“Normal” aging is typically accompanied by easier weight gain and, along with declining hormones and decreased physical activity can reduce muscle mass, lead to frailty and a higher prevalence of metabolic disorders.  This insidious, age-related loss of muscle mass is called sarcopenia.

In many respects, sarcopenia is to muscle what osteoporosis is to bone.  The typical American gains one pound of fat and loses a half pound of muscle yearly between age 30 and 60.  Deterioration of muscle and loss of muscular strength is a major reason elderly lose mobility and cannot remain living independently.  Although muscle mass and strength both decline with age, the declines do not correlate directly.  Muscular strength can be maintained for a decade or more after a noticeable amount of muscle mass has been lost. The most accurate predictor of functional decline in later life is a measure of muscular work, such as “power”; or the amount of work a muscle can accomplish in a given amount of time.  Strength is the maximal force a muscle can generate.  Power implies a component of velocity.  For example, muscular strength may help reduce injuries from falls in the elderly but if one trips, it is the immediate rapid movements that can prevent the fall.

Well recognized risk factors for sarcopenia include increasing age, diminishing hormones, low levels of physical activity, and inadequate nutrition.  Recent studies implicate oxidative stress as a significant risk factor for muscle wasting.[1]   Mitochondria, the microscopic power plants within every cell, convert fuel into energy.  One consequence of this energy production is the formation of free radicals, or reactive oxygen species, which are potentially harmful if produced in excess.  Mitochondrial efficiency also plays a role in free radical defense.  Exercise is the most proven method of increasing the efficiency of existing mitochondria as well as stimulating the production of additional mitochondria.  Increased mitochondrial density and number allow more energy to be produced, and more muscular work to be performed.  Lack of muscle mass or mitochondrial density predisposes individuals to weight gain, insulin resistance, type-2 diabetes, metabolic syndrome and frailty.

Research reveals that resistance training can counteract the decline in skeletal muscle mass, maintain motor skills and reduce the risk of metabolic syndrome.   Mitochondria within skeletal muscle are the primary target for carbohydrate and fat metabolism to produce energy. Maintaining adequate muscle mass and mitochondrial density is a proactive measure to offset the risk factors related to metabolic syndrome, such as obesity, elevated blood pressure and hemoglobin A1C levels (a measure of blood glucose control over time).[2]  It has been widely known that resistance training is critical in preventing osteoporosis. It is now clear that resistance training should also be recommended for type-2 diabetes and metabolic disorders.

 Rapid weight lifting, or an interval style resistance program, has been shown to increase muscular power output more dramatically than traditional resistance training.[3]  It is a misconception that higher intensity exercise is riskier and only suited to younger individuals.  An intensive exercise training program improves measures of physical function, such as strength, gait, balance and oxygen uptake better than a low intensity home exercise program in older adults.[4]  Generally oxygen uptake declines 10-15% per decade after age 20; with an accumulation of body fat and a decrease in habitual physical activity accounting for about half of that age-related decrease.  Oxygen uptake is a measure of aerobic fitness.  Deterioration in aerobic fitness may result in a loss of independence in later life by limiting one’s physical endurance.  A recent study demonstrated that long term regular exercise was associated with improved preservation of telomere length, which determines aging at a cellular level.[5]  Proper mitochondrial function is also crucial for aerobic performance.  As the site of energy production in the cell, mitochondria are critical for the function and endurance properties of muscle.[6]

 So what’s the message here?  Exercise is a key determinant of how well you will age, your risk for developing chronic diseases, how well and how long you will live and how long you can remain independent as you age.  But, it is not enough to do just one type of exercise, nor is it enough to occasionally go for a stroll.  Exercise requires you to put in some work, sweat, get out of breath.  Maintaining muscle mass, muscular strength, muscular power and endurance are all essential to aging more youthfully.   

[1] Jang Y, et al. “Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration” FASEB Journal, 2009

[2]Strasser B, Siebert U, Schobersberger W. “Resistance training in the treatmen of metabolic syndrome”. Sports Medicine, 40(5):397-415. May 2010

[3]  Fielding, RA, Katula, J, Miller, ME, Abbott-Pillola, K, at al. “Activity Adherence and Physical Function in Older Adults with Functional Limitations.” Medicine & Science in Sports & Exercise. 2007 (November); 39 (11): 1997-2004

[4] Binder E, Schechtman B, Ehsani A, et al. “Effects of exercise training on frailty in community-dwelling older adults: results of a randomized, controlled trial”. .J Am Geriatr Soc. 2002 Dec;50(12):2089-91.

[5] Werner C, Furster T, et al. “Beneficial Effects of Long Term endurance Exercise with Leukocyte telomere Biology. Circulation. 2009;120:S492.

[6] Calvo JA, Daniels, TG, et al. “Muscle-specific expression of PPAR(gamma) coactivator1(alpha) improves exercise performance and peak oxygen uptake”. J Appl Physio 2008; 104:1304-1312