Metabolic, ventilatory, and hygric physiology of the gracile mouse opossum (Gracilinanus agilis)

We present the first complete study of basic laboratory-measured physiological variables (metabolism, thermoregulation, evaporative water loss, and ventilation) for a South American marsupial, the gracile mouse opossum (Gracilinanus agilis). Body temperature (Tb) was thermolabile below thermoneutrality (Tb = 33.5°C), but a substantial gradient between Tb and ambient temperature (Ta) was sustained even at Ta = 12°C (Tb = 30.6°C). Basal metabolic rate of 1.00 mL O2 g-1 h-1 at Ta = 30°C conformed to the general allometric relationship for marsupials, as did wet thermal conductance (5.7 mL O2 g-1 h-1 °C-1). Respiratory rate, tidal volume, and minute volume at thermoneutrality matched metabolic demand such that O2 extraction was 12.4%, and ventilation increased in proportion to metabolic rate at low T a. Ventilatory accommodation of increased metabolic rate at low Ta was by an increase in respiratory rate rather than by tidal volume or O2 extraction. Evaporative water loss at the lower limit of thermoneutrality conformed to that of other marsupials. Relative water economy was negative at thermoneutrality but positive below Ta = 12°C. Interestingly, the Neotropical gracile mouse opossums have a more positive water economy at low Ta than an Australian arid-zone marsupial, perhaps reflecting seasonal variation in water availability for the mouse opossum. Torpor occurred at low Ta, with spontaneous arousal when . T b > 20°C. Torpor resulted in absolute energy and water savings but lower relative water economy. We found no evidence that gracile mouse opossums differ physiologically from other marsupials, despite their Neotropical distribution, sympatry with placental mammals, and long period of separation from Australian marsupials. © 2009 by The University of Chicago. All rights reserved.

Age and gender influence the cardiorespiratory function and metabolic rate of broiler chicks during normocapnia and hypercapnia

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

The Influence of Baseline Metabolic Rate and Exercise Training on Cardio-Respiratory Dynamics

Speeding the VO2 kinetics results in a reduction of the O2 deficit. Two factors might determine VO2 kinetics: oxygen delivery to muscle (Tschakovsky and Hughson 1999) and a muscle 'metabolic inertia' (Grassi et al. 1996). Therefore, in study 1 we investigated VO2 kinetics and cardiovascular system adaptations during step exercise transitions in different regions of the moderate domain. In study 2 we investigated muscle oxygenation and cardio-pulmonary adaptations during step exercise tests before, after and over a period of training. Study 1 methods: Seven subjects (26 ± 8 yr; 176 ± 5 cm; 69 ± 6 kg) performed 4 types of step transition from rest (0-50W; 0-100W) or elevate baseline (25-75W; 25-125W). GET and VO2max were assessed before testing. O2 uptake and were measured during testing. Study 2 methods: 10 subjects (25 ± 4 yr; 175 ± 9 cm; 71 ± 12 kg) performed a step transition test (0 to 100 W) before, after and during 4 weeks of endurance training (ET). VO2max and GET were assessed before and after of ET (40 minutes, 3 times a week, 60% O2max). VO2 uptake, Q and deoxyheamoglobin were measured during testing. Study 1 results: VO2 τ and the functional gain were slower in the upper regions of the moderate domain. Q increased more abruptly during rest to work condition. Q τ was faster than VO2 τ for each exercise step. Study 2 results: VO2 τ became faster after ET (25%) and particularly after 1 training session (4%). Q kinetics changed after 4 training sessions nevertheless it was always faster than VO2 τ. An attenuation in ∆[HHb] /∆VO2 was detectible. Conclusion: these investigations suggest that muscle fibres recruitment exerts a influence on the VO2 response within the moderate domain either during different forms of step transition or following ET.

Perinatal adaptation in mammals: the impact of metabolic rate

Mammalian birth is accompanied by profound changes in metabolic rate that can be described in terms of body size relationship (Kleiber's rule). Whereas the fetus, probably as an adaptation to the low intrauterine pO2, exhibits an "inappropriately" low, adult-like specific metabolic rate, the term neonate undergoes a rapid metabolic increase up to the level to be expected from body size. A similar, albeit slowed, "switching-on" of metabolic size allometry is found in human preterm neonates whereas animals that are normally born in a very immature state are able to retard or even suppress the postnatal metabolic increase in favor of weight gain and O2 supply. Moreover, small immature mammalian neonates exhibit a temporary oxyconforming behavior which enhances their hypoxia tolerance, yet is lost to the extent by which the size-adjusted metabolic rate is "locked" by increasing mitochondrial density. Beyond the perinatal period, there are no other deviations from metabolic size allometry among mammals except in hibernation where the temporary "switching-off" of Kleiber's rule is accompanied by a deep reduction in tissue pO2. This gives support to the hypothesis that the postnatal metabolic increase represents an "escape from oxygen" similar to the evolutionary roots of mitochondrial respiration, and that the overall increase in specific metabolic rate with decreasing size might contribute to prevent tissues from O2 toxicity.

Association between cerebral oxygen metabolic rate and the incidence of nosocomial pneumonia in head injury patients

The development of nosocomial pneumonia was monitored in 96 head-trauma patients requiring mechanical ventilation for up to 10 days. Pneumonia occurred in 28 patients (29.2%) or 53.9 cases per 1,000 admission days. The incidence of nosocomial pneumonia was negatively correlated with cerebral oxygen metabolic rate (CMRO$\sb2$) measured during the first five days. The relative risk of nosocomial pneumonia for patients with CMRO$\sb2$ less than 0.6 umol/gm/min is 2.08 (1.09$-$3.98) times those patients with CMRO$\sb2$ greater than 0.6 umol/gm/min. The association between cerebral oxygen metabolic rate and nosocomial pneumonia was not affected by adjustment of potential confounding factors including age, cimetidine and other infections. These findings provide evidences underlying the CNS-immune system interaction. ^

Characterization of the interaction between local cerebral metabolic rate for glucose and acid -base index in ischemic rat brain employing a double-isotope methodology

The association between increases in cerebral glucose metabolism and the development of acidosis is largely inferential, based on reports linking hyperglycemia with poor neurological outcome, lactate accumulation, and the severity of acidosis. We measured local cerebral metabolic rate for glucose (lCMRglc) and an index of brain pH--the acid-base index (ABI)--concurrently and characterized their interaction in a model of focal cerebral ischemia in rats in a double-label autoradiographic study, using ($\sp{14}$C) 2-deoxyglucose and ($\sp{14}$C) dimethyloxazolidinedione. Computer-assisted digitization and analysis permitted the simultaneous quantification of the two variables on a pixel-by-pixel basis in the same brain slices. Hemispheres ipsilateral to tamponade-induced middle cerebral occlusion showed areas of normal, depressed and elevated glucose metabolic rate (as defined by an interhemispheric asymmetry index) after two hours of ischemia. Regions of normal glucose metabolic rate showed normal ABI (pH $\pm$ SD = 6.97 $\pm$ 0.09), regions of depressed lCMRglc showed severe acidosis (6.69 $\pm$ 0.14), and regions of elevated lCMRglc showed moderate acidosis (6.88 $\pm$ 0.10), all significantly different at the.00125 level as shown by analysis of variance. Moderate acidosis in regions of increased lCMRglc suggests that anaerobic glycolysis causes excess protons to be generated by the uncoupling of ATP synthesis and hydrolysis. ^

Seawater carbonate chemistry and length, weight, survival rate, metabolic rate of coral reef fish Amphiprion melanopus in a laboratory experiment

Carbon dioxide concentrations in the surface ocean are increasing owing to rising CO2 concentrations in the atmosphere. Higher CO2 levels are predicted to affect essential physiological processes of many aquatic organisms, leading to widespread impacts on marine diversity and ecosystem function, especially when combined with the effects of global warming. Yet the ability for marine species to adjust to increasing CO2 levels over many generations is an unresolved issue. Here we show that ocean conditions projected for the end of the century (approximately 1,000 µatm CO2 and a temperature rise of 1.5-3.0 °C) cause an increase in metabolic rate and decreases in length, weight, condition and survival of juvenile fish. However, these effects are absent or reversed when parents also experience high CO2 concentrations. Our results show that non-genetic parental effects can dramatically alter the response of marine organisms to increasing CO2 and demonstrate that some species have more capacity to acclimate to ocean acidification than previously thought.

Sea urchins in a high CO2 world: partitioned effects of body-size, ocean warming and acidification on metabolic rate

Body-size and temperature are the major factors explaining metabolic rate, and the additional factor of pH is a major driver at the biochemical level. These three factors have frequently been found to interact, complicating the formulation of broad models predicting metabolic rates and hence ecological functioning. In this first study of the effects of warming and ocean acidification, and their potential interaction, on metabolic rate across a broad body-size range (two-to-three orders of magnitude difference in body mass) we addressed the impact of climate change on the sea urchin Heliocidaris erythrogramma in context with climate projections for east Australia, an ocean warming hotspot. Urchins were gradually introduced to two temperatures (18 and 23 °C) and two pH (7.5 and 8.0), and maintained for two months. That a new physiological steady-state had been reached, otherwise know as acclimation, was validated through identical experimental trials separated by several weeks. The relationship between body-size, temperature and acidification on the metabolic rate of H. erythrogramma was strikingly stable. Both stressors caused increases in metabolic rate; 20% for temperature and 19% for pH. Combined effects were additive; a 44% increase in metabolism. Body-size had a highly stable relationship with metabolic rate regardless of temperature or pH. None of these diverse drivers of metabolism interacted or modulated the effects of the others, highlighting the partitioned nature of how each influences metabolic rate, and the importance of achieving a full acclimation state. Despite these increases in energetic demand there was very limited capacity for compensatory modulating of feeding rate; food consumption increased only in the very smallest specimens, and only in response to temperature, and not pH. Our data show that warming, acidification and body-size all substantially affect metabolism and are highly consistent and partitioned in their effects, and for H. erythrogramma near-future climate change will incur a substantial energetic cost.

The dual effect of normobaric hypoxia on heart rate variability and substrate partitioning following interval cycling

Recent studies have shown the importance of the beat-by-beat changes in heart rate influenced by the autonomic nervous system (ANS), or heart rate variability (HRV). The purpose of this study was to examine the lasting effects of hypoxic exercise on HRV, and its influences on substrate usage. Results from this study could lead an increased understanding on this topic. Eight active healthy males (age: 31±11 years; height: 180±7 cm; weight: 83±8 kg; VO₂max (maximal oxygen consumption): 4.4±0.6 L•min⁻¹) underwent normoxic and hypoxic (FᵢO₂= 0.15) conditions during high-intensity interval (HIIT) cycling (70%-high interval, 35%-rest interval). Cycling intensity was determined by a peak power output cycling test. Each experimental session consisted of a basal metabolic rate determination, up to 45-minutes of HIIT cycling, and three 30-minute post-exercise metabolic rate measurements (spanning 3 hours and 15 minutes after exercise). During exercise, RPE was higher (p<0.01) and LAC (lactate) increased (p=0.001) at each point of time in hypoxia, with no change in normoxia. After hypoxic exercise, the SNS/PNS ratio (overall ANS activity) was significantly higher (p<0.01) and significantly decreased through time in both conditions (p<0.01). In addition, a significant interaction between time and conditions (p<0.02) showed a decrease in LAC concentration through time post-hypoxic exercise. The findings showed that a single bout of hypoxic exercise alters ANS activity post-exercise along with shifting substrate partitioning from glycolytic to lipolytic energy production. The significant decrease in LAC concentration post-hypoxic exercise supports the notion that hypoxic HIIT induces a greater muscle glycogen depletion leading to increased fat oxidation to sustain glycogenesis and gluconeogenesis to maintain blood glucose level during recovery.

Modelling the associations between fat-free mass, resting metabolic rate and energy intake in the context of total energy balance

Peer reviewed

Interactions between energy intake and expenditure in the development and treatment of obesity.

Summary There are four interactions to consider between energy intake (EI) and energy expenditure (EE) in the development and treatment of obesity. (1) Does sedentariness alter levels of EI or subsequent EE? and (2) Do high levels of EI alter physical activity or exercise? (3) Do exercise-induced increases in EE drive EI upwards and undermine dietary approaches to weight management and (4) Do low levels of EI elevate or decrease EE? There is little evidence that sedentariness alters levels of EI. This lack of cross-talk between altered EE and EI appears to promote a positive EB. Lifestyle studies also suggest that a sedentary routine actually offers the opportunity for over-consumption. Substantive changes in non exercise activity thermogenesis are feasible, but not clearly demonstrated. Cross talk between elevated EE and EI is initially too weak and takes too long to activate, to seriously threaten dietary approaches to weight management. It appears that substantial fat loss is possible before intake begins to track a sustained elevation of EE. There is more evidence that low levels of EI does lower physical activity levels, in relatively lean men under conditions of acute or prolonged semi-starvation and in dieting obese subjects. During altered EB there are a number of small but significant changes in the components of EE, including (i) sleeping and basal metabolic rate, (ii) energy cost of weight change alters as weight is gained or lost, (iii) exercise efficiency, (iv) energy cost of weight bearing activities, (v) during substantive overfeeding diet composition (fat versus carbohydrate) will influence the energy cost of nutrient storage by ~ 15%. The responses (i-v) above are all “obligatory” responses. Altered EB can also stimulate facultative behavioural responses, as a consequence of cross-talk between EI and EE. Altered EB will lead to changes in the mode duration and intensity of physical activities. Feeding behaviour can also change. The degree of inter-individual variability in these responses will define the scope within which various mechanisms of EB compensation can operate. The relative importance of “obligatory” versus facultative, behavioural responses -as components of EB control- need to be defined.