Hypoxic ventilatory response

Hypoxic ventilatory response (HVR) is the increase in ventilation induced by hypoxia that allows the body to intake and process oxygen at higher rates. It is initially elevated in lowlanders who travel to high altitude, but reduces significantly over time as people acclimatize. In biological anthropology, HVR also refers to human adaptation to environmental stresses resulting from high altitude. Hypoxic ventilatory response (HVR) is the increase in ventilation induced by hypoxia that allows the body to intake and process oxygen at higher rates. It is initially elevated in lowlanders who travel to high altitude, but reduces significantly over time as people acclimatize. In biological anthropology, HVR also refers to human adaptation to environmental stresses resulting from high altitude. In mammals, HVR invokes several physiological mechanisms. It is a direct result of the decrease in partial pressure of oxygen in arterial blood, and leads to increased ventilation. The body has different ways of coping with acute hypoxia. Mammals that rely on pulmonary ventilation will increase their ventilation to account for the lack of oxygen reaching the tissues. Mammals will also experience decreases in aerobic metabolism and oxygen demand, along with increases in ATP production. The physiological mechanisms differ in effect and in course of time. HVR is time dependent and can be divided into two phases: the first (0–5 minutes) of ventilation increase, and the second (5–20 minutes) of slow decline. The initial increase in ventilation from HVR is initiated by the carotid bodies, which are bilaterally located at the port of brain circulation. Carotid bodies contain oxygen-sensitive cells that become more active in response to hypoxia. They send input to the brainstem which is then processed by respiratory centers. Other mechanisms include hypoxia-inducible factors, particularly HIF1. Hormonal changes have also been associated with HVR, particularly those that affect the functioning of the carotid bodies. As HVR is a response to decreased oxygen availability, it shares the same environmental triggers as hypoxia. Such precursors include travelling to high altitude locations and living in an environment with high levels of carbon monoxide. Combined with climate, HVR can affect fitness and hydration. Especially for lowlanders who traverse past 6000 meters in altitude, the limit of prolonged human exposure to hypoxia, HVR may result in hyperventilation and ultimately the deterioration of the body. Oxygen consumption is reduced to a maximum of 1 liter per minute. Travelers acclimatized to high altitudes exhibit high levels of HVR, as it provides advantages such as increased oxygen intake, enhanced physical and mental performance, and lower susceptibility to illnesses associated with high altitude. Adaptations in populations living at high altitudes range from cultural to genetic, and vary among populations. For example, Tibetans living at high altitudes have a more sensitive hypoxic ventilatory response than do Andean peoples living at similar altitudes, even though both populations exhibit greater aerobic capacity compared to lowlanders. The cause of this difference is most likely genetic, although developmental factors may also contribute. The first stage of the hypoxic ventilatory response consists of the initial reaction to a hypoxic environment leading up to the peak known as short-term potentiation (STP). The process is induced by a decrease in oxygen partial pressure in blood. Type I glomus cells of carotid bodies detect the change in oxygen levels and release neurotransmitters towards the carotid sinus nerve, which in turn stimulates the brain, ultimately resulting in increased ventilation. The period of increased ventilation varies among different individuals but typically lasts under ten minutes. STP is the increase in ventilation after the acute hypoxic response and the eventual return of ventilation to its equilibrium after carotid sinus nerve stimulation, which causes a slowing in heart rate. This mechanism usually lasts between one and two minutes. STP is most apparent in tidal volume or the amplitude of phrenic neural output. STD is a temporary jump in respiratory frequency at the beginning of carotid chemo afferent stimulation or a temporary drop in respiratory frequency at the end of chemo afferent stimulation. This mechanism lasts from a span of several seconds to a few minutes. STP has only been found in the respiratory frequency of phrenic nerve stimulation, which produces contraction of the diaphragm.