Our second session is Exercise Science for the Neuromuscular Clinician, a Physiatrist's Approach with Dr. Gautam Malhotra. Dr. Malhotra is Clinical Associate Professor of Physical Medicine and Rehabilitation at the Rutgers New Jersey Medical School Kessler Program. Let's enjoy his informative talk. Thanks to the AANEM for having the faith in me to present this challenging topic to the advanced practice provider community who are routinely treating these neuromuscular patients. I want to warn you that my slides may be a little intimidating because I wanted to share as much explanation and reference as possible. But focus on me, focus on the pictures and what I tell you rather than getting lost in the slide material. My goal is to first give you a solid understanding of what PM&R physicians know about exercise science in normal humans, you and me, which will better inform a summary of the existing scientific evidence of exercise for neuromuscular conditions. My name is Gautam Malhotra. I have no disclosures except that I do not routinely manage patients with rare neuromuscular disorders. I do diagnose them and routinely use exercise for common neuromuscular conditions at the New Jersey VA where I work full-time. I also enjoy a part-time private practice. I'm a graduate of the very same program where I am now a clinical associate professor actively teaching at the bedside and didactics of general physiatry and electrodiagnostic principles. I genuinely love helping and meeting people so feel free to reach out to me with any questions any time. Let's quickly review what we mean when we say neuromuscular. Projection is in teal here and it begins with a stimulus in the periphery that travels through nerves and plexuses to reach the cell bodies located in the dorsal root ganglia right here, just outside the spinal cord. Another exonal projection goes up the spinal cord and then synapses abound within the brain. Conversely, the motor pathway, in red here, begins with a thought in the brain. An upper motor neuron crosses over and synapses with a lower motor neuron in the anterior horn of the spinal cord. The axon traverses the ventral root, plexuses, peripheral nerves, and then causes movement. This whole motor pathway is what we're going to spend our time thinking about today so let's deepen this discussion. Semantically, neuromuscular diagnoses typically do not involve the central nervous system. That is, the brain and spinal cord. So let's focus on the peripheral. The term motor unit refers to the anterior horn cell, its axonal projections, and all of its associated terminals, junctions, and muscle fibers. Here you see two motor neurons projecting to a muscle belly. The blue one has many neuromuscular junctions with a set of muscle fibers interdigitating between muscle fibers belonging to another motor neuron. I'm going to spend some time on reviewing muscles since exercise science requires a solid understanding of it. The purpose of muscles is to move and or stabilize bones. So here you see a bone and the tendon is a non-contractile tissue that attaches the bone to a muscle and transmits force or tension to the bone. The muscle belly is what we see with our eyes and it has a name like biceps. Each belly is a bundle of bundles, as you can see here, and the bundles are called fascicles. The fascicle is a bundle of muscle fibers, each of which is a single multinucleated muscle cell and the cell is packed with these myofibrils or myofilaments, which themselves are comprised of filaments. Under the microscope, we can see these thick and thin filaments repeating. Each is called a sarcomere and is the muscle's histological unit of contraction. If we look at the sarcomere, the way the muscle shortens is that the thin filaments interdigitate with and slide along the thick filaments. This is called the sliding filament theory. For this to happen, when calcium attaches to troponin, it moves tropomyosin out of the way so that myosin can interact with actin. This is called the power stroke and obviously requires ATP or energy, so that was probably the fastest summary possible of what you learned in biology and histology. But since we are going to talk about myopathies eventually, I just want to point out that the muscle cell has a complex meshwork of filaments called a cytoskeleton. This is important to maintain the cell's structure, but also functions to transmit the forces of muscle contraction to the membrane. The dystrophin protein complex is important for that transfer of force from the cytoskeleton to the cell membrane. It also helps to strengthen the muscle's fibers and protect them from injury as muscles contract and relax. I'm not unaware of how dry this may seem, but the point is that a problem with any of these proteins can basically lead to a myopathy. So if we're moving, we need energy and that basically means ATP or other phosphates in blue here. When you first move, that's what you're using. There's a whole bunch of that just sitting around in the muscle and that gets used up first. As you continue moving, glycolysis converts sugar to energy. This is anaerobic metabolism. If you keep moving, mitochondria can then use oxygen to squeeze out every last bit of energy from the byproducts of glycolysis. The yield on this aerobic energy use is phenomenal compared to anaerobic. So the more your muscles can use this aerobic oxidative process, the more efficient the system is at doing work. We'll talk more about this when discussing exercise, but after a certain point, there are only so many mitochondria and more work is powered by anaerobic systems. So here we get to combine what we learned. Whether the muscle fiber is going to be good at using oxygen or not is determined by the motor neuron that innervates it. One way we can determine this is by staining them. Type 1 fibers have lots of oxygen using mitochondria and citric acid cycle enzymes. Type 2b fibers pretty much only use glycolysis, and then type A are somewhere in the middle doing both. There are a bunch of muscle stem cells lying around waiting to help out in case of injury or exercise, and that comes up later. When staining, we get this beautiful mosaic of interposed type 1s and 2s, but if a motor neuron is damaged or dies, its neighboring motor neuron will collaterally sprout to adopt the orphaned muscle fibers. Unfortunately, we lose the mosaic when this happens. Muscle makes an enormous contribution to the body mass. Other than movement, it offers protection, heat and energy production, metabolic regulation, etc. But today, what we're really interested in is the generation of movement and force. So let's get to the good stuff now. In my mind, the way I see this is the way you have normal muscle the way I just described it for you, and if you do stuff with it, you get stuff. And my goal is to define all of that for you in a practical way. Aerobic exercise will lead to aerobically conditioned muscles, lifting weights and push-ups will lead to strength, and stretching will lead to better flexibility. On the other hand, this slide is the essence of PM&R. If you don't use it, you lose it. You'll notice I've put some familiar forms of inactivity here. Inactivity leads to deconditioning, weakness or loss of strength, and contracture or loss of range of motion. Physical inactivity is the fourth leading independent risk factor for death caused by non-communicable diseases. Let's start with one of the easier concepts. If you stretch, you get flexibility, and if you don't, you lose it. So these terms may feel interchangeable to you, but they mean different things to a physiatrist or a therapist. The noun form of range of motion designates the measurable limits you can move at a joint. Flexibility is how much of this you can do without pain. Mobilization moves a joint through its range of motion without applying a deforming force, while stretching defines any activity that does apply a deforming force along the rotational or translational planes of motion of a joint. You can either observe the range of motion, or actually measure it with one of these devices. Believe it or not, there are lots of ways to stretch. Passive is what you normally think of as stretching. Isometric means you're also firing the muscle. PNF is more complicated and requires a therapist. Dynamic is like the woman on the left with repeated movements going back and forth there. Ballistic is this on steroids and can cause injury, so we don't recommend it. And the kitten stretching here is just too cute, even for a dog lover like me. So this is all the good stuff, but what happens if we don't move? Contracture is comprised compromised motion, and it can be due to lots of things. Joints can get hurt or lock up. It's not directly related, but I wanted to digress a moment. These pictures here, well basically joints develop because we move when we're embryos in our mommies. Loading and unloading and motion all cause the synovial fluid to suck and squeeze like a sponge to offer nutrition. When we don't do this, like say in this rabbit who was immobilized for 6 and then 12 weeks, the bones become degenerated like someone with moderate osteoarthritis. So not moving is bad for joints. Contracture can also occur if the connective tissue or skin congeals up. If you don't move, the connective tissue surrounding the muscle shortens and eventually, slowly the muscle loses sarcomeres, contributing to contracture. So that's the good and the bad of motion. Let's talk about strength and weakness from a muscle perspective. I'd like to clarify some vocabulary about muscles generating force. When it's done quickly, when force is generated quickly, it's called strength. And when you fail, it's called weakness. When you can do it many times or over a long period of time, it's called endurance. And if you can't, it's fatigue. When a muscle generates force without changing length, it's called an isometric contraction. When the contraction is accompanied by a change in length, it can be shortening, which is concentric, or lengthening, which is eccentric. When you use a machine to enforce a constant speed of motion, that's called isokinetic contraction, and it's only really used for research. Most of us measure static strength with manual muscle testing, which is technically called the Classification of the Medical Research Council of Great Britain. The one repetition maximum is the max weight you can lift once and fatigue out. Prescriptions for strengthening can be based on a percentage of this. Isokinetic is the research stuff I told you about before. And then you can use various equipment to objectively measure strength. We call it resistance exercise when strengthening the muscles by lifting weights or using machines. Using higher weights is more effective, but if someone is injured or really debilitated, you might opt for low weights with more repetitions. Progressive resistive exercise, or the DeLorme Protocol, starts by figuring out your 10 repetition maximum weight. That's the amount of weight you can just lift 10 times before fatiguing out. You use that to then figure out 50%, 75%, or full amounts of weight for 10 reps each. The Oxford program is the reverse, and the DAPRE is sometimes known as pyramid training and is similar to DeLorme but decreases the number of reps. I've included a summary of the American College of Sports Medicine guidelines for healthy folks as well. The early strength gains you see when you start resistance training, they're really a reflection of optimizing your motor neurons in the brain, the spinal cord, and the periphery. I'm showing the rackets here, kicking together, to convey how much stronger we get when our neurons similarly fire in synchrony. As resistance training proceeds, the various myofibrillar proteins ramp up in production until the muscle cell starts bursting at the seams. Those type IIc stem cells I was telling you about earlier also contribute to hypertrophy. The IIb cells start building more oxidative machinery, collateral blood vessels grow, and transcription of glucose transporters increase to make exercise Mother Nature's metformin. So if you don't move, loss of strength or weakness occurs. This is referred to as disuse atrophy. Your body says, why am I putting any energy into this organ if it's not being used? So right away, with immobilization, bed rest, you start preferentially losing sarcomeres in your oxidative anti-gravity muscle fibers. The collagen doesn't break down, so you have all this extra collagen and you get stiffness. This is in contrast to atrophy from nerve injury, like I showed you before. All the muscle fibers belonging to that axon will wither away unless collateral sprouting occurs, and then you lose that mosaic pattern which we talked about. If you have a myopathy, proximal muscles tend to be affected more. What about just getting older? At this point, we think it's a combination of the disuse issues and less of the youthful stimulating factors in the body. We briefly mentioned tendon before. This family medicine paper shows healthy tendon with the collagen all pristine and organized, but with inactivity you get degeneration, or tendinosis. The term tendinitis refers to acute inflammation, which this does not represent. So finally, we get to cardio. Since this can be a difficult topic to navigate at first, I'm hoping to simplify the literature on this for you now. Cardio is really called dynamic exercise, which is any repetitive rhythmical movement of large muscle groups, and it should be enough work to overcome your muscle's aerobic ability. It should be often enough to turn on the genes, ideally daily. It's only going to benefit the muscles that are actually worked out. Basically you have to break a sweat. You can measure the intensity by looking at heart rate, asking how hard they think they're working, or by the settings on the machine. There are three parts to a workout. Start with a five minute warm up to get the blood flowing, and loosen up the joints. Then you go do the hard work for about a half hour. Finally, don't just stop, decrease to a mild pace so that you don't get venous pooling. I have personal experience with this. When my wife and I first went back to the treadmill in the gym, we stopped after 30 minutes. Babe, are you dizzy? Yes. Turn the treadmill back on. That's called venous pooling. The blood that should be going to our brains is hanging out in our legs. That means we're out of shape. Anyway, I just want to orient you to these curves where the x-axis is how hard you're working and the y-axis represents how much oxygen your body is consuming. As you can see, this is a linear relationship and plateaus at a certain point. Always start on the left at rest when your body is at its lowest metabolic demand. Then look all the way to the right, and that's the workload where your mitochondria can no longer use any of the extra oxygen the blood is sending over to them. This is your aerobic capacity, or anaerobic threshold, and it's what we want to improve with conditioning exercises. Everything in between here is submaximal exercise. This is an important term for neuromuscular rehabilitation. Submaximal exercise is everything between rest and maximal. Here's the story that no one tells you. During a bout of exercise, your moving muscles need oxygen and energy so the vessels to the muscles open up nice and big. This decreases peripheral resistance so less blood is sent to the gut and kidneys because we don't need to pee or digest right now while we're exercising. The autonomic nervous system kicks in to get your heart beating faster and harder. This keeps increasing until you max out. A lot of the energy used by the muscle is released as heat through the skin, so imagine this is in your advanced neuromuscular patients. It certainly might raise some concerns in them. That's why it can be a good idea to get a baseline exercise tolerance test to see how much they can safely tolerate. Briefly, there are all sorts of ways you can test them. Then you can create an individualized exercise prescription allowing an optimal level of training without exposing the patient to undue risk. So you're a good girl and you follow your prescribed regimen that you'll get. More and more blood vessels are going to the muscles, better insulin sensitivity, and best of all, more mitochondria and more optimized mitochondria show up as you do your exercise. I'm sure you already know all the benefits of exercise already. The cardiovascular benefits are that your maximum aerobic capacity and cardiac output increase so you can do more with the oxygen you're given, and this puts less demand on your heart. And yeah, you feel good too. Now the bad news. If you don't move, it's awful. All of your body systems are jacked up as you can see from this table on the left. You get osteoporotic, orthostatic, swollen, you get ulcers, your chem seven is going to be out of whack, you're going to be constipated, your VQ mismatch occurs, sleep disturbance, compression neuropathies, and the muscles we kind of already talked about. When all of this happens, it's called deconditioning. It's your body's normal reaction to not moving, to not use resources when they're not needed. In the early 1900s, people were put to bed rest. Based on what we know now, I tell my patients that bed rest is poison. And unfortunately, our neuromuscular population is afflicted with this. So that's my whirlwind presentation of exercise science as it will relate to the neuromuscular research out there. It essentially boils down to the body having a continuum of responses to the type and amount of activity it is exposed to. Okay, on to the second part. Now we talk about actual exercise in neuromuscular disorders. So now that you have some understanding of the exercise science, we can move on to what the literature has to say about exercise in neuromuscular disorders. It's such an exciting time with abundant advances in the field. Although there are a lot of studies, unfortunately we don't have enough strong evidence from randomized controlled trials with sufficient sample size to give exact prescribing information for specific diagnoses. What we do know is that generally, moderate intensity, aerobic exercise, and physical activity are a requirement. At the end, I'll give you some very practical advice after making the case for exercise. Just to beat a dead horse, this is a hard topic to study because there are generally less people with neuromuscular diseases. So they usually get lumped together as if they're just one type of patient, which they very clearly are not. And to make matters worse, not everyone uses the same type or dose of exercise. And finally, not everyone is measuring the same way or the same thing to reliably inform on outcomes. The first thing everyone wants to know is if it's safe for them to exercise. Well, what's great about exercise is that there is a challenge to the body that wakes up our genetics to create a better physical version of things, as I showed you before. The concern is that the disease process may cause the patient with, let's say, ALS to have difficulty with recovery, or the muscular dystrophy patient not to be able to recover from the tearing of the muscles because of underlying dysfunction. But the good news is that a common theme exists, where they all seem to tolerate at least a moderate amount of exercise without adverse effect. I spoke extensively with Virginia Kudritsky. She's a therapist who's worked with many ALS patients in Seattle. She agrees with the literature that muscles should be grade 3 or more if you're going to do resistance training. That means anti-gravity. This aligns with the recommendations in the literature. And this is really important because the science has shown that neuromuscular patients have more sedentary time per day when age and BMI are matched to controls, whether they exercise or not. So they're more sedentary whether they exercise or not. We already talked extensively about the problems within activity. So exercise becomes even more important in these individuals with neuromuscular diseases whose primary symptoms are weakness, fatigue, and muscle atrophy. Our neuromuscular patients fall frequently as a result of weakness and sensory impairment associated with their disease. And these impairments can be positively affected by therapeutic exercise. So another case for doing exercise in neuromuscular patients. They also have many painful regions due to the secondary musculoskeletal issues incurred. And exercise can help prevent this too. So in general, we can say that there are benefits of exercise for them, including decreasing falls, decreasing pain, addressing the deconditioning associated with an activity. Resistance training, aerobic exercise training, range of motion activities, and bracing at various points in the natural evolution of the disease may prolong ambulation, increase strength, and reduce the progression of many neuromuscular diseases. The gain in muscle function is related to the initial muscle strength. So it's important to start right away before they lose more strength. Ideally, the training needs to be optimized according to the patient's initial strength and function. The type, frequency, intensity, and the desired goals of exercise are likely to differ depending on the muscle group being trained. It's also important that it's individualized to fit with their own motivation and daily life activities. Since too much exercise may lead to poor compliance, Virginia recommends dialing it back, modifying or even stopping if the patient is feeling excessive intensity and duration of fatigue from the exercise. So I just want to clarify what I mean when I'm talking about neuromuscular conditions. And this is the way I teach my trainees when they're first learning. I organize the conditions based on the proximal to distal site of primary pathology. We start most proximally with motor neuron disorders like ALS. Next are the anatomical sites of lesions such as root, plexus, or specific nerve issues. Polyneuropathies are next, which can be further subdivided as axonal or demyelinating. Neuromuscular junction disorders such as Lambert-Eaton, botulism, and myasthenia gravis. And finally, muscle pathology of different causes, myopathies. So let's go through what the literature says about each of these categories. And we'll start with motor neuron diseases. There is a lot out there about exercise and ALS, so I'm going to focus on ALS. Is it safe in ALS? Generally, yes. In transgenic mice programmed to get ALS, although high-intensity endurance training didn't start ALS any earlier, it did progress their decline quicker. But then vigorous exercise didn't change anything in a different study. It's controversial whether the energy is like gas in a tank each day. One study showed no difference in fatigue from exercising. Another one may have found it to be even neuroprotective. So overall, let's say it's safe, but maybe don't push too hard. Officially, there are two randomized controlled trials that the Cochrane literature search included and couldn't detect a benefit or harm. One meta-analysis found cardio but not strength training benefits. And exercise was the only thing, the only thing that actually reduced spasticity in ALS. Studies have found improvements in functioning, functional scoring, pulmonary function tests, and Ashworth scales. Almost all of them agree that it slowed down deterioration. So overall, it's a good thing, and I'll give you practical approaches at the end of this section. The therapist I told you about, Virginia, emphasizes that in ALS, exercise is the most effective at maintaining function, even beyond all of the meds that we have out there. Stretching should start immediately and never ever stop. If you have to pick one, go with cardio over resistance training. The literature she references suggests a wide range of sub-maximal training intensity. But practically, it should be intense enough to carry out a conversation but not necessarily sing. It was fascinating that she pointed out sit-to-stand is most likely to carry over to function. So she recommends adding 10 sit-to-stands at breakfast, 10 at lunch, 10 at dinner. For resistance training, she sticks to training the big muscles, emphasizing good form, and she aims for 12 to 15 reps with multiple sets. Finally, the exercise should not be done at the expense of life activities. She also does respiratory muscle training with them using an inspirometer. So to me, this is probably the most practical slide that you're going to get from me on exercise in the neuromuscular population. Anatomical injuries to single nerves or the plexuses will not be covered in this lecture. I'll summarize to say that there is strong evidence for using exercise in radiculopathy, not so much out there for plexopathy, and there are also many not-so-great papers for various mononeuropathies. Peripheral neuropathies, on the other hand, have some interesting things to point out. For peripheral neuropathies in general, the Cochrane database found evidence that exercise improved strength but not functional ability. Chemotherapy-induced neuropathies has mixed evidence but overall seems to help with balance, endurance, and strength. Some even improved paresthesias. Charcot-Marie-Tooth disease, one of the uniform demyelinating neuropathies, improved strength, pain, fatigue, and type 1 fiber diameter with exercise. The one I see the most is diabetic neuropathy, where there is a lot more trial evidence. You all know it's a complex mechanism leading to this toxic neuropathy. I found it fascinating that axons were found to increase in numbers after exercise in diabetics. You don't have to worry about increasing their symptoms, falls, or foot wounds. Balance seems to respond well. Strength training is meh. Weight-bearing is better than non-weight-bearing for endurance exercise. Exercise improved strength and function in multiple studies. On to the neuromuscular junctionopathies. We can break these diseases up into sites of pathology. Presynaptic like Lambert-Eaton and botulism, synaptic space issues like organophosphate toxicity, and the more commonly encountered post-synaptically mediated myasthenia gravis. There is evidence that age degenerates and exercise regenerates the neuromuscular junction. So maybe exercise could be good for those with neuromuscular junction pathology. The exercise for myasthenia gravis literature has been bursting and bustling this past decade. One thing we know is that even though they may exercise, their baseline is more sedentary for some reason. You can apply regular guidelines to stable myasthenics. Pre-op exercise seems to improve post-thymectomy outcomes. Fatigue doesn't seem to improve with exercise. Moderate intensity exercise improved muscle strength, endurance, daily functioning, motor amplitudes, respiratory muscle function, and was safe overall. There was an interesting case report of a runner with myasthenia gravis who completed an ultra-endurance event with the help of his medical team. The bottom line is exercise is safe and beneficial in myasthenia gravis. The last category is our myopathies. Exercise in inflammatory myopathies used to be discouraged for fear of exacerbating inflammation. The accumulated evidence supports safety and efficacy of exercise in polymyositis and dermatomyositis, although data are more inconclusive for efficacy in patients with IBM. I see more of the inclusion body myositis in my own practice. Moderate intensity resistance may improve strength and function without increasing inflammation and downregulation of genes regulating inflammation and fibrosis in muscle tissue. So overall a good thing in your inflammatory myopathies. There is a ton out there about hereditary muscular dystrophies. Exercise predictably helps in all the ways we already said. Intensive muscle contractions, particularly when including an eccentric component, can tear muscles. Specifically, it damages the muscle's cytoskeleton more than in able-bodied subjects. So this is something you may want to keep as a caveat in hereditary dystrophies. Limb girdle, fascio-scapulohumeral dystrophy, and myotonic dystrophies also all show benefit without damage. Both nuclear and mitochondrial mutation types of McCardell's glycogen myopathy improve with exercise, even though previously they were advised to avoid it for fear of rhabdo. And exercise in mitochondrial myopathies seem to optimize the mitochondria without any adverse effects. So if you've made it this far, I'm glad and grateful for your attention. I think it's fair to say that the bottom lines are straightforward. The literature can't be definitive, because we just don't have the numbers to say things with supreme specificity. We used to worry that exercise will make these patients worse, but mostly it's not only safe, it's really helpful. Push for cardio and stretching, and maybe think a bit about the resistance training before you prescribe it. Especially if you learn nothing else from this, when you talk to your patients, you can be a cheerleader by telling them that there are plenty of good reasons to incorporate exercise into their lives. Just to round out the picture of who I am, this is my family, my colleagues, my bitmoji, the Optimus Prime costume I made for Comic Con, me with Weird Al Yankovic, and some silly stuff. This is just so you know, I'm a people person underneath all the official dry medical stuff. And that's the end. I do have some extra slides, which I say slides for geeks and nerds. And I hope you enjoyed this presentation. Thank you to the AANEM for having me join. Hey there, hopefully you're still awake. No questions in the text chat. My goal was to get everyone to just understand the science behind exercise. And then the literature has all been summarized for you so that you can then tell them it's okay to do it and they very well should do it. And the idea is to inform you so that you have that confidence. So I see someone said, so far we are advising for similar stretching, etc. I also advise for modified Tai Chi for ALS. You mentioned in this disuse atrophy, there was an increase in collagen. Is there more formation of collagen or is that relative to the amount of muscle cells? Great question. And yes, you are correct. The amount of collagen increases a little bit. But I think the fact that the ratio changes makes it stiffer. I think also the quality of the collagen does change in terms of how much type one and type two are there. This is nice. Had a couple of questions. Some of you are still out there. I'll just keep yapping while you guys write stuff. It was pretty interesting to see how much the body responds, even in neuromuscular conditions, to exercise. And it's turning on and off of genes. It's response to mechanical shear forces, etc. So it's pretty helpful. So the question is, any thoughts on why exercise doesn't improve fatigue in myasthenia gravis? I think given the mechanism of myasthenia gravis, where the end plate potentials just don't build up enough to cause the contractions that are needed, I think that may be why. I think you'd need to get more. But we did talk about how the neuromuscular junctions degenerate less or get reversed in regular age-related situations. But maybe it's just not enough to overcome what's needed. I'm speculating. This is not written in the literature anymore. So that's my speculation. I would think, though, that subjective fatigue probably does improve, just because you've got better oxygen utilization and better performance from the muscles. If someone doesn't mind responding, was this basically a review for you, or did you feel that this added something new? A lot of review, but did learn. OK. Hopefully, now you have references for the things you already knew. It was a review and new information, which is very helpful. OK, great. Yeah, this was, I think, a first time that this was offered. Strong review, but definitely good to hear the evidence-based medicine behind recommending exercise. Yeah. And I think, hopefully, the fear of prescribing exercise, maybe that's been affected a little. In fact, it's almost like the onus is on you, and your duty is to push for exercise. Thank you very much, everybody. Thank you very much for your time today. I think that that was a really good reminder to everyone, even us, to exercise more often, right? If we're prescribing it, we should also be doing it ourselves. I really appreciate your time today. Thank you, everyone, for attending. We'll see you next week for week six of six. Yes, same time, same place. Thank you, Dr. Malhotra. If anybody has any questions for you, they can contact us at AANEM to get more information or contact information for any of the speakers. So thank you so much. Enjoy the rest of your afternoon. Take care.

exercise science

neuromuscular clinician

muscle structure and function

exercise effects on muscle types

exercise safety for neuromuscular disorders

exercise impact on specific conditions

exercise prescriptions