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Effects of bedrest 3: musculoskeletal and immune systems, skin and self-perception


Exploring what happens to the musculoskeletal and immune systems, skin and self-perception in patients confined to bed, and what nurses should look out for

This article has been updated

The evidence in this article is no longer current

  • Click here for an updated and expanded article on the immune system
  • Click here for an updated and expanded article on the muscles, joints and mobility
  • Click here for an updated and expanded article on bones, skin and self-perception


This is the third article in the series exploring the adverse effects of prolonged bedrest and immobility. In this final article, the effects on the musculoskeletal and immune systems, skin and self perception are examined.

Citation: Nigam Y et al (2009) Effects of bedrest 3: musculoskeletal and immune systems, and skin. Nursing Times; 105; 23, early online publication.

Authors: John Knight, Yamni Nigam and Aled Jones are lecturers, School of Health Science, Swansea University.

  • This article has been double-blind peer-reviewed


Bedrest is often necessary for healing injured or diseased parts of the body. However, it is now well established that extensive periods of bedrest can cause harm to the rest of the body.

The most obvious effects of long periods of immobility are seen in the musculoskeletal system, with the loss of muscle strength and endurance, and bone weakening. Bones undergo a progressive loss in mass through a condition known as disuse osteoporosis.

Immobility is also linked with altered skin integrity and can affect the immune system.

The musculoskeletal system

The musculoskeletal system (with the help of the central nervous system) provides mobility and the ability to carry out normal daily activities. Any muscle weakness or joint and bone stiffness through immobility or disuse has an impact on these functions and may also increase the risk of injury or infection.


Disuse of the muscles leads to atrophy and a loss of muscle strength at a rate of around 12% a week (Jiricka, 2008). After 3–5 weeks of bedrest, almost half the normal strength of a muscle is lost.

Skeletal, voluntary muscle mainly consists of two types of fibres – slow-twitch (type 1) and fast-twitch (type 2).

Slow-twitch fibres contract slowly and produce large amounts of energy to enable them to keep going for a long time. They also house large amounts of myoglobin (a protein that stores oxygen) and contain numerous blood capillaries and mitochondria, which make them very resistant to fatigue.

These fibres are predominantly found in the muscles of the neck and back where they help to maintain posture. They are also abundant in the soleus muscle of the lower leg and aid endurance activities such as long-distance running.

Fast-twitch muscle fibres contract quickly but rapidly get tired. They contain little myoglobin and relatively few mitochondria. Found in large numbers in the muscles of the arm these fibres are perfectly adapted for rapid movements but consume lots of energy. Since they are not able to generate sufficient energy for a continuous supply of adenosine triphosphate (ATP), they tire easily.

Long periods of immobility have different effects on these two types of muscle fibres. Studies have been conflicting on whether one type atrophies faster than the other (Topp et al, 2002; Kannus et al, 1998). However, it is known that fibre atrophy occurs and leads quickly to a loss of strength and mass in the postural muscles of the back, legs and arms.

In elite athletes, inactivity after injury or immobilisation rapidly affects the size and aerobic capacity of both fibre types. In endurance athletes, type 1 fibres are mainly affected, while in sprinters it is the type 2 fibres that atrophy (Lorenz and Campello, 2001).

Atrophy can occur after only a short period of immobility. One study found that 72 hours of limb immobilisation can cause atrophy of type 1 and type 2 fibres by 14% and 17% respectively (Lindboe and Platou, 1984). It appears that the larger and better trained the muscle, the faster the loss of muscle strength, and the quicker the deconditioning process (Jiricka, 2008).

The first muscles to become weak are those in the lower limbs that normally resist gravitational forces in the upright position. Skeletal muscles lose tone when the feet no longer bear weight.

This stiffening and shrivelling of muscles leads to a dramatic reduction in muscle mass and this, along with loss of fat, may be responsible for the weight loss that sometimes accompanies bedrest.

In general, extensor muscles (such as the quadriceps femoris at the front of the thigh), which have a prime postural role, atrophy to a greater extent than flexor muscles (such as hamstrings).

When muscles are immobilised, they shorten. A programme of immediate or early motion may prevent muscle atrophy. However, atrophy of the quadriceps muscle (which occurs through the forced immobility of a rigid plaster cast) cannot be reversed through the use of isometric exercises (where joint angle and muscle length do not change) (Lorenz and Campello, 2001).

The number of sarcomeres (muscle filaments) decreases when muscles are kept in a shortened position. The extent of atrophy is significantly increased if the muscle is kept in the contracted position.

The reduced oxidative capacity of the mitochondria means that muscles tire more easily, and increased muscle fatigue is associated with reduced muscle blood flow and red cell volume. The activity of oxidative enzymes falls, leading to a drop in the extraction of oxygen by the muscle.

Dietrich (2000) showed that immobilisation of the elbow joint for five weeks caused a 35–41% reduction in elbow extension strength. After five weeks of strict bedrest, Gogia et al (1988) found that muscles showed a remarkable decrease in strength (Fig 1).

It takes about four weeks to recover from atrophy caused by immobility – a slower process than recovery from direct muscle trauma (Halar, 1994). Disuse weakness is reversed at a rate of only 6% per week with exercise.

Complete rest will also result in decreased endurance levels through reduced muscle strength, metabolic activity and circulation. This can cause a sense of fatigue, affecting the patient’s motivation and leading to a vicious cycle of greater inactivity (Dittmer and Teasell, 1993). In stroke paralysis or in patients whose limbs are immobilised by splinting, muscles atrophy by around 30–40%.

Totally degenerated muscles, for example in patients with peripheral nerve injury, can lose as much as 95% of their bulk, and muscle fibres are permanently replaced by fat and connective tissue.

In a study of six male patients, researchers found that, after 14 days of bedrest, there was a decrease in leg and whole body lean mass (Ferrando et al, 1996). Measurements showed that this was because of a 50% drop in muscle protein synthesis.

Muscle wasting is caused by an imbalance between protein synthesis and breakdown. Muscle atrophy is reflected in increased nitrogen in the urine, and the muscle breakdown that accompanies enforced bedrest can yield as much as 8g of protein loss per day (Seregin et al, 1964). Muscle wasting is also generally associated with increased plasma concentrations of the stress hormone cortisol.

Fitts et al (2007) showed that the negative effects of bedrest on human skeletal muscle fibres were ameliorated by dietary protein supplementation. The same study also showed that simulating an increase in levels of plasma cortisol to mimic the levels reached in a patient in hospital, caused an increase in muscle protein catabolism so breakdown exceeded synthesis. This caused greater atrophy and loss of force in the muscle fibres tested.

The physiological changes in neural control also contribute to the deterioration of muscle strength and endurance. Motor unit recruitment (the progressive activation of a muscle by successive recruitment of contractile units) is diminished, as is the ability to activate all motor units during contractions in inactive patients.

Changes in electrical activity in the muscles and a decrease in the strength of the neuromuscular junction have also been reported, explaining further the fatigue seen in disused muscles. Decreased levels of ATP and glycogen stores, and a reduced ability of the muscles to immobilise fatty acids, are also seen.

Disuse of muscle may also have detrimental effects on neuromuscular function. The loss of muscle strength is often greater than the degree of atrophy. This may also be due to an inability to recruit the motor unit properly – in essence the body ‘forgets’ how to properly coordinate motor function.

Backache and fatigue during convalescence are often due to disuse atrophy of underlying muscles rather than the disease or disorder resulting in the bedrest. Postural and locomotive muscles lose their tension-generating capacity, and paraspinal and abdominal muscles become weak if not used.

The upper extremities may escape significant atrophy if self-care activities are continued.

Connective tissue

Tendons, ligaments and articular cartilage require motion to stay healthy and will therefore undergo changes when patients are immobile.

Changes in the structure and function of connective tissue become apparent four to six days after immobility begins and these changes remain even after normal activity has been resumed. Most of these changes are due to altered structure of collagen fibres.

Tendons are stiff fibres connecting muscle onto bone. About 20 days of bedrest reduces the stiffness of tendons and increases their viscosity (Kubo et al, 2003). This affects transmission from muscle fibres to bone and reduces the ability to produce dynamic force, resulting in a weaker and more exhausted patient.

Ligament complexes are affected biomechanically, biochemically and morphologically by immobility. Experiments show that ligament stiffness and load-bearing ability drop to 69% and 61% below normal respectively, and that ligaments do not return to normal after one year (Zarrins, 1982).


Any decrease from the normal range in parts of the body responsible for motion – for example joints, ligaments, tendons and related muscles – is known as a contracture (Montague et al, 2005). It can be transient, such as morning stiffness after eight hours of sleep in a curled-up position, which can be easily corrected by stretching in the opposite direction.

However, 2–3 weeks of immobilisation will produce a much firmer contracture, and this is a frequent complication of bedrest. Muscle atrophy plays a part in the development of contractures because of the abnormal shortening and weakening of the muscle.

Contractures can develop over joints, often when there is an imbalance in the muscle strength of opposing muscle groups.

If allowed to progress, a contracture may go on to involve the muscles, tendons, ligaments and joint capsule, causing a stiff joint, limited in its full use and range of motion. An example is contracture of the knee after plaster immobilisation to treat a fractured tibia.

The basic component of connective tissue is the protein collagen, which is arranged in fibres. In areas that move frequently, the fibres are in a loosely coiled arrangement that permits normal stretching and activity. Immobilisation causes them to change into a mass of shortened, straightened and more densely packed fibres (Corcoran, 1991), and these changes can occur after less than one day. In 2–3 weeks a firmer contracture develops. After 2–3 months of immobility, surgical correction may be needed.

Immobility can cause a fibro-fatty infiltration of joints that can develop into strong adhesions and destroy cartilage. In peri-articular connective tissue, increased cross-linking between existing collagen and new abnormal type 1 collagen deposited in the matrix adds to contracture formation.

A common problem associated with bedrest and immobility is foot drop contracture deformity, which results in the inability to place the heel on the ground, or to raise the foot at the ankle. The commonest cause is entrapment of the common peroneal nerve at the neck of fibula at the top of the calf. Improper positioning, infrequent passive exercise or inadequate support produce a shortening of the Achilles tendon (Springhouse, 2006). The condition presents a limp-like, weak foot that causes difficulty in walking. Once a patient regains mobility, the shortened Achilles tendon can be put under undue strain and may rupture.

Contractures may be prevented through proper positioning and body alignment, and the use of straps and supports. Carrying each joint through its full range of motion at least once every eight hours is the key to prevention.


The primary function of bone is mechanical support for body tissues and muscles, and to maintain mineral homeostasis by providing a reservoir of calcium, phosphorous and magnesium salts (Marieb, 2008).

In the skeleton, most of the calcium and phosphorus are present as crystals of hydroxyapatite, the deposition and orientation of which are influenced by mechanical stresses on the bone (Montague et al, 2005). When there is little force acting on the body for any length of time, a drastic reduction in the mineral content of bone tissue is seen, leading to a fall in bone density and reduced strength. This is known as disuse osteoporosis.

Maintaining normal bone function depends on two types of cells: osteoblasts, which are responsible for building the osseous matrix of bone, and osteoclasts, which break down existing bone matrix. Bone is a dynamic tissue, and in normal levels of health and activity a constant equilibrium of bone formation and reabsorption is reached.

Osteoblasts rely on the stress of mobility and weight bearing to perform their function. During immobility and bedrest, the process of building new bone stops, but the osteoclasts still break down bone, resulting in a loss of bone density, leaving the bone structure soft and weak. Even ordinary forces such as those encountered during wheelchair transfers, physical therapy activities or minor falls may cause fractures (Corcoran, 1991).

Alarmingly, the mineral content of bone tissue can change so that the rate of calcium loss from bone begins to exceed the rest of deposition (Corcoron,1991). In just a few days of bedrest, plasma calcium levels rise and, by the third day, there are measureable increases in urinary losses of calcium. If immobility continues, this can lead to the formation of calcium-containing kidney stones (urolithiasis).

A diet high in calcium will not improve bone uptake of calcium – instead, it will add to the excess calcium already excreted in the urine. In some, calcium will be deposited in soft tissues (a condition called heterotopic calcification or myositis ossificans). This can occur in muscles, vessel walls or cardiac valves, where it may interfere with joint or muscle function, or even affect cardiovascular function.

Calcium clearance is 4–6 times higher than normal within three weeks of total immobilisation. Hypercalcaemia can develop, affecting neurones and smooth muscle. Anorexia, nausea and vomiting may occur.

Bone is generally classified into two types: cortical bone, also known as compact bone; and trabecular bone, also known as spongy bone. Cortical bone is dense and is found in the shaft of long bones. Trabecular bone is much more porous and is found in the end of long bones, in vertebrae and in flat bones such as the pelvis.

During immobility, both cortical and trabecular bone are lost. Since the loss is predominantly of trabecular bone it occurs mainly in weight-bearing bones such as the vertebrae, the long bones of the legs, the heels and wrists. Bone mineral density of the vertebral column decreases by about 1% per week of bedrest, nearly 50 times that of normal age-related bone loss.

With bedrest, patients develop soft spongy bones that can easily compress, become deformed or fracture. People with disuse osteoporosis experience pain when they begin weight-bearing activities again.

Between 24% and 40% of the mass of the heel bone is lost during 36 weeks of bedrest (Bortz, 1984). Lost bone mass is not regained for some weeks after muscle mass and strength have returned to normal, and this adds to the risk of fracture (Bloomfield, 1997).

Early mobility and physiotherapy are essential to prevent disuse osteoporosis. In postmenopausal women, bone loss is particularly rapid in the femoral neck, increasing the risk of fracture (Milton and Riggs, 1983).


The skin protects underlying muscles, bones and internal organs, as well as being involved in temperature regulation and sensation.

Immobility is the factor most likely to put an individual at risk of altered skin integrity (Wilkinson, 2000).

Normally, to relieve discomfort, individuals automatically shift their weight off pressure areas every few minutes, even during sleep. However, immobile patients or those with decreased sensation cannot do this, resulting in prolonged pressure on skin capillaries and, ultimately, the death of skin tissue.

The only areas of the body where skin is designed to bear weight are the soles of the feet. However, during bed rest, a large surface area of skin bears weight and is in constant contact with the bed.

Areas where skin is stretched tautly over bony prominences are at the highest risk of breakdown. Here, the possibility of ischaemia is at its greatest because skin capillaries are compressed between the bone and a hard surface such as a bed or chair (Gulanick and Myers, 2006). Impaired flow of lymph and blood causes ischaemic lesions commonly known as pressure ulcers.

Prolonged pressure (greater than capillary pressure of 32mmHg) can result in ischaemia and necrosis of underlying tissues. The longer the duration and the greater the magnitude of pressure, the higher the chance of developing a pressure ulcer. Microscopic changes to skin tissue have been observed with pressures of 70mmHg after only two hours.

Repositioning a recumbent patient in bed will cause additional forces of friction and shear, pulling weakened skin over muscles and bony ridges. Also, skin next to bed sheets perspires, leading to moist bed linen and creating an ideal environment for bacterial reproduction (Rubin, 1988).

Pressure ulcers occur most in immobilised older patients, people in critical care settings and those with spinal cord injuries. One study reported pressure ulcers in 25–80% of patients with spinal cord injuries, with resulting complications accounting for up to 8% of deaths in this group (Dittmer and Teasell, 1993). The prevalence of pressure ulcers increases significantly with age – 70% occur in patients older than, who can acquire them within two weeks of admission to hospital (Dittmer and Teasell, 1993).

About 95% of all pressure ulcers occur at five sites: the sacrum, ischial tuberosity, greater trochanters, heels and ankles (Fig 2). They tend to occur mainly on the sacrum and heels in supine patients, and on the ischial tuberosity in sitting or reclining patients.

Prevention is better than cure for pressure ulcers and can be done by frequent position change, meticulous skin care, early assessment of risk factors, and careful, continuous observation.

To alleviate pressure, relieving devices and interventions such as air-fluidised beds or alternating pressure air mattresses may help, but turning the patient every two hours is a safe and simple measure.

Egg-crate foam mattresses and protective foot cradles provide additional protection, but getting the patient out of bed and as mobile as possible is the best prevention for pressure ulcers.

The immune system

Changes in immune responses have been reported after bedrest, and, although most studies have focused on conditions facing astronauts during space flight, there is overlap in the immune response of astronauts and those of patients exposed to prolonged bedrest.

One of the most significant findings concerns the reactivation of latent viruses. A study by Sonnenfeld et al (2007) found that the Epstein-Barr virus was reactivated in subjects exposed to a 60-day bedrest, with a dramatically increased viral load. Maintenance of viral latency is largely determined by the patient’s immune status, and numerous studies relate viral reactivation to an immunocompromised or immunosuppressed state.

The other major effect of bedrest on the immune system appears to be on the production of cytokines. These chemical messengers regulate the immune response in various ways, including stimulating the production of immune cells (leucocytes) or mediating inflammation.

The production of interleukins (IL) seems to be most affected by bedrest. A decrease in the production of IL-2 (responsible for growth, proliferation and activation of T and B lymphocytes and natural killer cells) has been found in patients confined to bed, which may contribute to lower levels of immunity. Increased levels of IL-1β have also been reported. This is a pro-inflammatory messenger and it may also be involved in bone mineral loss.

Also, there are some reports of a significant decrease in the level of circulating plasma antibodies (Craven and Hirnle, 2008; Shearer et al, 2009.

If prolonged bedrest itself is a major cause of reduced immunity, this has yet to be scientifically determined. There is still a considerable lack of research on this area.

The perception of ‘self’

Immobility and the associated changes in body composition described above can also affect the self-concept of patients. The self is one of the central concepts in psychology and self-concept is described as a stable set of beliefs about one’s qualities and attributes (Taylor, 1999).

Related to this is self-esteem, which refers to the feeling of self-worth, and is a central component of psychological well-being (Walker et al, 2007).

Self-concept and self-esteem are made up of a person’s body image, achievement, social functioning and self-identification.

Although levels of self-esteem and self-concept are relatively stable within people, particular events such as sudden or chronic illness can produce drastic changes. Prolonged bedrest, which causes both a decrease in body function and altered appearance, can lead to patients having to re-evaluate their physical self.

Studies of hospitalised patients indicate that body image plummets during illness (Taylor, 1999). It can affect:

  • The achieving self – prolonged bedrest threatens valued aspects of achievement through work or hobbies. Many people draw satisfaction from their jobs and interests, and this sense of satisfaction is potentially threatened if they are unable to do them;
  • The social self – interactions with friends and family can be a vital source of self-esteem and emotional support. A breakdown in this support system can have unhelpful consequences for the patient’s sense of identity within a family or other social network;
  • The private self – bedrest creates a dependency on others and the resulting loss of independence and the strain of imposing on others can be a major threat to the private self.


The three articles in this series have covered the effects of bedrest and immobility on the various organs and systems of the body. Exploring just how detrimental immobility can be on the body’s systems should dispel the notion that bedrest may be a favourable choice. Although bedrest is still a chosen and perhaps necessary intervention in many cases, as soon as a patient is ready, the resumption of even minor activity and movement is in their best interest.

Key points

  • Immobilisation may lead to atrophy of muscle and associated structures, leading to a loss in muscle strength and endurance
  • Patients who are confined to bed are prone to contractures and loss of bone mass, with accompanying disuse osteoporosis
  • Patients subject to prolonged bedrest may suffer from impaired skin integrity, resulting in the development of pressure sores
  • Prolonged bedrest may damage aspects of self-perception and body image

Readers' comments (2)

  • How do we explain bears who hibernate for long periods without any harmful effects?

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  • Nice work.....I have enjoyed going through your papers.

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