Maximal oxygen uptake in four species of small mammals

Pasquis, P; Lacaisse, A; Dejours, P

doi:10.1016/0034-5687(70)90078-2

Cited by 120 publications

(40 citation statements)

References 5 publications

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“…The evolution of flight in bats was a major factor leading to the success of this amazing group of mammals, although the evolution of this ability has required complex changes in the anatomy of these animals. In addition to other important factors, such as changes in bone density and development of the wings, bat flight also requires a significantly higher metabolic rate, a rate well above the maximum capable by other similar-sized terrestrial mammals during exercise (2,6,46). Aerobic metabolism by mitochondria plays a vital role as the energy production centers of cells The OXPHOS pathway of mitochondria has adaptively evolved to meet the demands of changing environmental and physiological conditions.…”

Section: Resultsmentioning

confidence: 99%

Adaptive evolution of energy metabolism genes and the origin of flight in bats

Shen

Lü

Zhu

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

260

225

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Bat flight poses intriguing questions about how flight independently developed in mammals. Flight is among the most energyconsuming activities. Thus, we deduced that changes in energy metabolism must be a primary factor in the origin of flight in bats. The respiratory chain of the mitochondrial produces 95% of the adenosine triphosphate (ATP) needed for locomotion. Because the respiratory chain has a dual genetic foundation, with genes encoded by both the mitochondrial and nuclear genomes, we examined both genomes to gain insights into the evolution of flight within mammals. Evidence for positive selection was detected in 23.08% of the mitochondrial-encoded and 4.90% of nuclearencoded oxidative phosphorylation (OXPHOS) genes, but in only 2.25% of the nuclear-encoded nonrespiratory genes that function in mitochondria or 1.005% of other nuclear genes in bats. To address the caveat that the two available bat genomes are of only draft quality, we resequenced 77 OXPHOS genes from four species of bats. The analysis of the resequenced gene data are in agreement with our conclusion that a significantly higher proportion of genes involved in energy metabolism, compared with background genes, show evidence of adaptive evolution specific on the common ancestral bat lineage. Both mitochondrial and nuclearencoded OXPHOS genes display evidence of adaptive evolution along the common ancestral branch of bats, supporting our hypothesis that genes involved in energy metabolism were targets of natural selection and allowed adaptation to the huge change in energy demand that were required during the origin of flight.Chiroptera | genetic foundation | mitochondria | OXPHOS B ats are perhaps the most unusual and specialized of all mammals, as flight is their main mode of locomotion. Although there are several gliding mammals that are able to glide from tree to tree (such as the flying squirrel, gliding possums, and colugos), bats are the only mammal capable of sustaining level flight (1). The evolution of flight in bats was a major factor leading to the success of this amazing group (2, 3). A number of adaptations to flight found in birds are not shared by mammals, thus Darwin in the Origin of Species (Chapter 5) (4) proposed that the evolution of a flying bat from an insectivorous terrestrial mammal was too difficult to imagine.Bat flight is a highly complex functional system from a morphological, physiological, and aerodynamic perspective (5). As in birds, bat flight requires a metabolic rate that is 3-5 times greater than the maximum observed during exercise in similar-sized terrestrial mammals (2, 6). Hence, a significant metabolic barrier must separate volant from nonvolant vertebrates (6). Therefore, we speculate that energy metabolism is among the primary factors that influenced the development of flight in bats.The respiratory chain of the mitochondrial produces 95% of the adenosine triphosphate (ATP) needed for locomotion. The enzymes involved in oxidative phosphorylation (OXPHOS) are composed of multisubunit complexes that a...

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Section: Resultsmentioning

confidence: 99%

Adaptive evolution of energy metabolism genes and the origin of flight in bats

Shen

Lü

Zhu

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

260

225

View full text Add to dashboard Cite

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“…V O 2 max in untrained mice has been reported to range from ϳ80 to 260 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 , and RER at V O 2 max from 0.91 to 1.28 (13,14,31,32,36,38,40). However, there are differences in these studies regarding test protocols, equipment, body masses, strains, age, sex, and how accustomed the mice were to the methods.…”

Section: Discussionmentioning

confidence: 99%

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Kemi

Loennechen

Wisløff

et al. 2002

Journal of Applied Physiology

244

265

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. Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy. J Appl Physiol 93: 1301-1309. First published May 24, 2002 10.1152/japplphysiol.00231.2002-Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored and call for an effective and wellcharacterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (V O2 max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent V O2 max with 0.98 test-retest correlation was found at 25°treadmill grade. Running for 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of V O2 max and 2 min at 50% (adjusted to weekly V O2 max testing) increased V O2 max to a plateau 49% above sedentary females and 29% in males. Running economy improved in both sexes, and echocardiography indicated significantly increased left ventricle posterior wall thickness. Ventricular weights increased by 19-29 and 12-17% in females and males, respectively, whereas cardiomyocyte dimensions increased by 20-32, and 17-23% in females and males, respectively; skeletal muscle mass increased by 12-18%. Thus the model mimics human responses to exercise and can be used in future studies of molecular mechanisms underlying these adaptations. maximal oxygen uptake; work economy; respiratory exchange ratio; cardiomyocyte; allometric scaling SEVERAL NOVEL SIGNALING PATHWAYS of pathological cardiac hypertrophy have been unveiled in the powerful model of mechanical overloading by thoracic aorta constriction in genetically modified mice (8,22). Thus far, the molecular mechanisms of adaptive cardiac hypertrophy in response to physiological stimuli remain virtually unexplored because of a paucity of effective and well-controlled experimental models in this species. Ideally, the outcome should mimic typical results of exercise training in humans, e.g., increased maximal oxygen uptake (V O 2 max ) and work economy (21). In healthy individuals, increased exercise capacity is dependent on functional and structural adaptations in skeletal muscle, blood vessels, and heart. Cardiac adaptation includes increased ventricular chamber volumes and weights, cardiomyocyte hypertrophy, increased cardiac output, and improved contractile function measured in isolated cardiomyocytes and in the intact heart (2, 3).At present, there are few well-controlled endurance training studies in mice. Training is usually carried out as voluntary exercise regimens, with little control of exercise intensity and the individual's fitness level. Voluntary wheel running is most frequently used. V O 2 max has been shown to increase by 12-30% after a 7-to 12-wk period of free wheel running (11,40). The latter study also demonstrated a 6% decreased respiratory exchange ratio (RER) at V O 2 max in trained mice. Exercise capacity and adaptations have al...

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“…It is clear that during maximal exercise some mammals (such as man and dog) can increase their myocardial energy flux more than 5-fold, and the values become near to the maximum oxidative phosphorylation capacity of their hearts [134,135]. We have estimated, on the basis of their mitochondrial volume fraction and the knowledge that 1 g of mitochondria consumes about 4 ml O 2 /min [6,135], that human hearts have an oxidative capacity in excess of 200 mW g Ϫ1 and would It is interesting to note that rodents have a very reduced exercise tolerance compared with man's [136]. This is manifest as a much-reduced ability to increase heart rate, although rodents can undoubtedly double the work output per beat (see Table 3b).…”

Section: Basal Metabolism Mechanical Efficiency and Species Difmentioning

confidence: 93%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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The cardiac basal metabolism is the rate of energy expenditure of the quiescent myocardium. It is also called the resting metabolism or the arrested heart metabolism. It has been measured in numerous ways, and in vivo there is good evidence that it accounts for about 1/5 to 1/3 of the total energy flux. The difficulty arises, however, when the heart is stopped because the magnitude of the basal metabolism depends, as blood viscosity, on how and under what physiological condition it is measured. It is possible for the in vivo basal value to fall to less than 1/5 of its original value without cellular damage or to increase to values 5 times greater than its probable in vivo magnitude (i.e., to rise to values in excess of the energy flux of the normally beating heart) by altering the composition of the perfusion medium. We have written on this subject several times [1][2][3], but believe that developments in knowledge now make it possible for us to speculate in a more informed manner. Since several million openheart operations are performed on arrested hearts worldwide each year, it would seem imperative that we understand the cellular mechanisms that can change the magnitude of basal metabolism.A. V. Hill [4] has pointed out that in examining physiological activities, it is necessary to assume a baseline from which some quantity or rate can be measured. If the energy flux produced by the beating heart were very large compared with the energy flux of the arrested heart, baseline ambiguity would be relatively unimportant. But this is not so in regard to the heart; its basal metabolism is high. Within a species, the basal metabolism of cardiac tissue is several-fold higher than the resting metabolism of skeletal muscle and is an order of magnitude greater than the resting metabolism of amphibian skeletal muscle.Species differences are clearly evident in the magnitude of cardiac basal metabolism, and we believe that the major reason for these differences relates to the leakiness of cell membranes, such as those of the sarcolemma and sarcoplasmic reticulum and those of Japanese Journal of Physiology, 51, 399-426, 2001 Key words: whole hearts, isolated preparations, biochemical contributors, modifiers, species difference, temperature, substrate, hypoxia. Abstract:We endeavor to show that the metabolism of the nonbeating heart can vary over an extreme range: from values approximating those measured in the beating heart to values of only a small fraction of normal-perhaps mimicking the situation of nonflow arrest during cardiac bypass surgery. We discuss some of the technical issues that make it difficult to establish the magnitude of basal metabolism in vivo. We consider some of the likely contributors to its magnitude and point out that the biochemical reasons for a sizable fraction of the heart's basal ATP usage remain unresolved. We consider many of the physiological factors that can alter the basal metabolic rate, stressing the importance of substrate supply. We point out that the protective effect of hypothermia ...

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Maximal oxygen uptake in four species of small mammals

Cited by 120 publications

References 5 publications

Adaptive evolution of energy metabolism genes and the origin of flight in bats

Adaptive evolution of energy metabolism genes and the origin of flight in bats

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Cardiac Basal Metabolism.

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