How does Sports Training Restructure the Brain?

Originally published on the PLOS Neuroscience Community

The impact of regular exercise on the body is obvious. It improves cardiovascular fitness, increases strength and tones muscle. While these transformations are visible to the naked eye, changes to brain structure and function by physical activity occur behind the scenes and are therefore less understood. It’s not news that the brain is wonderfully plastic, dynamically reorganizing in response to every sensory, motor or cognitive experience. One might imagine therefore, that elite athletes–who train rigorously to perfect specialized movements–undergo robust neural adaptations that support, or reflect, their exceptional neuromuscular skills. Different sports, invoking different movements, will target unique neural substrates, but most physical activities similarly rely on regions that are key for eliciting, coordinating and controlling movement, such as the motor cortex, cerebellum and basal ganglia. In a new study published in Experimental Brain Research, Yu-Kai Chang and colleagues explored how microstructure in the basal ganglia reflects training and skill specialization of elite athletes.

Runners, martial artists and weekend warriors

The study enrolled groups of elite runners and elite martial artists, along with a control group of non-athletes who only engaged in occasional, casual exercise. Although both groups of athletes were highly trained (averaging over four hours of training daily), their uniquely specialized skills were key for determining whether basal ganglia structure varied by sport or by athletic training generally. The groups did not differ in terms of basic physical attributes, demographics or intelligence, but as expected, the athletes were more physically fit than the controls.

Measuring microstructure

The researchers focused on the basal ganglia, a set of nuclei comprising the caudate, putamen, globus pallidus, substantia nigra and subthalamic nuclei, since these structures serve critical roles in preparing for and executing movements and learning motor skills.

Structures of the basal ganglia

Structures of the basal ganglia

They used diffusion tensor imaging (DTI), which measures how water flows and diffuses within the brain. Since water diffusion is determined by neural features like axon density and myelination, it is more sensitive to finer-scale brain structure than traditional MRI approaches that measure the size or shape of brain regions. Fractional anisotropy (FA) and mean diffusivity (MD) are common metrics to assess, respectively, the directionality and amount of diffusion. Typically, higher FA and lower MD are thought to reflect higher integrity or greater organization of white matter.

Globus pallidus restructures in athletes

The basal ganglia microstructure of the athletes and controls were remarkably similar, with one exception. The internal globus pallidus showed lower FA and a trend for higher MD in the athletes than the non-athletes, but there were no differences between the runners and martial artists.

This result in intriguing for two reasons. First, it’s notable that both athletic groups showed a similar magnitude difference from non-athletes. Thus, acquiring and refining skilled movements more generally, rather than any particular movement pattern unique to running or martial arts, may restructure the globus pallidus. As study author Erik Chang explains,

“With the current results, we can only speculate that the experience of high intensity sport training, but not sport-specific factors, would trigger the localized changes in DTI indices we observed.”

This would make sense, considering the area is an important output pathway of the basal ganglia, broadly critical for learning and controlling movements. It’s likely that other regions may undergo more specialized adaptations to sport-specific training. Chang expects that future studies using a whole-brain approach with “distinctions between sport types and reasonable sample size would find cross-sectional differences or longitudinal changes in brain structure related to motor skill specialization.”

Second, although we expect athletic training to enhance regional brain structure, the reduced FA and increased MD observed in these elite athletes would commonly be considered signs of reduced white matter integrity. This is somewhat surprising in light of other studies reporting positive correlations between physical fitness and white matter integrity in non-professional athletes and children. But as Chang points out, “Professional sport experience is quite different from leisure training.” Although unexpected, this finding aligns well with similar reports that intensive training in dancersmusicians and multilinguals is associated with reduced gray or white matter volume or reduced FA. Why would this be? For starters, DTI doesn’t directly measure axonal integrity or myelination–only water diffusion. So while sports training has some clearly reorganizing effect on basal ganglia, we can’t yet infer what changes are occurring at the neuronal level. One interesting possibility is that the development of such expertise involves neuronal reorganization or pruning as circuits become more specialized and efficient. Chang cautions that their findings “could reflect the manifestation of an array of factors, including increased neural efficiency, altered cortical iron concentration in the elite athletes, or other training-specific/demographic variables.”

In the broader context, this study is a striking example of why care is warranted in interpreting neuroplasticity. Depending on the study conditions, the same intervention–here, athletic training–can apparently remodel the brain in opposing directions. This is an important reminder that although we like to assume that bigger is better in terms of brain structure, this is not always true, highlighting the need to more deeply explore exactly how and why these neural adaptations occur. Chang eagerly anticipates that future studies incorporating “HARDI (High-angular-resolution diffusion imaging) and Q-ball vector analysis, together with larger sample sizes and longitudinal design, will be very helpful in revealing finer microscopic structural differences among different types of elite athletes.”

References

Chang YK, Tsai JH, Wang CC and Chang EC (2015). Structural differences in basal ganglia of elite running versus martial arts athletes: a diffusion tensor imaging study. Exp Brain Res. doi: 10.1007/s00221-015-4293-x

Chaddock-Heyman L, et al. (2014). Aerobic fitness is associated with greater white matter integrity in children. Cortex. 54:179-89. doi: 10.1016/j.cortex.2014.02.014

Elmer S, Hänggi J and Jäncke L (2014). Processing demands upon cognitive, linguistic, and articulatory functions promote grey matter plasticity in the adult multilingual brain: Insights from simultaneous interpreters. Front Hum Neurosci. 8:584. doi: 10.3389/fnhum.2014.00584

Hänggi J, Koeneke S, Bezzola L and Jäncke L (2010). Structural neuroplasticity in the sensorimotor network of professional female ballet dancers. Hum Brain Mapp. 31(8):1196-206. doi:10.1002/hbm.20928

Imfeld A, et al. (2009). White matter plasticity in the corticospinal tract of musicians: a diffusion tensor imaging study. Neuroimage. 46(3):600-7. doi: 10.1016/j.neuroimage.2009.02.025

Tseng BY, et al. (2013). White matter integrity in physically fit older adults. Neuroimage. 82:510-6. doi: 10.1016/j.neuroimage.2013.06.011

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A call for acceptance of career polygamy in science

Throughout my academic career from undergrad to my current postdoc, I’ve been perplexed by my atypical relationship with science. Yes, research and I have maintained a long, passionate love affair, but an affair apparently unlike those enjoyed by my colleagues. My unconventional attitude towards my work has served as a disconcerting voice that I’m just not cut out for a serious scientific career. I’ll certainly never win a Nobel, probably won’t publish in Science and may never even hold a faculty position. This reality has never really bothered me, but my lack of bother has been a subtle source of concern.

Only now, as a postdoc years into my Neuroscientific career, am I beginning to understand what makes my love affair with science so unusual. It’s by no means less genuine or less impassioned than those of colleagues madly pursuing tenure-track jobs; rather, it’s set apart by its polygamous nature. I get enthralled by new theories, overwhelmed with the excitement of shiny new data, and bore friends and family with my ecstatic ramblings about my research. I am a scientist for no other reason than I love it. However, it’s not the only object of my affection. I have never been, and probably never will be, able to suppress my love for so many other facets of life. A monogamous relationship with Neuroscience would just never suffice for me.

20131007-001611Since I was a teenager, a certain passage from Sylvia Plath’s the Bell Jar has always haunted me. She shared her predicament of being unable to choose a single fig – a life path, and as her indecision gripped her the figs wilted, leaving her starving and without a future. I’ve long been distraught by this similar fear of foregoing any one of my many dreams, wavering among so many enticing options and failing to commit to one whole-heartedly. As did Sylvia, I too considered this a flaw … a characteristic that would hold me back and prevent me from attaining my goals. As I’m finally understanding that these scattered passions or lack of focus – call it what you will – lie at the heart of my atypical approach to my work, I am also finally accepting that this is not necessarily a flaw.

“Good” scientists come in all shapes and sizes, but common to all is a sincere curiosity, a longing for answers and a rigorous devotion to unveiling them. Although these are precisely the factors that originally drew me to Neuroscience, I have always struggled with the conviction that I must not love my work quite enough – or at least not as much as the rock-stars around me, spending grueling hours in the lab, aiming for the highest impact-factor journals and power-networking with the bigwigs in their field. To a certain degree, these are crucial elements of a successful research trajectory, and I too have worked hard, held my research quality to the highest standards, and of course reveled in the rewards of grants and publications. But I have worked equally hard outside of the lab. Throughout grad school and my postdoc, I’ve allowed myself to pick several of those ripe, juicy figs and have savored every one of them. I’m not talking about the conventional concept of work-life balance that we’ve come to accept – at least superficially – is essential for job satisfaction. I’m referring more specifically to work-work balance. I indulge my writing addiction through freelance writing and editing and won’t hesitate to take on other side-projects as I’m so inspired. These endeavors are often neuro-related, but sometimes sprout from my obsession with running and fascination with sports physiology and biomechanics. These extra-neuro pursuits are as much “work” as my research, and I approach them all with the same intensity and devotion. They have not limited my productivity as a Neuroscientist, but have actually fostered it, by keeping me fresh, motivated and engaged with novel perspectives within and beyond the science community.

I’ve been blessed with both graduate and postdoc advisers who’ve been remarkably supportive of my promiscuous work habits, which has doubtlessly contributed to my own recent acceptance of my choices. Yet, I suspect my fortune is the exception rather than the rule, with the admission of this sort of behavior being met with disapproval or condemnation in many labs. In the current academic environment, time spent outside lab or even (gasp!) enjoying yourself is too often considered a sign of laziness or lack of drive. Tales of researchers working themselves to poor health or even suicide are rampant. It’s not clear how a field based on incentives so beautiful as curiosity and understanding has become so ugly, but it’s far time this trend is reversed. Outside interests or other professional pursuits should not be sources of guilt, and are not – contrary to common belief – prohibitive of a flourishing scientific career. Any culture that discourages the nurturing of broad interests can be toxic, stifling both personal growth and, ironically, professional development and productivity.

While there is certainly nothing wrong with the driven pursuit of a focused scientific career – and I strongly admire my dedicated colleagues who have chosen this path – it’s time we reject the myth that this is the only honorable or effective route to scientific success. As a first step, I’m embracing my relationship with Neuroscience, idiosyncrasies and all, and proudly proclaiming that we’ve been polygamous all along.

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San Diego Barefoot Running Workshops

I’m thrilled to announce … the first in a series of FREE San Diego Barefoot Running Workshops!

SDBRW_053115_3pm
THE MOTIVATION

This past International Barefoot Running Day, the small crew of San Diego barefoot runners gathered to share our love for natural running. This was my third consecutive year celebrating #IBRD and each year I come away with a renewed appreciation for the barefoot running community and new insights into how to maximally reap the benefits of the practice. Each of us have come from distinct backgrounds, have traversed unique paths and have made our own discoveries along the way, but we’ve all arrived at the same conclusion … Barefoot running is the way for us. For several months I’ve been toying with the idea of how best to share the lessons I’ve garnered from barefoot running with others in the hopes that they too may experience similar joy and growth. Reuniting with other barefooters last weekend reaffirmed the conviction that sharing these experiences and supporting others in their barefoot journeys is a worthy endeavor. As such, I’d like to invite you to participate in my San Diego Barefoot Running Workshop Series. These workshops are crafted with the novice barefooter in mind, but will ideally also serve as a welcoming environment for all – even lifelong barefooters – to nurture their evolution as strong, healthy, empowered runners.

WORKSHOP FORMAT AND AIMS

This first (beta-series, if you will) of workshops will comprise five meet-ups, each session focusing on a unique aspect of barefoot-running form, training and lifestyle. Each session will involve discussion and drills, and will conclude with a short fun-run to put into practice what we’ve learned. These runs will be designed to develop technique, rather than speed or endurance, so they will be short, easy and appropriate for runners of all levels. The workshops will be spaced apart (between two to four weeks) to allow runners sufficient time between sessions to incorporate lessons into their training. They will be casual, interactive and collaborative, with the hope that all participants will share their knowledge and experiences, and continue to learn from one another. The ultimate aim is to re-discover the pure, basic joy of running, by reinforcing natural movement patterns, learning safe training practices and increasing awareness of our bodies and environment.

Workshop #1 will take place Sunday, May 31 at 3 pm in Balboa Park.

We’ll meet at the Founder’s statue at the northwest corner of Balboa and El Prado. Please wear comfortable clothing (but leave your shoes at home!) and bring any hydration or supplies that you’d like. We’ll schedule the time, frequency and location of future workshops based on feedback from this first session. If you have suggestions for topics you’d like covered or how these workshops should be organized, please comment below. If you plan to attend (which I hope you do!) please RSVP at the Facebook event page, and please pass this along to other runners or barefoot enthusiasts. I’m looking forward to sharing the joys of barefoot running with you!

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A New Mechanism for Neurovascular Coupling in FMRI

Originally published on the PLOS Neuroscience Community

Although fMRI is the most commonly used tool for detecting human brain activity, the blood oxygen level dependent (BOLD) signal does not directly reflect neuronal activity, but instead, measures changes in blood flow and oxygen metabolism. This “neurovascular coupling” – the translation of neural to vascular signals – lies at the core of fMRI’s utility as a proxy for neural activity, yet there’s still uncertainty over exactly how neural processes drive vascular signals. The neural-to-vascular link is largely obscured by the complex cascade of events involved in neural activity, including glucose metabolism, oxygen consumption, neurotransmitter release and recycling, and changing membrane potentials. Past research has pointed to astrocytes as key players in the neurovascular coupling game, as these cells envelop both neurons and blood vessels. A key signaling molecule, both within astrocytes and between astrocytes and other cells, is ATP, best known for its role as the “cellular energy currency.” In their recent paper published in the Journal of Neuroscience, Jack Wells, Isabel Christie and colleagues explored the physiological mechanisms by which astrocytes might serve as the neurovascular interface of fMRI. Their study tested whether astrocytic purines – including ATP and its products ADP and AMP – are critical for the BOLD response.

ATP is key to eliciting the BOLD response

The authors speculated that, if astrocytic ATP mediates the vascular response to neural activity, blocking ATP should impair the BOLD signal. In normal rats, electrically stimulating one forepaw induces a BOLD response and ATP release in the somatosensory cortex of the opposite side of the brain. Therefore, to test if ATP is required for the BOLD response, they first disrupted ATP on only one side of the somatosensory cortex, and then stimulated both forepaws. They expressed TMPAP, which breaks down purines, into one side of the forepaw region of the rats’ somatosensory cortices, and a control into the other side. Oddly enough, although these vectors weren’t cell-specific, they were mainly expressed in astrocytes – but not neurons – a convenient pattern for testing the selective role of astrocytes in neurovascular coupling.

As expected, the BOLD response to forepaw stimulation was typical in control somatosensory cortex. But the signal was reduced in cortex expressing TMPAP (see Figure, A left and B top). This suggested that purine signaling is indeed important for a normal BOLD response. But what if the altered signal resulted from some other effect of the TMPAP expression, besides the intended purine reductions? For instance, breaking down ATP and its products could lead to build-up of the inhibitory neurotransmitter adenosine, which could interfere with normal neural activity. The authors repeated the experiment, this time using an adenosine antagonist to block any effects of adenosine accumulation. The results were the same. The BOLD response was reduced with TMPAP and did not normalize by blocking adenosine (see Figure, A right and B bottom), confirming that the effect wasn’t simply an artifact of adenosine build-up.

Group activation maps (A) and response curves (B) show that the BOLD response to forepaw stimulation is reduced after blocking purine signaling (TMPAP), compared to control (EGFP). The effect remains even after accounting for adenosine build-up with the adenosine antagonist DPCPX. From Wells et al., 2015.

Group activation maps (A) and response curves (B) show that the BOLD response to forepaw stimulation is reduced after blocking purine signaling (TMPAP), compared to control (EGFP). The effect remains even after accounting for adenosine build-up with the adenosine antagonist DPCPX. From Wells et al., 2015.

Does ATP support neural and vascular signaling or just their coupling?

If astrocytic purine signaling is truly involved in the translation of neural activity to a cerebrovascular response, interfering with purines should diminish the BOLD effect (as they showed), but neural activity and the background vascular state should remain unchanged. Indeed, multiunit recordings showed that TMPAP did not affect the neural response to forepaw stimulation, and arterial spin labeling indicated no change in resting blood flow or vascular reactivity.

Astrocytic ATP: One piece of the puzzle

Results from each of these experiments provided a critical piece of the neurovascular puzzle, illustrating the role of astrocytic purines in the series of events translating neural activity to the BOLD response. Together, they suggest that ATP signaling in astrocytes is critical for a normal vascular response to neural activity, but importantly, is not needed for either neural or vascular function alone. In other words, astrocytic ATP selectively underlies the coupling of neural and vascular activity.

It’s important to note that, although these findings show that ATP is important for neurovascular coupling, it’s unlikely this is the only mechanism supporting the BOLD response. While this study doesn’t directly trace the intricate events by which ATP mediates neurovascular coupling, the authors offer several plausible pathways. ATP is known to trigger calcium responses in astrocytes, which – through a series of downstream processes – could cause vascular effects like blood vessel dilation that are key to the BOLD response. However, ATP does not just support communication between astrocytes, but is also involved in neuron-to-astrocyte and astrocyte-to-blood vessel signaling. Any of these interactions could feasibly explain why ATP is required for the vascular response to neural activity. Of course, we can’t rule out the influence of ATP in neurons, which also may modulate vascular function independent of astrocytes. Although TMPAP was primarily expressed in astrocytes, this wasn’t exclusive; it’s possible that ATP levels were also reduced in neurons and may have affected the BOLD response in distinct ways.

Many questions remain regarding the physiological origins of the BOLD response to neural activity. However, these findings from Wells, Christie and colleagues help to solidify the role of astrocytes, and to introduce ATP as a key player, in the neurovascular coupling game.

References

Wells JA, Christie IN et al. (2015). A Critical Role for Purinergic Signalling in the Mechanisms Underlying Generation of BOLD fMRI Responses. J Neurosci 35(13):5284-92. doi: 10.1523/JNEUROSCI.3787-14.2015

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The structure-function paradox: Thoughts from a barefoot-curious reader

One perk I’ve enjoyed since starting this blog has been connecting with like-minded readers … runners, barefooters and scientists. Occasionally readers will reach out with their personal stories or questions (which I love!) The other day I received an email from a reader curious about the importance of toe and metatarsal alignment for foot health. His insights into foot biomechanics, enthusiasm for optimizing his own barefoot experience, and curiosity for the best path to do so – were striking. As he raised some interesting questions that are relevant for anyone considering transitioning to a barefoot lifestyle, I’m sharing his message, along with my response, below (note that I’ve removed his name for privacy and have trimmed the email for brevity).

I’d like to say thank you so much for documenting your experience, it is an invaluable source of information. I have great investment in this movement for myself (patellar tendonitis, fallen arches), and my family (bunion sufferers). I’m going to cut right to the chase. You seem very knowledgeable about the biomechanics of the foot, and I feel there is a significant sliver in the venn— diagram between our two philosophies. What about our toes alignment with our metatarsal shafts?

This is an idea that I see very rarely addressed among barefoot runners. I’m not sure how much of this information you’re familiar with, probably all of it but just in case I’m going to breeze through it. The shod VS the unshod life, a developed condition. I feel like this is so often ignored. In my rehabilitation from conventional footwear, I’ve been made aware of the deformation that has taken place in my bones and tendons that has bent my big toe inward, bent my small toes outward, and given me hammertoe. Why do I see so few barefoot runners addressing this? I work everyday to stretch and re-align my great toe into its natural place, a continuation of the metatarsal shaft, so that it can once again be in its place of maximum support.

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I even invested in a product that re-alignes my toes back to the way they were, so as to, over time, affect the bone and tendon structure, pushing them back into alignment. But seeing your story, how you came through without the use of these, and how your toe alignment between 2011 and 2012 didn’t seem to change much. In your recent pictures it’s hard to discern the alignment of your toes, have you seen a difference since 2012?

Does this idea hold water to you at all or do you consider something else entirely more important than alignment. I would love to know, I’ve been trying to make sense of going completely barefoot, but with my great toe alignment (about the same as yours in 2012) it just doesn’t make sense to me, I feel like I’d be putting weight on a delicate system that no longer is in the proper alignment to do its job properly. Am I completely off the mark? Any thoughts would be extremely appreciated.

I love this last picture, and it is the most profound and affirming to me, a (mostly) un-contacted tribe within the amazon. Their toes are my every day goal. I know little biomechanics, but this has philosophy has resonated with me. Am I wasting my time with this? Is this new information to you? What made you feel your path was best?

AmazonTribe

MY RESPONSE:

Thanks for your email. I love hearing from others with a shared interest in natural, barefoot living. Indeed, I’m aware of the deformations shoes make on our feet, and that toe separators can help reverse this (I actually have some myself).

I think the answer to most of your questions lies in your goal. If your main aim is simply to realign your bone structure, then sure, work on this just the way you are. For me, better toe/metatarsal alignment has been an incidental consequence of pursuing my other goals – overall healthier, stronger feet that allow me to move the way my body is meant to. So there are two, albeit related, issues here: structure and function. You seem very focused on changing your foot structure, but for what purpose? If it’s so that your foot (and body) will also move better, the best way to achieve that is simply to use your feet the way they’re meant to be used. By going barefoot as much as possible you will quickly build muscle, tendon and bone strength and as a consequence, your foot shape will also change.

I gave up shoes four years ago and have indeed noticed major changes since then. The toe splay hasn’t been dramatic, but my arches have become strong and high and my feet and ankles have gone from soft and dainty looking, to thick, toned and defined. This sounds odd, but my feet have become my favorite physical asset – I’m proud of their transformation into powerful, beautiful structures. At this point, I could care less how my toes splay, since my feet are functioning magnificently, allowing me to walk and run for miles on end, pain-free and carefree!

You’re concerned that you could injure yourself by going barefoot if your bone alignment isn’t perfect. This is a slight possibility, but easily avoided by simply listening to your body. I would be concerned less about proper alignment than general foot weakness. The risks of walking or running barefoot excessively before you’re ready come from inadequate strength, and the only way to strengthen your feet is to use them! Sure, going out and sprinting a 5k for your first barefoot run will injure you. Instead, go for a short walk until your feet start to fatigue. Then call it a day. Or run around the block for 2 minutes. Give yourself enough rest to allow your feet to recover and rebuild before you try again. Over time, you’ll be able to walk further, run longer and start noticing remarkable changes in how your feet feel, look and function. When I gave up shoes in 2011 I couldn’t walk barefoot more than a few minutes before my feet hurt. I walked barefoot for a couple years to build up base strength, then began running barefoot – literally starting by running one block. I now regularly run 40-45 miles a week barefoot.

I seem to have written a novel, but this is an important and interesting topic for me! My last tidbit of advice is to not over-think it … just enjoy the improved sensory experience and awareness your feet give you and savor the growth, however gradual it may be. Happy barefooting!

What are your thoughts on the relative importance of foot structure and function, and how they influence one another?

I love hearing my readers’ experiences and questions, so please don’t hesitate to reach out!

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The shoulder-hip rotation equation

Stabiliity. Mobility. Activation. Relaxation. Each of these features has its place in a strong, efficient running stride. Yet, an excess or lack of one at the wrong place in the gait cycle can seriously throw off a runner’s biomechanics. Through some recent trials and experimentation of my own, I’ve learned how profoundly true this is for a proper kinematic balance throughout the core, extending from the pelvis up through the abs, back and shoulders.

Those who’ve been following my blog will be aware of my history of hamstring and foot injuries. I’ve struggled with disproportionate left hip/hamstring tension and tendinopathy for years, and have sustained beyond my fair share of right foot fractures and tendinoses. While these issues are more or less under control due to gradually improving biomechanics, more mindful training and frequent self-care (massage, ART and physical therapy), they continue to linger as minor annoyances on most runs. A couple weeks ago, my physical therapist performed a gait analysis to get to the source of these longstanding imbalances.

She noted three main issues:

1) Excessive left shoulder rotation. I tend to pull my left shoulder back too much right before left foot-strike. The arms should swing in the sagittal plane, but there should be minimal rotation at the shoulders.

Left shoulder rotates excessively

Left shoulder rotates excessively

2) Insufficient right leg drive. Compared to my left leg, my right leg does not come up as high during the swing phase. I can feel this while running, as if the leg is dragging behind me instead of driving back powerfully. In fact, I have a tendency to occasionally stub my right big toe due to my inability to lift.

Right leg lifts lower than left

Right leg lifts lower than left

3) Externally rotated right foot. When the foot strikes, it tends to land with the toes pointed outward. I am also keenly aware of this error, as it feels like the entire right leg is uncontrollably turned out.

Right foot rotates outward

Right foot rotates outward

Mental trick FAIL

For the past week, I’ve attempted to consciously correct each of these biomechanical errors in turn … without success. Efforts to stabilize my shoulders left me with excess tension from the neck down, through the shoulder and back. Empowering my right leg drive felt unnatural and exhausting, and turning my right foot inward was even more awkward and resulted in lateral ankle pain. Form correction FAIL.

My physical therapist prescribed some drills to ingrain proper shoulder and foot motor-memory; yet these changes will take time and I wanted a quick fix. I knew something major was off with my gait, so I launched my own investigation. I came across an article discussing the balance between shoulder and pelvic rotation (which I can no longer track down) that struck a chord. Excessive amounts of shoulder rotation, they explained, may signal insufficient hip rotation. If the hips are too rigid, the upper body compensates. Prior to my long run this week, I practiced this simple exercise to reinforce what proper pelvic rotation should feel like … and to no surprise, this was a novel sensation for my typically rigid running hips.

Mental trick SUCCESS!

Throughout my long run, I repeatedly checked in with my form, this time drawing on some new tools in my belt. Rather than forcefully immobilizing my upper body, I focused on relaxing the shoulders, keeping the neck extended, and leading with the chest. I increased my forward full-body lean and was cautious not to overstride. Most critically, I experimented – for the first time – with exaggerating my pelvic rotation. As my left leg began to swing back, I let the hip pull back with it … this was a remarkably new sensation, but felt fluid and right. I was suddenly able to attain much greater leg extension that usual, without force or effort. Further exploring the movement, I discovered that emphasizing rotation on the left compared to the right seemed to balance and better align my hips. The pattern of tension that typically evolves over my long runs – extending from my lower back down through the left glutes and hamstring – was oddly absent. Not only was my left leg moving with new-found fluidity, but my right leg had inadvertently gained strength and alignment as well. By increasing my left pelvic rotation, my right leg and foot were now freed to glide naturally through their stride. Without effort, the right foot was now striking straight and both legs were driving back with equal strength.

So how does a runner know how to balance stability with mobility? When during the gait cycle to relax and when to engage? It’s truly a delicate balance, and one that doesn’t always come naturally. Injuries that cause compensatory movement, or years of running with even slight dysfunction can further exacerbate and ingrain poor motor patterns. Critically, as each runner is unique in terms of structure and function, there is no one-size-fits-all biomechanical prescription. Even running experts agree there’s no “perfect” form, and it can be risky to change your form unnecessarily. My advice to you, runner, is to experiment with your gait if there’s a preexisting problem. Then, play with various adjustments and assess your body’s response until you hone in on changes that benefit you.

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This is your Brain on Wine: FMRI Signals of Alcohol Content

Originally published on the PLOS Neuroscience Community

In today’s burgeoning wine industry, winemakers are in constant search of ways to perfect their product and achieve an edge over the competition. Complicating the challenge of producing a bottle that we’re sure to select at our next fine dining experience is the variability across palates. The individuality and unpredictability of sensory experiences – which may further be manipulated by context or expectations – make predicting a wine’s appeal a daunting task. In a dream world, winemakers could peer directly into the brain to examine the biological response to a smoky syrah or a spicy zinfandel. Such a tool could theoretically empower producers to target their wine characteristics to not just the psychological, but also the physiological response to a wine. In their study recently published in PLOS ONE, Frost and colleagues sought to accomplish just this, using functional MRI to assess brain responses to a wine’s flavor attributes.

Rather than assess relatively subjective features like fruitiness, tannins or fullness, the researchers focused on alcohol content, a more objective – and therefore easier to quantify – property. Twenty-one “inexperienced” wine drinkers (they imbibed less than once per week) participated in four wine-tasting sessions while undergoing functional MRI. During each session, they alternated among sipping a tasteless solution, a low-alcohol red wine (13-13.5%) and a high-alcohol red wine (14.5-15%). A different pair of low- and high-alcohol wines, matched on flavor, was tasted in each session. A post-scan taste-test confirmed that participants could not tell the difference between the low- and high-alcohol wines of each pair, as they rated their tastes as essentially identical.

Frost and colleagues identified 30 brain regions of interest that were activated by drinking wine, regardless of alcohol content. This set of areas was then further tested for effects of alcohol. Of these regions, only the right insula and right cerebellum were differentially activated by alcohol level, demonstrating greater activity to the low- than high-alcohol wines. Surprisingly, no regions preferentially activated to more alcoholic wines.

This is your brain on wine. The right insula (left) and right cerebellum (right) were more active when participants drank low- than high-alcohol wines. Adapted from Frost et al., 2015.

This is your brain on wine. The right insula (left) and right cerebellum (right) were more active when participants drank low- than high-alcohol wines. Adapted from Frost et al., 2015.

The cerebellum is known to be involved in sensorimotor processing, which could reasonably account for its activation by subtle differences in alcohol perception. However, both the insula and cerebellum have been shown to be modulated by taste, activating to more intense flavors and feelings of satiety. Shouldn’t high-alcohol wines – which are arguably more intense– therefore more heavily engage these regions? The authors dug deeper into the literature to interpret these unexpected findings.

They propose that because these areas are involved in “cognitive modulation of sensory perception” and “coordinating the acquisition of sensory information,” the lower alcohol wines might have “induced a greater attentional orienting and exploration of the sensory attributes.”

Yet there’s one tiny hole in this explanation, at least when considering the current evidence alone. We could reasonably link activation of these regions to flavor intensity or taste perception if there were some associated behavioral indication that the wines elicit distinct sensory experiences. However, the participants in fact report no perceptible taste difference between the two classes of wines. This discrepancy between the subjective perceptual experiences and brain responses suggests that the observed insular and cerebellar effects may reflect some sensory aspect of wine-tasting that lies below conscious awareness.

Although the researchers don’t directly discuss this possibility, it’s worth exploring. Since the difference in alcohol content between the wine types was notably small (just ~1.5%), it’s not surprising that the participants couldn’t detect a taste difference. It would be interesting to see whether the activations would be more robust to a wider gap in alcohol levels, or might track with a continuum of alcohol content. Furthermore, the study participants were “inexperienced” wine drinkers. Perhaps the taste differences would have been perceptible – or the brain responses stronger – in a sample of connoisseurs with more “refined palates.” As the evidence stands, we can’t conclude whether the BOLD responses indeed reflect effects of wine taste perception that were simply too subtle and hence immeasurable here, or instead relate to lower-level, unconscious sensory processes.

So what do these findings mean for the winemaker looking to neuroscience for a marketing advantage? It’s safe to assume that manipulating the alcohol content of a wine will indeed affect brain physiology (in fact, the known influence of alcohol on the BOLD signal raises concern over confounds between the wine conditions). However, it’s unclear how this brain response relates to a wine drinker’s sensory experience, let alone preference for one wine over another.

As blogger Neuroskeptic points out in his recent commentary on the study, “it’s not clear whether a brain scan is the best way to approach the question of whether high alcohol is overpowering. Surely the same thing could be demonstrated using a taste test.”

Despite these considerations, Frost and colleagues establish a solid stepping-stone to further explore the complex relationship between a wine’s flavor profile and consumers’ gustatory and neural responses. More importantly for wine-lovers everywhere, their study offers a key first step towards unraveling how and why that bold, oaky cabernet beats a merlot any day.

References

Bower JM et al. (1981). Principles of Organization of a Cerebro-Cerebellar Circuit. Brain Behav Evol 18:1-18. doi:10.1159/000121772

Frost R et al. (2015). What Can the Brain Teach Us about Winemaking? An fMRI Study of Alcohol Level Preferences. PLOS ONE. doi: 10.1371/journal.pone.0119220

Plassmann H et al. (2008). Marketing actions can modulate neural representations of experienced pleasantness. Proc Natl Acad Sci 105(3):1050-4. doi:10.1073/pnas.0706929105

Small DM et al. (2003). Dissociation of Neural Representation of Intensity and Affective Valuation in Human Gustation. Neuron 39(4):701-11. doi:10.1016/S0896-6273(03)00467-7

Smeets PAM et al. (2006). Effect of satiety on brain activation during chocolate tasting in men and women. Am J Clin Nutr 83(6):1297-1305.

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Return to racing, bare and proud!

As I crossed the finish line of the San Diego Half Marathon this past Sunday, I choked back the tears as a powerful flood of emotion overcame me. Two years ago at this time, I was recovering from my second metatarsal stress fracture, just one of a series of severe injuries that kept me sidelined from racing – and nearly from running at all. Over the previous two years, I had tried – and failed – to treat my torn achilles, peroneal and extensor tendonitis, hip bursitis, metatarsal stress reaction and two fractures, by experimenting with every therapy in the books and every shoe available (seriously, you should have seen my shoe rack). My running accomplishments had rapidly diminished from regular marathons to hobbling a few painful miles at best. Each successive injury was followed by yet another, sending me faster into a downward spiral of intensifying hopelessness, as it appeared that my running days were nearing their end.

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Running rebirth

There was a deeper imbalance that was untreatable by rest, physical therapy or new shoes. It was time to hit the reset button and retrain myself to run … from scratch. When I vowed to give up shoes a year and a half ago (September 7, 2013 to be exact) I was terrified. This meant intentionally reducing my mileage to frustratingly low levels and risking more broken bones or worse (as the media promised, with headlines to the tune of “Barefoot Running Can Cause Injuries, Too” and “Barefoot Running Injuries: Doctors See Health Problems Ranging From Stress Fractures To Pulled Calf Muscles“). Although I had been dabbling in running barefoot for a year or so prior, I had approached it as a casual occasional training tool to improve my form, not to mention have a little childlike fun on the side! It seemed unsustainable for the distances and regularity I had been logging and longed to return to. Yet, as every conventional option had failed me, the novelty and craziness of barefoot running offered just the glimmer of hope I needed.

As I progressed through my barefoot journey, the initial apprehension quickly wore off. The requisite patience was offset both by the thrill of running painlessly and freely, as well as by the small, victorious milestones along the way. I vividly remember the satisfaction of completing my first barefoot mile, the giddiness after my first 5-miler and the astonishment after finishing my first 10-miler. The experiment was working!

Racing: The missing piece

Yet, although I had overcome the chronic injuries and – most importantly – had regained my love for running, there was still a missing piece to my inner runner. Due to the incessant injuries, followed by the gradual transition to barefoot running, I hadn’t seriously raced since my last marathon over three years ago. I knew from others’ experiences that returning to full performance (in terms of distance and speed) after switching from shod to barefoot running can take years – around a decade by some estimates. While I dreamed of returning to racing, I was admittedly terrified. Foremost, my barefoot training required a new level of control and precaution, forcing me to limit my terrain mostly to smooth pavement and concrete, and to abandon speed and distance goals. But further, racing for me has always been a chance to explore and test my physical and mental limits. Barefoot racing was uncharted territory and I feared the disappointment if I were to fail that test.

Soon, this race anxiety was overpowered by annoyance with the anxiety, and fed up with my complacency, I took the plunge. My body may never be “perfectly” barefoot-race-ready, but my mind was itching to race. With more excitement than perhaps for any past race, I spontaneously registered for the San Diego Half Marathon, just a couple weeks out. I had been warned by a fellow barefoot runner of some rough spots, but refused to check out the course in advance. Ignorance can indeed be bliss. I was anxious enough, and preferred to bask in blind eagerness than further worry myself.

Taper despair

To my despair, a week from race day as I began to taper, I developed an odd forefoot issue: tight, burning metatarsal heads and painful, tingly first and second toes (I suspect this was related to clumsily wacking my foot on a curb weeks prior, but we’ll never know). The two days before the race, the ‘injury’ peaked and I was hobbling in pain. The mental battle raged, as I weighed the risks and benefits of showing up at the starting line – a painful, miserable, slow run, versus intense disappointment and regret.

Race morning, my foot still ached. But I had to try. The buzz at the starting line reaffirmed my decision, as the shared anticipation amongst the running community flooded me with excitement.

Mile 1: My big toe ached. “Already? Ugh. Why I am I here again?” By mile 2 the pain was gone.

Mile 3: A rough stretch of nasty road. What would have typically ripped up my feet now barely fazed me as I focused intently on light, relaxed form.

Mile 5: Drained and anxious. My foot had been acting up around mile 4-5 in my training runs, and I anticipated the end of my race was near. “This race was such an idiotic decision. I’m injured and tired … there’s just no way this will end well. I’ll most certainly end up more severely hurt, and for what? To prove that I can race barefoot?” But the energy of the runners and spectators propelled me forward, and the constant stream of “Barefoot … thats awesome!” and “Look, she’s barefoot!” reminded me that not only could I do it, I was doing it.

Mile 6.5: Half way already? The foot still felt fine.

Mile 9: After an ugly stretch of not-so-well maintained pavement crossing the 5 freeway, “the hill” appeared. As the 300-foot ascent began and runners around me began to walk, I savored the smooth concrete under my feet as I climbed steadily. But as I peaked to flat ground, I felt a painful ‘pebble’ under my big toe. After a couple of minutes I pulled aside to wipe it away, but there was no pebble. My already finicky flexor tendon had apparently been irritated by the hill, but with only 3 miles to go, I had to push through.

Mile 11: The course weaved through my neighborhood, and as I passed by the cheering onlookers at my typical weekend coffee spot, the pride hit me. I could have been one of those spectators myself, sipping my tea with regret. But not today.

To the finish: Perhaps the most frustrating stretch of the race was the downhill finish. I felt exceptionally strong, but had put on some slight breaks to avoid tearing up the quads, calves and of course, feet.

13.1: I crossed the finish line with deeper gratitude than at perhaps any other race. Compared to my shod days, I hadn’t run particularly fast, and the distance was nothing remarkable, but I had broken another type of PR. After years of being sidelined by injury, I was back in the game. That missing piece to my inner runner was finally found. I was no longer transitioning to barefoot running … I was there. I was a real runner once again … strong, healthy and basking in the post-race passion of the running community that I so missed.

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Mapping Memory Circuits with High-Field FMRI

Originally posted on the PLOS Neuroscience Community

How we create and recall memories has long fascinated scientists, spurring decades of research into the brain mechanisms supporting memory. These studies overwhelmingly point to the hippocampus as an essential structure for memory formation; yet despite these efforts, we still don’t fully understand how hippocampal circuits transform stimulus input into stored memories, in part due to several fundamental methodological challenges.

The most commonly used functional imaging method in humans, fMRI, neither measures neural activity directly nor attains ideal spatiotemporal resolutions. Although more powerful, invasive techniques can be used in animals, it’s arguable whether they can be applied to assess higher cognitive functions like episodic memory, as the jury’s out on whether this process is uniquely human or shared with animals. However, recent neuroimaging advances are rapidly narrowing the power gap between invasive and non-invasive techniques, helping to reconcile findings across animal and human studies. In particular, high-field, high-resolution fMRI in humans is becoming more feasible, permitting sub-millimeter spatial resolution. Although the BOLD signal from fMRI only approximates the neural signal, such methodological advances get us one step closer to imaging neural activity during cognitive functions like memory formation. A team of researchers recently took advantage of high-field fMRI to investigate sub-region and layer-specific memory activity in the medial temporal lobe, an area critical for long-term memory acquisition.

The hippocampal-entorhinal circuit

Within the medial temporal lobe, the entorhinal cortex (EC) and hippocampus (including subfields dentate gyrus, CA1, CA2 and CA3) make up a well-characterized circuit, in which superficial EC layers project to the dentate gyrus and CA1 via the perforant path, on to CA3 via mossy fibers, to CA1 via schaffer collaterals, and finally return back to the deep layers of the EC. We know this circuit is important for memory, as the hippocampus is essential for memory encoding and other processes that presumably support memory, including novelty detection or pattern separation and completion. However, the mapping of these functions onto human entorhinal-hippocampal pathways is incomplete. 

The entorhinal-hippocampal circuit

The entorhinal-hippocampal circuit

Imaging memory with high-field fMRI

To examine how novelty and memory signals are distributed along the EC-hippocampus circuit, Maass and colleagues conducted high-resolution (0.8 mm isotropic voxels) 7T fMRI while participants performed an incidental encoding task. The subjects viewed a series of novel and familiar scenes during scanning, and later completed a surprise memory recall test on the scenes they had previously seen. This allowed the researchers to assess brain activity related to novelty – by comparing novel and familiar trials – as well as activity related to successful memory encoding – by comparing trials that were subsequently remembered and forgotten. On each subject’s structural brain image, they parcellated the EC into superficial input layers and deep output layers, and segmented the hippocampus into CA1 and a combined dentate gyrus/CA2/CA3 region (DG/CA2/3). 

Segmentation of entorhinal cortex layers (left) and hippocampal subfields (right). Maass et al., 2014.

Segmentation of entorhinal cortex layers (left) and hippocampal subfields (right). Maass et al., 2014.

Double-dissociation of novelty and encoding signals

Across participants, novel scenes activated DG/CA2/3, whereas successful encoding activated CA1, and the strength of this CA1 signal predicted retrieval accuracy. Next, Maass and colleagues looked at subject-level voxel-wise activity, which preserves high spatial resolution by eliminating the need for smoothing and across-subject averaging. Using multivariate Bayes decoding, which can be used to compare the log evidence that various regions predict a particular cognitive state, they evaluated whether EC or hippocampal regions predict novelty and memory encoding. As illustrated by the relative log evidences in the below graphs, DG/CA2/3 (A right) and CA1 (B right) respectively signaled novelty and encoding, consistent with their group-level findings. But this analysis further showed that superficial EC (the input layers to the hippocampus) and deep EC (the output layers from the hippocampus) also respectively predicted novelty (A left) and encoding (B left). What’s more, superficial EC and DG/CA2/3 functionally coupled during novelty processing, whereas deep EC and CA1 coupled during encoding. 

Multivariate Bayes decoding predicts novelty and encoding from entorhinal cortex and hippocampal activity. Maass et al., 2014.

Multivariate Bayes decoding predicts novelty and encoding from entorhinal cortex and hippocampal activity. Maass et al., 2014.

In essence, these findings suggest a division of labor across the EC-hippocampal circuit, where hippocampal input pathways participate in novelty detection, and output pathways transform these signals for memory storage. The researchers offer a model in which information about stimulus identity feeds in from upstream regions such as the perirhinal and parahippocampal cortices, which are known to process object and scene identity. Hippocampal pattern separation or comparator computations might then be performed to both assess novelty and reduce interference between stimulus representations, transforming the novelty signal into output for long-term storage. This explanation for how hippocampal circuits process a stimulus representation is reasonable, considering that DG/CA3 is important for pattern separation, and CA1 has been proposed as a neural comparator, processes which may determine the memory fate of a stimulus representation.

Cautions and caveats

A segregation of function across EC layers and hippocampal subfields does not necessarily imply that these mappings are mutually exclusive. For instance, it’s likely that output pathways still carry a novelty signal, and memory formation may begin earlier in the processing stream than detected here. Despite the impressive resolution in this study, allowing fine segmentation of cortical layers and subregions, noise and artifact are inherent concerns for any fMRI study. As the BOLD signal is a crude estimate of neural activity, there may well be a ceiling to the power of high-field fMRI, even with the most rigorous methods. How accurately these region- and layer-specific signals map onto memory functions therefore remains to be validated. And of course, we can’t infer directionality, causality or any direct relationship to neural activity from fMRI alone. It’s tempting to interpret early circuit activity as an input signal and late activity as an output signal, or to assume that the BOLD response reflects excitatory neural activity; however, we’ll need more direct neuroimaging tools to trace the flow of neural signal and confirm these speculations.

Together, Maass and colleagues’ study advances the field of cognitive neuroscience on two fronts. First, it helps bridge the gap between robust yet invasive imaging tools and non-invasive but less powerful approaches commonplace in human imaging studies. Their successful application of high-field fMRI demonstrates the feasibility of assessing human brain activity with sub-millimeter resolution, paving the way for the standardization and refinement of these tools. Second, and perhaps most critically, it allows us to peer into the brain at previously impossible scales to view the live hippocampal circuit hard at work, processing and engendering memories. While past fMRI studies have effectively shown where memories are woven together, these findings refine this anatomical precision to bring us one step closer to understanding how hippocampal circuits accomplish this feat.

First author Anne Maass kindly offered to answer a few questions about her research. Here is a brief interview with Maass and her colleagues.

Are there unique methodological concerns to consider when using high-field, high-resolution fMRI?

The increased signal-to-noise ratio provided by MRI at 7T enables us to acquire fMRI data at an unprecedented level of anatomical detail. However, ultra high-field fMRI is also more vulnerable to distortions and susceptibility-related artifacts and the negative effect of motion increases with resolution.

In particular, the anterior medial temporal lobe regions, such as the entorhinal cortex and perirhinal cortex, are often affected by susceptibility artifacts. Nevertheless, an optimized 7T protocol as we used in our study can reduce (but not fully eliminate) these signal dropouts and distortions, e.g. by the very small voxel size, shorter echo times as well as optimized shimming and distortion correction. We therefore had to manually discard functional volumes with visible dropouts and distortions.

The analysis of high-resolution functional data raises additional challenges, for instance the precise coregistration of structural and functional (often partial) images or the normalization into a standard space, which is usually done for group comparisons. In our study, we aimed to evaluate functional differences between entorhinal and hippocampal layers and subregions. We thus manually defined our regions of interest and chose a novel approach that enables to use the individual (raw) functional data to achieve highest anatomical precision.

Have other studies examined the hippocampal-entorhinal circuit during memory encoding or novelty detection using more direct neural imaging tools, for example, with intracranial EEG? If so, how do they align with your findings?

Although there have been several intracranial EEG recording studies in humans that investigated functional coupling between hippocampus and EC (i.e. Fernandez et al., 1999), to our knowledge, these studies have not been able to look at deep versus superficial EC or at specific hippocampal subfields.

Your findings have obvious implications for memory disorders. Have you done any work investigating how the hippocampal-entorhinal memory circuit is disrupted in Alzheimer’s or other dementias?

To investigate layer-specific processing in aging or neurodegenerative diseases is of course of particular interest as aging seems to affect particularly entorhinal input from superficial EC layers to the dentate gyrus and also taupathology in Alzheimer’s disease emerges in the superficial EC layers, subsequently spreading to particular hippocampal subregions or layers (i.e. CA1 apical layers). However, high-resolution fMRI at 7T is particularly challenging in older people. The high probability of exclusion criteria (e.g. implants) complicates subject recruitment and stronger subject movement increases motion artefacts. So far we have collected functional data at 7T in healthy older people with 1mm isotropic resolution that we are currently analyzing. In addition, further studies are planned that focus on changes in intrinsic functional connectivity of the hippocampal-entorhinal network in early Alzheimer’s disease.

What further questions do your results raise regarding hippocampal memory pathways, and do you have plans to follow-up on these questions with future studies?

One further question that we are currently addressing is how hippocampal and neocortical connectivity with the EC is functionally organized in humans.

While the rodent EC shows a functional division into lateral and medial parts based on differential anatomical connectivity with parahippocampal and hippocampal subregions, almost nothing is known about functional subdivisions of the human EC.

In addition to characterizing entorhinal functional connectivity profiles in young adults, we also want to study how these are altered by exercise training. Finally, we aim to resolve how aging affects object vs. scene processing (and pattern separation) in different components of the EC and subfields of the hippocampus.

References

Dere E et al. (2006). The case for episodic memory in animals. Neurosci Biobehav Rev 30(8):1206-24. doi:10.1016/j.neubiorev.2006.09.005

Fernandez G et al. (1999). Real-Time Tracking of Memory Formation in the Human Rhinal Cortex and Hippocampus. Science 285(5433):1582-5. doi:1 0.1126/science.285.5433.1582

Friston K et al. (2008). Bayesian decoding of brain images. Neuroimage 39(1):181-205. doi:10.1016/j.neuroimage.2007.08.013

Maass A, et al. (2014). Laminar activity in the hippocampus and entorhinal cortex related to novelty and episodic encoding. Nat Commun 5:5547. doi:10.1038/ncomms6547

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PRP: A shot full of miracles

Four and a half weeks ago I couldn’t bend over, extend my leg in front of me or sit for more than a few minutes without a deep pain in the butt. Four and a half weeks ago I got my first injection of platelet-rich plasma (PRP) to treat a chronic hamstring tendinopathy. I was desperate and eager, but also very skeptical. “You’re a perfect candidate for the treatment,” my doctor encouraged me. “We’ve had incredible success with cases just like yours.” I wanted so badly to believe him, but didn’t want to face the disappointment if it didn’t work. This was my last resort. I had tried every other treatment in the books – ART, physical therapy, massage, dry needling, you name it – none of it helped. So why would PRP? What would I do if it didn’t work?

Platelet-rich plasma: The nitty-gritty

I covered the procedure in detail previously, but to summarize, I received three injections into the injured hamstring, each spaced a week apart. The first was intensely painful, but each subsequent shot was noticeably more tolerable. Despite my doctor’s advice to avoid running completely, I continued running throughout the treatment and recovery, albeit at a slightly reduced mileage (I’ve been logging roughly 25-35 miles/week, compared to my typical 40-45 miles/week). At no point did I feel the running set me back, and if anything, I suspect the gentle activity may have helped stimulate healing.

So, did it work, you ask?

Fast forward to today, and I can confidently say I’ve experienced a medical miracle. I’m by no means 100%, but in just a month I’ve witnessed dramatic, objective improvement and continue to improve daily. For the first couple of weeks, I really wanted to feel an effect and at points convinced myself I felt something. In retrospect, these early notions were most certainly a placebo effect. However, right around two weeks – after my final treatment  – the wishful thinking turned into an undeniable reality. Since then I’ve developed 1) increased range of motion, 2) remarkable strength, and 3) essentially no pain running. Even my ART and massage therapists were astounded at how different … healthier … my tissue felt. So I guess it’s really not just in my head?

Welcome back, Gumby!

I’ve always been flexible … almost too flexible for a runner. But that range of motion disappeared with my recent hamstring flare-up, and I haven’t been able to bend over without intense pain in seven months. Today, I can easily touch my toes (pain-free and without fear of ripping my hamstring!) and can almost do the splits, just like my typically Gumby-esque self.

Return of strength

The tearing in my hamstring left me not only tight and inflexible, but also weak. I’ve been unable to do simple exercises that engage the hamstring, like reverse planks and hamstring curls. Today, my bad leg is still weaker than my good, but I can hold a single-legged reverse plank without collapsing in pain. Now that‘s progress!

Goodbye pain!

The last tidbit of evidence that I’m legitimately improving is the joyous absence of pain while running! Sure, I still feel tight. My stride occasionally shortens, especially with fatigue or during the last couple miles of a long run. But I no longer have to stop mid-run to jam my fist into my cramping butt. Perhaps the most wondrous perk of the this miraculous healing process has been regaining those blissful miles of meditative escape. Instead of cringing in anxious anticipation of when my hamstring will throw a tantrum, or of when my hip will lock up and my feet will refuse to turn over, I can once again float along, physically fluid and mentally free.

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