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Putting the Maximus Back Into Gluteus

As humans, one of our most distinct features is the presence of round mass of muscle located on the posterior aspect of our hips. This muscle mass is commonly known as the gluteus maximus (GM). It provides us with many different qualities. These qualities range from a perceived enhanced physical appearance to proper control of our lower extremities in everyday functional activities and protection from injury.

In the health and fitness industry, the emphasis is generally placed upon its cosmetic qualities, one of the top requests of a client seeking the assistance of a fitness professional. Count the times you have heard the phrase, “I’d like to firm up my butt.” As such, a fitness professional should have a comprehensive understanding of this muscle, how its works, what causes it to work improperly and leads to altered appearance and, most importantly, how to fix it.

The key is to implement a systematic, progressive, integrated training program that compiles all aspects of training into one neat package with a purpose. The beauty of creating a properly integrated training program is that while you are striving to fix the altered appearance of this muscle, you will simultaneously enhance its functional capacity.

This is a very important concept to note. In order to change the characteristics of a muscle (size, shape or strength), you must get the muscle to function properly. This means proper neuromuscular communication. If a proper neuromuscular connection is not established, it will create dysfunctions not only in the specific muscle but also throughout the entire kinetic chain. By addressing the neuromuscular needs of your clients, you will increase their quality of life and help them to achieve their desired goals more effectively, which will ultimately make you a more successful trainer.

Defining Key Terms

Regardless of the goal, all clients must achieve optimal neuromuscular efficiency to ensure the highest level of performance with a minimal amount of breakdown. The NASM defines neuromuscular efficiency as the ability of all muscles in the kinetic chain (agonists, antagonists, synergists, stabilizers and neutralizers) to work together to produce force, reduce force and dynamically stabilize force in all planes of motion.

The kinetic chain is simply defined as the interdependent operation of the soft tissue system (muscle, tendon, ligament and fascia), the nervous system and the articular system. In other words, these three major systems in the body operate together to allow for proper movement patterns to occur (neuromuscular efficiency). A deficiency in any one of these systems will produce faulty recruitment patterns and place an increased demand on tissues in the body. This can further lead to early fatigue and eventual injury.

Therefore, training for any goal must involve a comprehensive understanding of some key aspects of the kinetic chain that are necessary for proper program development. These include functional anatomy and biomechanics, common causes of disruption in neuromuscular efficiency and, most importantly, how to correct them through program design. In the following article, we will address the GM with respect to these key aspects and their impact on performance.

Functional Anatomy and Biomechanics

As seen in Figure 1 below, the GM originates from the thoracolumbar fascia, iliac crest, sacrum, sacroiliac ligaments, coccyx and sacrotuberous ligament. It attaches into the iliotibial tract (IT-band) or fascia lata and the gluteal tuberosity of the femur.


Posterior View Lateral View
Figure 1. The Gluteus Maximus

Traditional functional anatomy and biomechanics places the emphasis on concentric muscle actions where muscles are viewed as “working” when they shorten or decrease a joint angle. However, this is an isolated view of muscle action and does not demonstrate the integrated functional capacity that muscles must forgo to ensure proper and efficient movement. All muscles operate within a muscle action spectrum consisting of concentric (acceleration), eccentric (deceleration) and isometric (dynamic stabilization) actions. Therefore, both the traditional and integrated function of the GM must be illuminated to demonstrate its importance and contribution to everyday functional movements.

Concentric Action

Concentrically, the GM accelerates (produces force) hip extension and assists in the production of hip external rotation and abduction. From a functional biomechanical perspective, this has also been termed supination. This simply means that with the foot fixed (on the ground) the hip, knee and ankle/foot complex will concurrently extend, abduct and externally rotate when producing force or acting in a concentric manner. Therefore, the description of hip extension, abduction and/or external rotation as a separate action is merely for simplicity. With a fixed foot, they will all occur together.

To demonstrate this, simply stand with your feet on the ground and squeeze your glutes, externally rotating your hips. Notice that your knees and ankle/foot complex follow into external rotation.

Some examples of concentric GM actions with the foot unfixed (not on the ground) would be a swimmer’s kicking action or a figure skater extending the leg (hip extension, external rotation and abduction) behind them prior to a jump.

However, in everyday life, we rarely extend, externally rotate or abduct the hip when the foot is not fixed on the ground, and thus supination becomes a much more functional description of how the GM works. Examples of supination occur during walking, running, standing up from a seated position and climbing stairs. In the sagittal plane, the GM exerts a posterior pull on the pelvis and acts to extend the hip by pulling the trunk into an upright position (extension). GM activity increases with increased force production such as walking on an incline, running or sprinting.

Other examples of supination that are more frontal and transverse plane dominant include:

Essentially, any activity that requires triple extension (hip and knee extension and ankle plantar flexion) involves concentric action (supination) of the GM.

Eccentric Action

Eccentrically, the GM decelerates (reduces force) hip flexion, hip internal rotation and hip adduction prior to and during the single-leg stance phase of gait. From a functional biomechanical perspective, this has also been termed pronation. This simply means that with the foot fixed (on the ground) the hip, knee and ankle/foot complex will concurrently flex, adduct and internally rotate when reducing force or acting in an eccentric manner. Therefore, the description of hip flexion, adduction and/or internal rotation as a separate action is merely for simplicity. With a fixed foot, they will all occur together.

In everyday functioning, the GM works eccentrically both with the foot unfixed as well as fixed. As mentioned above, this can be demonstrated during walking or running. As the leg swings forward, the GM assists the biceps femoris in deceleration of hip flexion prior to the foot making contact with the ground. By slowing the forward swing of the femur, the tibia will continue to swing forward, extending the knee and allowing for a proper foot placement on the ground in relation to the body.

Once the foot is in contact with the ground and pronation begins, the GM must then help to decelerate the forward momentum of the trunk (hip flexion) in the sagittal plane, hip adduction in the frontal plane and internal rotation of the femur and tibia in the transverse plane. Thus the GM has a direct influence on the knee and foot/ankle complex as well as the hip.

An example of a sagittal plane dominant eccentric action of the GM includes the deceleration of the lower extremity (pronation) with every step a sprinter or jogger takes. A frontal plane dominant example would include decelerating the lead leg during the lateral shuffling of an offensive lineman down the line of scrimmage or side stepping through a crowd. A transverse plane dominant example would include decelerating the internal rotation of the front leg (hip) of a batter swinging the bat or a person rinsing dishes and turning to put them on the sink to dry.

Dynamic Stabilization

In a stabilization capacity, the GM assists in dynamically stabilizing the knee via the IT band as well as the sacroiliac joint (SI joint) via the latissimus dorsi and the sacrotuberous ligament.

As previously mentioned, the GM provides frontal and transverse plane control of the knee by decelerating internal rotation and adduction of the femur and tibia. Dynamically, it stabilizes the knee by preventing increased internal rotation during the transition from pronation (eccentric) to supination (concentric).

This is achieved in part by the insertion of the GM into the extensive fascial network of the IT band that allows for increased tension and stability at the hip and knee. Stabilization at the knee as a result of GM activity is also attributed to the synergistic function of its upper fibers with those of the gluteus medius assisting in the deceleration of femoral adduction.

With respect to the SI joint, the GM provides stabilization in concert with its interconnection to the latissimus dorsi and the sacrotuberous ligament.

Again, using the walking cycle to illustrate this action, as the foot strikes the ground and proceeds into the mid-stance phase, the GM increases in activation (tension). This is the transition from pronation (eccentric deceleration) into supination (concentric acceleration), which is the motion necessary to accelerate the leg and propel the body forward. The increase in GM activation coupled with the activation of the contralateral latissimus dorsi from the back swing of the arm (shoulder extension), create an increased tension in the thoracolumbar fascia and sustained tension in the sacrotuberous ligament that act to stabilize the SI joint. This has also been termed the posterior oblique system.

Synergists and Antagonists

The central nervous system (CNS) is designed to produce movement through the selection of muscles in groups. Simply stated, no muscle works alone to produce movement. Thus the main muscle or agonist (prime mover) must rely on help from other assistant muscles. These assistant muscles are termed synergists.

Muscles that are synergists to the GM include the hamstring, erector spinae and adductor magnus predominantly in the sagittal plane, the gluteus medius and minimus predominantly in the frontal plane and the hip external rotators and latissimus dorsi predominantly in the transverse plane.

In order to properly accelerate and decelerate joint motion in all directions, it is necessary to have opposing prime movers or muscles that act opposite of each other. These muscles are termed antagonists. This is much like a giant two-man saw used by lumberjacks to cut down a tree. In order to make the saw move properly, there must be opposing forces (people) working with one another. Person #1 pushes the saw (concentric action) while person #2 must allow the saw to be pushed (eccentric action) in order to move the saw into a position that it can then be pushed back by person #2.

Muscles that are antagonists to the GM include the iliopsoas and rectus femoris predominantly in the sagittal plane and the adductors predominantly in the frontal and transverse planes. Comparing muscles to the lumberjack example, the GM and the iliopsoas are the two people maneuvering the saw and the hip joint is the tree. This concept will become more important when reviewing common causes of disruption in neuromuscular efficiency and how to correct them in the second and third parts of this series.


  1. Clark MA. Integrated training for the new millennium. Thousand Oaks, CA: National Academy of Sports Medicine; 2001.
  2. Panjabi MM: The stabilizing system of the spine. Part 1. Function, dysfunction, adaptation, and enhancement. J Spinal Disord 1992; 5:383-9.
  3. Bullock-Saxton JE: Muscles and Joint: Inter-Relationships with pain and movement dysfunction. University of Queensland. Course Manual, 1997.
  4. Chaitow L: Muscle Energy Techniques. New York: Churchill Livingstone; 1997.
  5. Clark MA. A scientific approach to understanding kinetic chain dysfunction. Thousand Oaks, CA. The National Academy of Sports Medicine; 2001.
  6. Janda V, Vavorova M: Sensory Motor Stimulation. Brisbane, Australia: Body Control Systems; 1990.
  7. Edgerton VR, Wolf S, Roy RR. Theoretical basis for patterning EMG amplitudes to assess muscle dysfunction. Med Sci Sports Exerc 1996; 28(6):744-51.
  8. Fischer FJ, Houtz SJ. Evaluation of the function of the gluteus maximus muscle: An electromyographic study. Ann Phys Med 1968; 47:182-91.
  9. Clark MA. Human movement science. Thousand Oaks, CA. The National Academy of Sports Medicine; 2001.
  10. The National Academy of Sports Medicine. Lower body muscular anatomy. Thousand Oaks, CA: The National Academy of Sports Medicine; 2000.
  11. Porterfield JA, DeRosa C: Mechanical Low Back Pain; Perspectives in functional anatomy. Philadelphia: WB Saunders; 1998.
  12. Valsilyeva, LF, Lewit K. Diagnosis of muscular dysfunction by inspection. In: Liebenson C (ed.). Rehabilitation of the spine. Baltimore, Williams and Wilkins, 1996.
  13. Travell JG, Simons DG. Myofascial pain and dysfunction: The trigger point manual. Volume 2. Philadelphia: Lippincott Williams & Wilkins; 1999.
  14. Bronner S. Functional rehabilitation of the spine: The lumbo-pelvis as a key point of control. In: Brownstein B, Bronner S (eds.). Functional movement in orthopedic and sports physical therapy. New York: Churhill Livingston Inc.; 1997.
  15. Clark MA. Integrated core stabilization training. Thousand Oaks, CA. The National Academy of Sports Medicine; 2001.
  16. Gray GW: Chain Reaction Festival. Wynn Marketing. Adrian, MI 1996.
  17. Oddsson L, Thorstensson A. Task specificity in the control of intrinsic trunk muscles in man. Acta Physiol Scand 1990; 139(1):123-31.
  18. Tokuhiro A, Nagashima H, Takechi H. Electromyographic kinesiology of lower extremity muscles during slope walking. Arch Phys Med Rehabil 1985; 66(9):610-3.
  19. Greenlaw RK. Function of muscles about the hip during normal level walking. Thesis. Kingston, Ontario: Queens University; 1979.
  20. Zimmermann CL, Cook TM, Bravard MS, Hansen MM, Honomichl RT, Karns ST, Lammers MA, Steele SA, Yunker LK, Zebrowski RM. Effects of stair-stepping exercise direction and cadence on EMG activity of selected lower extremity muscle groups. J Orthop Sports Phys Ther 1994; 19(3):173-80.
  21. Watkins RG, Dennis S, Dillin WH, Schnebel B, Schneiderman G, Jobe F, Farfan H, Perry J, Pink M. Dynamic EMG analysis of torque transfer in professional baseball pitchers. Spine 1989; 14(4):404-8.
  22. Hertling D, Kessler RM. Management of common musculoskeletal disorders. 3rd edition. Philadelphia: Lippincott Williams & Wilkins; 1996.
  23. Montgomery WH, Pink M, Perry J. Electromyographic analysis of hip and knee musculature during running. Am J Sports Med 1994; 22:272-8.
  24. Winter D. Foot trajectory in human gait: A precise and multifactorial motor control task. Phys Ther 1992; 72:45-53.
  25. Lyons K, Perry J, Gronley JK, Barnes L, Antonelli D. Timing and relative intensity of hip extensor and abductor muscle action during level and stair ambulation. Phys Ther 1983; 63(10):1597-1605.
  26. Inman VT, Ralston HJ, Todd F. Human walking. Baltimore: Williams & Wilkins; 1981.
  27. Ericson MO, Nisell R, Ekholm J. Quantified electromyography of lower-limb muscles during level walking. Scand J Rehabil Med 1986; 18(4):159-63.
  28. Ayyappa E. Normal human gait. Ortho Phys Ther Clin North Amer 2001; 10(1):115.
  29. Dostal WF, Soderberg GL, Andrews JG. Actions of hip muscles. Phys Ther 1986; 66(3):351-61.
  30. Gross J, Fetto J, Rosen E. Musculoskeletal examination. Malden, MA: Blackwell Sciences, Inc.; 1996.
  31. Shiavi R. Electromyographic patterns in normal adult locomotion. In: Schmidt GL (ed.). Gait in rehabilitation. New York: Churchill Livingstone; 1990.
  32. Vleeming A, Stoeckart R, Snidjers CJ, Stoeckart R, Stijnen T. Load application to the sacrotuberous ligament: Influences on sacroiliac joint mechanics. Clin Biom 1989; 4:204.
  33. Vleeming A, Pool-Gougzwaard AL, Stoeckart R, van Windergarden JP, Snidjers CJ. The posterior layer of the thoracolumbar fascia: Its function in load transfer from spine to legs. Spine 1995; 20:753.
  34. Vleeming A, Snijders CJ, Stoeckart R, Mens JMA. The role of the sacroiliac joints in coupling between spine, pelvis, legs and arms. Chapter 3. In Vleeming a, Mooney V, Dorman T, Snijders C, Stoeckart R editors. Movement, stability and low back pain. London: Churchill livingstone; 1997.
  35. Snijders CJ, Vleeming A, Stoeckart R, Mens JMA, Kleinrensink GJ. Biomechanics of the interface between spine and pelvis in different postures. Chapter 6. In Vleeming a, Mooney V, Dorman T, Snijders C, Stoeckart R editors. Movement, stability and low back pain. London: Churchill livingstone; 1997.
  36. Mooney V, Pozos R, Vleeming A, Gulick J, Swenski D. Coupled motion of contralateral latissimus dorsi and gluteus maximus: Its role in sacroiliac stabilization. Chapter 7. In Vleeming a, Mooney V, Dorman T, Snijders C, Stoeckart R editors. Movement, stability and low back pain. London: Churchill livingstone; 1997.
  37. Mooney V. Sacroiliac joint dysfunction. Chapter 2. In Vleeming A, Mooney V, Dorman T, Snijders C, Stoeckart R editors. Movement, stability and low back pain. London: Churchill livingstone; 1997.
  38. Lee D. Instability of the sacroiliac joint and the consequences for gait. Chapter 18. In Vleeming A, Mooney V, Dorman T, Snijders C, Stoeckart R editors. Movement, stability and low back pain. London: Churchill livingstone; 1997.
  39. Lee D. The pelvic girdle. London: Churchill Livingstone; 1999.
  40. Gracovetsky SA. Linking the spinal engine with the legs: A theory of human gait. Chapter 20. In Vleeming A, Mooney V, Dorman T, Snijders C, Stoeckart R editors. Movement, stability and low back pain. London: Churchill livingstone; 1997.
  41. Soderberg GL, Dostal WF. Electromyographic study of three parts of the gluteus medius muscle during functional activities. Phys Ther 1978; 58(6):691-6.
  42. Kelso JAS. Dyanmic Patterns. The self-organization of brain and behavior. Cambridge, MA: The MIT Press; 1995.
  43. Newton RA. Neural systems underlying motor control. In Montgomery PC, Connoly BH editors. Motor control and physical therapy: Theoretical framework and practical applications. Hixson, TN: Chatanooga Group, Inc; 1991.
  44. Rose DJ. A multi level approach to the study of motor control and learning. Needham Heights, MA: Allyn & Bacon; 1997.