Hey Readers! I am so thankful that you are here! This blog post is part IV of my gluteal amnesia series. In this series, I am taking a deep dive into the world of gluteal amnesia. If you have not read the earlier parts of this series, I recommend that you go back and read those parts first (click here for part I; click here for part II; click here for part III).
As we have discussed, gluteal amnesia is a term coined by Dr. Stuart McGill, and it refers to reduced activation, strength, and/or size in the gluteal muscles as a result of pain, poor posture, or lack of use. Your gluteal muscles are responsible for creating much of the movement in the hip joint, especially hip extension and hip abduction. When the gluteal muscles are weak and/or underactive, it causes other muscles in your body to pick up the slack from your "sleepy" glutes. This added work puts these helper muscles at risk for injury and/or pain. For efficient movement and posture in your body, you want the right muscle to fire at the right time and with the right amount of force. In this installment, I will go over what happens neurologically between the gluteal muscles and the nervous system in gluteal amnesia. Specifically, I will address the following:
The neuromuscular junction
Before we dive deeper into things, let's chat briefly about how the human nervous system generally works. Your nervous system is quite plastic, meaning that it can, and does, change in response to the input it receives. New neurons (and subsequently the connections they make) tend to be produced in response to experiences that are often considered “healthy” (e.g. exercise, learning something new, etc.), whereas fewer neurons are produced in response to "unhealthy" behaviors (e.g. sedentary lifestyle, stress, alcohol, sleep deprivation, etc.). Your nervous system is also very efficient in the connections it makes to muscles, glands, and other neurons. If neural connections are not needed, the nervous system will not continue to maintain those pathways and connections, causing denervation, or a loss of nerve supply. Conversely, if your nervous system deems certain neural connections to be important, not only will it use energy to maintain those connections, but it will also use energy to increase the number of neural connections present, known as innervation.
In gluteal amnesia, the neural drive (aka connections or synapses), to the glutes can decrease, typically due to pain, poor posture, or lack of use (e.g. chronic sitting). This decreased neural drive can accompany, or even cause, muscle atrophy (see part III for more detail on muscle atrophy). In gluteal amnesia, your gluteal muscles essentially “forget” how to activate maximally because the neural impulses reaching these muscles are greatly reduced. Let's now dig a little deeper into what potentially could happen between the nerves and gluteal muscles in Gluteal Amnesia.
The Neuromuscular Junction
A discussion about the neural control of muscle tissue is not complete without discussing what the neuromuscular junction (NMJ) is and what happens there. The NMJ is the place where the end of a motor neuron (i.e. a neuron that tells a muscle to generate force) meets a muscle cell. More specifically, the NMJ is where the motor neuron forms a synapse (i.e. the site of transmission of electrical nerve impulses from one cell to another) with the muscle cell, and in reality, the NMJ is really a small space between the two different cells.
Motor neurons, similar to other neuron types, consist of a cell body, short projections known as dendrites (which receive information from other neurons), and long projections known as axons (which send information to other neurons, muscle cells, and glands).
The NMJ is where the axon terminal of a motor neuron (i.e. the ends of an axon) synapses with the muscle cell (pictured below).
One motor neuron can have multiple axonal projections, thereby innervating many muscle cells. A single motor neuron and all the muscle cells it synapses with is known as a motor unit. Quick side note - exercise actually enhances motor unit recruitment and synchronization for optimal muscle functioning. Okay, back on track.
Your synapses, including the NMJ, undergo constant change and remodeling (generally referred to as "neuromuscular plasticity") in response to the demands placed upon it. Decades ago, the current thinking was that your nervous system was relatively static and would not change. However, this line of thinking has been disproven repeatedly. Your nervous system is actually quite plastic and is constantly changing to adapt to the stimuli it is experiencing. In the case of gluteal amnesia, neuroplasticity suggests that the gluteal muscles could become denervated (i.e. lose neural connections) as a result of pain, poor posture, and/or lack of use. If this denervation occurs, it can be challenging to correctly and efficiently activate the gluteal muscles, and it also can stimulate atrophy pathways in the gluteal muscle cells (see part III for more information on this). Conversely, neuromuscular plasticity also suggests that neural connections to the gluteal muscles can improve with the right stimulation, such as exercise and muscle use.
Muscle Denervation in Gluteal Amnesia
So, what actually can happen to the NMJ in gluteal amnesia? That's a fabulous question! There are several factors to discuss. Denervation, or a loss of nerve supply, results from a loss of synaptic contacts between the motor neuron and muscle at the NMJ. This is the opposite of synaptogenesis, which is defined as the generation of new synapses (discussed in the next section). In denervation, you might see reduced numbers of motor units, muscle atrophy, and/or functional impairment in the muscle. Denervation in skeletal muscles can occur from injury, healthy aging, poor posture, dysfunctional movement patterns, and/or muscle disuse. Injury, poor posture, and muscle disuse are all correlated with gluteal amnesia. Let's discuss each one of these factors in more detail.
Injury. When a neuromuscular injury occurs, two things can happen that can ultimately lead to denervation. First, injury can disrupt the axon of the motor neuron by interfering with axonal transport (i.e. transportation of proteins and such along the axon), which causes degradation of the axon. The degraded axon then gets "eaten" (or digested) by specific cells, known as phagocytic cells. Recall, the axon of the motor neuron is what makes contact with the muscle cell. If the axon has been digested by phagocytic cells, it is no longer available to communicate with the muscle cell - hence, denervation.
Second, the inflammation that accompanies an injury brings excess fluid into the injured area. This excess fluid interferes with the functioning of sensory neurons (i.e. neurons that send information to the brain and spinal cord), impeding effective sensory integration (i.e. making sense of all sensory stimuli), and potentially leading to muscle inhibition. Your nervous system detects the inflammation and altered sensory processing at the injured muscle, and to protect you from further damage, it inhibits the muscle or area that was injured. Essentially, the nervous system is like, “Whoa! What the heck is happening here?! Until we figure it out, shut this injured area down.” In the case of gluteal amnesia caused by injury, your nervous system quite literally inhibits the motor neurons to the gluteal muscles. This makes it much more difficult for you to activate your gluteal muscles. This inhibition is usually not permanent.
Poor posture. Poor static posture interferes with efficient neuromuscular signaling within the entire human movement system because poor posture can cause muscle imbalances. A muscle imbalance is when a muscle's resting length becomes altered. In a muscle imbalance, muscles on one side of a joint become shortened (and hence, overactive) while muscles on the other side of the joint become lengthened (and hence, underactive), and this can pull the joint out of its optimal alignment.
In a muscle imbalance, the neural drive to the shortened muscles actually increases (because your nervous system "thinks" you need these muscles more than you actually do), while the neural drive to the lengthened muscles decreases (because your nervous system "thinks" you do not need these muscles as often as you actually do). For example, when the hip flexors are too tight (which is super common in gluteal amnesia, especially from a sedentary lifestyle), it can decrease the amount of neural connections at the gluteal muscles (antagonist to the primary hip flexors). Thus, the poor posture created from sitting too much or standing with poor posture (e.g. excessive anterior pelvic tilt), can actually affect neural signaling to certain muscles in your body.
Poor dynamic posture (i.e. posture during movement) can interfere with neuromuscular signaling as well. Flawed movement patterns can actually alter the firing order of the muscles in complex movements. For example, with dysfunctional movement, prime movers (such as the glutes in certain hip movements) may be slow to activate, while synergists (such as the hamstrings) may incorrectly activate first to complete the movement of the hip. This can be very confusing for your nervous system and could result in denervation to certain muscles, while increasing innervation to other muscles (recall, your nervous system will not use energy to maintain pathways that it does not think you need). Regarding gluteal amnesia, when your gluteal muscles are weaker than normal, it can cause you to move your body in ways that are not necessarily natural or functional. For example, when standing up from a chair, your gluteal muscles should activate in order to extend your hips. However, weak glutes may cause your nervous system to recruit your low back or hamstring muscles to complete the task. As discussed throughout this series, synergist muscles (i.e. helpers) are not built to complete the task of another muscle. Thus, after time, these muscles become susceptible to overuse injuries.
Lack of use. Muscle disuse can result in denervation. When a muscle is not used for whatever reason (e.g. sedentary lifestyle, cast immobilization, etc.), neural connections to that muscle begin to diminish. Here again, this is because the nervous system is very efficient and economical. Using energy to support synaptic contacts that are not really needed by the body is not something that the nervous system is typically wired to do. Neuronal connections at the NMJ do not survive if they are not adequately stimulated with novel, and challenging, experiences. If you sit most of the day, the synaptic connections between your nervous system and gluteal muscles will begin to die off. This decreased neural drive is how your gluteal muscles “forget” how to activate. The number of synapses at the neuromuscular junction can decrease because your nervous system "thinks" that you do not need those connections anymore. This is a prime example of the principle known as “use it or lose it” in the neuroscience world - if you do not use your neuronal connections, you will lose them. Remember that foreign language class you were required to take in high school? If you didn't continue to speak in that language, you likely have lost most of that information. Again, this is because your nervous system is not programmed to energetically maintain connections you do not appear to need.
The good news is that research has shown that physical exercise and novel learning experiences (including motor learning, which occurs during exercise) can prevent, or reverse, muscle denervation. The next section will take a deeper look at muscle innervation.
Thousands of new neurons are produced every day throughout most of your life, and more than half of these new cells die within just a few weeks of being born if there is not sufficient learning or challenge imposed on them. However, it turns out that many, if not most, of these new neurons can be rescued from death by engaging in neurophysiological activities that are new and/or challenging, such as motor learning. Motor learning is the change in ability to execute a motor skill as a result of practice or experience. Motor learning reflects structural and functional changes made both to the nervous system and the muscular system.
Regarding the gluteal muscles, this may involve engaging in novel and/or challenging exercises aimed at strengthening or stabilizing the glutes (part V of this series will go over some of these exercises in more depth). Indeed physical exercise can induce neuroplasticity and structural changes in the nervous system. It is proposed that one of the mechanisms behind these changes is the expression, secretion, and downstream signaling of neurotrophic factors, such as Brain Derived Neurotrophic Factor (BDNF).
Neurotrophins, of which BDNF is an example, regulate important neurobiological processes such as neurogenesis (i.e. development of new neurons), synaptogenesis (i.e. new synapse formation), and protein synthesis. Many types of cells synthesize and release BDNF including, microglial cells (i.e. cells in the nervous system that remove damaged neurons and infections), T and B lymphocytes (i.e. immune cells), skeletal muscle cells, monocytes (i.e. a type of white blood cell), and glutamatergic neurons (i.e. neurons that release the excitatory neurotransmitter, glutamate).
Physical activity increases peripheral BDNF levels in healthy humans, and many studies have shown that both acute AND chronic exercise is associated with increased blood levels of BDNF. Lactate, which is produced during exercise, is positively correlated with BDNF levels; however, the exact interaction between lactate and BDNF levels is not yet well resolved. There are some theories, but that is out of the scope of this series. What is agreed upon is that physical exercise increases lactate levels. The increased lactate levels somehow lead to an increase in BDNF levels. BDNF can then enhance neuroplasticity via neurogenesis, synaptogenesis, and protein synthesis. Regarding gluteal amnesia, physical activity, especially exercises that target the gluteal muscles (which will be discussed in part V of this series) can lead to increased BDNF levels. BDNF can then act to stabilize the current synapses at the NMJ in the gluteal muscles AND it can help support the growth of new synapses at the NMJ. This leads to improved communication between the brain the gluteal muscles, which can improve stability, strength, and power in functional movements, ultimately leading to more exercise. This entire cycle has the potential to limit, or even prevent, the effects of gluteal amnesia.
The NMJ is the location where a motor neuron synpases with a muscle cell. The axons of motor neurons can actually synpase with multiple muscle cells. A motor neuron and all of the muscle fibers (or cells) that it innervates is known as a motor unit. Muscle and nervous tissue is constantly undergoing change, known as neuroplasticity. When synpases at the NMJ are lost, it is known as denervation. Denervation can occur for many reasons, including healthy aging, injury, poor posture, and lack of muscle use. The nervous system is highly efficient, and it will not invest energy to maintain synapses that are not needed on a regular basis. Not using your gluteal muscles sends the message to your nervous system that you do not need those neural connections in the glutes, so your nervous system stops maintaining them and they die off. Poor posture can cause some muscles to be longer than normal and other muscles to be shorter than normal. This leads to the tighter muscles having increased neural drive and the lengthened (and weaker) muscles having decreased neural drive. This occurs because your nervous system responds accordingly to the demands, or lack thereof, that you place on it. The good news is that your muscle innervation can increase with exercise and appropriate stimulation to the muscles. Denervation in gluteal amnesia does not appear to be permanent. By contrast, physical exercise can lead to enhanced neural communication at the NMJ via the effects of BDNF. When you engage in novel and/or challenging exercises, your body produces and secretes higher levels of BDNF. BDNF is known for increasing the number of neurons and synapses in your body as well as increasing protein synthesis. Thus, physical exercise appears to be the best way to ward off gluteal amnesia. Part V of this series will go over various exercises and lifestyle practices that can help to prevent gluteal amnesia.
Please note, the information presented in this blog series is not meant to diagnose gluteal amnesia or treat active cases of gluteal amnesia. After reading this series, if you have concerns about your gluteal muscles, please follow up with your physician, physical therapist, or sports medicine doctor. If you have been diagnosed with gluteal amnesia, please continue to heed the advice of the medical professional that evaluated you. Also, please keep in mind that I have simplified some anatomical and biological information, so I can keep the focus on gluteal amnesia as best I can. If you feel like you need more thorough descriptions and explanations, please refer to my reference list at the end of each installment in this series. Also, a special thanks to my amazing husband for doing all of the artwork for this post. Matt - you truly are a very talented artist.
As always, the information presented in this blog post is derived from my own study of neuroscience, human movement, anatomy, and yoga. If you have specific questions about your gluteal muscles, please consult with your physician, physical therapist, or private yoga teacher. If you are interested in private yoga sessions with me, Jackie, you can book services on my website ("Book Online" from the menu at the top of the page), or you can email me at email@example.com for more information about my services. Also, please subscribe to my website so you can receive my weekly newsletters (scroll to the bottom of the page where you can submit your email address). This will help keep you "in-the-know" about my latest blog releases and other helpful yoga and wellness information. Thanks for reading!
~Namaste, Jackie Allen, M.S., M.Ed., CCC-SLP, RYT-200, RCYT, NASM-CPT
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