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Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 5

Deconditioning and physical inactivity are risk factors for atherosclerosis and cardiovascular disease. The cardiovascular impact of deconditioning is very well characterized and has been described in my previous posts. However, there are also a number of other system deficits induced by deconditioning.

Musculoskeletal system has the most obvious decline in response to deconditioning. A person can lose 10-20% of muscle strength in one week or bed rest. Thigh muscles can lose 3% of mass within seven days. Muscle loss is greatest in the lower back and weight bearing muscles of the legs.

After three days of continuous bed rest, contractures can form. This is the result of connective tissue and muscles being kept in a shortened position. After three weeks of bed rest, the connective tissue around joints changes to stabilize the joint in a shortened position.

Osteoporosis can occur in deconditioned patients. This is called “disuse osteoporosis” as it occurs because the bones are not bearing weight. When the bones are not bearing weight, the pressure of the body and gravity is not applied to the bones. This causes the bone cells to be resorbed at an abnormal rate, with liberated calcium entering the blood stream. After twelve weeks of bed rest, bone density can be almost 50% less. This effect is most pronounced in the long bones. Cartilage degeneration and osteoarthritis can also occur, along with a variety of other bone specific complications.

Frequent episodes of bed rest can also increase the risk of blood clots forming. This in turn can cause pulmonary embolism, in which a blood clot blocks one of the arteries in the lungs.

Bed rest causes a number of pulmonary concerns as well. Over time, reduced muscle strength and endurance causes less movement of the diaphragm, intercostal and abdominal muscles. Mucous becomes trapped in the airways and impaired cilia are unable to move it out. This can cause a cough and eventually develop into pneumonia.

Deconditioned patients often experienced decreased appetite, lower gastric secretion, constipation, impaired absorption and atrophy of the mucosa and glands in the GI tract. Excretion of water and salt is increased. 15-30% patients on bedrest develop kidney stones and urinary tract infection is not uncommon. Deconditioned patients have less lean body mass and develop more fat. Nitrogen metabolism becomes disordered and minerals and electrolytes are excreted more quickly than appropriate.

Frequent bed rest can compress peripheral nerves, especially the perineal and ulnar nerves. Cognition is also affected. These patients find focusing difficult and judgment and problem solving impaired. Pain threshold becomes lowered, making pain worse. Anxiety, fear and depression are more commonly found in deconditioned patients than in the general population. Sensory processing is affected, increasing the auditory threshold so that sounds must be louder to be heard correctly.

Bed rest can also affect the patient’s circadian rhythm, temperature and sweating response and provoke glucose intolerance. A number of hormones, including thyroid, adrenal and pituitary hormones, undergo altered metabolism and regulation. After two weeks of bed rest, two weeks of resumed activity is needed before glucose behavior returns to base line.



Bleeker, Michiel W.P., et al. Vascular adaptation to deconditioning and the effect of an exercise countermeasure: results of the Berlin Bed Rest study. Journal of Applied Physiology (2005); 99(4); 1293-1300.

Parsaik A., et al. Deconditioning in patients with orthostatic intolerance. Neurology 2012; 79; 1435.

Sung-Moon Jeong , Gyu-Sam Hwang , Seon-Ok Kim , Benjamin D. Levine , Rong Zhang. Dynamic cerebral autoregulation after bed rest: effects of volume loading and exercise countermeasures. Journal of Applied Physiology 2014 Vol. 116 no. 1, 24-31.