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Sidestepping Sarcopenia: Avoiding the Loss of Muscle Mass

From early middle age on, most of us lose muscle mass. It’s not inevitable – a very physically active lifestyle can delay or prevent this – but people who are physically inactive lose up to 5% of their muscle mass per decade from age 30.

Publisert: 09.04.2015 - Endret: 09.04.2015

This age-related loss of muscle mass, known as sarcopenia, affects over 20% of 60-70 year-olds and half of those over age 75. As numbers of elderly folk increase, the socio-economic costs of ill health caused by sarcopenia have become very significant. The most recent (2004) survey of US costs put them as high as $26 billion per year (Janssen et al ’04). In 2008 the Centers for Disease Control named sarcopenia as one of the top five biggest health risks facing the US population. The EU has adopted a similar position.

Sarcopenia patients offer suffer from other related medical conditions. When the loss of muscle mass has led to a loss of mobility and appetite, osteoporosis and general wasting often co-present as the so-called “frailty syndrome.” If calorie intake has been preserved, sarcopenia generally presents with obesity (‘sarcobesity’) and with diabetes (‘metobesity’).

This explains why sarcopenia is associated not only with the falls that cause fractures, but also with complications of diabetes, including a raised risk of vascular disease, heart attacks, strokes, blindness, liver and kidney disease and a range of gastrointestinal cancers. In short, sarcopenia contributes to the entire ageing process, and in the process inflicts a substantial burden of morbidity and mortality (Parr et al ’13).

Sarcopenia is at the center of all these diseases because muscle is not just a way of moving our bodies. It is also a highly important metabolic organ, and is critically involved in blood glucose control and plasma lipid profiles.

For example, when we consume carbohydrates and insulin kicks in, some glucose is taken up by the liver and stored as glycogen. In a fit and physically active person, the bulk of blood glucose is taken up and used as fuel in the skeletal muscles. If muscle mass has fallen, the capacity of muscle to take up and ‘burn’ glucose is dramatically compromised.

This contributes to insulin resistance, glycative stress, chronic inflammation, wide spread tissue damage and accelerated ageing. Similarly, loss of muscle bulk and functionality impairs the muscles’ ability to remove LDL cholesterol from the circulation, creating an atherogenic plasma profile.

The causes of sarcopenia include:

  • Endocrine shift: the menopause and viropause trigger hormone shifts that degrade muscle in women and men
  • Sedentary lifestyle: a risk factor for sarcopenia and many other disorders (ie Owen et al ‘10)
  • Chronic inflammation: a vicious cycle, whereby chronic inflammation drives muscle breakdown and the build-up of adiposity drives inflammation.
  • Dysnutrition (ie Vandewoude et al ’12): insufficient protein & the co-factors required to build muscle protein. Also, fast foods cooked at high temperatures contain high levels of pro-inflammatory compounds
  • Smoking: another cause of chronic inflammation

By examining the causes of sarcopenia we can begin to design programs that will delay or even prevent this core element of the ageing process. This will improve quality of life in the elderly, increase their independence, reduce their needs for health care and cut health care costs. The optimal protective strategy includes resistance exercise and enhanced nutrition.

When nutrition alone cannot meet the body’s requirements, nutritional supplementation may help. 

When there is a loss of muscle mass, Testofen may provide support. Testofen is a fenugreek extract standardized to 50% Fenuside. Fenugreek is a well-known, versatile herb that contains over 100 phytochemical constituents, including Furostanol Saponins and Steroidal Saponins. While fenugreek has multiple health applications, the active constituents included in Testofen have been shown to increase muscle mass and support healthy energy levels.



  1. Chen MB, Zhang Y, Wei MX, Shen W, Wu XY, Yao C, Lu PH. Activation of AMP-activated protein kinase (AMPK) mediates plumbagin-induced apoptosis and growth inhibition in cultured human colon cancer cells. Cell Signal. 2013 May 25.
  2. Holloszy JO. Regulation of Mitochondrial Biogenesis and GLUT4 Expression by Exercise. Compr Physiol. 2011 Apr;1(2):921-40.
  3. Janssen I, Shepard DS, Katzmarzyk PT, Roubenoff R The healthcare costs of sarcopenia in the United States. J Am Geriatr Soc. 2004 Jan;52(1):80-5.
  4. O`Neill HM. AMPK and Exercise: Glucose Uptake and Insulin Sensitivity. Diabetes Metab J. 2013 Feb;37(1):1-21.
  5. Owen N, Sparling PB, Healy GN, Dunstan DW, Matthews CE. Sedentary behavior: emerging evidence for a new health risk. Mayo Clin Proc. 2010 Dec;85(12):1138-41.
  6. Parr EB, Coffey VG, Hawley JA. `Sarcobesity`: a metabolic conundrum. Maturitas. 2013 Feb;74(2):109-13. 
  7. Sanchis-Gomar F. Sestrins: novel antioxidant and AMPK-modulating functions regulated by exercise? J Cell Physiol. 2013 Aug;228(8):1647-50.
  8. Vandewoude MF, Alish CJ, Sauer AC, Hegazi RA.J Malnutrition-sarcopenia syndrome: is this the future of nutrition screening and assessment for older adults? Aging Res. 2012; 2012:651570.
  9. Yang X, Huang N. Berberine induces selective apoptosis through the AMPK?mediated mitochondrial/caspase pathway in hepatocellular carcinoma. Mol Med Rep. 2013 May 31. 


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