A decreased respiratory drive can also be the result of metabolic alkalosis, a state of decreased carbon dioxide in the blood
Central sleep apnea. During sleep, the breathing centers of the brain can pause their activity, leading to prolonged periods of apnea with potentially serious consequences. Hyperventilation followed by prolonged breath-holding. This hyperventilation, attempted by some swimmers, reduces the amount of carbon dioxide in the lungs. This reduces the urge to breathe. However, it also means that falling blood oxygen levels are not sensed, and can result in hypoxemia. Physical states
A variety of conditions that physically limit airflow can lead to hypoxemia. Suffocation, including temporary interruption or cessation of breathing as in obstructive sleep apnea, or bedclothes may interfere with breathing in infants, a putative cause of SIDS. Structural deformities of the chest, such as scoliosis and kyphosis, which can restrict breathing and lead to hypoxia. Muscle weakness, which may limit the ability of the diaphragm, the primary muscle for drawing new air into lungs, to function. This may be a result of a congenital disease, such as motor neuron disease, or an acquired condition, such as fatigue in severe cases of COPD. Environmental oxygen
In conditions where the proportion of oxygen in the air is low, or when the partial pressure of oxygen has decreased, less oxygen is present in the alveoli of the lungs. The alveolar oxygen is transferred to hemoglobin, a carrier protein inside red blood cells, with an efficiency that decreases with the partial pressure of oxygen in the air. Altitude.
Exercise
Exercise-induced arterial hypoxemia occurs during exercise when a trained individual exhibits an arterial oxygen saturation below 93%. It occurs in fit, healthy individuals of varying ages and genders. Adaptations due to training include an increased cardiac output from cardiac hypertrophy, improved venous return, and metabolic vasodilation of muscles, and an increased VO2 max. There must be a corresponding increase in VCO2 thus a necessity to clear the carbon dioxide to prevent a metabolic acidosis. Hypoxemia occurs in these individuals due to increased pulmonary blood flow causing:

Reduced capillary transit time due to an increased blood flow within the pulmonary capillary. Capillary transit time (tc), at rest is around 0.8s, allowing plenty of time for the diffusion of oxygen into the circulation and the diffusion of CO2 out of the circulation. After training, the capillary volume is still the same however cardiac output is increased, resulting in a decreased capillary transit time, reducing to around 0.16s in trained individuals at maximal work rates. This does not give sufficient time for gas diffusion and results in a hypoxemia. Intrapulmonary arteriovenous shunts are dormant capillaries within the lungs that become recruited when venous pressures become too high. They are normally located within deadspace area where gas diffusion does not occur, thus the blood passing through does not become oxygenated resulting in a hypoxemia.