Supplements
A component of sarcopenia is the loss of ability for aging skeletal muscle to respond to anabolic stimuli such as amino acids, especially at lower concentrations. However, aging muscle retains the ability of an anabolic response to protein or amino acids at larger doses. Supplementation with larger doses of amino acids, particularly leucine has been reported to counteract muscle loss with aging. Exercise may work synergistically with amino acid supplementation.β-hydroxy β-methylbutyrate (HMB) is a metabolite of leucine that acts as a signalling molecule to stimulate protein synthesis. It is reported to have multiple targets, including stimulating mTOR and decreasing proteasome expression. Its use to prevent the loss of lean body mass in older adults is consistently supported in clinical trials. More research is needed to determine the precise effects of HMB on muscle strength and function in this age group. Epidemiology
The prevalence of sarcopenia depends on the definition used in each epidemiological study. Estimated prevalence in people between the ages of 60-70 is 5-13% and increases to 11-50% in people more than 80 years of age. This equates to >50 million people and is projected to affect >200 million in the next 40 years given the rising population of older adults. Public health impact
Sarcopenia is emerging as a major public health concern given the increased longevity of industrialized populations and growing geriatric population. Sarcopenia is a predictor of many adverse outcomes including increased disability, falls and mortality. Immobility or bed rest in populations predisposed to sarcopenia can cause dramatic impact on functional outcomes.
The most common causes are (in no particular order) infections, interstitial lung disease, and pulmonary oedema. Diagnosis
Type 1
Type 1 respiratory failure is defined as a low level of oxygen in the blood (hypoxemia) with either a standard (normocapnia) or low (hypocapnia) level of carbon dioxide (PaCO2) but not an increased level (hypercapnia). It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. The fundamental defect in type 1 respiratory failure is a failure of oxygenation characterized by:

This type of respiratory failure is caused by conditions that affect oxygenation, such as:

Low ambient oxygen (e.g. at high altitude)
Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism)
Alveolar hypoventilation (decreased minute volume due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease); this form can also cause type 2 respiratory failure if severe. Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia or ARDS)
Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt)

Type 2
Hypoxemia (PaO2 <8kPa or normal) with hypercapnia (PaCO2 >6.0kPa). The basic defect in type 2 respiratory failure is characterized by:

Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the buildup of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be eliminated.