were also higher than those of the LBD subjects, i.e. 35% and 23%, respectively. VO&inf2; max and RO were similar between the study groups, suggesting that the elevated REE of the patients with abdominal adiposity were likely not the result of their greater muscle mass or differences in substrate utilization. CONCLUSION: fat distribution affects REE in morbidly obese premenopausal females, and further research is needed to identify the various entities regulating REE in the morbidly obese.

Energy expenditure in obese women before and during weight loss, after refeeding, and in the weight-relapse period

In 10 moderately obese women, 24-h energy expenditure (24EE) was measured in a respiration chamber under four conditions: 1) before weight loss (body weight = 77.9 kg), 2) during weight loss (63.9 kg), 3) after realimentation (62.5 kg), and 4) 6-15 mo after the study diet with ad libitum diet (67.7 kg). The 14 +/- 8 kg (mean +/- SD) weight loss produced a decrease in 24EE of 1498 +/- 1138 kJ/d (P < 0.001), ie, a decrease of weight of 107 kJ.kg body wt-1.d-1. The subsequent 24EE (conditions 3 and 4) remained lower than the value before weight loss. A significant correlation was found between changes before and after weight regain in basal respiratory quotient (RQ) and the spontaneous rate of body-weight gain after cessation of the period of low energy intake (r = 0.89, P < 0.01); this suggests that the value of the postabsorptive RQ may be a predictor of relapse of weight gain. After discontinuation of the low energy diet, an elevated postabsorptive RQ shows that the endogenous lipid oxidation is low, a condition favoring weight gain.

Substrate oxidation errors during combined indirect calorimetry-hyperinsulinemic glucose clamp studies

The procedure of indirect calorimetry is often combined with the hyperinsulinemic, euglycemic clamp technique so that intracellular rates of glucose oxidation (G ox), fat oxidation (F ox), and energy expenditure (EE) can be determined at different insulin concentrations and rates of whole-body glucose uptake. In order to perform these calculations, rates of protein oxidation (P ox) must be known and are usually estimated from urinary nitrogen (N) excretion. The use of urinary N assumes that this measurement accurately reflects P ox and is unaltered by the glucose clamp technique. To examine these assumptions and determine potential errors in rates of G ox, F ox, and EE with this method, eight healthy subjects each had basal urinary N excretion determined on 4 different days and during a 300 pmol/m 2/min hyperinsulinemic, euglycemic clamp. Mean basal urinary N excretion was 6.4 ± 1.6 mg/min. Within individuals, basal urinary N was highly variable on the 4 different days with a mean coefficient of variation (CV) of 36% ± 18%. Over the range of basal respiratory quotient (RQ) values in this study (0.78 to 0.85) the day-to-day variation in basal urinary N resulted in potential errors of 11% to 23% for G ox, 16% to 24% for F ox, but minimal effects (≤ 1%) on EE. During the hyperinsulinemic, euglycemic clamp, RQ increased to 0.95 or greater, while urinary N excretion, rather than decreasing as expected, increased by 47% (6.4 ± 1.6 to 9.4 ± 2.8 mg/min) due in part to increases in urea clearance from 37.5 ± 6.7 to 75.2 ± 12.4 mL/min ( P < .025). This increased urinary N excretion had minimal influence on F ox and EE, but underestimated G ox by up to 5% at RQ less than 0.95. A more accurate estimate of urinary N excretion during hyperinsulinemic clamps may be obtained by correcting for changes in urea clearance. These results indicate that basal urinary N excretion is highly variable and influenced by hyperinsulinemic glucose clamps. Thus, urinary N excretion, particularly during the basal state, may not accurately reflect changes in P ox and can lead to substantial erros in G ox and F ox.

Familial growth retardation, renal aminoaciduria and cor pulmonale: I. Description of a new syndrome, with case reports

A syndrome, apparently previously undescribed, characterized by growth retardation, poor muscular development, scanty adipose tissue, recurrent pulmonary infection, atelectasis and right ventricular hypertrophy has been found in three of six children of asymptomatic parents. Two children died suddenly in the first decade. The survivor has, in addition, aminoaciduria without hyperaminoacidemia, increased plasma unesterified fatty acid concentration, a low basal respiratory quotient and evidence of alveolar hypoventilation with resultant cor pulmonale.