Optimal hematocrit for maximal exercise performance in acute and chronic erythropoietin-treated mice

In small resident bird species living at northern latitudes, winter cold acclimatization is associated with an increase in pectoral muscle size and haematocrit level, and this is thought to drive the seasonal increase in summit metabolic rate (Ṁ sum , a measure of maximal shivering thermogenic capacity). However, evidence suggesting that pectoral muscle size influences Ṁ sum is correlational and the link between haematrocrit level and Ṁ sum remains to be demonstrated. We experimentally tested the relationship between pectoral muscle size and Ṁ sum by manipulating muscle size using a feather clipping protocol in free-living wintering black-capped chickadees (Poecile atricapillus). This also allowed us to investigate the link between haematocrit and thermogenic capacity. After a first series of measures on all birds, we cut half of the flight feathers of experimental individuals (N=14) and compared their fat and pectoral muscle scores, Ṁ sum and haematocrit level at recapture with their previous measures and with those of control birds (N=17) that were captured and recaptured at comparable times. Results showed that: (1) experimental birds developed larger pectoral muscles than control individuals and (2) mass-independent Ṁ sum was up to 16% higher in birds expressing large pectoral muscles. Ṁ sum was also positively correlated with haematocrit, which was not affected by the experimental manipulation. These findings demonstrate that, for a given body mass, large pectoral muscles are associated with a higher Ṁ sum in black-capped chickadees and that oxygen carrying capacity likely supports thermogenesis in this species.

Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Phenotype manipulations confirm the role of pectoral muscles and haematocrit in avian maximal thermogenic capacity

Petit

Vézina

2013

“…Under normoxia, a moderately increased Hct augments arterial O 2 content and therefore enhances aerobic capacity (Ekblom and Hermansen, 1968;Kanstrup and Ekblom, 1984;Ekblom and Berglund, 1991). However, the highest attainable Hct is not necessarily associated with the highest attainable aerobic power output (Crowell et al, 1959;Crowell and Smith, 1967;Villafuerte et al, 2004;Schuler et al, 2010). This is because the associated increase in blood viscosity produces a higher peripheral vascular resistance that might compromise Q, thereby reducing V O2,max (Guyton and Richardson, 1961;Connes et al, 2006).…”

Section: Erythropoeitic Activitymentioning

confidence: 98%

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

Storz

Scott

Cheviron

2010

353

343

SummaryHigh-altitude environments provide ideal testing grounds for investigations of mechanism and process in physiological adaptation. In vertebrates, much of our understanding of the acclimatization response to high-altitude hypoxia derives from studies of animal species that are native to lowland environments. Such studies can indicate whether phenotypic plasticity will generally facilitate or impede adaptation to high altitude. Here, we review general mechanisms of physiological acclimatization and genetic adaptation to high-altitude hypoxia in birds and mammals. We evaluate whether the acclimatization response to environmental hypoxia can be regarded generally as a mechanism of adaptive phenotypic plasticity, or whether it might sometimes represent a misdirected response that acts as a hindrance to genetic adaptation. In cases in which the acclimatization response to hypoxia is maladaptive, selection will favor an attenuation of the induced phenotypic change. This can result in a form of cryptic adaptive evolution in which phenotypic similarity between high-and low-altitude populations is attributable to directional selection on genetically based trait variation that offsets environmentally induced changes. The blunted erythropoietic and pulmonary vasoconstriction responses to hypoxia in Tibetan humans and numerous high-altitude birds and mammals provide possible examples of this phenomenon. When lowland animals colonize high-altitude environments, adaptive phenotypic plasticity can mitigate the costs of selection, thereby enhancing prospects for population establishment and persistence. By contrast, maladaptive plasticity has the opposite effect. Thus, insights into the acclimatization response of lowland animals to high-altitude hypoxia can provide a basis for predicting how altitudinal range limits might shift in response to climate change.

“…However, results of several empirical and theoretical studies suggest that increasing the Hb concentration of partially saturated blood is not an ideal long-term solution to the problem of chronic hypoxemia because the associated increase in blood viscosity produces an elevated peripheral vascular resistance that can compromise cardiac output (Guyton and Richardson, 1961;Bullard, 1972;McGrath and Weil, 1978;Winslow and Monge, 1987;Monge and León-Velarde, 1991;Connes et al, 2006;Schuler et al, 2010;Storz, 2010). Studies of humans at high altitude have suggested that the optimal Hb concentration at rest and at exercise may actually be quite close to the typical sea level value (Winslow, 1988;Villafuerte et al, 2004), or perhaps only slightly higher (Reeves and León-Velarde, 2004), and it is well documented that excessive polycythemia is a causal factor in the development of chronic mountain sickness (Winslow et al, 1985;Winslow and Monge, 1987;Monge and León-Velarde, 1991;Rivera-Ch et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Phenotypic plasticity in blood-oxygen transport in highland and lowland deer mice

Tufts

Revsbech

Cheviron

et al. 2012

SUMMARYIn vertebrates living at high altitude, arterial hypoxemia may be ameliorated by reversible changes in the oxygen-carrying capacity of the blood (regulated by erythropoiesis) and/or changes in blood-oxygen affinity (regulated by allosteric effectors of hemoglobin function). These hematological traits often differ between taxa that are native to different elevational zones, but it is often unknown whether the observed physiological differences reflect fixed, genetically based differences or environmentally induced acclimatization responses (phenotypic plasticity). Here, we report measurements of hematological traits related to blood-O 2 transport in populations of deer mice (Peromyscus maniculatus) that are native to high-and low-altitude environments. We conducted a common-garden breeding experiment to assess whether altitude-related physiological differences were attributable to developmental plasticity and/or physiological plasticity during adulthood. Under conditions prevailing in their native habitats, high-altitude deer mice from the Rocky Mountains exhibited a number of pronounced hematological differences relative to low-altitude conspecifics from the Great Plains: higher hemoglobin concentrations, higher hematocrits, higher erythrocytic concentrations of 2,3-diphosphoglycerate (an allosteric regulator of hemoglobin-oxygen affinity), lower mean corpuscular hemoglobin concentrations and smaller red blood cells. However, these differences disappeared after 6weeks of acclimation to normoxia at low altitude. The measured traits were also indistinguishable between the F 1 progeny of highland and lowland mice, indicating that there were no persistent differences in phenotype that could be attributed to developmental plasticity. These results indicate that the naturally occurring hematological differences between highland and lowland mice are environmentally induced and are largely attributable to physiological plasticity during adulthood. Supplementary material available online at