Having discussed metabolism in an evolutionary context, the collection moves on to address metabolic demands in a variety of circumstances. Considering the energetic costs of communication, Philip Stoddard from Florida International University, USA and Vielka Salazar from Cape Breton University, Canada describe how some animals invest little in signalling while others expend more of their energy budget on signalling than on the rest of their energy demands. Focusing on gymnotiform electric fish (p. 200), the duo explain that the fish can rapidly modulate signal power in response to social conditions and say that ‘territorial or sexually selected species may be under selective pressure to boost signal power’. Males expend more energy than females on both signal production and cellular metabolism, but the more a male spends on signals, the less he spends on cellular metabolism. This apparent trade-off suggests that males are up against an intrinsic limit on total metabolic output.
Moving on to consider human energy budgets, Ted Garland and colleagues from various US institutes and The Netherlands discuss potential ways of increasing our activity to combat the modern obesity epidemic (p. 206). Recommending that we spend less time in sedentary activities, such as watching television, Garland considers the lessons that we can learn about the physiological effects of activity from mice that have been selectively bred for voluntary exercise. Explaining that the brain's endocannabinoid system may play an important role in the control of voluntary activity in mice, Garland and his colleagues warn that, in addition to adjusting our activity levels, we may have to alter our eating habits too, as ‘energy expenditure is not necessarily tightly coupled to energy intake during relatively short-term exposure’.
While the energy budgets of obese humans are tipped so that they expend significantly less energy than they ingest, many other creatures' metabolic outputs are routinely stretched to the limit. But what imposes this limit? This is the question that has intrigued John Speakman at the University of Aberdeen, UK for much of the past decade. Working on mice, Speakman explains that the period when a lactating mother feeds her young is one of the most intense and sustained periods of metabolic output that any creature can endure. With Elzbieta Król, he tested whether the mothers were peripherally limited (by the sum of the maximum energetic outputs of all tissues) or limited by the amount of heat that they can dissipate (p. 230). Shaving the lactating mice, the duo found that the limit that had prevented the mothers from increasing their metabolic output beyond a certain level had risen, suggesting that the mother's ability to dissipate heat limited the amount of energy that she could expend. Speakman and Król say, ‘the heat dissipation limit and peripheral limitations are likely to be important to all animals, but to different extents’.
Another factor that contributes to energy budgets is the production of metabolic heat through nonshivering thermogenesis. During World War II, mice were found to adapt to life in cold rooms. Brown fat was later identified as the source of nonshivering thermogenesis, which allowed the rodents to survive in the cold without shivering. Barbara Cannon and Jan Nedergaard from Stockholm University, Sweden explain that a mitochondrial protein, uncoupling protein 1 (UCP1), is the thermogenic protein (p. 242) that produces heat by discharging the mitochondrial proton gradient. Also, high fat diets trigger nonshivering thermogenesis, leading to the suggestion that the rodents could use brown fat to ‘combust excess energy in the diet and thus not become obese’. More recently, the discovery that adult humans have brown fat has led to an increased interest in the role of nonshiverng thermogenesis in human metabolism and obesity. However, the duo raise concerns about the conclusions drawn from animal studies that are routinely conducted at temperatures below the animal's thermoneutral zone; i.e. at temperatures where diet-induced thermogenesis would not be revealed due to thermoregulatory thermogenesis. They recommend that future studies be conducted at the animals' thermoneutral temperatures (29–30°C) in order to ‘identify agents and genes important for human energy balance’.