179
Chapter eight: Fasting
The assumption is that regenerating skin in warmer waters provides a net energy savings
despite the additional locomotory costs and extended fast that it requires.
Potential energetic savings can be realized through decreases in activity levels, thermoregulatory costs, and Resting Metabolic Rate (Cherel et al. 1988). Reduced physical activity will obviously lower energy use, however, the option to do so is highly dependent on
concurrent behavioral requirements. For example, baleen whales that undertake seasonal
migrations between calving and foraging grounds may experience extended fasting periods while coping with substantial locomotory costs. These migrations can be unbelievably
extensive; humpback whales (including mothers and calves) migrating from Antarctic
feeding grounds to Pacific wintering areas off the coast of Central America travel approximately 8300 km.
In some mammals, thermoregulatory costs may be curtailed by either a controlled
decrease in core body temperature, or a decrease in the defended (effective) core body
mass. Such thermoregulatory adaptations may manifest rapidly at the onset of the fast, but
there is little evidence for this among marine mammals due to their expansive insulation.
Metabolic depression is a term for the decrease in Resting Metabolic Rate (RMR)—the
total energy requirements of an inactive animal within its thermoneutral zone. It is often
cited as a common physiological adaptation to periodic food shortages among many species (Keys et al. 1950) that serves to limit rates of mass loss despite insufficient energy
intake (Guppy and Withers 1999). This strategy may be key to maximizing protein sparing during extended fasts (Henry et al. 1988), by limiting glucose consumption rates and,
therefore, catabolism of protein for gluconeogenesis. Among vertebrates, rapid depression
of RMR is often observed early in the fast, leading to a new steady state fasting level (i.e., the
amount of energy expended per kg body mass). As mass-specific RMR remains constant,
subsequent decreases in overall (or absolute) metabolic rate throughout the fast are due to
decreasing body mass. There are also indications of increasing metabolic rate toward the
end of the natural fasting period, as cell and tissues are prepared for the resumption of
foraging and digestion.
Depressed RMR can occur by at least three avenues: selective loss of metabolically
active tissue, downregulation of energetically expensive processes, and reduction of cellular metabolism. While protein catabolism and loss of lean tissue will reduce total metabolism (versus loss of metabolically inert lipids), mass-specific decreases in metabolism can
most effectively be produced by targeted catabolism of an animal’s most energy-demanding tissues. One common strategy is to shrink portions of the digestive tract, which represents a large portion of total body mass and requires continuous turnover of the cell lining,
which is relatively expensive to maintain. Fortunately, during periods of fasting, the gut
is not required and can be “restructured” when food again becomes available. The kidney
is another metabolically expensive organ. However, unlike the gut, there is no evidence
that the kidney becomes physically smaller during fasts. This is partly due to its complexity, and partly due to the fact that it is still required to process metabolic waste, and to
help maintain fluid and electrolyte homeostasis through resorption of endogenous electrolytes and body water (see Chapter 7). However, energy is saved if the level of processing
through the kidney is significantly reduced during fasts (usually measured as changes in
glomerular filtration rate), due to decreased protein turnover and increased water conservation. Metabolic depression can also occur through downregulation of cellular processes.
This hypometabolic state is not the result of major biochemical reorganization (Guppy
and Withers 1999) but results from molecular controls operating at a level “above” that of
allosteric regulation of enzymes and “below” that of gene expression. The net result is a
“coordinated inactivation of many cellular processes” (Storey and Storey 2004).
Chapter eight: Fasting
The assumption is that regenerating skin in warmer waters provides a net energy savings
despite the additional locomotory costs and extended fast that it requires.
Potential energetic savings can be realized through decreases in activity levels, thermoregulatory costs, and Resting Metabolic Rate (Cherel et al. 1988). Reduced physical activity will obviously lower energy use, however, the option to do so is highly dependent on
concurrent behavioral requirements. For example, baleen whales that undertake seasonal
migrations between calving and foraging grounds may experience extended fasting periods while coping with substantial locomotory costs. These migrations can be unbelievably
extensive; humpback whales (including mothers and calves) migrating from Antarctic
feeding grounds to Pacific wintering areas off the coast of Central America travel approximately 8300 km.
In some mammals, thermoregulatory costs may be curtailed by either a controlled
decrease in core body temperature, or a decrease in the defended (effective) core body
mass. Such thermoregulatory adaptations may manifest rapidly at the onset of the fast, but
there is little evidence for this among marine mammals due to their expansive insulation.
Metabolic depression is a term for the decrease in Resting Metabolic Rate (RMR)—the
total energy requirements of an inactive animal within its thermoneutral zone. It is often
cited as a common physiological adaptation to periodic food shortages among many species (Keys et al. 1950) that serves to limit rates of mass loss despite insufficient energy
intake (Guppy and Withers 1999). This strategy may be key to maximizing protein sparing during extended fasts (Henry et al. 1988), by limiting glucose consumption rates and,
therefore, catabolism of protein for gluconeogenesis. Among vertebrates, rapid depression
of RMR is often observed early in the fast, leading to a new steady state fasting level (i.e., the
amount of energy expended per kg body mass). As mass-specific RMR remains constant,
subsequent decreases in overall (or absolute) metabolic rate throughout the fast are due to
decreasing body mass. There are also indications of increasing metabolic rate toward the
end of the natural fasting period, as cell and tissues are prepared for the resumption of
foraging and digestion.
Depressed RMR can occur by at least three avenues: selective loss of metabolically
active tissue, downregulation of energetically expensive processes, and reduction of cellular metabolism. While protein catabolism and loss of lean tissue will reduce total metabolism (versus loss of metabolically inert lipids), mass-specific decreases in metabolism can
most effectively be produced by targeted catabolism of an animal’s most energy-demanding tissues. One common strategy is to shrink portions of the digestive tract, which represents a large portion of total body mass and requires continuous turnover of the cell lining,
which is relatively expensive to maintain. Fortunately, during periods of fasting, the gut
is not required and can be “restructured” when food again becomes available. The kidney
is another metabolically expensive organ. However, unlike the gut, there is no evidence
that the kidney becomes physically smaller during fasts. This is partly due to its complexity, and partly due to the fact that it is still required to process metabolic waste, and to
help maintain fluid and electrolyte homeostasis through resorption of endogenous electrolytes and body water (see Chapter 7). However, energy is saved if the level of processing
through the kidney is significantly reduced during fasts (usually measured as changes in
glomerular filtration rate), due to decreased protein turnover and increased water conservation. Metabolic depression can also occur through downregulation of cellular processes.
This hypometabolic state is not the result of major biochemical reorganization (Guppy
and Withers 1999) but results from molecular controls operating at a level “above” that of
allosteric regulation of enzymes and “below” that of gene expression. The net result is a
“coordinated inactivation of many cellular processes” (Storey and Storey 2004).