Lower Respiratory Exchange Ratio Research Articles

Respiratory and metabolic responses during exercise and skeletal muscle morphology in obesity

Obese subjects need additional energy to move larger bodies and a greater amount of O2 to accomplish an equal external work-load than lean subjects. Moreover, obesity is characterized by a marked insulin resistance, which may modify metabolic responses to physical exercise. We measured the respiratory and metabolic responses to a progressive ergometric test in a group of 10 men obese and in 10 lean controls. Muscle biopsies of the left quadriceps were performed to study correlations between metabolic responses and muscle morphology. Oxygen consumption, carbon dioxide production and the respiratory exchange ratio (RER) were assessed, as were plasma concentrations of K+ and catecholamines in the basal state (rest) and during the last 30 s of each work load at exercise. Lactic acid was also measured. Obese subjects achieved a lower maximal power output (129 vs. 140 W) and a significantly lower anaerobic threshold (82 vs. 114 W, p<0.05). RER was significantly lower in the obese group, and catecholamines rose earlier and with a lower peak in correspondence of maximal power outputs. K+ and lactic acid levels increased in both groups, although significantly less in obese subjects. The main feature of muscle specimens from obese subjects was hypertrophy of the fibers, present in 9 of 10 cases, and increased amounts of neutral lipids (Oil Red O staining), present in 7 of 10 individuals. Low RER in obese subjects indicated a condition of insulin resistance, which persisted during physical activity. We conclude that fats are the fuel preferred by obese individuals during strenuous exercise.

Aggravated hypoxia during breath-holds after prolonged exercise

Hyperventilation prior to breath-hold diving increases the risk of syncope as a result of hypoxia. Recently, a number of cases of near-drownings in which the swimmers did not hyperventilate before breath-hold diving have come to our attention. These individuals had engaged in prolonged exercise prior to breath-hold diving and it is known that such exercise enhances lipid metabolism relative to carbohydrate metabolism, resulting in a lower production of CO(2) per amount of O(2 )consumed. Therefore, our hypothesis was that an exercise-induced increase in lipid metabolism and the associated reduction in the amount of CO(2) produced would cause the urge to breathe to develop at a lower P O(2), thereby increasing the risk of syncope due to hypoxia. Eight experienced breath-hold divers performed 5 or 6 breath-holds at rest in the supine position and then 5 or 6 additional breath-holds during intermittent light ergometer exercise with simultaneous apnoea (dynamic apnoea, DA) on two different days: control (C) and post prolonged sub-maximal exercise (PPE), when the breath-holds were performed 30 min after 2 h of sub-maximal exercise. After C and before the prolonged submaximal exercise subjects were put on a carbohydrate-free diet for 18 h to start the depletion of glycogen. The respiratory exchange ratio ( RER) and end-tidal P CO(2), P O(2), and SaO(2) values were determined and the data were presented as means (SD). The RER prior to breath-holding under control conditions was 0.83 (0.09), whereas the corresponding value after exercise was 0.70 (0.05) ( P <0.01). When the three apnoeas of the longest duration for each subject were analysed, the average duration of the dynamic apnoeas was 96 (14) s under control conditions and 96 (17) s following exercise. Both P O(2) and P CO(2) were higher during the control dynamic apnoeas than after PPE [PO(2) 6.9 (1.0) kPa vs 6.2 (1.2) kPa, P <0.01; P CO(2) 7.8 (0.5) kPa vs 6.7 (0.4) kPa, P <0.001; ANOVA testing]. A similar pattern was observed after breath-holding under resting conditions, i.e., a lower end-tidal P O(2) and P CO(2) after exercise (PPE) compared to control conditions. Our findings demonstrate that under the conditions of a relatively low RER following prolonged exercise, breath-holding is terminated at a lower P O(2) and a lower P CO(2) than under normal conditions. This suggests that elevated lipid metabolism may constitute a risk factor in connection with breath-holding during swimming and diving.

Residual effects of prior exercise and recovery on subsequent exercise-induced metabolic responses

Data on the metabolic responses to repeated endurance exercise sessions are limited. Thus, the aims of this study were to examine (1) the impact of prior exercise on metabolic responses to a subsequent exercise session and (2) the effect of different recovery periods between two daily exercise sessions on metabolic responses to the second bout of exercise. Nine male elite athletes participated in four 25-h trials: one bout of exercise (ONE), two bouts of exercise separated by 3 h of rest and one meal (SHORT), two bouts of exercise separated by 6 h of rest and two meals (LONG), and a trial with no exercise (REST). All exercise bouts consisted of 10 min cycling at 50% followed by 65 min at 75% of maximal O2 uptake. Compared to no prior exercise (ONE), a previous bout of exercise (SHORT) was followed by higher mean O2 uptake, heart rate (HR), rectal temperature (TR), excess post-exercise oxygen consumption and lower respiratory exchange ratio (R) during and after a similar exercise session 3 h later. A longer rest interval between the two exercise bouts (6 h versus 3 h) and an additional meal resulted in a decrease in O2 uptake, HR, TR and an increase in R during the second bout of exercise, but no effects on post-exercise metabolism were found. Thus, augmented metabolic stress was observed when strenuous exercise was repeated after only 3 h of recovery, but this was attenuated when a longer recovery period including an additional meal was provided between the exercise sessions.

The Menstrual Cycle or Oral Contraceptive Pill

1911 Substrate utilisation during exercise differs between the oral contraceptive pill (OCP) and normal menstrual cycle (NMC) such that OCP users metabolise fewer carbohydrates and oxidise a greater proportion of fat than women in the luteal phase of the NMC 1. There is, however, an increasing consensus that aerobic capacity is impaired with OCP use 2. PURPOSE: Given that exogenous female steroid hormones seem to reduce aerobic capacity but have the potential to alter energy substrate utilisation compared to endogenous female steroid hormones this study aimed to compare the effects of these hormones during the NMC and OCP, on exercise status in young (18–30 yrs), sedentary women. METHODS: Twenty-three women taking a monophasic OCP and fourteen women with normal menstrual cycles (NMC) performed incremental cycle ergometer exercise to exhaustion and 20 min steadystate exercise at 75% VO2peak. RESULTS: Maximal power output and endurance time to exhaustion were higher in the OCP group. Oxygen uptake (VO2, L·min−1) was significantly higher in the OCP group from 40% − 100% VO2peak (P < 0.05). The OCP group had a higher oxygen pulse (ml·beat−1) and a lower respiratory exchange ratio at all levels of exercise intensity (P < 0.01) in the incremental test. During both exercise tests the OCP group were deriving more energy from lipid (P < 0.01) than the NMC group and there was no difference between the groups in terms of heart rate and rate of perceived exertion. CONCLUSIONS: Exercise status defined by aerobic capacity and endurance performance is increased in young, sedentary women taking an OCP and the results suggest this could be due to a both an improvement in stroke volume and a greater dependence on fat metabolism associated with exogenous steroid hormone administration.

The Menstrual Cycle or Oral Contraceptive Pill

1911 Substrate utilisation during exercise differs between the oral contraceptive pill (OCP) and normal menstrual cycle (NMC) such that OCP users metabolise fewer carbohydrates and oxidise a greater proportion of fat than women in the luteal phase of the NMC 1. There is, however, an increasing consensus that aerobic capacity is impaired with OCP use 2. PURPOSE: Given that exogenous female steroid hormones seem to reduce aerobic capacity but have the potential to alter energy substrate utilisation compared to endogenous female steroid hormones this study aimed to compare the effects of these hormones during the NMC and OCP, on exercise status in young (18–30 yrs), sedentary women. METHODS: Twenty-three women taking a monophasic OCP and fourteen women with normal menstrual cycles (NMC) performed incremental cycle ergometer exercise to exhaustion and 20 min steadystate exercise at 75% VO2peak. RESULTS: Maximal power output and endurance time to exhaustion were higher in the OCP group. Oxygen uptake (VO2, L·min−1) was significantly higher in the OCP group from 40% − 100% VO2peak (P < 0.05). The OCP group had a higher oxygen pulse (ml·beat−1) and a lower respiratory exchange ratio at all levels of exercise intensity (P < 0.01) in the incremental test. During both exercise tests the OCP group were deriving more energy from lipid (P < 0.01) than the NMC group and there was no difference between the groups in terms of heart rate and rate of perceived exertion. CONCLUSIONS: Exercise status defined by aerobic capacity and endurance performance is increased in young, sedentary women taking an OCP and the results suggest this could be due to a both an improvement in stroke volume and a greater dependence on fat metabolism associated with exogenous steroid hormone administration.

Effect of dietary lipid on response to exercise: relationship to metabolic adaptation.

The aim of the present study was to relate changes in muscle oxidative capacity and free fatty acid flux in response to oil supplementation to fuel utilisation during subsequent exercise of varying intensities. Following 10 weeks of oil supplementation there was an increased capacity for fat utilisation during low and moderate intensity exercise as indicated by a lower respiratory exchange ratio (RER) (P<0.05). We suggest that this was contributed to by a parallel increase in the oxidative capacity of muscle as indicated by a significant increase in the activity of muscle citrate synthase (CS) (P<0.05) and trend towards an increase in beta-Hydroxy acyl CoA dehydrogenase (beta-HAD), (P>0.05). In addition, low and moderate intensity exercise was associated with an exercise-induced increase in plasma free fatty acids (FFA) and there was an increased facility for uptake of FFA by working muscle from circulating triglycerides, as suggested by an increase in TL activity (P<0.01). The response to oil supplementation varied between individual horses and the magnitude of response, during the low intensity exercise test, in terms of difference in RER was correlated to the increase in CS activity (r2 = 0.95, P<0.05) following oil supplementation. There was no similar significant correlation with respect to FFA, TL or beta-HAD activity (P>0.05). The hypothesis in this study was that the metabolic adaptation to oil supplementation, in terms of exercise response, was related to individual increases in the activities of CS, beta-HAD or TL. However, the relationship between these parameters was unequivocal and requires further investigation, ideally with a larger group of horses.

Substrate utilization during endurance exercise in men and women after endurance training

We investigated the effect of endurance training on whole body substrate, glucose, and glycerol utilization during 90 min of exercise at 60% peak O2 consumption (VO2(peak)) in males and females. Substrate oxidation was determined before and after 7 wk of endurance training on a cycle ergometer, with posttesting performed at the same absolute (ABS, W) and relative (REL, VO2(peak)) intensities. [6,6-2H]glucose and [1,1,2,3,3-2H]glycerol tracers were used to calculate the respective substrate tracee flux. Endurance training resulted in an increase in VO2(peak) for both males and females of 17 and 22%, respectively (P < 0.001). Females demonstrated a lower respiratory exchange ratio (RER) both pretraining and posttraining compared with males during exercise (P < 0.001). Glucose rate of appearance (R(a)) and rate of disappearance (R(d)) were not different between males and females. Glucose metabolic clearance rate (MCR) was lower at 75 and 90 min of exercise for females compared with males (P < 0.05). Glucose R(a) and R(d) were lower during exercise at both ABS and REL posttraining exercise intensities compared with pretraining (P < 0.001). Females had a higher exercise glycerol R(a) and R(d) compared with males both pre- and posttraining (P < 0.001). Glycerol R(a) was not different at either the ABS or REL posttraining exercise intensities compared with pretraining. We concluded that females oxidize proportionately more lipid and less carbohydrate during exercise compared with males both pre- and posttraining, which was cotemporal with a higher glycerol R(a) in females. Furthermore, endurance training resulted in a decrease in glucose flux at both ABS and REL exercise intensities after endurance exercise training.

Gender differences in substrate metabolism during endurance exercise.

Females show a lower respiratory exchange ratio (RER) than males during submaximal endurance exercise, which translates into a proportionately lower carbohydrate and higher fat oxidation. Data from rodents show that 17-beta-estradiol may mediate these metabolic differences. 17-beta-estradiol supplementation in humans is less convincing; however, two studies found a reduction in glucose rate of appearance during exercise. No difference is found between genders in muscle glycogen content; however, lipid content in muscle is higher in females. Evidence shows that short chain OH-acyl CoA-dehydrogenase (SCHAD) maximal enzyme activity is higher in females. The rate of leucine oxidation is lower in females at rest and during endurance exercise. This is not apparently related to gender differences in branched chain-2-oxo-dehydrogenase (BCOAD) activity in skeletal muscle, which may implicate hepatic control. Important muscle proteins to examine in future research are hormone sensitive lipase, the enzymes of beta-oxidation, and fatty acid transporters.

Targeted Disruption of the β2 Adrenergic Receptor Gene

beta-Adrenergic receptors (beta-ARs) are members of the superfamily of G-protein-coupled receptors that mediate the effects of catecholamines in the sympathetic nervous system. Three distinct beta-AR subtypes have been identified (beta1-AR, beta2-AR, and beta3-AR). In order to define further the role of the different beta-AR subtypes, we have used gene targeting to inactivate selectively the beta2-AR gene in mice. Based on intercrosses of heterozygous knockout (beta2-AR +/-) mice, there is no prenatal lethality associated with this mutation. Adult knockout mice (beta2-AR -/-) appear grossly normal and are fertile. Their resting heart rate and blood pressure are normal, and they have a normal chronotropic response to the beta-AR agonist isoproterenol. The hypotensive response to isoproterenol, however, is significantly blunted compared with wild type mice. Despite this defect in vasodilation, beta2-AR -/- mice can still exercise normally and actually have a greater total exercise capacity than wild type mice. At comparable workloads, beta2-AR -/- mice had a lower respiratory exchange ratio than wild type mice suggesting a difference in energy metabolism. beta2-AR -/- mice become hypertensive during exercise and exhibit a greater hypertensive response to epinephrine compared with wild type mice. In summary, the primary physiologic consequences of the beta2-AR gene disruption are observed only during the stress of exercise and are the result of alterations in both vascular tone and energy metabolism.

Effect of elevated blood FFA levels on endurance performance after a single fat meal ingestion.

This study was designed to examine the effect of elevated blood free fatty acid (FFA) levels on carbohydrate (CHO) oxidation and cycling performance after ingesting a single fat meal (FM). Four hours before cycling exercise, nine trained males consumed either a FM (4711 kJ; 30% CHO, 61% fat, and 9% protein) or control meal (CM) (4877 kJ; 58% CHO, 31% fat, and 11% protein). The intensity of exercise employed was 67% of the maximal oxygen consumption (VO2max) for the first 120 min of exercise, followed by an increase to 78% VO2max. The FM ingestion significantly (P < 0.05 and P < 0.01) elevated serum FFA levels above those resulting from CM ingestion almost throughout the entire exercise. A significantly (P < 0.05 and P < 0.01) lower respiratory exchange ratio in the FM versus the CM trials was observed during the first hour of exercise. This was accompanied by a significantly greater amount of fat oxidized at 20 (P < 0.01) and 60 min (P < 0.05) of FM trials and a significantly smaller amount of CHO oxidized at 20 min (P < 0.05) of FM trials. However, endurance time and work production did not differ between the FM (141 +/- 8 min, 134333 +/- 6049 kg x m (SEM)) and CM (138 +/- 5 min, 131450 +/- 4737 kg x m) trials. Also, there were no significant differences in oxygen consumption, heart rate, and perceived exertion or in glucose, lactate, and triglyceride levels in the blood. These results suggest that the elevated blood FFA levels after a single FM ingestion reduce CHO oxidation early in exercise, but this decrease in CHO oxidation would not be adequate enough to contribute to an increased endurance.

ACUTE ADAPTATION TO ISOCALORIC HIGH-FAT FEEDING PREDICTS MAINTENANCE OF BODY COMPOSITION IN FEMALE RATS 243

The goals of this study were to; 1) examine the acute effect of increased fat intake on oxygen consumption (VO2) and respiratory exchange ratio (RER) in rats fed isocalorically, and 2) relate short-term changes in RER to long-term changes in body fat (BF). We hypothesized that the 24-hr RER observed after 7 days on an isocaloric high-fat (iso-HF) diet would predict BF changes with chronic elevation of dietary fat. Forty-four mature female Sprague-Dawley (SD) rats were fed a low-fat diet (12% Kcal fat) ad libitum for 3-wk, then divided into groups matched for weight and food intake. 24-hr VO2 and RER were measured by indirect calorimetry during 8-hr of fasting and 16-hr of food access. Rats were then meal-fed diets providing 12, 18, 24, 30, or 36% Kcal as fat (food quotient, FQ =.92,.90,.88,.87, and.85, respectively) in amounts equal to baseline energy intake. All diets provided 21% Kcal from protein and increased fat replaced carbohydrate. VO2 and RER were assessed after 7 days on iso-HF, and BF and fat pads were measured at 16 wk. Baseline RER was characteristically low during fasting and elevated during feeding; baseline 24-hr RER was similar to FQ (p > 0.05). After 1 week of iso-HF feeding, VO2 was unchanged while a lower RER during feeding produced a decrease in 24-hr RER that was proportional to the change in FQ (r2 = 0.99, p = 0.001). The change in RER reflects acute adaptation and maintenance of substrate balance with iso-HF, which would predict no change in BF, and indeed there was no effect of fat intake on body mass, BF or fat pad weights after 16 wk. The results of this study demonstrate that body composition is maintained in mature female SD rats despite elevated fat intake when fat utilization acutely adapts to match fat intake, as is predicted by early changes in RER with increased dietary fat.

Improved aerobic power by detraining in basketball players mainly trained for strength

Six male basketball players (18 ± 0.2 years old), all playing on the same team, performed two incremental, cycle ergometer exercises while connected to an instrumental apparatus from which cardiocirculatory, respiratory, and metabolic variables were recorded. The first test (T1) was performed at the height of the game season when athletes were in full training, mainly doing strength exercises. The second test (T2) was performed 5 months after T1, when they were detrained. In T2 with respect to T1 the following parameters were higher, anaerobic threshold (11%), maximum work rate (13%), maximum oxygen consumption (27%), maximum pulmonary ventilation (16%), maximum oxygen pulse (26%), and end‐tidal partial carbon dioxide pressure tension at the maximum work rate (11%); still at maximum work rate, the following were lower respiratory exchange ratio (‐8%), ventilatory equivalent of oxygen (‐9%), and end‐tidal partial oxygen tension (‐6%). These data indicated that in the detrained condition relative to the ful...

Quantification of carbohydrate oxidation by respiratory gas exchange and isotopic tracers

Estimates of glucose oxidation measured by indirect respiratory calorimetry and by [U-13C]glucose tracer were compared as a function of respiratory exchange ratio (RER) in 14 studies performed on 9 healthy adult subjects. RER was varied between 0.7 and 1.04, either by fasting or by infusing glucose. 13C enrichment of plasma glucose and expired CO2 were measured by mass spectrometry. The two methods gave similar results when the nonprotein respiratory quotient (NPRQ) was between 0.76 and 0.90. Glucose oxidation by the tracer method was quantified to be higher than that by respiratory calorimetry when NPRQ was < 0.76; it was lower than the respiratory calorimetry estimate when NPRQ was > 0.90. The discrepancy between the two methods at low RER may represent the contribution of gluconeogenesis, whereas, at high RER, the discrepancy may be the consequence of lipogenesis. We conclude that respiratory calorimetry and [13C]glucose tracer give comparable results only in a narrow range of RER. These data are important when the disposal of glucose is compared using these techniques in different metabolic states with varying respiratory quotients.

Exercise intensity: effect on postexercise O2 uptake in trained and untrained women

Despite many reports of long-lasting elevation of metabolism after exercise, little is known regarding the effects of exercise intensity and duration on this phenomenon. This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal O2 consumption (VO2max)] on 3-h recovery of oxygen uptake (VO2). VO2 and respiratory exchange ratios were measured by open-circuit spirometry in five trained female cyclists (age 25 +/- 1.7 yr) and five untrained females (age 27 +/- 0.8 yr). Postexercise VO2 measured at intervals for 3 h after exercise was greater (P less than 0.01) after exercise at 50% VO2max in trained (0.40 +/- 0.01 l/min) and untrained subjects (0.39 +/- 0.01 l/min) than after 70% VO2max in (0.31 +/- 0.02 l/min) and untrained subjects (0.29 +/- 0.02 l/min). The lower respiratory exchange ratio values (P less than 0.01) after 50% VO2max in trained (0.78 +/- 0.01) and untrained subjects (0.80 +/- 0.01) compared with 70% VO2max in trained (0.81 +/- 0.01) and untrained subjects (0.83 +/- 0.01) suggest that an increase in fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P less than 0.05) after 50% VO2max in trained (147 +/- 4 mg/min) and untrained subjects (133 +/- 9 mg/min) compared with 70% VO2max in trained (101 +/- 6 mg/min) and untrained subjects (85 +/- 7 mg/min).

Metabolic responses to exercise after fasting.

Fasting before exercise increases fat utilization and lowers the rate of muscle glycogen depletion. Since a 24-h fast also depletes liver glycogen, we were interested in blood glucose homeostasis during exercise after fasting. An experiment was conducted with human subjects to determine the effect of fasting on blood metabolite concentrations during exercise. Nine male subjects ran (70% maximum O2 consumption) two counterbalanced trials, once fed and once after a 23-h fast. Plasma glucose was elevated by exercise in the fasted trial but there was no difference between fed and fasted during exercise. Lactate was significantly higher (P less than 0.05) in fasted than fed throughout the exercise bout. Fat mobilization and utilization appeared to be greater in the fasted trial as evidenced by higher plasma concentrations of free fatty acids, glycerol, and beta-hydroxybutyrate as well as lower respiratory exchange ratio in the fasted trial during the first 30 min of exercise. These results demonstrate that in humans blood glucose concentration is maintained at normal levels during exercise after fasting despite the depletion of liver glycogen. Homeostasis is probably maintained as a result of increased gluconeogenesis and decreased utilization of glucose in the muscle as a result of lowered pyruvate dehydrogenase activity.

Influence of physical training on the fuel-hormone response to prolonged low intensity exercise

The effects of physical training on the fuel-hormone response to prolonged (3 hr), low intensity cycle ergometer exercise (40% maximal aerobic power) which in the untrained state fails to produce a rise in blood lactate, was examined in six healthy male subjects. The training program consisted of one hour cycle ergometer exercise performed 4 times weekly for 6 weeks and resulted in a 19% increase in maximal aerobic power. Prior to training, prolonged low intensity exercise resulted in a 20% decline in plasma glucose, a 2.5-fold rise in plasma free fatty acids (FFA), a 7-fold rise in plasma epinephrine, a 3-fold elevation in plasma norepinephrine, and a 2.5-fold rise in plasma glucagon. Following training, the exercise-induced decline in glucose was 60% less than before training, the elevations in plasma FFA and norepinephrine were respectively, 45% and 90% less than before training and no significant increment in plasma norepinephrine and glucagon was observed. Training also blunted the exercise-induced elevations in circulating ketones and growth hormone and resulted in a lower respiratory exchange ratio during exercise. The data indicate that training markedly diminishes the fuel-hormone perturbations associated with low intensity exercise and in the face of a lessened increment in plasma FFA results in a greater utilization of fat and less dependence on carbohydrate during the exercise.

Insulin binding to monocytes in trained athletes: changes in the resting state and after exercise.

Insulin binding to monocytes was examined in trained athletes (long distance runners) and in sedentary control subjects in the resting state and after 3 h of exercise at 40% of maximal aerobic power. At rest, specific binding of 125-I-insulin to monocytes was 69% higher in athletes than in sedentary controls and correlated with maximal aerobic power. The increase in insulin binding was primarily due to an increase in binding capacity. During acute exercise, insulin binding fell by 31% in athletes but rose by 35% in controls. The athletes had a smaller decline in plasma glucose and a lower respiratory exchange ratio during exercise than did controls. We conclude that physical training increases insulin binding to monocytes in the resting state but results in a fall in insulin binding during acute exercise. Changes in insulin binding in athletes thus may account for augmented insulin sensitivity at rest as well as a greater shift from carbohydrate to fat usage during exercise than is observed in untrained controls.