Comprising up to 50% of most species' body mass, skeletal muscle is the largest organ in many creatures' bodies. Skeletal muscle also consumes a significant proportion of the body's metabolic budget. Every tissue's metabolic rate is dramatically affected by changes in temperature, which makes metabolic adaptation in skeletal muscle especially important for creatures whose body temperatures are dictated by their environment. The review by Hans-Otto Pörtner describes functional adaptations of fish muscle to icy polar waters (p. 2217). Both Arctic and Antarctic species have compensated for their reduced aerobic function by packing their muscle tissue with mitochondria and lipid fuel at the expense of fewer contractile elements into each muscle cell. But Antarctic species, which only survive a very narrow range of temperatures, have also reduced their oxygen demand by reducing their mitochondrial metabolic rate.

Fish that face seasonal temperature variations have to adapt over a much shorter time frame than their polar relatives. Carp survive equally well in temperate and near-freezing waters as the seasons change. By looking at the ATPase activity of the myosin component of muscle from fish that were acclimated to both warm and cold temperatures, Shugo Watabe explains that the muscles from cold carp switch to a conformationally flexible form of myosin,which maintains muscle performance even at low temperatures(p. 2231). But altered protein expression patterns aren't the only approach to altering muscle function at the cellular level. Helge Guderley and Julie St-Pierre explain that when the going gets cold, ectotherms have two choices. They either become less active,to conserve energy, or they lower their metabolic rate. By taking a close look at mitochondria from ectothermal fish muscle, Guderley and St-Pierre agree with many of Pörtner's assessments about cold adapted muscle, but add that the mitochondria of fish with low metabolic rates have improved their efficiency by dropping the proton leakage rate(p. 2237).

Many muscles generate heat, either by shivering or running the mitochondria backwards. Heat generation has probably been a major selective pressure on many muscles, but in Steve Katz's review, he explains that the heater muscles developed by some ectothermic fish might not have evolved specifically to generate warmth (p. 2251). In Katz's words It may be that heterothermy really is nothing more than a happy accident after all.'

How hummingbirds keep warm is another intriguing question, because they lack brown fat, which most mammals use to generate heat. The mitochondria in mammalian brown fat generate heat by switching from being net ATP producers to net ATP consumers, through a class of protein called the uncoupling proteins(UCP). Eduardo Bicudo describes how the tiny birds probably maintain their body temperature by generating heat with their skeletal muscle mitochondria(p. 2267). He has evidence that the mitochondria in hummingbird muscle express an uncoupling protein,UCP1, which he believes contributes to the muscle's role as a thermogenic organ.

Although UCP1 is involved in heat production, it's less clear how other uncoupling proteins affect metabolism. Patrick Schrauwen describes a UCP homologue, UCP3, found in human skeletal muscle. At times when energy conservation is essential because food is scarce, the levels of proteins that leak protons across the mitochondrial inner membrane should drop, but he finds increased levels of UCP3. He believes that UCP2 and UCP3 don't contribute to metabolic regulation, but they are implicated in disorders such as obesity and diabetes (p. 2275). Hoppeler adds that with the recent increase in the incidence of metabolic disorders, it is clear that the body's largest metabolic organ plays the major part in diseases caused by inactivity. Understanding how muscle interacts with other aspects of our physiology is a major goal if we are to combat the present epidemic of inactivity related disease.

Hibernation and inactivity pose a different set of challenges to skeletal muscle. Frogs that pass the winter in cold, hypoxic water turn down their aerobic respiration largely through metabolic suppression in their skeletal muscle. Bob Boutilier turned to mitochondria in hibernating frogs to find out how the dormant amphibians conserve ATP and lower metabolic costs. Working with Julie St-Pierre, they analysed how mitochondrial function responded to hibernation and found that many key mitochondrial enzymes had a lower activity than the mitochondria of active summer frogs(p. 2287). As well as conserving ATP, Australian frogs that aestivate in mud baked hard by the desert sun, somehow protect their muscles from wasting during the long months in their rocky tomb, ready to begin moving as soon as the rains arrive. These amphibians downregulate their metabolic rate while they are inactive, and Nick Hudson believes that this in turn protects the frog's muscles from wasting during their long wait (p. 2297).

Having discussed muscle from every possible perspective, Ian Johnston returns to locomotion to conclude the collection, discussing the relationship between thermal plasticity and locomotory performance in species that experience continual temperature fluctuations(p. 2305). Johnston explains that although he doesn't find any simple relationships between whole-animal performance and muscle phenotype', he points out that the extent of muscle plasticity is also dependent on developmental state. He finds that some species' juvenile and adult tissues respond differently to a single stimulus,suggesting that muscle signal transduction pathways also change at different stages of development, adding another tier to muscles phenomenally plastic properties.