Liver glucagon receptors (GluR): effect of exercise and fasting on binding characteristics, GluR-mRNA, and GluR protein content in rats.

The purpose of the study was to investigate the effects of acute exercise and fasting on glucagon receptor (GluR) binding characteristics, GluR-mRNA, and protein content in rat liver. Liver homogenates were prepared and plasma membranes were purified by aqueous 2-phase affinity partitioning in rats fed at rest (control) and after 180 min of swimming exercise and 24 h of fasting (7 rats/group). Saturation curve of plasma membranes incubated with [125I]-glucagon showed significant higher GluR density following exercise and fasting than in the control group (8.19±0.29 and 8.01±0.65 vs. 3.09±0.12 pmol/mg of proteins, respectively). When compared to control rats, GluR Kd was also higher following exercise and fasting (0.46±0.05 and 0.56±0.13 vs. 0.33±0.05 nM, respectively; significantly different for fasting only). Expression of GluR-mRNA and protein content were both significantly higher (~100% and ~90%, respectively) following the 24-h fast than in the control rats, but not following exercise. These results, in line with the literature showing an increased sensitivity of the liver to glucagon following exercise and fasting, indicate that an increased density of GluR on plasma membranes can be obtained by 2 complementary mechanisms: externalization of pre-existing GluR from intracellular pools operative in response to the prolonged exercise, and de novo synthesis of GluR operative only in response to fasting. The reduction in plasma insulin concentration and/or depletion of liver glycogen stores, which results from both prolonged exercise and fasting, could be involved in the control of these mechanisms.

Rm62, a DEAD-box RNA helicase, complexes with DSP1 in Drosophila embryos.

Two main classes of proteins, Polycomb group (PcG) and Trithorax group (TrxG), play a key role in the regulation of homeotic genes. These proteins act in multimeric complexes to remodel chromatin. A third class of proteins named Enhancers of Trithorax and Polycomb (ETP) modulates the activity of TrxG and PcG, but their role remains largely unknown. We previously identified an HMGB-like protein, DSP1 (Dorsal Switch Protein 1), which was classified as an ETP. Preliminary studies have revealed that DSP1 is involved in multimeric complexes. Here we identify a DEAD-box RNA helicase, Rm62, as partner of DSP1 in a 250-kDa complex. Coimmunoprecipitation assays performed on embryo extracts indicate that DSP1 and Rm62 are associated in 3- to 12-h embryos. Furthermore, DSP1 and Rm62 colocalize on polytene chromosomes. Consistent with these results, a mutation in Rm62 enhances a null mutation of dsp1 and also mutations of trxG or PcG, suggesting that Rm62 has characteristics of an ETP. We show here for the first time that an RNA helicase is involved in the maintenance of homeotic genes.

Effect of a 20-day ski trek on fuel selection during prolonged exercise at low workload with ingestion of 13C-glucose.

Fuel selection was measured in five subjects (36.0 +/- 10.5 years old; 87.3 +/- 12.5 kg; mean +/- SD) during a 120-min tethered walking with ski poles (1.12 l O(2) min(-1)) with ingestion of (13)C-glucose (1.5 g kg(-1)), before and after a 20-day 415-km ski trek [physical activity level (PAL) approximately 3], using respiratory calorimetry, urea excretion, and (13)C/(12)C in expired CO(2) and in plasma glucose. Before the ski trek, protein oxidation contributed 9.7 +/- 1.6% to the energy yield (%En) while fat and carbohydrate (CHO) oxidation provided 73.5 +/- 5.5 and 16.7 +/- 6.5%En. Plasma glucose was the main source of CHO (52.9 +/- 9.5%En) with similar contributions from exogenous glucose (27.2 +/- 3.1%En), glucose from the liver (25.6 +/- 8.3%En) and muscle glycogen (20.9 +/- 4.0%En). Endogenous CHO contributed 46.6 +/- 3.9%En. Following the ski trek %En from protein, fat, CHO, exogenous glucose and endogenous CHO were not significantly modified (10.1 +/- 1.3, 15.8 +/- 6.7, 74.1 +/- 6.5, 28.7 +/- 3.0 and 45.5 +/- 7.5%En, respectively) but the %En from plasma glucose and glucose from the liver (41.1 +/- 3.6 and 12.4 +/- 4.0%En) were reduced, while that from muscle glycogen increased (33.0 +/- 4.5%En). These results show that in subjects in the fed state with glucose ingestion during exercise, CHO is the main substrate oxidized, with major contributions from both exogenous and endogenous CHO. Following a ~3-week period of prolonged low intensity exercise, the %En from protein, fat, CHO, exogenous glucose and endogenous CHO were not modified. However, the %En from glucose released from the liver was reduced (possibly due to an increased insulin sensitivity of the liver) while that from muscle glycogen was increased.

Muscle glycogen oxidation during prolonged exercise measured with oral [13C]glucose: comparison with changes in muscle glycogen content.

Plasma glucose and muscle glycogen oxidation during prolonged exercise [75-min at 48 and 76% maximal O(2) uptake (Vo(2 max))] were measured in eight well-trained male subjects [Vo(2 max) = 4.50 l/min (SD 0.63)] using a simplified tracer technique in which a small amount of glucose highly enriched in (13)C was ingested: plasma glucose oxidation was computed from (13)C/(12)C in plasma glucose (which was stable beginning at minute 30 and minute 15 during exercise at 48 and 76% Vo(2 max), respectively) and (13)CO(2) production, and muscle glycogen oxidation was estimated by subtracting plasma glucose oxidation from total carbohydrate oxidation. Consistent data from the literature suggest that this small dose of exogenous glucose does not modify muscle glycogen oxidation and has little effect, if any, on plasma glucose oxidation. The percent contributions of plasma glucose and muscle glycogen oxidation to the energy yield at 48% Vo(2 max) [15.1% (SD 3.8) and 45.9% (SD 5.8)] and at 76% Vo(2 max) [15.4% (SD 3.6) and 59.8% (SD 9.2)] were well in line with data previously reported for similar work loads and exercise durations using conventional tracer techniques. The significant reduction in glycogen concentration measured from pre- and postexercise vastus lateralis muscle biopsies paralleled muscle glycogen oxidation calculated using the tracer technique and was larger at 76% than at 48% Vo(2 max). However, the correlation coefficients between these two estimates of muscle glycogen utilization were not different from zero at each of the two work loads. The simplified tracer technique used in the present experiment appears to be a valid alternative approach to the traditional tracer techniques for computing plasma glucose and muscle glycogen oxidation during prolonged exercise.

Substrate source utilization during moderate intensity exercise with glucose ingestion in Type 1 diabetic patients.

Substrate oxidation and the respective contributions of exogenous glucose, glucose released from the liver, and muscle glycogen oxidation were measured by indirect respiratory calorimetry combined with tracer technique in eight control subjects and eight diabetic patients (5 men and 3 women in both groups) of similar age, height, body mass, and maximal oxygen uptake, over a 60-min exercise period on cycle ergometer at 50.8% (SD 4.0) maximal oxygen uptake [131.0 W (SD 38.2)]. The subjects and patients ingested a breakfast (containing approximately 80 g of carbohydrates) 3 h before and 30 g of glucose (labeled with 13C) 15 min before the beginning of exercise. The diabetic patients also received their usual insulin dose [Humalog = 9.1 U (SD 0.9); Humulin N = 13.9 U (SD 4.4)] immediately before the breakfast. Over the last 30 min of exercise, the oxidation of carbohydrate [1.32 g/min (SD 0.48) and 1.42 g/min (SD 0.63)] and fat [0.33 g/min (SD 0.10) and 0.30 g/min (SD 0.10)] and their contribution to the energy yield were not significantly different in the control subjects and diabetic patients. Exogenous glucose oxidation was also not significantly different in the control subjects and diabetic patients [6.3 g/30 min (SD 1.3) and 5.2 g/30 min (SD 1.6), respectively]. In contrast, the oxidation of plasma glucose and oxidation of glucose released from the liver were significantly lower in the diabetic patients than in control subjects [14.5 g/30 min (SD 4.3) and 9.3 g/30 min (SD 2.8) vs. 27.9 g/30 min (SD 13.3) and 21.6 g/30 min (SD 12.8), respectively], whereas that of muscle glycogen was significantly higher [28.1 g/30 min (SD 15.5) vs. 11.6 g/30 min (SD 8.1)]. These data indicate that, compared with control subjects, in diabetic patients fed glucose before exercise, substrate oxidation and exogenous glucose oxidation overall are similar but plasma glucose oxidation is lower; this is associated with a compensatory higher utilization of muscle glycogen.

[Evaluation of the analytical performances of CRP Diasys reagent on Roche Hitachi 917]. / Evaluation des performances analytiques du réactif CRP Diasys sur Roche Hitachi 917.

C reactive protein, the most sensible acute phase protein of inflammation and the labororatory should perform CRP testing on a continous 24 hour basis. The measurement is mainly performed by immunoturbimetry and immunonephelemetry methods available on multiparametric biochemical analyzer. In this study, we evaluated the analytical performances, precision and exactitude, of the CRP Diasys reagent on Roche Hitachi 917. The results were compared to those obtained with a CRP latex immunoassay (Roche). The reagent showed high analytical characteristics and especially a significant precision in a large range of CRP levels including low levels between 1 and 3 mg/L. Although this reagent is not considered as a high-sensitive CRP reagent, the measurement quality obtained in the 1-3 mg/L range allows an utilization as a cardiovascular risk predictor.

Plasma glucose kinetics and response of insulin and GIP following a cereal breakfast in female subjects: effect of starch digestibility.

BACKGROUND/OBJECTIVES: Foods with high contents of slowly digestible starch (SDS) elicit lower glycemic responses than foods with low contents of SDS but there has been debate on the underlying changes in plasma glucose kinetics, that is, respective contributions of the increase in the rates of appearance and disappearance of plasma glucose (RaT and RdT), and of the increase in the rate of appearance of exogenous glucose (RaE) and decrease in endogenous glucose production (EGP). SUBJECTS/METHODS: Sixteen young healthy females ingested in random order four types of breakfasts: an extruded cereal (0.3% SDS: Lo-SDS breakfast) or one of three biscuits (39-45% SDS: Hi-SDS breakfasts). The flour in the cereal products was labeled with (13)C, and plasma glucose kinetics were measured using [6,6-(2)H2]glucose infusion, along with the response of plasma glucose, insulin and glucose-dependent insulinotropic peptide (GIP) concentrations. RESULTS: When compared with the Lo-SDS breakfast, after the three Hi-SDS breakfasts, excursions in plasma glucose, the response of RaE, RaT and RdT, and the reduction in EGP were significantly lower (P<0.05). The amount of exogenous glucose absorbed over the 4.5-h postprandial period was also significantly lower by ~31% (P<0.001). These differences were associated with lower responses of GIP and insulin concentrations. CONCLUSIONS: Substituting extruded cereals with biscuits slows down the availability of glucose from the breakfast and its appearance in peripheral circulation, blunts the changes in plasma glucose kinetics and homeostasis, reduces excursions in plasma glucose, and possibly distributes the glucose ingested over a longer period following the meal.

The NssBF element, a sequence of the Drosophila melanogaster retrotransposon 1731 potentially implicated in transcriptional repression and replication.

The nuclear single-stranded DNA binding factor (NssBF) has been characterized as a nuclear protein that binds to a 26 nucleotides sequence in the long terminal repeat (LTR) of the Drosophila melanogaster 1731 retrotransposon. This sequence, called NssBF element, was analysed by gel retardation experiments using wild-type and mutated oligonucleotides. In vitro transcription experiments were performed and suggest that NssBF element binding protein(s) represses transcription through the 1731 promoter. Furthermore, computer assisted sequence comparisons put forward a possible role of this element and/or its associated DNA binding proteins in replication.

Promoter activity of the 1731 Drosophila retrotransposon in a human monocytic cell line.

The resemblance between retrotransposons and retroviruses suggests an evolutionary relationship and indicates that they may share common transcription factors. We have analyzed the behaviour of the Drosophila 1731 retrotransposon promoter in the human monocytic U937 cell line. We show that the long terminal repeat (LTR) of 1731 promotes CAT (chloramphenicol acetyl transferase) activity in these cells, in which it is enhanced by phorbol esters. Using gel mobility assays, we detected a human nuclear protein that binds in the U3 region of the LTR in a sequence-specific manner. Its precise target was determined by a DNase I footprinting experiment.

Isolation and characterization of novel mutations of the Broad-Complex, a key regulatory gene of ecdysone induction in Drosophila melanogaster.

Seven new alleles of the Broad-Complex gene of Drosophila melanogaster, which encodes a family of four zinc finger protein isoforms BR-C Z1, Z2, Z3 and Z4, were generated by transposase-induced mobilization of a P[Zw] element inserted in either the first intron downstream from the P165 promoter or the exon encoding the Z2-specific zinc finger domain. They were characterized by genetic complementation tests, molecular mapping and cytogenetic analysis of their effect on ecdysone-induced puffing and BR-C proteins binding to polytene chromosomes. Four mutations that correspond to three overlapping deletions and one tandem insertion of the P[Zw] element are located in the intron. They provide evidence that regulatory elements essential for a correct expression of the BR-C Z2 and BR-C Z3 transcripts are located within the intron downstream from the P165 promoter. Three mutations correspond to internal deletions of the locus and exhibit a complete loss of all BR-C(+) genetic functions in the complementation and cytogenetic tests. They thus provide well characterized new amorphic reference alleles of the BR-C gene. The precise cytogenetic location of more than 300 binding sites of BR-C proteins on larval salivary gland polytene chromosomes was determined by immunostaining using specific antibodies. Sites were found in big ecdysone inducible puffs, constitutively active small puffs as well as interbands. A complete list of the major sites on all four salivary gland polytene chromosomes of BR-C(+) larvae is presented.

Electrophysiological evidence for a shared representational medium for visual images and visual percepts.

Does mental imagery involve the activation of representations in the visual system? Systematic effects of imagery on visual signal detection performance have been used to argue that imagery and the perceptual processing of stimuli interact at some common locus of activity (Farah, 1985). However, such a result is neutral with respect to the question of whether the interaction occurs during modality-specific visual processing of the stimulus. If imagery affects stimulus processing at early, modality-specific stages of stimulus representation, this implies that the shared stimulus representations are visual, whereas if imagery affects stimulus processing only at later, amodal stages of stimulus representation, this implies that imagery involves more abstract, postvisual stimulus representations. To distinguish between these two possibilities, we repeated the earlier imagery-perception interaction experiment while recording event-related potentials (ERPs) to stimuli from 16 scalp electrodes. By observing the time course and scalp distribution of the effect of imagery on the ERP to stimuli, we can put constraints on the locus of the shared representations for imagery and perception. An effect of imagery was seen within 200 ms following stimulus presentation, at the latency of the first negative component of the visual ERP, localized at the occipital and posterior temporal regions of the scalp, that is, directly over visual cortex. This finding provides support for the claim that mental images interact with percepts in the visual system proper and hence that mental images are themselves visual representations.

Metabolic availability of oral glucose during exercise: a reassessment.

The purpose of this study was to reassess the metabolic availability of oral glucose during prolonged exercise in man, using 13C-labeling and a computation procedure (J Appl Physiol 69:1047-1052, 1990) that correctly takes into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates (Rendo). These changes are due to glucose ingestion associated with exercise. Each of the seven subjects completed three 2-hour periods of exercise at 67% maximum oxygen consumption (VO2max) on an ergocycle, with ingestion of water (1,000 mL) or 60 g (in 1,000 mL water) of 13C-labeled glucose at two levels of enrichment (13C/12C = 1.11482% and 1.13303%). As expected, Rendo significantly increased from rest to exercise with water ingestion (1.09888% +/- .00196% to 1.09970% +/- .00175%) and with glucose ingestion (1.10002% +/- .00159%) due to changes in the respective contributions of endogenous carbohydrates and fat to energy requirements as assessed by the respiratory exchange ratio (RER). When changes in Rendo were taken into account, the estimated amount of exogenous glucose oxidized was 38.8 +/- 10.3 g. Much higher values were found when Rendo at rest or during exercise with water ingestion were used in the computation (42.3 +/- 10.3 to 65.1 +/- 20.5 g) according to the commonly used method. Examination of data in the literature indicates that the reported oxidation rate of exogenous glucose (g/min) is significantly related to oxygen consumption (VO2) (L/min; r = .592) and that exogenous glucose contributes approximately 14% to 17% to the energy requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

An electrophysiological study of the mental rotation of polygons.

Reaction times and event-related potentials (ERPs) were recorded during a task requiring subjects to decide whether two sequentially presented polygons had the same shape regardless of differences in orientation. Reaction times increased approximately linearly with angular departure from upright orientation, which suggests that mental rotation was involved in the comparison process. The ERPs showed, between 665 and 1055 ms, a late posterior negativity also increasing with angular disparity from upright, which we assumed to reflect mental rotation. Two other activities were exhibited, from 265 to 665 ms, which may be related either to an evaluation of the stimulus or a predetermination of its orientation, and from 1055 to 1600 ms attributed to the decision process.

Mathematical analysis of running performance and world running records.

The objective of this study was to develop an empirical model relating human running performance to some characteristics of metabolic energy-yielding processes using A, the capacity of anaerobic metabolism (J/kg); MAP, the maximal aerobic power (W/kg); and E, the reduction in peak aerobic power with the natural logarithm of race duration T, when T greater than TMAP = 420 s. Accordingly, the model developed describes the average power output PT (W/kg) sustained over any T as PT = [S/T(1 - e-T/k2)] + 1/T integral of T O [BMR + B(1 - e-t/k1)]dt where S = A and B = MAP - BMR (basal metabolic rate) when T less than TMAP; and S = A + [Af ln(T/TMAP)] and B = (MAP - BMR) + [E ln(T/TMAP)] when T greater than TMAP; k1 = 30 s and k2 = 20 s are time constants describing the kinetics of aerobic and anaerobic metabolism, respectively, at the beginning of exercise; f is a constant describing the reduction in the amount of energy provided from anaerobic metabolism with increasing T; and t is the time from the onset of the race. This model accurately estimates actual power outputs sustained over a wide range of events, e.g., average absolute error between actual and estimated T for men's 1987 world records from 60 m to the marathon = 0.73%. In addition, satisfactory estimations of the metabolic characteristics of world-class male runners were made as follows: A = 1,658 J/kg; MAP = 83.5 ml O2.kg-1.min-1; 83.5% MAP sustained over the marathon distance. Application of the model to analysis of the evolution of A, MAP, and E, and of the progression of men's and women's world records over the years, is presented.

A theoretical analysis of the effect of altitude on running performance.

A theoretical analysis of the effect of altitude on running performance is presented using a mathematical model we have recently described and validated (J. Appl. Physiol. 67: 453-465, 1989). This model relates the average power output available over a given running time for a given combination of anaerobic capacity, maximal aerobic power, and endurance capability. For short sprinting distances, the contribution of aerobic metabolism to the energy requirement is small and the speed sustained is high. The reduction of maximal aerobic power with altitude is, thus, negligible, whereas the reduction of aerodynamic resistance is beneficial. Accordingly the performance steadily increases with altitude (e.g., average speed for 100 m at Mexico City is 101.9% of the average speed at sea level). On the other hand, the reduction in maximal aerobic power with altitude is associated with a reduction in performance over middle and long distances (800 m to marathon). For 400 m an improvement in performance is observed up to an altitude of approximately 2,400-2,500 m (average speed approximately 101.4% of sea level speed). Beyond this altitude the reduction in air density cannot compensate for the reduction in maximal aerobic power, and the performance deteriorates. Tables of performances equivalent to the current world records for selected altitudes ranging from 0 to 4,000 m are proposed.

Increase in blood bradykinin concentration after eccentric weight-training exercise in men.

The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects. Eccentric exercise (5 x 10 leg presses at 120% maximal voluntary concentric contraction) resulted in muscle damage and inflammation, as suggested by the significant increase in serum creatine kinase activity (from 204 +/- 41 to 322 +/- 63 U/l 12 h postexercise) and by severe lasting pain, which also peaked at 12 h postexercise. Blood BK and des-Arg(9)-BK concentrations were measured by competitive enzyme immunoassays using highly specific polyclonal rabbit IgG. Des-Arg(9)-BK concentration was not modified (preexercise: 44 +/- 14 pmol/l; pooled postexercise: 47 +/- 4 pmol/l). In contrast, BK concentration significantly increased immediately after the exercise session (68 +/- 9 vs. 42 +/- 3 pmol/l preexercise) and returned to basal values at 12, 24, and 48 h (pooled value: 40 +/- 4 pmol/l). This observation suggests that the inflammatory process due to eccentric exercise-induced muscle damage could be mediated in part by BK.

Oral [13C]glucose oxidation during prolonged exercise after high- and low-carbohydrate diets.

The effect of a diet either high or low in carbohydrates (CHO) on exogenous 13C-labeled glucose oxidation (200 g) during exercise (ergocycle: 120 min at 64.0 +/- 0.5% maximal oxygen uptake) was studied in six subjects. Between 40 and 80 min, exogenous glucose oxidation was significantly higher after the diet low in CHO (0.63 +/- 0.05 vs. 0.52 +/- 0.04 g/min), but this difference disappeared between 80 and 120 min (0.71 +/- 0.03 vs. 0.69 +/- 0.04 g/min). The oxidation rate of plasma glucose, computed from the volume of 13CO2 produced the 13C-to-12C ratio in plasma glucose at 80 min, and of glucose released from the liver, computed from the difference between plasma glucose and exogenous glucose oxidation, was higher after the diet low in CHO (1.68 +/- 0.26 vs. 1.41 +/- 0.17 and 1.02 +/- 0.20 vs. 0.81 +/- 0.14 g/min, respectively). In contrast the oxidation rate of glucose plus lactate from muscle glycogen (computed from the difference between total CHO oxidation and plasma glucose oxidation) was lower (0.31 +/- 0.35 vs. 1.59 +/- 0.20 g/min). After a diet low in CHO, the oxidation of exogenous glucose and of glucose released from the liver is increased and partly compensates for the reduction in muscle glycogen availability and oxidation.

Oxidation of a glucose polymer during exercise: comparison with glucose and fructose.

The purpose of this study was to compare the oxidation of 13C-labeled glucose, fructose, and glucose polymer ingested (1.33 g.kg-1 in 19 ml.kg-1 water) during cycle exercise (120 min, 53 +/- 2% maximal O2 uptake) in six healthy male subjects. Oxidation of exogenous glucose and glucose polymer (72 +/- 15 and 65 +/- 18%, respectively, of the 98.9 +/- 4.7 g ingested) was similar and significantly greater than exogenous fructose oxidation (54 +/- 13%). A transient rise in plasma glucose concentration was observed with glucose ingestion only. However, plasma insulin levels were similar with glucose and glucose polymer ingestions and significantly higher than with water or fructose ingestion. Plasma free fatty acid and glycerol responses to exercise were blunted with carbohydrate ingestion. However, fat utilization was not significantly different with water (82 +/- 14 g), glucose (60 +/- 3 g), fructose (59 +/- 11 g), or glucose polymer ingestion (60 +/- 8 g). Endogenous carbohydrate utilization was significantly lower with glucose (184 +/- 22 g), glucose polymer (187 +/- 31 g), and fructose (211 +/- 18 g) than with water (239 +/- 30 g) ingestion. Plasma volume slightly increased with water ingestion (7.4 +/- 4.5%), but the decrease was similar with glucose (-7.6 +/- 5.1%) and glucose polymer (-8.2 +/- 4.6%), suggesting that the rate of water delivery to plasma was similar with the two carbohydrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of 13C substrates for metabolic studies in exercise: methodological considerations.

The purpose of this study is to outline a common mistake made when the rate of oxidation of exogenous substrates during prolonged exercise is computed using 13C naturally labeled substrates. The equation proposed and commonly used in the computation does not take into account that exercise and/or exogenous substrate ingestion modifies the composition of the mixture of endogenous substrates oxidized and, consequently, the isotopic composition of CO2 arising from oxidation of endogenous substrates. The recovery of 13C and the amount of exogenous substrate oxidized are thus overestimated. An adequate procedure for the computation of exogenous substrate oxidation taking into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates is suggested. Results from a pilot experiment (4 subjects) using this procedure indicate that over 2 h of exercise (66% of maximal O2 uptake), with ingestion of 60 g of glucose, 39 +/- 4 g of glucose were oxidized. Estimates made without taking into account changes in isotopic composition of CO2 arising from oxidation of endogenous substrates range between 70 +/- 8 and 44 +/- 3 g depending on 1) the isotopic composition of exogenous glucose and 2) the isotopic composition of expired CO2 taken as reference (rest or exercise without glucose ingestion). These observations suggest that results from previous studies of exogenous substrate oxidation during exercise using 13C labeling should be used with caution.

Plasma catecholamines in the aorta and the phrenicoabdominal vein in exercising dogs.

Plasma epinephrine and norepinephrine concentrations were measured in the aorta and phrenicoabdominal vein in five dogs at rest and during short-duration mild- and moderate-intensity exercise and during prolonged mild-intensity exercise. Plasma epinephrine and norepinephrine concentrations increased with exercise in both the aorta and the phrenicoabdominal vein. Plasma epinephrine concentration was much higher in the phrenicoabdominal vein than in the aorta (24-43 times). Plasma epinephrine concentrations in the aorta and phrenicoabdominal vein were significantly correlated (r = 0.88). This confirms that peripheral epinephrine concentration is a reliable index of the activity of the adrenal medulla during exercise. The epinephrine-to-norepinephrine ratio in the phrenicoabdominal vein was stable (4:1) throughout the experimental protocol, suggesting that the proportion of the two amines released by the adrenal medulla did not vary through this range of adrenal activity in dogs.