For a trainer to produce optimal results in their clients, the kinetic chain (soft tissue, nerves and joints) must be operating with maximal neuromuscular efficiency (see Part 1 for definition). With respect to the gluteus maximus (GM), this means that it must be activated in the right manner at the right time and in the proper sequence with its synergists. If this does not occur, the recruitment pattern of the client’s musculature can be altered and will lead to compensation, altered appearance and eventually injury.
Changing appearance and ultimately avoiding injury in a client is paramount for a trainer. However, in order to produce successful results, the trainer must gain an understanding of some common predisposing factors that contribute to decreased neuromuscular efficiency and lead to altered muscle recruitment and appearance.
One of the most common causes of decreased neuromuscular efficiency in the GM is brought about through a concept known as reciprocal inhibition. Reciprocal inhibition is a principle whereby a tight muscle will cause decreased neural input to its functional antagonist. Electromyographic (EMG) data has demonstrated that tight muscles have a propensity to activate (simulate concentric action) easier and at times when they would normally remain less active. From a mechanical perspective, a tight muscle will also limit the range of motion that its antagonist can move through. In the case of the GM, a tight iliopsoas (see Figure 1 below) will mechanically cause a decrease in hip extension as well as neurologically cause decreased neural drive to the GM.
When the neural drive of the GM is decreased, it will no longer produce the same amount of force with the proper timing. Thus in order to maintain the same productivity of a given movement pattern (i.e., hip extension), the synergists (hamstrings, adductor magnus and erector spinae) must take up the slack. This concept is known as synergistic dominance.
Synergistic dominance produces a movement that occurs with altered neurological and mechanical control. The synergists (hamstrings, adductor magnus and erector spinae) take over the role of prime movers, and the nervous system will now respond to them as such by increasing their neural drive (activity). Concurrently, the GM is limited mechanically by a tight iliopsoas (hip flexor) to move through its functional range of motion (hip extension) and thus can not be utilized as much during movement. Furthermore, the nervous system decreases the neural drive to the GM.
Figure 1. Gluteus Maximus
The National Academy of Sports Medicine. Lower body muscular anatomy. Thousand Oaks, CA: The National Academy of Sports Medicine; 2000. Adapted from A.D.A.M.® Software, Inc.
Mechanisms for Injury
These disruptions (reciprocal inhibition and synergistic dominance) in neuromuscular efficiency can lead to a decrease in the activity of the GM. This can eventually lead to atrophy and/or a saggy appearance of the buttocks. With the GM working at a decreased capacity via reciprocal inhibition, the synergists are now called upon to act as a prime mover (synergistic dominance). They do not, however, have the proper characteristics mechanically or neurologically to sustain this performance. More stress is now being placed upon the hamstrings, adductor magnus and IT-band, with less force being absorbed from the foot and ankle complex, knee, hip and low back. This can often lead to the client who complains of or demonstrates hamstring and groin tightness, foot/ankle pain, knee pain and/or low back pain.
The result of a disruption in the neuromuscular efficiency of the kinetic chain has been explored. As a trainer, however, it is imperative to delineate some of the real-life common causes of these disruptions so that they may be better addressed in the program design for your clients. One of the prime causes that has already been alluded to is a tight iliopsoas or hip flexor complex. Tightness in the hip flexors can be brought about in a number a ways:
1. Sustained or repetitive movements involving hip flexion
- Prolonged sitting or sleeping in the fetal position
Another common cause of disruption in neuromuscular efficiency has been demonstrated as a direct result of joint dysfunction or injury. Three specific injuries and/or dysfunctions that are quite common include:
- Stubbed or dysfunctional toe
- Ankle sprains
- Low back pain
Stubbed or Dysfunctional Toe
The big toe is a vital component to proper walking mechanics. Normal walking motion at the big toe is to dorsiflex (toe bends up or back toward the body) as the body roles forward over the foot to push off. Proper dorsiflexion allows the knee and hip to extend and the ankle to plantarflex (triple extension). Stubbing your toe or even wearing narrow shoes can create inflammation and pain that leads to muscle inhibition and causes a joint dysfunction. If the big toe cannot perform proper dorsiflexion, the hip cannot go into full extension and will prematurely flex. This places an increased demand on the iliopsoas, and now we’re right back to an overactive hip flexor complex causing reciprocal inhibition to the GM.
Looking at ankle injuries, research has demonstrated that there is a disruption in the sensory feedback from the injured ankle that can lead to decreased stability and altered recruitment. Specifically, recruitment of the GM has been shown to be altered (delayed) during hip extension. Another interesting finding made by these researchers was the fact that not only was there a disruption in the recruitment to the GM on the injured ankle side but to the GM on the uninjured side as well.
Low Back Pain
Low back pain (LBP) effects approximately 80% of all adults. In, turn, LBP has been shown to be associated with dysfunction of the deep stabilizing muscles of the lumbar spine. Weakness of these stabilizing muscles of the spine will cause the kinetic chain to increase recruitment of the iliopsoas to stabilize the spine (due to its attachment onto the lumbar vertebrae). As a result, the iliopsoas receives increased neural drive from the nervous system, causing it to become tight. Again, this leads to the reciprocal inhibition of the GM.
When viewing the list of causes of a tight hip flexor complex, it should be apparent as to the ease and commonness with which this can occur. Let’s look at a typical client:
- Spends approximately eight hours a day sleeping
- Spends another eight to ten hours sitting at work and driving
- Spends another couple of hours sitting in front of a television or computer at home
- There is an 80% chance that they have LBP
- Incidence of a stubbed toe in their past or wears narrow shoes (like a dress shoe)
- Has had a sprained an ankle in the past
Any one of these can lead to a hip flexor complex that is overly tight and creating reciprocal inhibition to the GM or directly to an inhibited GM via injury. This can result in the inability to properly recruit the GM. In turn, this will decrease the proper firing pattern of the GM with its synergists, as well as force output and appearance. Therefore, anyone who is trying to get bigger, stronger, faster or change the appearance of their GM (which is basically everyone) will not be maximizing their efforts. In fact, they are putting themselves at a greater risk by placing an increased demand on other components in the kinetic chain that are not capable of performing the same functions as the GM. This is evident by the high incidence of the described injuries listed above.
In the final part of this series, we will look at how to create a proper programming strategy to correct imbalances and create a strong, firm, functional GM.
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