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Sarcopenia: What it is and how to best combat it

As people age, strength becomes an, if not the most, important factor in their quality of life. Indeed, as people become weaker, there are many physiological characteristics taking place, such as coordination, frailty, and lost resilience. What often follows are psychological characteristics like remembering how strong you once were or feeling unsafe being home alone. These characteristics leads to an overall decrease in quality of life and an increased risk of morbidity and mortality (1,2,3,4,5).

-So what takes place as people become physically weaker?-

Well, when people become stronger, two main physiological characteristics take place:

1) The nervous system begins to learn how to coordinate muscle tissue appropriately and efficiently, and

2) The muscle tissues being innervated begin to increase in size (Hypertrophy).

Therefore, when you get weaker, the same physiological effects occur, but in the opposite and undesirable direction.

-So how does Sarcopenia relate into the equation?-

Well, Sarcopenia is the age-related loss of muscle. It is prevalent in about 10% of the population greater than 60 years old and rises to >50% in people over 80 years old. Deterioration of muscle begins to take place at around 30 years of age in untrained individuals. The rate of muscle loss is alarming as well, as some reports have indicated ~1% muscle atrophy every passing year and accelerates as you get older (1).

The results or Sarcopenia reach further than muscle atrophy alone. First, as mentioned previously, innervation of the muscles are required for a contraction to take place. However, when the nervous system is not acting on the tissues to contract and apply a force, the skeletal muscle tissue begins to decompose. To make matters worse, when muscles contract, tendons pull on the attached bone and can therefore signal for bone adaptation. However, if motor units stop firing and muscles atrophy to the point of no challenging tension to the bones, bone mineral density loses adaptation and begins to break down. This in turn results in Osteoporosis, or significant bone loss. The trifecta of decreased motor unit recruitment, muscle atrophy or sarcopenia, and osteoporosis often accelerates into each other and can result in other issues down the road (1,2,3,4).

-In simple terms: you use it or you lose it.-

For examples,

Body fat gain can increase due to lost activity done from locomotion, which will decrease due to the systems responsible for movement (that is, the skeletal muscle tissue and the skeletal system) breaking down. More specifically, activity levels help with caloric expenditure. If expenditure decreases with the same caloric intake, a net increase of calories will be stored. And since muscle is atrophying, most of the caloric surplus will become stored in adipose tissue, or body fat (4).

Type-2 diabetes can also result from poor nutrition partitioning that takes place within muscle cells. Notably, muscle cells can store sugars ingested as Glycogen.The larger those cells are, the more Glycogen can be stored. The bodies ability to handle blood glucose well via Insulin driving glucose properly into cells is known as cell sensitivity and is much desired. However, if muscle cells are very small and have atrophied, Glycogen storage is weak and can therefore have a significant impact in Insulin sensitivity. This in turn can create cellular resistance, hyperglycemia, and Type-2 Diabetes. Down the road, type-2 diabetes is shown to increase significant risks of cardiovascular disease, kidney disease, and cerebrovascular incidences (strokes), all of which are also correlated to sarcopenia (3,4).

Testosterone also decreases with sarcopenia due to the lack of receptors required to upkeep the motor units that were originally in place. Testosterone place an important factor in motor firing and muscle growth. However, as Sarcopenia takes place, Testosterone naturally decreases in response to the loss of muscle and strength (2,3,4).

Lastly, hip and other stress fractures are at much higher risk of occurring. Due to the lack of coordination, trips can occur at a higher rate. Further, catching a trip requires muscles to react and contract at a high rate. This ability is limited when significant muscle atrophy and sarcopenia has occurred (1,2). Lastly, some hip breaks have been shown to occur at the junction where the muscle tendon attaches into the hip bone, indicating a break from too much stress at the tendon to the bone. This occurs from very significant bone loss, which has resulted from a loss of forceful muscular contractions that act on the bone (4).

With the knowledge of what can occur as we age, there are things to do to prevent such a downward spiral to occur. Most notably, preventing and even reversing strength loss can promote a higher life expectancy, quality of life, and independence (1,3). Compound exercises such as squats, deadlifts, and presses are not discriminatory against anyone of any age and should be included in a routine for anyone building strength. Utilizing fast coordinated movements can effectively improve motor unit recruitment and produce neural stimulation (1,2,5). Exercises such as fast sit-to-stands, ball throws, and coordinated hip rotations can be utilized for better coordination.

However, Exercises in which requires excessive balancing may prove to be counter productive, and there are several reasons for this:

1) Exercises that do not react directly with the floor do not translate well into everyday activity. If you only use the floor throughout the day, then you should exercise off the floor as well (this is known as the principle of specificity).

2) If force production (strength) is limited from balance, then maximal motor unit recruitment is inhibited and thereby defeats the purpose of coordination based activity. For example, balancing on the ball will prove difficult relative to any of the exercises being added on top of the ball.

3) Injury in training usually results from a requirement of standing on a modality rather than the exercise itself. For example, twisting the ankle trying to stand on a Bosu ball will be a higher risk than the squats that are performed on the ball.

4) Strength already requires balance. Let's analyze this in an extreme case: If someone can squat 600 pounds, what is the likelihood of poor coordination? I am willing to bet he/she will have no problem staying on any apparatus simply because of the strength they have developed. On the flip side, how many people solely engaged in balancing modalities will be capable of squatting anywhere near 600 pounds? The fallacy of putting balance in front of strength training greatly limits both outcomes, and that is because being strong already requires balance through proper motor unit recruitment.

You can also check out my opinion about "functional training" related to resistance training.

Including days of strength training will not only make you feel better, you will also reduce your chances of Sarcopenia and other effects due to the age related muscle loss!


1. Fragala, MS, Cadore, EL, Dorgo, S, Izquierdo, M, Kraemer, William, J, Peterson, MD, and Ryan, ED. Resistance Training for Older Adults: Position Statement From the National Strength and Conditioning Association. Journal of Strength and Conditioning Research, 2019, 33(8), 2019-2052.

2. Aagaard, P, Suetta, C, Caserotti, P, Magnusson, SP, and Kjær, M. Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure. Scandinavian Journal of Medicine & Science in Sports. 2010;20(1), 49-64.

3. Dodds, RM, Granic, A, Robinson, SM, and Sayer, AA. Sarcopenia, long‐term conditions, and multimorbidity: findings from UK Biobank participants. Journal of Cachexia, Sarcopenia and Muscle. 2019.

4. EVANS WJ. Reversing sarcopenia: how weight training can build strength and vitality. Geriatrics. 1996;51(5):46-54.

5. Marcell, T, Hawkins, S, & Wiswell, R. Leg strength declines with advancing age despite habitual endurance exercise in active older adults. Journal of Strength and Conditioning Research, 2014, 28(2), 504–513.

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