Hibernation is a deeply regulated physiological state that allows certain mammals to survive periods of extreme cold and resource scarcity. This process is not merely a deep sleep but an active, controlled transition into a state of profound hypothermia and hypometabolism. The body effectively lowers its internal thermostat and suppresses nearly all major functions to conserve energy. This survival strategy involves a coordinated biological slowdown that is radically different from the uncontrolled, life-threatening hypothermia seen in non-hibernating mammals.
Acute Systemic Depression
The most immediate and apparent change upon entering torpor is the decline in core body temperature, which is actively regulated through the lowering of the thermoregulatory set point. For small hibernators, body temperature can drop from a normal range near 37°C down to just 2°C to 5°C, or even as low as -2.9°C in the Arctic ground squirrel. This controlled cooling is a pre-programmed homeostatic shift, allowing the body to defend this new, much lower temperature against further drops.
The cardiovascular system undergoes a slowdown known as bradycardia. A ground squirrel’s heart rate, which is normally around 200 to 400 beats per minute (BPM) during its active state, plummets to a mere 3 to 10 BPM during deep torpor. This reduction in heart rate significantly lowers the pressure and output of the circulatory system. The body must manage the resulting increase in blood viscosity at cold temperatures to prevent clotting, a challenge that non-hibernators cannot tolerate.
Respiration enters a state of bradypnea and periodic apnea. The breathing rate can fall from an active rate of over 100 breaths per minute down to just 4 to 6 breaths per minute. Some species exhibit long periods of apnea, where breathing ceases for several minutes at a time. This drastically reduced ventilation matches the body’s minimal oxygen demand, limiting the work of the respiratory muscles.
Metabolic Rate Reduction and Fuel Dynamics
The systemic slowdown is a consequence of metabolic suppression. The metabolic rate is reduced by 95% to 98% compared to the active state, meaning an animal can survive for months on its stored reserves. While the effect of cold temperature (known as the Q10 effect) naturally slows biochemical reactions, hibernation involves an active, temperature-independent suppression of metabolism that begins before the body temperature drops significantly.
The body achieves this suppression by down-regulating energy-intensive processes like transcription and translation, effectively putting cell maintenance on hold. This involves mechanisms like the regulated inhibition of mitochondrial respiration. For instance, the activity of key energy consumers like the \(\text{Na}^+-\text{K}^+-\text{ATPase}\) pump is significantly suppressed.
The body also executes a shift in its primary fuel source. Hibernators rely predominantly on lipid (fat) metabolism, moving away from carbohydrates. Lipids are ideal because they have a high energy density and, crucially, their breakdown produces metabolic water, which helps prevent dehydration over extended periods of inactivity. This shift is regulated by upregulating enzymes like pyruvate dehydrogenase kinase isoenzyme 4 (\(\text{PDK}4\)), which effectively suppresses the use of glucose and channels the body toward fatty acid oxidation.
The hibernation period is punctuated by periodic arousals, where the animal rapidly raises its body temperature back to a near-normal level of approximately \(37^\circ\text{C}\). This rapid rewarming requires a burst of metabolic activity, often exceeding the peak metabolic rate of an active animal. Heat is generated through non-shivering thermogenesis, primarily by brown adipose tissue (BAT), which is densely packed with mitochondria. During the initial, rapid phase of arousal, the body temporarily shifts back toward carbohydrate and glycerol metabolism because these fuels are more efficient under the limited oxygen supply of the rapidly rewarming tissues, before returning to fat-based metabolism once fully aroused.
Adaptive Cellular and Molecular Protection
To survive the cycles of extreme cold, low oxygen, and reduced blood flow, hibernators possess cellular and molecular safeguards. The brain, which is vulnerable to ischemia-reperfusion injury, is protected by a state of neuroprotection. This involves changes in gene expression that stabilize neuronal membranes and prevent the build-up of oxidative stress.
Despite months of complete inactivity, hibernating mammals exhibit resistance to muscle atrophy. They achieve this by regulating protein turnover and reducing the breakdown of muscle proteins. This mechanism often involves the suppression of catabolic pathways and the modulation of factors like myostatin, a negative regulator of muscle growth, which allows them to maintain muscle mass and function.
Hibernators alter the lipid composition of their cell membranes, increasing the proportion of polyunsaturated fatty acids to maintain membrane fluidity and prevent rigidification in the cold. Specialized enzyme systems are either selectively maintained or modified to function efficiently at low temperatures.
The immune system is managed throughout the hibernation cycle. While many immune functions are temporarily suppressed during the deep torpor phase, a restoration of immune activity occurs during the periodic arousal bouts. This restoration allows the animal to repair cellular damage and fight off potential infections before re-entering the hypometabolic state.