Increment In Oxygen Consumption Research Articles

Metabolic long‐term monitoring of transcorneal electrical stimulation in retinitis pigmentosa

AbstractPurpose: Transcorneal electrical stimulation (TES) is a new therapeutical approach for retinitis pigmentosa (RP). With progression of RP, degeneration of photoreceptors results in lower oxygen consumption of the retina. Retinal oximetry (RO) is a noninvasive method to analyse oxygen saturation in retinal vessels and has shown promising short‐term results as a therapy monitoring tool for TES. The aim of our study was to measure the long‐term effects of TES on RO parameters over a period of 3 years (3Y).Methods: A total of 18 eyes of 9 subjects (5♀ 4♂) suffering from RP were examined at baseline (BL), 6 months, and 3Y of TES (OkuStim®) treatment. TES was performed for 30 min once a week at 200% of the individual phosphene threshold simultaneously on both eyes. The oxygen saturation was examined at BL and following TES therapy with the oxygen saturation tool of the Retinal Vessel Analyser (IMEDOS Systems UG, Jena, Germany). The global oxygen saturation parameters (in %), within 1.0–1.5 optic‐disc diameters from the disc margin, in retinal arterioles (A‐SO2) and venules (V‐SO2) were measured and their difference (A‐V SO2) was calculated. In addition, we recorded the diameters in the main arterioles (D‐A) and venules (D‐V). ANOVA‐based linear mixed‐effects models were employed for statistical analysis using SPSS®.Results: After 3Y of TES treatment both the mean A‐SO2 (from 96.35 ± 12.76% to 100.89 ± 5.87%, p = 0.22) and V‐SO2 (from 62.20 ± 11.55% to 64.55 ± 8.24%, p = 0.77) increased slightly. The A‐V SO2, which corresponds to the oxygen consumption of the retina, presented also with a slight increment from 34.15 ± 9.68% at BL to 36.23 ± 7.71% without reaching statistical significance (p = 0.27). TES also did not appear to alter the vascular diameter parameters, D‐A and D‐V (p > 0.05).Conclusions: Our long‐term observations indicate that TES therapy in RP might lead to a slight increment in oxygen consumption of the retina. However, a larger cohort and longer duration may be needed to adequately power a follow‐up study and to confirm this trend reflecting a possible benefit of TES for RP.

Anti-inflammaging effects of black soybean and black rice mixture extract by reprogramming of mitochondrial respirations in murine macrophages

• Aging exacerbates the inflammatory responses in both M1 and M2 BMDMs, for which the phenomenon was termed as inflammaging. • Mitochondrial oxygen consumption in BMDMs was increased by black rice and black bean mixture extract (BBME) in aged-mice. • Increment in oxygen consumption by BBME further drove macrophage subsets into M2-like anti-inflammatory phenotypes. Chronic, persistent, low-grade inflammation in the elderly is termed ‘inflammaging’ and is one of the main causes of age-related diseases. Although the detailed molecular mechanisms of inflammaging are poorly understood, its amelioration by modulating macrophage phenotypes is of high interest. As a dietary approach, it was previously reported that black soybean ( Rhynchosia nulubilis ) and black rice ( Oryza sativa L.) contain potent bioactive components that aid in the mitigation of several metabolic diseases. The current study investigated whether dietary intervention of black soybean and black rice mixture extract (BBME) modulates inflammaging through functional and/or phenotypic alteration of mitochondrial respiration in bone marrow-derived macrophages (BMDMs). Administration of BBME not only inhibited the expression of inflammatory mediators, but also enhanced anti-inflammatory cytokines. BBME further regulated mitochondrial respiration in M1/M2 BMDMs. These results suggest BBME as a dietary modulator for prevention or amelioration of diseases related to inflammaging.

Metabolic Long-Term Monitoring of Transcorneal Electrical Stimulation in Retinitis Pigmentosa

Introduction: Transcorneal electrical stimulation (TES) is a new therapeutical approach for retinitis pigmentosa (RP). With progression of RP, degeneration of photoreceptors results in lower oxygen consumption of the retina. Retinal oximetry (RO) is a noninvasive method to analyze oxygen saturation in retinal vessels and has shown promising short-term results as a therapy monitoring tool for TES. The aim of our study was to measure the long-term effects of TES on RO parameters over a period of 3 years (3Y). Methods: A total of 18 eyes of 9 subjects (5♀ 4♂) suffering from RP were examined at baseline (BL), 6 months, and 3Y of TES (OkuStim®) treatment. TES was performed for 30 min once a week at 200% of the individual phosphene threshold simultaneously on both eyes. The oxygen saturation was examined at BL and following TES therapy with the oxygen saturation tool of the Retinal Vessel Analyser (IMEDOS Systems UG, Jena, Germany). The global oxygen saturation parameters (in %), within 1.0–1.5 optic-disc diameters from the disc margin, in retinal arterioles (A-SO₂) and venules (V SO₂) were measured and their difference (A-V SO₂) was calculated. In addition, we recorded the diameters in the main arterioles (D-A) and venules (D-V). ANOVA-based linear mixed-effects models were employed for statistical analysis using SPSS®. Results: After 3Y of TES treatment both the mean A-SO₂ (from 96.35 ± 12.76% to 100.89 ± 5.87%, p = 0.22) and V SO₂ (from 62.20 ± 11.55% to 64.55 ± 8.24%, p = 0.77) increased slightly. The A-V SO₂, which corresponds to the oxygen consumption of the retina, presented also with a slight increment from 34.15 ± 9.68% at BL to 36.23 ± 7.71% without reaching statistical significance (p = 0.27). TES also did not appear to alter the vascular diameter parameters, D-A and D-V (p > 0.05). Conclusion: Our long-term observations indicate that TES therapy in RP might lead to a slight increment in oxygen consumption of the retina. However, a larger cohort and longer duration may be needed to adequately power a follow-up study and to confirm this trend reflecting a possible benefit of TES for RP.

Melatonin Supplementation Decreases Hypertrophic Obesity and Inflammation Induced by High-Fat Diet in Mice.

Obesity results from critical periods of positive energy balance characterized by caloric intake greater than energy expenditure. This disbalance promotes adipose tissue dysfunction which is related to other comorbidities. Melatonin is a low-cost therapeutic agent and studies indicate that its use may improve obesity-related disorders. To evaluate if the melatonin is efficient in delaying or even blocking the damages caused by excessive ingestion of a high-fat diet (HFD) in mice, as well as improving the inflammatory profile triggered by obesity herein, male C57BL/6 mice of 8 weeks were induced to obesity by a HFD and treated for 10 weeks with melatonin. The results demonstrate that melatonin supplementation attenuated serum triglyceride levels and total and LDL cholesterol and prevented body mass gain through a decreased lipogenesis rate and increased lipolytic capacity in white adipocytes, with a concomitant increment in oxygen consumption and Pgc1a and Prdm16 expression. Altogether, these effects prevented adipocyte hypertrophy caused by HFD and reflected in decreased adiposity. Finally, melatonin supplementation reduced the crown-like-structure (CLS) formation, characteristic of the inflammatory process by macrophage infiltration into white adipose tissue of obese subjects, as well as decreased the gene expression of inflammation-related factors, such as leptin and MCP1. Thus, the melatonin can be considered a potential therapeutic agent to attenuate the metabolic and inflammatory disorders triggered by obesity.

Short-pulse neodymium:yttrium–aluminium garnet (Nd:YAG 1064 nm) laser irradiation photobiomodulates mitochondria activity and cellular multiplication of Paramecium primaurelia (Protozoa)

Few studies exist to explore the potential photobiomodulation (PBM) effect of neodymium:yttrium–aluminium garnet (Nd:YAG) laser irradiation using a flat-top handpiece delivery system. In this study, we explored the photobiomodulation effect of that laser, on Paramecium primaurelia. The parameters for the different study groups were: 0.50W, 10Hz, 100msp, 30J/cm2; 0.75W, 10Hz, 100msp, 45J/cm2; 1.00W, 10Hz, 100msp, 60J/cm2; 1.25W, 10Hz, 100msp, 75J/cm2 and 1.50W, 10Hz, 100msp, 90J/cm2. Our results suggest that only the parameter 0.5W, 10Hz, 100msp, 30J/cm2 positively photobiomodulates the Paramecium cells inducing an increment in oxygen consumption, endogenous ATP synthesis and fission rate rhythm. Applying the laser energy with parameters of 1.25W, 10Hz, 100msp, 75J/cm2 and 1.50W, 10Hz, 100msp, 90J/cm2, induce adverse effect on the Paramecium cells, which protect themselves through the increase in Heat Shock Protein-70 (HSP70). The data presented in our work support our assumption that, when using appropriate parameters of irradiation, the 1064nm Nd:YAG laser with flat-top handpiece could be a valuable aid for effective clinical application of PBM.

Patterns of oxygen consumption during simultaneously occurring elevated metabolic states in the viviparous snake Thamnophis marcianus.

Snakes exhibit large factorial increments in oxygen consumption during digestion and physical activity, and long-lasting sub-maximal increments during reproduction. Under natural conditions, all three physiological states may occur simultaneously, but the integrated response is not well understood. Adult male and female checkered gartersnakes (Thamnophis marcianus) were used to examine increments in oxygen consumption (i.e. V̇(O2)) and carbon dioxide production (i.e. V̇(CO2)) associated with activity (Act), digestion (Dig) and post-prandial activity (Act+Dig). For females, we carried out these trials in the non-reproductive state, and also during the vitellogenic (V) and embryogenic (E) phases of a reproductive cycle. Endurance time (i.e. time to exhaustion, TTE) was recorded for all groups during Act and Act+Dig trials. Our results indicate that male and non-reproductive female T. marcianus exhibit significant increments in V̇(O2) during digestion (∼5-fold) and activity (∼9-fold), and that Act+Dig results in a similar increment in V̇(O2) (∼9- to 10-fold). During reproduction, resting V̇(O2) increased by 1.6- to 1.7-fold, and peak increments during digestion were elevated by 30-50% above non-reproductive values, but values associated with Act and Act+Dig were not significantly different from non-reproductive values. During Act+Dig, endurance time remained similar for all of the groups in the present study. Overall, our results indicate that prioritization is the primary pattern of interaction in oxygen delivery exhibited by this species. We propose that the metabolic processes associated with digestion, and perhaps reproduction, are temporarily compromised during activity.

Acute and chronic contractile activity-induced adaptations in muscle and mitochondrial function

Exercise training is a potent stimulus for favourable phenotypic adaptations in muscle, including the induction of mitochondrial biogenesis. Although the occurrence of organelle expansion in response to chronic muscle use is accepted, the cellular events governing this remodeling are undefined. Thus, the purpose of this dissertation was to examine the acute and chronic contractile activity-induced adaptations in skeletal muscle and mitochondrial function in young and old animals. The intracellular signals associated with contractile activity are important for the induction of downstream phenotypic plasticity. In study 1, we investigated the influence of muscle oxygen consumption and reactive oxygen species (ROS) production on kinase signaling. The results demonstrate that mitochondrial content influenced the rate of ROS production in resting muscle. Furthermore, several protein kinases were differentially sensitive to increments in oxygen consumption, and this sensitivity was also related to the muscle mitochondrial volume. In study 2, we further explored the effect of mitochondrial content on the acute contraction-induced kinase signaling in skeletal muscle. We found that mitochondrial content was inversely related to kinase activation in resting skeletal muscle. Moreover, training-induced increases in mitochondrial volume were associated with an attenuated adaptive signaling response subsequent to a single bout of contractions, suggesting a mitochondrially mediated mechanism regulating training-elicited muscle remodeling. The aim of study 3 was to examine the effect of age on the acute exercise-induced signaling response. Skeletal muscle from old animals exhibited pathophysiological properties, including reduced force production, fatigue resistance, mitochondrial content, and ATP-synthesizing ability, all characteristic of aging-associated sarcopenia. This condition was correlated with an attenuated signaling response to acute exercise, which was dependent on muscle mitochondrial content. Study 4 assessed the adaptive plasticity of mitochondria in young and old animals after chronic muscle use. We found that the mitochondria from aged animals were able to adapt favourably to a period of chronic contractile activity, despite an attenuated signaling response after each individual bout of exercise. However, the adaptive plasticity of aged animals was lower than that observed in young animals. These findings underscore the importance of daily physical activity in the maintenance and improvement of health for individuals of all ages.

Enhanced Cellular Respiration in Cells Exposed to Doxorubicin

Doxorubicin executes topoisomerase II mediated apoptosis, a process known to result in mitochondrial dysfunction, such as the leakage of cytochrome c and the opening of mitochondrial permeability transition pores (PTP). To further define the effects of doxorubicin on cell metabolism, we measured cellular respiration, cellular ATP, DNA fragmentation, and cytochrome c leakage in Jurkat (supersensitive), human leukemia-60 (HL-60, sensitive), and HL-60/MX2 (resistant) cells following exposure to 1.0 microM doxorubicin for 30 min. The measurements were made after 24 h of exposure to the drug. In Jurkat and HL-60 cells, doxorubicin treatment increased cellular mitochondrial oxygen consumption and ATP content by 2-3-fold. The increment in oxygen consumption was blocked by the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone (zVAD-fmk) and by the PTP inhibitor cyclosporin A. In HL-60/MX2 cells, which are resistant because of a reduced topoisomerase II activity, doxorubicin treatment was without effect on either respiration or ATP content, suggesting that topoisomerase II was essential for induction of apoptosis and stimulation of respiration and ATP content. The conclusion that both of the latter processes were products of oxidations in the mitochondrial respiratory chain was supported by the further observation that rotenone and sodium cyanide inhibited oxygen consumption and substantially lowered ATP content in the treated and untreated cells. Thus, oxidative phosphorylation is enhanced in cells briefly incubated with doxorubicin for as long as 24 h post drug exposure despite apoptosis-associated mitochondrial insults caused by the drug.

Experimental discrimination between proton leak and redox slip during mitochondrial electron transport.

By measuring the relationship between protonmotive force and the increment in oxygen consumption by mitochondria treated with submaximal amounts of uncoupler, we have experimentally tested four different models of imperfect coupling of oxidative phosphorylation. The results show that the increased rate of oxygen consumption at high protonmotive force is explained entirely by the dependence on protonmotive force of the passive proton leak conductance of the mitochondrial inner membrane. There is no measurable contribution from redox-slip reactions in the proton pumps caused by high protonmotive force. Neither is there any contribution from increased proton conductance of the membrane or increased redox slip in the respiratory chain caused by high turnover rates of the complexes.

Oxidative cost of breathing in the turtle Chrysemys picta bellii

We estimated the cost of breathing of turtles by measuring ventilation and oxygen consumption during air breathing and CO2 breathing. We assumed that any increment in oxygen consumption due to hypercapnic hyperpnea was due to the metabolic cost of the increased breathing. Six turtles were studied while breathing air and then 5% CO2 in air after at least 12 h breathing each gas. For the measurements, the turtles were submerged unrestrained in water at 20 degrees C and were free to raise their heads into a ventilated chamber. Tidal volumes were measured by the pressure changes in the chamber, and oxygen consumption was measured by conventional open-circuit respirometry. Ventilation increased markedly during CO2 breathing up to 50 times the control level, but oxygen consumption increased only slightly. Assuming no depression in nonventilatory metabolism, our data indicate an oxidative cost of breathing on the order of 1% of the total metabolic rate at rest. This is far less than the 15-20% cost predicted from published work (Kinney et al., Respir. Physiol. 31: 327-332, 1976) on a closely related species of turtle and is consistent with earlier work in our laboratory. We conclude that the cost of breathing in turtles is low, similar to other air-breathing vertebrates, and therefore the existing notion that turtle breathing is expensive and inefficient should be discarded.

Insulin Resistance after Surgery: Normalization by Insulin Treatment

1. Injury is known to be associated with variable degrees of tissue insensitivity to insulin. We measured insulin resistance in a group of non-obese, glucose-tolerant patients undergoing major elective surgery with an uncomplicated post-operative course. 2. Shortly after surgery, hyperglycaemia (7.3 +/- 0.6 versus 4.2 +/- 0.3 mmol/l glucose pre-surgery, mean +/- SEM, P less than 0.01) with normal insulin concentrations (73 +/- 15 versus 64 +/- 18 pmol/l) suggested the presence of insulin resistance. Counter-regulatory hormones were raised, whole-body protein oxidation was doubled (P less than 0.01) and energy expenditure was up by 18% (P less than 0.01). 3. Insulin sensitivity was quantified by clamping plasma glucose concentrations at 5.6 mmol/l during 24 h of total parenteral nutrition (15% protein, 55% glucose and 30% fat, supplying 1.25 times the measured resting energy expenditure) with a variable infusion of exogenous insulin. After surgery, eight times more insulin was needed than before surgery (14.14 +/- 1.15 versus 1.78 +/- 0.29 pmol min-1 kg-1, P less than 0.001) to maintain euglycemia. 4. After surgery, stimulation of net carbohydrate oxidation (18.8 +/- 1.4 versus 17.2 +/- 1.8 mumol min-1 kg-1 preoperatively, not significant), suppression of lipolysis and lipid oxidation and inhibition of ketogenesis occurred to the same extent as before surgery. Of the infused nutrients, the glucose was all oxidized, amino acids replaced endogenous protein losses (= neutral nitrogen balance) and lipids were stored. Insulin administration caused no further increment in oxygen consumption or energy expenditure.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxygen consumption for K+ uptake during post‐stimulatory activation of Na+, K(+)‐ATPase in perfused rat mandibular gland.

1. In order to determine the stoichiometry of K+ uptake and ATP consumption by Na+, K(+)-ATPase in the isolated, perfused mandibular gland of the rat, oxygen consumption and net K+ uptake from the vascular side were measured during the recovery period following K+ depletion by stimulation with acetylcholine in combination with ouabain. 2. Acetylcholine (10(-6) M) induced fluid secretion and an initial, transient release of K+ from the gland. Addition of ouabain suppressed salivary fluid secretion and caused an additional, dose-dependent, transient release of K+. 3. With acetylcholine (10(-6) M), the oxygen consumption of the gland increased to 62.4 +/- 4.2 microliters/(g min) from a resting value of 12.9 +/- 1.2 microliters/(g min). The increased oxygen consumption was suppressed by ouabain, in a dose-dependent fashion. 4. Withdrawal of acetylcholine and ouabain induced a net uptake of K+ and, simultaneously, an increase in oxygen consumption. The cumulative K+ uptake and the increment of oxygen consumption during the recovery period were dependent on the concentration of used ouabain. 5. The rates of K+ uptake and ATP hydrolysis were compared during recovery, assuming that six moles of ATP were hydrolysed for each mole of oxygen consumed. The data obtained during the later phase of the recovery lay on a single straight line with a slope of 1.8 for each of the various concentrations of ouabain, suggesting that the relationship between K+ uptake and energy consumption was linear. 6. Assuming the K+:ATP stoichiometry of the Na+, K(+)-ATPase to be 2:1, K+ would appear to be transported with ca 90% efficiency by Na+, K(+)-ATPase in the rat mandibular gland. Using 1.8-2.0 as a K+/ATP stoichiometry, the rate of primary active K+ uptake and the corresponding passive K+ efflux during secretion were estimated to be 20-22 mumol/(g min) from the oxygen consumption and the net K+ flux. 7. The passive K+ efflux was estimated, from the initial rate of K+ release caused by addition of 10(-3) M-ouabain, to be 30 mumol/g min). The discrepancy between the estimated active K+ uptake and passive K+ release (8-10 mumol/(g min] could be attributed to a secondary active K+ uptake process such as Na(+)-K(+)-2Cl-symport.

老人の呼吸困難とその対策

It is certainly difficult to understand the clinical significance of dyspnea or breathlessness among the elderly, though this symptom is quite routine. Setting a conjugate of the dyspnea index as an indicator of ventilatory reserve ratio, its distribution was tested along an age abscissa upon the twenty senile dyspnea and demonstrated almost all of them below the 30% level. Their arterial blood oxygen tensions were grouped onto the severity rank of dyspnea, clarifying that some senile lived of no complaint by the blood oxygen tensions within the range of pulmonary insufficiency, despite there some reluctant by the normal blood gas tensions. In order to comprehend this evidence, the dyspnea was dissected into several raising factors, each of which was examined the manner how a set of organs in the respiratory system of the elderly to be concerned under aging effects and to be detected in measurement. Respiratory center drive behaves in response to the efficacy of ventilation apparatus, so in resting state it supports by minimum activity without sensation of breathing difficulty, but at needs it works more even in dyspnea, the sensation of which deepens less itself together with increment of oxygen consumption. Considerable causes of this symptom for the senile may be due to hyperventilation syndrome, lung embolism after bone fracture, diabetic pulmonary capillopathy and hypophosphatemia. The treatments of senile dyspnea shall require the exact estimation of causal seriousness and not only attain improvement of pulmonary impairments and its accessory setups but also psychophysical rehabilitations upon rational nutrient preservation.

The regulation of lipogenesis by thyroid hormone and its contribution to thermogenesis.

We have used the tritiated water method to quantitate the effects of thyroid hormone on lipogenesis in the rat and then determined the contribution of this process to thyroid hormone-induced thermogenesis. After thyroid hormone administration to hypothyroid animals, fatty acid synthesis rose after a lag time of 12-16 h and reached a plateau after 4-5 days. This is consistent with the kinetics of an increase in oxygen consumption measured by others in similar animals. A diurnal variation was maintained in all thyroid states, with the peak value in the middle of the dark period being 3-fold higher than the nadir. Fatty acid synthesis in the livers of hyperthyroid animals was 3- to 4-fold higher than that in euthyroid rats, which, in turn, was 3- to 5-fold higher than the rate observed in hypothyroid rats. Slightly smaller but similar fold increases were measured in epididymal fat. A stimulation of fatty acid synthesis by thyroid hormone was also measured in the rest of the carcass, with hyperthyroid rates being twice those in hypothyroid animals. The contribution of the liver was much greater in hyperthyroid rats (34% of total fatty acid synthesis) than in hypothyroid animals (5%). The energy costs of this synthesis were calculated and compared to published values for total oxygen consumption in different thyroid states. Thus, 6-10% of the total increment in oxygen consumption between hyperthyroid and hypothyroid animals could be attributed to lipogenesis, depending on which published figures were used. About 3% of this increment was due to the liver alone.

Hypoxemia During Hemodialysis: A Critical Review of the Facts

The literature describing the fall in PaO2 during dialysis is intensively and critically reviewed. This phenomenon is related to both the type of membrane used (cellulosic v noncellulosic membrane), and to the composition of the dialysate (acetate v bicarbonate). It appears that a ventilation/perfusion mismatch due to pulmonary leukostasis can, in part, explain hypoxemia in patients dialyzed with cellulosic membranes. This phenomenon is especially apparent in patients with preexisting pulmonary abnormalities. However, hypoventilation remains the major cause of hypoxemia. This hypoventilation is mainly due to CO2 consumption during acetate metabolism (acetate dialysis), or alkalinization of the blood (bicarbonate dialysis). The metabolic consequences of acetate metabolism, and of bicarbonate and CO2 losses through the dialyzer are critically analyzed. The cause for the increment in oxygen consumption during acetate dialysis is examined. Finally, the respective role of these combined factors are described and used to explain the changes in VCO2, VO2, respiratory quotient (RQ), and PaO2 reported in the literature during dialysis against acetate and/or bicarbonate.

Effects of exercise and intermittent cold exposure on shivering and nonshivering thermogenesis in rats.

The effects of both exercise training and intermittent cold acclimation on heat production (shivering and nonshivering thermogenesis (NST)) in rats were studied. Warm-acclimated rats (housed at 24 degrees C, WA) and intermittently cold-acclimated rats (exposed daily to -5 degrees C for 2 h, CA) were forced to run (25 m.min-1 for 1 h) every day (WA-T and CA-T). WA and CA left sedentary (WA-S and CA-S) served as controls. Norepinephrine (NE)-induced thermogenic capacity assessed from the increment of oxygen consumption (VO2) and colonic temperature (Tc) were measured 4 weeks after commencing acclimation and exercise training. The thermogenic capacity was greater in CA than in WA. However, in WA, WA-T responded to NE less than WA-S, whereas the response of CA-T and CA-S did not differ. Wet weight of interscapular brown adipose tissue (IBAT) and its protein (and dry matter--regarded to be highly representative of protein) content were larger in CA than in WA. Respective sedentary and exercised groups of rats had similar IBAT protein (and dry matter) content although tissue weight was lighter in WA-T than in WA-S. Lipid content of IBAT was also larger in CA than in WA. IBAT of WA-T had less lipid compared to that of WA-S while no difference was seen between CA-S and CA-T. Shivering activity during acute cold (4 degrees C) exposure was less in CA compared to WA and there was no difference between respective groups of exercised and sedentary rats. Propranolol, a blocker of NE-dependent NST, eliminated the difference in shivering among these four groups. When exposed to severe cold (-10 or -20 degrees C), the fall in Tc of rats fasted for 18 h was greater in WA than in CA. CA-T showed a greater decrease in Tc than CA-S during -20 degrees C exposure while it did not differ during -10 degrees C exposure. On the other hand, Tc of WA-T and WA-S did not differ significantly during either cold exposure period. These results suggest that exercise training in rats housed at 24 degrees C suppresses NE-dependent NST whereas another nonshivering thermogenic mechanism (NE-independent) may compensate this suppression. However, NE-dependent NST of WA-S and WA-T did not parallel protein (dry matter) content of IBAT; no difference existed in IBAT protein between these two groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Defective thermoregulatory thermogenesis in monosodium glutamate-induced obesity in mice

We have studied thermoregulatory thermogenesis in mice rendered obese by neonatal administration of monosodium glutamate (MSG) and in saline treated controls. At 12 weeks of age MSG-treated mice maintained on a chow diet and housed at 24 °C, exhibited hypertrophy of brown adipose tissue (BAT) compared to controls (65% increase in wet weight and lipid content, no difference in DNA content). Acute cold exposure (4 °C for two hours) resulted in a significantly greater fall in core temperature in MSG-treated than control mice. After cold exposure to 4 °C for six hours, control animals mobilized BAT lipid whereas MSG-treated animals did not. Both groups showed comparable increments in oxygen consumption in response to exogenous norepinephrine. The above changes were qualitatively the same for both male and female animals. The following conclusions were reached: (1) MSG-treated mice have defective cold induced thermogenesis, indirect evidence suggests this results from impaired activation of thermogenic mechanisms in BAT; (2) the defect responsible for this lies extrinsic to BAT; and (3) the quantitative significance of defective thermoregulatory thermogenesis for the development of obesity in these mice is uncertain.

Cardiorespiratory effects of respiratory protective devices during exercise in well-trained men.

The effects of a filtering device, an air-line breathing apparatus and a self-contained breathing apparatus ( SCBA ) on pulmonary ventilation, oxygen consumption and heart rate were studied in 12 well-trained firemen aged 21-35 years. Their average maximal oxygen consumption (VO2 max) was 64.9 ml X min-1 X kg-1. Sequential tests without and with the respirator were performed on a treadmill. The continuous test contained five components, each of which lasted 5 min: sitting at rest, walking at 20%, 40%, and 60% of the individual VO2 max, and recovery sitting. During the higher submaximal work levels and recovery, ventilation, heart rate, and oxygen consumption in particular increased more with respirators than without them. At the highest work level the increments in oxygen consumption caused by the respirators were 13%, (8.7 ml X min-1 X kg-1), 7% (4.4 ml X min-1 X kg-1), and 20% (12.7 ml X min-1 X kg-1) of VO2 max. All three respirators hampered respiration, resulting in hypoventilation. The additional effort of breathing and the weight of the apparatus (15 kg with the SCBA ) increased the subjects' cardiorespiratory strain so clearly that the need for rest periods and the individual's work capacity when the respirators are worn must be carefully considered, particularly with the SCBA .

Cardiovascular changes associated with treadmill running in the Pekin duck.

Six adult white Pekin ducks were trained to run on a treadmill for 10 min at a speed of 1.43 km h-1. O2 consumption, CO2 production, breathing rate, blood gas tension and pH, sciatic and carotid blood flows and colonic and skin temperatures were measured in the experiments. A 2.6 times increase in oxygen consumption was observed when going from resting on the treadmill to exercise. The increased oxygen delivery was achieved by a 61% increase in cardiac output and a 51% increase in the arterio-venous oxygen content difference. Probably the reported resting oxygen consumption was higher than a true resting level causing the increment in oxygen consumption to be more correctly 3.6 times the resting level. Sciatic and carotid blood flow increased by 3.7 times and 2.3 times, respectively, during exercise. At cessation of exercise, the carotid blood flow decreased very rapidly, while the sciatic blood flow decreased more slowly. An increased web temperature above the exercise level was seen in the post-exercise period. The results suggest that the ducks prefer to use non-evaporative heat loss in the post-exercise period, respiratory evaporative cooling being of minor importance. this strategy may be correlated to the small internal heat load induced by the running (body temperature increased by only 0.3 degrees C.

Calorigenic response in obese and nonobese women

The calorigenic response to a high protein test meal was studied in women with a history of childhood onset obesity. Obese and nonobese individuals were fasted overnight and basal oxygen consumptions determined the following morning. A semisynthetic 823 kcal high protein test meal was ingested within a 1-hr period followed by hourly determinations of oxygen consumption and plasma levels of insulin, free fatty acids, triglycerides, glucose, amino acids, and urea nitrogen. Amino acid levels increased faster and to a higher plateau in the nonobese group, while insulin levels increased and eventually decreased in a similar fashion in both groups. No differences in basal metabolic rate were detected. The postprandial increment in oxygen consumption was significantly less among the obese subjects. Diminished calorigenesis after each meal would result in accumulation of extra calories provided that caloric consumption is not appropriately decreased. These data suggest that a physiological aberration of energy metabolism may contribute to the development of childhood onset obesity.