Diet, phylogeny, and basal metabolic rate in phyllostomid bats

Aside from the pervasive effects of body mass, much controversy exists as to what factors account for interspecific variation in basal metabolic rates (BMR) of mammals; however, both diet and phylogeny have been strongly implicated. We examined variation in BMR within the New World bat family Phyllostomidae, which shows the largest diversity of food habits among mammalian families, including frugivorous, nectarivorous, insectivorous, carnivorous and blood-eating species. For 27 species, diet was taken from the literature and BMR was either measured on animals captured in Brazil or extracted from the literature. Conventional (nonphylogenetic) analysis of covariance (ANCOVA), with body mass as the covariate, was first used to test the effects of diet on BMR. In this analysis, which assumes that all species evolved simultaneously from a single ancestor (i.e., a star phylogeny), diet exerted a strong effect on mass-in-dependent BMR: nectarivorous bats showed higher mass-independent BMR than other bats feeding on fruits, insects or blood. In phylogenetic ANCOVAs via Monte Carlo computer simulation, which assume that species are part of a branching hierarchical phylogeny, no statistically significant effect of diet on BMR was observed. Hence, results of the nonphylogenetic analysis were misleading because the critical values for testing the effect of diet were underestimated. However, in this sample of bats, diet is perfectly confounded with phylogeny, because the four dietary categories represent four separate subclades, which greatly reduces statistical power to detect a diet (= subclade) effect. But even if diet did appear to exert an influence on BMR in this sample of bats, it would not be logically possible to separate this effect from the possibility that the dietary categories differ for some other reason (i.e., another synapomorphy of one or more of the subclades). Examples such as this highlight the importance of considering phylogenetic relationships when designing new comparative studies, as well as when analyzing existing data sets. We also discuss some possible reasons why BMR may not coadapt with diet. © by Urban & Fischer Verlag.

Loss of the Ability to Control Right-to-Left Shunt Does Not Influence the Metabolic Responses to Temperature Change or Long-Term Fasting in the South American Rattlesnake Crotalus durissus

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

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)

Resting heart rate and auditory evoked potential

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.

Resting heart rate and incident heart failure and cardiovascular mortality in older adults: role of inflammation and endothelial dysfunction: the PROSPER study

Resting heart rate is a promising modifiable cardiovascular risk marker in older adults, but the mechanisms linking heart rate to cardiovascular disease are not fully understood. We aimed to assess the association between resting heart rate and incident heart failure (HF) and cardiovascular mortality, and to examine whether these associations might be attributable to systemic inflammation and endothelial dysfunction.

QTc interval and resting heart rate as long-term predictors of mortality in type 1 and type 2 diabetes mellitus: a 23-year follow-up

We evaluated the association of QT interval corrected for heart rate (QT(c)) and resting heart rate (rHR) with mortality (all-causes, cardiovascular, cardiac, and ischaemic heart disease) in subjects with type 1 and type 2 diabetes.

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.

[Calculating the basal metabolic rate and severe and morbid obesity]

The aim of this study was to evaluate the currently available predictive equations for basal metabolic rate (BMR) in subjects with obesity class II and III, and to assess the contribution by the components of a two-compartment model of body composition, namely the lean body mass (LBM) and the fat mass (FM) to the prediction. A second objective was to examine the reliability of the Harris Benedict equation in obese subjects, especially with a weight > or = 120 kg.

[Is resting heart rate a cardiovascular risk factor?]

During recent years, resting heart rate was not considered as a cardiovascular risk factor. However, new evidences have showed that resting heart rate is an important prognostic factor for sudden cardiac death and heart failure in the general population, and especially among patients with known cardiac disease. Interestingly, resting heart rate not only predicts cardiac mortality but also all-cause mortality. The most common pathophysiological explanation is related to the fact that increased heart rate increases myocardial oxygen consumption and in parallel reduces coronary blood flow (reduction in the diastolic duration).