The Road to Recovery is Neither Short Nor Fast

You have got to be kidding me.  2 years. 24 months.  That is the amount of time that it can take cartilage to form, mature, and adapt to the stresses I’ll likely place on it.  Microfracture surgery forms new cartilage and rather than replace cartilage and hence the recovery is excruciatingly slow, long, important, and individualized.  The recovery will depend on location, size, depth, quality of surrounding cartilage, age, BMI, health, nutrition, goals, motivation, surgery success, and more. Basically, it is highly individualized – so one must recognize that the existing evidence and information out there (this blog post included) is not 100% applicable to your situation.  Still, I hope to provide some insights into my thought process about recovery as I progress through the different stages of recovery.  There will likely be many ups and downs through the process as well, which will hopefully prove instructive (read: Amelia Boone’s great recent blog post highlighting how to persevere in the up and down process of recovery).

Currently, I am in phase 1 of the recovery, the (chondrocyte) proliferation phase.  After the surgeon poked a few holes in my femur the bone marrow hopefully formed a clot over the area which cartilage was missing.  The goal here is to have those stem cells turn into the best possible cartilage making chondrocyte cells as possible.  Not all chondrocytes are the same, studies have shown that some are better than others, just as some muscle cells, neurons, or endothelial cells are “better” than others.  With microfracture one of the reasons inferior firbrocartilage forms normally instead of matching the existing superior articular cartilage is because the chondrocytes that form in the blood clot are inferior to the chondrocytes which reside in existing high quality articular cartilage.  Thus, one of my strategies is to use interventions which either make superior chondrocytes and to keep the chondrocytes from dying off if at all possible during this initial 4-6 week phase of recovery.  My second strategy is to mitigate the many negative side effects of nearly zero load and essentially having my left leg immobilized for the this first 4-6 weeks.  Limb immobilization can cause atrophy of skeletal muscle, connective tissue, metabolic capacity, and overall loss of cardiovascular fitness.

To do so I have researched and adopted 3 strategic approaches which I hope will work together to improve the quality of my newly developed cartilage and lessen the negative impacts of no weight bearing. They are:

  • Mechanical stimulation
  • Nutritional supplementation
  • Passive heat


Mechanical Stimulation

6-8 hours/day. 6-8 weeks. Let’s start with mechanical stimulation.  There is good biological rationale for that mechanical stimulation increases the number of chondrocyte cells formed from stem cells and the quality of these cells as determined by the type and quantity of collagen and proteoglycans secreted by these cells.  The way I am doing this is continuous passive motion or CPM.  Evidence in animals clearly shows that 6-8 hours/day of CPM machine decreases the loss of proteoglycans, increases the formation of chondrocytes, may increase blood flow to the joint (the cartilage normally received very little blood flow and thus nutrients), may lower inflammation, allows more chondrocyte protective proteins to be formed, and overall better recovery (here, here).  However, most of the studies don’t say exactly how much CPM time is ideal or if CPM works better for specific types or sizes of cartilage defects (here).  Again, it’s individual.  Irrespectively of the limitations, my goal has been mechanical stimulation through mainly CPM with a move towards limited partial weight bearing starting at 2 weeks.  I started CPM movement the day after my surgery and have been very consistent with 6-8 hours/day in the “machine”.  I will likely continue for another 3 weeks for 6 weeks total.


Nutritional Approaches

Besides eating fresh foods, non-processed foods, low glycemic index foods, and a variety of vegetables and meats I have a few added supplement strategies not normally applied on a day to day basis.

Push Protein (20-30 grams/meal):  This is a basic one. Every meal should have 20 – 30 grams of high quality protein.  Typically for me its eggs in the morning, a protein shake (without added sugar) for lunch, and some sort of meat (chicken, pork, grass feed ground beef) for dinner on a salad.  See a review here.

Glucosamine and Chondroitin Supplements (2 x per day, 1.5 & 1.2 g respectively. Kirkland USP certified brand):  The literature on glucosamine and chondroitin is unequivocal to say the least.  Typically, this supplement is used for osteoarthritis to protect against further cartilage degradation rather than rebuilding the cartilage.  Still, while I am non-load bearing I can except that the existing cartilage may degrade without normal loading.  Glucosamine and chondroitin are reported to reduce the expression of cartilage degrading proteins (MMP-3) and inflammatory proteins that are detrimental to chondrocyte cell health as well.  (References here, here)

Curcumin (Meriva-SF, 500mg 2x day): Curcumin is a compound found in turmeric and actually has extensive research documenting its effects.  The major biological effect of curcumin is to reduce inflammation and cell division across many different tissues.  My specific interest is because of reports that it reduces the progression of osteoarthritis (reference here), improve chondrocyte cell survival, reduce inflammation, and prevent collagen degradation (reference here).  Other evidence suggests that curcumin may improve the differentiation of chondrocytes, critical to a successful microfracture surgery (reference here and here). There is also evidence it prevents weight gain and metabolic dysfunction following cessation of exercise (here).

Gelatin (~10g/day): The synthesis of soft tissue such as cartilage, ligaments, and tendons suffer from low blood flow.  Recently the role of the amino acid proline in stimulating ligament collagen formation was shown in a wonderful set of very applied studies by Dr. Keith Baar at UC-Davis (reference here).  Most of the gels used in joints use a gelatin like matrix to improve the cellular environment for chondrocyte health and differentiation (reference here, here, .  While I did not have a matrix put into my knee, I am putting plenty of jello into my body in hopes that some of the gelatin finds its way to my developing chondrocytes. In addition I am hoping that the gelatin mitigates some of the loss of connective tissue occurring due to non-weight bearing for an extended period of time.


Passive Heat (Sauna)

4-5 times/week, 20 – 40 minutes, 150 – 170 Degrees Fahrenheit. The last part of my current therapy is sauna time.  I think the sauna is a useful tool for most people and has many, many different beneficial effects.  My rationale is based on studies that have shown:

  • Increased in aerobic capacity and fitness, without training. Likely due to increase blood volume. (here)
  • Increased expression of cellular protective proteins, heat shock proteins, which are also associated with increased longevity and removal of damaged proteins (here)
  • Increased differentiation of stem cells into chondrocytes (here)
  • Heat shock protein can increase in chondrocytes (here)
  • Decreased in atrophy and better muscle function in response to non-weight bearing (here).

My dose is based on the idea that you need to be uncomfortably hot to raise your core temperature to an appropriate stimulus level. While in the sauna I started to include small exercises to keep my heart rate up at a level I typically see on a steady state aerobic run for 10-15 minutes.



 There are problems with many of the studies used as rationale above.  Some are in animals and cell culture models, while others use a small number of people or people with very different condition than I have.  I’ll never know whether my exact protocol is better or worse than any other.  I can’t live my life as repeated experiments to find out definitively what the best approach is.  Instead, I have developed a plan that I think gives me at least a better chance of improving my long-term outcome.  That placebo alone is worth the trouble of researching and implementing such a plan. So I continue to sit in my continuous passive motion machine, eating my jello, and preparing for my next sauna session while visualizing healthy abundant chondrocytes laying down plenty of articular-like cartilage.


Additional Selected References

Ohira, T., Higashibata, A., Seki, M., Kurata, Y., Kimura, Y., Hirano, H., … Furukawa, S. (2017). The effects of heat stress on morphological properties and intracellular signaling of denervated and intact soleus muscles in rats. Physiological Reports, 5(15), e13350.

Hedley, A. M., Climstein, M., & Hansen, R. (2002). The effects of acute heat exposure on muscular strength, muscular endurance, and muscular power in the euhydrated athlete. Journal of Strength and Conditioning Research, 16(3), 353–8. Retrieved from

Scoon, G. S. M., Hopkins, W. G., Mayhew, S., & Cotter, J. D. (2007). Effect of post-exercise sauna bathing on the endurance performance of competitive male runners. Journal of Science and Medicine in Sport, 10(4), 259–62.

Miyabara, E. H., Nascimento, T. L., Rodrigues, D. C., Moriscot, A. S., Davila, W. F., AitMou, Y., … Mestril, R. (2012). Overexpression of inducible 70-kDa heat shock protein in mouse improves structural and functional recovery of skeletal muscles from atrophy. Pflügers Archiv – European Journal of Physiology, 463(5), 733–741.

Tsuchida, W., Iwata, M., Akimoto, T., Matsuo, S., Asai, Y., & Suzuki, S. (2017). Heat Stress Modulates Both Anabolic and Catabolic Signaling Pathways Preventing Dexamethasone-Induced Muscle Atrophy In Vitro. Journal of Cellular Physiology, 232(3), 650–664.

Kuhlenhoelter, A. M., Kim, K., Neff, D., Nie, Y., Blaize, A. N., Wong, B. J., … Roseguini, B. T. (2016). Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 311(2), R377–R391.

Isaka, S., Someya, A., Nakamura, S., Naito, K., Nozawa, M., Inoue, N., … Kaneko, K. (2017). Evaluation of the effect of oral administration of collagen peptides on an experimental rat osteoarthritis model. Experimental and Therapeutic Medicine, 13(6), 2699–2706.

Shaw, G., Lee-Barthel, A., Ross, M. L., Wang, B., & Baar, K. (2017). Vitamin C–enriched gelatin supplementation before intermittent activity augments collagen synthesis. The American Journal of Clinical Nutrition, 105(1), 136–143.

Henrotin, Y., Clutterbuck, A. L., Allaway, D., Lodwig, E. M., Harris, P., Mathy-Hartert, M., … Mobasheri, A. (2010). Biological actions of curcumin on articular chondrocytes. Osteoarthritis and Cartilage, 18(2), 141–149.

stErZi, silvia, GiordaNi, laura, MorroNE, M., lENa, E., MaGroNE, G., scarpiNi, claudia, … foti, calogero. (n.d.). The efficacy and safety of a combination of glucosamine hydrochloride, chondroitin sulfate and bio-curcumin with exercise in the treatment of knee osteoarthritis: a randomized, double-blind, placebo-controlled study. Retrieved from

Kjaer, M., Jørgensen, N. R., Heinemeier, K., & Magnusson, S. P. (2015). Exercise and Regulation of Bone and Collagen Tissue Biology. In Progress in molecular biology and translational science (Vol. 135, pp. 259–291).

Teich, T., Pivovarov, J. A., Porras, D. P., Dunford, E. C., & Matthew Laye, by. (2017). Curcumin limits weight gain, adipose tissue growth, and glucose intolerance following the cessation of exercise and caloric restriction in rats. J Appl Physiol.

Ko, J.-Y., Sun, Y.-C., Li, W.-C., & Wang, F.-S. (2016). Chaperonin 60 regulation of SOX9 ubiquitination mitigates the development of knee osteoarthritis. Journal of Molecular Medicine, 94(7), 755–769.

Chen, J., Li, C., Wang, S., Schmitt, G., & Madry, H. (2014). Periodic Heat Shock Accelerated the Chondrogenic Differentiation of Human Mesenchymal Stem Cells in Pellet Culture. PLoS ONE, 9(3), e91561.

Gracitelli, G. C., Moraes, V. Y., Franciozi, C. E., Luzo, M. V, & Belloti, J. C. (2016). Surgical interventions (microfracture, drilling, mosaicplasty, and allograft transplantation) for treating isolated cartilage defects of the knee in adults. In G. C. Gracitelli (Ed.), Cochrane Database of Systematic Reviews. Chichester, UK: John Wiley & Sons, Ltd.

Karnes, J. M., Harris, J. D., Griesser, M. J., & Flanigan, D. C. (2013). Continuous Passive Motion following Cartilage Surgery: Does a Common Protocol Exist? The Physician and Sportsmedicine, 41(4), 53–63.

Wilk, K. E., Macrina, L. C., & Reinold, M. M. (2010). Rehabilitation following Microfracture of the Knee. Cartilage, 1(2), 96–107.

Howard, J. S., Mattacola, C. G., Romine, S. E., & Lattermann, C. (2010). Continuous Passive Motion, Early Weight Bearing, and Active Motion following Knee Articular Cartilage Repair. Cartilage.



The Decision – Microfracture Surgery

I’ve written more about injuries on my blog lately than I have about training or science or life.  It’s just where I am in life.  As I write this my left leg is strapped into a continuous passive movement (CPM) machine repeatedly going from 0 to 90 and back to 0 degrees.  My leg is restless and as I glance at my stopwatch I see that I still have another 90 minutes of this tortured mechanical and completely painless hell before I reach my goal of 6 hours for the day.  Its repetitive and boring, but yet it is also necessary, like much of recovering from an injury and subsequent surgery.

Continuous Passive Movement in the Tiny Home with Coffee and Charlie

As I prepared for surgery my scientific curiosity came out in full force.  After my first MRI, I consumed every article with the words chondromalacia (cartilage loss) and surgery (see pubmed list here).  It drove me crazy that there is not a single best practice for this and that each of the approaches have major drawbacks.  We can edit out genetic diseases, but can’t fix cartilage?

My injury (likely) began in Scotland (skip ahead a bit if you want injury only details).  After a successful return to competitive ultras culminated with a win at the Highland Fling I decided I needed to explore more of the Highlands before attending the wedding of friends from my Copenhagen days which brought me to the northern parts of the UK.  Northern it was, and in May that meant some significant snow at a mere 1200 ft.  My goal was a 25-mile loop through the Highlands, but 4 miles in I was post-holing and moving at an inexcusably slow pace, which I vowed to make up for with aggressive downhill running.  Poor strategy and my unnecessary risk taking resulted in a nasty fall in which I hit my left knee directly on the granite rock.  With a gash of several inches that required stitches, but only received steri strips (I should have taken advantage of government healthcare), my running on the trip was done.  In the back of my head I was worried that I did something more than cosmetic.  That sort of impact does not go unpunished.

Fast forward several months and an occasional twinge would make its way into my left knee, but never pain and never causing me to stop.  The fall semester of 2015, my first teaching, I was so busy it was near impossible to train.  That spring I vowed to run “the” local race and managed to get into decent shape, but would be stopped from full on training by a left knee pain that would come on following a hard training session and reliable disappear with a few days off.  My race suffered from the same pain a mile from the top of the climb.  Time off, a trip to Europe, and then retraining again while in Boston I suffered the same pain, stopping me from running and lingering into my walks for several days.

Upon returning to Boise I vowed to get the problem fixed.  My MRI showed an area of bone-on-bone contact where a small (2-3 mm) area of cartilage was gone.  I also may have had some meniscus damage.  The surgeon recommended no surgery.  I could walk with no pain and could run 30-40 minutes several times a week pain free.  As I already knew from my own research there were no good options and no guarantees.  Lifestyle adjustments first.  I’d become a more rounded endurance athlete – I could live without running as long as hiking, biking, and new sports like skiing and climbing could fill the gap.

My first MRI following a 9 mile run meant to make the area angry showed a small cartilage defect and swelling of the bone.

I suffered again through a busy Fall and managed to break my thumb cross country skiing.  But my knee was still hurting and not just running.  Skiing and walking seemed to aggravate it. WTF, was I just overly sensitive?  It was getting to the point of altering my quality of life.  A weekend backpacking trip pain-free was impossible and so come spring I sought additional opinions.  All opinions (those with an MD behind their name and mine) agreed that surgery was a good option and that the best of the worst options was a microfracture surgery.

So why are they all bad options? Well we are born with a specific type of cartilage in our joints called articular cartilage.  This cartilage has the property of being able to absorb repetitive shock and allows gliding of bones against each other for the entirety of our lives, hopefully.  Those that suffer osteoarthritis (bone arthritis) have degraded cartilage that causes the bones to rub, become inflamed and painful.  Surgery for osteoarthritis is a temporary fix with many of moving on to total knee replacements, replacing the idea of restoring cartilage with removing the cartilage (and bone) altogether.  This is because the cartilage that they restore or replace is not identical to what was loss in one way or another. However, I’m optimistic that I am not headed down that path yet as my injury lacks the pathology of arthritis and was trauma induced.  Yet, the science is NOT super clear on this either!!!

Note that my cartilage lesion is in the 4-5mm range. So much smaller than the typical 1-5 cm.

Mircofracture surgery has been around for nearly 30 years with mixed success.  In a not uncommon story in modern medicine it was developed before scientists really understood why it works (you only have to show that something works for it to get approved by the FDA).  Now we know it works because of stem cells, or more specifically mesemchymal stem cells that are located in bone marrow.  The surgeon goes arthroscopically into the knee and creates small holes in the bone where the cartilage is missing (in my case the femur).  These holes allow the stem cell containing bone marrow to leak out of the bone and form a blood clot at the area of bone lacking the cartilage.  The stem cells then transform into another type of cell, a chondrocyte.  The chondrocytes are the cells in charge of cartilage.  The cells are embedded within the cartilage and secrete the collagen and proteoglycan proteins that make up the cartilage.  With microfracture we recruit and turn stem cells into chondrocytes that fill in the gap of cartilage.  Unfortunately, the chondrocytes recruited do not secrete the same mixture of collagen and proteoglycan proteins contained in that beautiful slick and strong articular cartilage.  Instead we get a different “type” of cartilage called firbogenetica cartilage.  But it works, for a while.  How long you might ask, and I certainly did? Well the data is not clear on that either.

So why did I choose microfracture if I knew it wasn’t going to make the right kind of cartilage (see a detailed review on the different techniques here).  Well there were a few reasons.  One is that it generally works and it works better for younger (<40), healthy, and normal weight individuals.  So I’m optimistic there. Second, it keeps all the other options on the table.  Other techniques involve taking a biopsy of cartilage from somewhere else and growing it up in the lab or putting it straight into the existing gap.  These techniques work well for larger gaps, but you can only do them once and the replacement cartilage doesn’t always stick.  Athletes have come back from microfracture before.  Several NBA and NFL players have returned to play following the procedure, but many don’t as well.   Most data actually shows no difference in outcomes with the various techniques in patient populations.  Studies do show that the inferior cartilage breaks down though and perhaps I will get 10 years out of my imposter articular cartilage.  Still all of this data is population based – I could be lucky and never have pain again, or in 4 years I might be under the knife again.  Large studies with lots of people don’t tell you exactly how your unique situations will respond.

My PhD mentor always told me that I could spend 26 years being active or focus on competitive 26.2 mile races, meaning I was to jeopardize my long-term health for a short term athletic goal?  However, I had running mentors who were older (and healthy) and that reasoning always felt like a false dichotomy and certain data does back that up. I certainly did not get here because of an over use injury but instead an underuse of my intellect.  But now the question does seem relevant.  When my doctor said that with this surgery I should be able to run again I was taken aback.  I had actually being riding my bike and coming to grasp with the idea of coaching rather than competing.  I was coming to grips with closing that door.  But now…I’m not so sure as like many of you and others it has become a part of my identity, my meaning, and my passion.  Not running has been a struggle, but then again 26 miles or 26 years.  As I move forward with rehab and I plan to share the process. That much is known even if the place that the process is leading me to is not.

Marcus Aurelius Quote. Definitely, can learn from the Stoics in this situation.

For more papers on various ways to deal with cartilage defects: