March 28, 2022 8 min read
Skeletal muscle is one of the most dynamic tissues of the human body. In humans, skeletal muscle comprises approximately 40 % of total body weight, contains 50–75 % of all body proteins, and accounts for 30–50 % of whole-body protein turnover.
Muscle is mainly composed of water (75 %), protein (20 %), and other substances including inorganic salts, minerals, fat, and carbohydrates (5 %).
Generally speaking, muscle mass depends on the balance between protein synthesis and degradation and both processes are sensitive to factors such as nutritional status, hormonal balance, physical activity/exercise, and injury or disease, among others.
The various protein compartments (structural, contractile, and regulatory) have received significant scientific attention because of their important contribution to mobility, exercise capacity, functioning, and health. 
What is the Function of Skeletal Muscle?
Skeletal muscle plays a major role in multiple bodily functions. From a mechanical point of view, the main function of skeletal muscle is to convert chemical energy into mechanical energy to generate force and power, maintain posture, and produce movement that influences activity, allows for participation in social and occupational settings, maintains or enhances health, and contributes to functional independence.
Skeletal muscle contributes to basal energy metabolism.
It serves as storage for important substrates such as amino acids and carbohydrates, the production of heat for the maintenance of core temperature, and the consumption of the majority of oxygen and fuel used during physical activity and exercise. Of particular interest is the role of skeletal muscle as a reservoir of amino acids needed by other tissues such as skin, brain, and heart for the synthesis of organ-specific proteins. 
In addition, amino acid release from muscle contributes to the maintenance of blood glucose levels during conditions of starvation. Skeletal muscle also plays a significant role in disease prevention and health because a decrease in muscle mass impairs the body’s ability to respond to stress and chronic illness.
How Skeletal Muscle Impacts Bone Health
According to the National Osteoporosis Foundation, approximately 10 million American adults (8 million women) have osteoporosis, and almost 35 million others have insufficient bone mass or osteopenia. Adults who do not perform resistance training may experience 1% to 3% reduction in bone mineral density every year of life. 
Logically, exercise interventions that promote muscle gain also may be expected to increase bone mineral density, and the majority of studies support this relationship.
Several longitudinal studies have shown significant increases in bone mineral density after 4 to 24 months of resistance training.
Research indicates that resistance exercise programs prevented or reversed approximately 1% bone loss per year (femoral neck and lumbar spine) in adult and older adult women. A more recent review revealed that resistance training increased bone mineral density between 1% and 3% (femoral neck and lumbar spine) in pre-menopausal and postmenopausal women. 
Although the majority of the research on resistance training and bone density has been conducted with older women, evidence reveals that young men may increase bone mineral density by 2.7% to 7.7% through resistance training. 
The range of bone mineral density change is related to different responses in different bones because the musculoskeletal effects of resistance training relatively are site specific.
The bulk of studies in this area support the notion that resistance training appears to be related positively with high bone mineral density in both younger and older adults and may have a more potent effect on bone density than other types of physical activity such as aerobic and weight bearing exercise.
How Skeletal Muscle Impacts Resting Metabolism
Resistance training stimulates increased muscle protein turnover and actually has a dual impact on resting metabolic rate. First, as a chronic response, resistance training results in greater muscle mass that demands more energy at rest for ongoing tissue maintenance.
A 2.2 lb increase in trained muscle tissue may raise resting metabolic rate by about 20 calories/day. 
Second, as an acute response, resistance training causes tissue microtrauma that necessitates relatively large amounts of energy for muscle remodeling processes that may persist for 72 hours after the training session. Research demonstrates significant increases in resting metabolic rate (~ 7%) after several weeks of resistance training. 
However, more recent studies have revealed a similar elevation in resting energy expenditure (5%-9%) for 3 days following a single bout of resistance training. 
How Skeletal Muscle Impacts Type 2 Diabetes
As the obesity problem increases so does the occurrence of type 2 diabetes. Experts predict that by the middle of this century, one of three adults will have diabetes. 
A recent review on aging, resistance training, and diabetes prevention concluded that resistance training may be an effective intervention approach for middle-aged and older adults to counteract age-associated declines in insulin sensitivity and to prevent the onset of type 2 diabetes. 
This position is supported by a vast amount of research studies, including those demonstrating improvements in insulin resistance and glycemic control. 
Resistance training also has been shown to reduce abdominal fat, which may be particularly crucial for diabetes prevention.
This is because insulin resistance seems to be associated with abdominal fat accumulation in aging adults. 
A recent review of pertinent research indicates that resistance training programs incorporating higher-volume and higher-intensity protocols may be more effective for improving insulin resistance and glucose tolerance compared with lower-volume and lower-intensity exercise protocols. 
Resistance training is associated with enhanced glucose and insulin homeostasis due to increases in muscle cross-sectional area and lean body mass, as well as qualitative improvements in muscle metabolic properties. 
There also is evidence that resistance training may be preferable to aerobic exercise for improving insulin sensitivity and for lowering HbA1c levels.
How to Increase & Strengthen Skeletal Muscle
Exercise training induces in muscle significant structural and metabolic changes that are exercise-type specific. Several signaling pathways activated during exercise have been identified that contribute to skeletal muscle growth and adaptation. 
Strength training results in an increased capacity to generate force, partly due to muscle hypertrophy, i.e. growth.
The main cause for hypertrophy is an increase in the size of individual muscle fibers due to increases in protein synthesis and the addition of myofilaments, myofibrils, and sarcomeres, which are the cellular components of skeletal muscle fibers.
This increase in size may occur from activation and fusion of satellite cells culminating in the addition of new muscle fibers.
One thing to take note of is that skeletal muscle is very adaptable, therefore in order to continue to add strength and muscle size; it’s crucial to incorporate some form of progressive overload. This ensures that your muscles are continually challenged in some degree.
Several factors and molecular pathways that regulate muscle mass and the hypertrophic response have been identified. 
Intense resistance training activates signaling pathways in both young and old individuals. One pathway includes activation of insulin-like growth factor-1 where it binds to its receptor on the muscle cell and induces protein synthesis. 
The second pathway involves myostatin which is a negative regulator of muscle mass.
The activation of satellite cells could play an important role in the muscle growth response.  In addition, several genes are activated during an acute bout of strengthening exercise training that contribute to muscle growth and this genetic response that leads to muscle growth is modulated by training. 
In order to stimulate muscle growth with exercise, dietary considerations are also extremely important.
A recent meta-analysis shows that the gains in muscle mass and strength with strength training can be augmented by protein supplementation in both young and older volunteers. 
It is quite interesting that amino acids activate the same IGF-1 signaling pathway activated by strength training mentioned in the previous paragraph.
Skeletal, Smooth, & Cardiac Muscle
The three types of muscle in your body are skeletal, smooth & cardiac muscle and will be briefly described below.
Skeletal muscle is an extremely dynamic and pliable tissue and impacts our health & well-being tremendously! Not only does it benefit our health in terms of weight management, bone density, metabolism, and more, but it also allows us to function better and have the strength for everyday activities.
As we age, this becomes extremely important as aging naturally causes loss of muscle tissue if you don’t do anything to preserve or build it. This leads to aging more rapidly and a host of other health complications.
1. Frontera, W.R. and J. Ochala, Skeletal muscle: a brief review of structure and function. Calcif Tissue Int, 2015. 96(3): p. 183-95.
2. Wolfe, R.R., The underappreciated role of muscle in health and disease. Am J Clin Nutr, 2006. 84(3): p. 475-82.
3. Foundation., N.O. Fast Facts. 2009.
4. Warren, M., et al., Strength training effects on bone mineral content and density in premenopausal women. Med Sci Sports Exerc, 2008. 40(7): p. 1282-8.
5. Going S, L.M., Osteoporosis and strength training. Am. J. Lifestyle Med, 2009. 3: p. 310-319.
6. Almstedt, H.C., et al., Changes in bone mineral density in response to 24 weeks of resistance training in college-age men and women. J Strength Cond Res, 2011. 25(4): p. 1098-103.
7. Strasser, B. and W. Schobersberger, Evidence for resistance training as a treatment therapy in obesity. J Obes, 2011. 2011.
8. Lemmer, J.T., et al., Effect of strength training on resting metabolic rate and physical activity: age and gender comparisons. Med Sci Sports Exerc, 2001. 33(4): p. 532-41.
9. Heden, T., et al., One-set resistance training elevates energy expenditure for 72 h similar to three sets. Eur J Appl Physiol, 2011. 111(3): p. 477-84.
10. Boyle, J.P., et al., Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence. Popul Health Metr, 2010. 8: p. 29.
11. Flack KD, D.K., Huber MAW, et al., Aging, resistance training, and diabetes prevention. J. Aging Res., 2011.
12. Eves, N.D. and R.C. Plotnikoff, Resistance training and type 2 diabetes: Considerations for implementation at the population level. Diabetes Care, 2006. 29(8): p. 1933-41.
13. Kohrt, W.M., et al., Insulin resistance in aging is related to abdominal obesity. Diabetes, 1993. 42(2): p. 273-81.
14. Phillips, S.M. and R.A. Winett, Uncomplicated resistance training and health-related outcomes: evidence for a public health mandate. Curr Sports Med Rep, 2010. 9(4): p. 208-13.
15. Bweir S, A.-J.M., Almalty AM, et al., Resistance exercise training lowers HbA1c more than aerobic training in adults with type 2 diabetes. Diab. Metab. Syndr, 2009. 1(27).
16. Lamon, S., M.A. Wallace, and A.P. Russell, The STARS signaling pathway: a key regulator of skeletal muscle function. Pflugers Arch, 2014. 466(9): p. 1659-71.
17. Russell, A.P., Molecular regulation of skeletal muscle mass. Clin Exp Pharmacol Physiol, 2010. 37(3): p. 378-84.
18. Schiaffino, S., et al., Mechanisms regulating skeletal muscle growth and atrophy. FEBS J, 2013. 280(17): p. 4294-314.
19. Blaauw, B. and C. Reggiani, The role of satellite cells in muscle hypertrophy. J Muscle Res Cell Motil, 2014. 35(1): p. 3-10.
20. Nader, G.A., et al., Resistance exercise training modulates acute gene expression during human skeletal muscle hypertrophy. J Appl Physiol (1985), 2014. 116(6): p. 693-702.
21. Cermak, N.M., et al., Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr, 2012. 96(6): p. 1454-64.