MY SOLUTION: I started this post several years ago. To anyone who might have benefited from it, I’m sorry I let it sit. I meant to come back and do a more complete job. But for the past few years (as of this writing in February 2020), I have had a working solution to my calf problems. I simply do a ~15-minute warm-up walk before each run, and I also do another brief (~5-min.) walk anytime my run is interrupted for more than 60 seconds or so. I don’t seem to need any of this when I’m out of shape. But when my calves are tight, this has been the solution for me. See the Updates section, toward the end (below), for recent additions.
I plan ahead, so as to prevent my route from requiring me to stop. For example:
If that short answer doesn’t work for you, then read on. I never did finish the research in this post. In several spots, especially toward the end, the text is disjointed and unfinished. I hope it helps nonetheless.
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I had my first calf attack — that is, a sharp pain in my calf while running — in 2006, when I was 50. At this writing in 2017, more than eleven years later, I was still dealing with it. This post presents information I accumulated and conclusions I reached, in the process of attempting to understand the problem and its solution.
The term “calf attack” is my shortened version of the “calf heart attack” term suggested by Runner’s World (Parker, 1996). Having experienced it, I could see why someone would compare it to a heart attack. It was a stabbing pain, like a heart attack, and, for purposes of running, it could be terminal. In Parker’s phrasing, you could “diddle around” with this for months, trying various cures that did not fix the problem. Although I usually had it in my right calf, sometimes I would also have it in my left calf. The two seemed independent; that is, having it in one calf did not seem to influence the other.
Note: I am not a medical professional. This post represents only a writeup of my efforts to understand my own calf pain.
Differential Diagnosis: Less Plausible Possibilities
I believed I had a simple muscle problem. Therefore, at first, I did not attempt to distinguish and rule out alternative possible explanations for my calf problems. This section came into existence when, in the interests of thoroughness, I went back and looked at other potential diagnoses.
A search for sources of information on possible causes of calf pain led to a seemingly endless variety of seemingly relevant materials. Brewer & Gregory (2012), Bonasia et al. (2015), and others (e.g., Goom & Pope, 2017; BMJ Best Practice, 2016; Nsitem, 2013; Medscape, 2015; Physiopedia, n.d.) identified many potential diagnoses.
Given the welter of possibilities and the inability to assess them without the aid of an MRI machine, I sympathized with the statement, by McCrory et al. (2002), that “Even for an astute clinician, distinction between the different medical causes may be difficult given that many of their presenting features overlap.” Nonetheless, at least the ones listed did not seem to fit very well with my impression of my problem. Note that I did not attempt a complete catalog of the maladies that may affect runners’ calves. This was just a summary and response to those that came up during my browsing.
- Stress fracture. There were two lower leg bones. The tibia (i.e., shin bone) was larger and located at the anterior medial side of the leg. (Anterior = front, as opposed to posterior, rear; medial = middle, inside, where the legs rub together, as opposed to lateral, outside, where the vertical stripe on a uniform would be.) The fibula was buried in the center of the leg, somewhat lateral and posterior to (i.e., outside and further back from) the tibia. Apparently the tibia and the fibula were both capable of sustaining stress fractures. OrthoInfo (2007) said stress fractures resulted from overuse — from, that is, continuing to engage in an activity “when muscles become fatigued and are unable to absorb added shock . . . often the result of increasing the amount or intensity of an activity too rapidly . . . [or] by the impact of an unfamiliar surface . . . [or] improper equipment.”
- Medial tibial stress syndrome (i.e., shin splints). Runner’s World (n.d.) said these, too, tended to result from increasing mileage too rapidly or abruptly changing an established workout regimen.
- Metabolic bone disease. Wikipedia characterized this as an umbrella term for a spectrum of disorders, most commonly resulting from abnormalities in levels of key minerals (e.g., calcium, phosphorus, magnesium, vitamin D).
- Arterial endofibrosis. A rare condition, with 90% of cases arising in the external iliac (i.e., groin) artery, occurring most often in the left side for competitive cyclists, in which pedaling eventually lengthens the artery and then causes it to kink or harden, resulting in weakness, cramping, and/or pain during maximum exertion (Fredericson & Tenforde, 2015, p. 103; Briscomb, n.d.).
- Saphenous nerve neuropathy. The saphenous nerve was a cutaneous (i.e., skin-oriented) sensory (i.e., not motor) nerve, running from the upper leg to the foot (Wikipedia). Damage to this nerve could result in anything from minor numbness to severe pain. Such damage could be caused by surgery (as in e.g., fasciotomy to relieve compartment syndrome; see Pyne et al., 2003) or entrapment syndrome.
- Popliteal artery entrapment syndrome. A rare condition (estimated 0.16% of population), existing from birth or developed over time, especially afflicting male athletes under 30, in which enlarged calf muscles compress the popliteal artery — that is, the main artery for the lower leg. Symptoms include aches, numbness, fatigue, and/or cramping in the calf, sometimes with swelling, arising at the same point (i.e., distance, time, level of exertion) in exercise, and fading a few minutes after exercise. See Cleveland Clinic; Wikipedia. Not to get ahead of the story, but this condition seemed most likely to involve the medial head of the gastrocnemius muscle (Wikipedia).
- Adventitial cystic disease. According to the Cleveland Clinic (n.d.), this was a rare, overwhelmingly male (generally young to middle-aged) condition in which a cyst would form in an artery (especially the popliteal artery) and block blood flow. Symptoms would include the symptoms of popliteal artery entrapment syndrome (above), along with leg pain or heaviness that would remain for up to 20 minutes after the end of walking or other exercise.
- Popliteal artery occlusive disease (PAOD) and peripheral arterial disease (PAD). Medscape (Shortell, 2017; Dominguez, 2016) and other sources did not make clear whether these two diagnoses were identical, related, or distinct. For example, in her article on PAOD, Shortell made several remarks about PAD, suggesting it was the same as PAOD. Either way, the general concept seemed to be that ischemia (i.e., insufficient blood flow) due to occlusion (i.e., blockage) could cause claudication (i.e., pain and/or cramping due to inadequate blood flow). According to the National Institutes of Health (NIH, 2016) and the Mayo Clinic (n.d.), the occlusion would usually be caused by atherosclerosis (i.e., the buildup of plaque) inside an artery, and it could be severe enough to result in gangrene and amputation. People especially at risk included the elderly, smokers, and those with cardiovascular diseases. Dominguez (2016) distinguished PAOD from several other maladies discussed here, and also from venous disease (characterized by dull ache at day’s end, not exacerbated by exercise), reflex sympathetic dystrophy (often related to a past trauma in the leg), and diabetic neuropathy.
- Intermittent claudication. As just indicated, claudication was a symptom, not a disease. Following the lead of the Mayo Clinic, I discuss it separately, here, for clarity. Sources distinguished chronic from acute claudication: the former would continue even when the person was at rest, and could include skin that looked bluish or felt cold; while the latter, more commonly called intermittent claudication, would tend to occur only during exercise. WebMD (n.d.) described the pain of intermittent claudication as a “tight, aching, or squeezing [or, according to the Mayo Clinic, weakness or burning] pain in the calf, foot, thigh, or buttock that occurs during exercise,” usually occurring after the same amount of exercise. That is, more strenuous exercise would tend to bring on the pain more quickly. WebMD said, “The average person with blockage of one major arterial segment in a leg can walk 90 to 180 meters (a football field or two) before pain starts.”
- Popliteal artery aneurysm. The University of Virginia (UVA) Heart & Vascular Center, n.d.), described an aneurysm as an outward bulge in the wall of an artery. The risk was that the weakened artery would rupture, introducing a blood clot that could require an amputation and/or potentially fatal bleeding. A popliteal aneurysm was a risk factor for those who smoked, had high cholesterol or blood pressure, had a bacterial infection, or had a previous blood-vessel reconstruction. If there were any symptoms, they would typically include pain behind the knee, edema (i.e., fluid buildup) in the lower leg, foot pain, or foot ulcers that did not heal.
- Popliteal artery dissection. UVA (n.d.) noted that arteries (including the popliteal) can be described as “dissected” when damage to their inner lining allows blood to separate their inner and outer layers, making them prone to burst. Ansari et al. (2016) said the cause of (in their case, abdominal) arterial dissection was not certain, but that it had been linked with a variety of conditions (e.g., hypertension, trauma, elastic tissue disorders).
- Entrapment syndromes generally. Medscape (Hollis, 2017) observed that the saphenous nerve was but one of many leg nerves that could become entrapped. For example, tarsal tunnel syndrome could result in heel pain. McCrory et al. (2002) proposed that dysfunction of the fascia (i.e., the fibrous tissue forming four compartments in the lower leg; see below) could be responsible for a variety of situations in which muscles, arteries, or nerves could be trapped and compressed, impairing their functioning.
- Deep vein thrombosis (DVT). According to the Mayo Clinic (2017), DVT could feature cramping or soreness, often starting in the calf; leg swelling; red or discolored skin; a feeling of warmth; or no symptoms at all. DVT would be caused by a blood clot that could break loose, float away to your lungs, and kill you. Often, it resulted from sitting or lying still for a long time (e.g., after a long plane flight, after surgery, during a long sickness), though there were many other possible causes (e.g., pregnancy, birth control pills, obesity, smoking, cancer, bowel disease, age over 60). Warning signs could include chest discomfort, dizziness, shortness of breath, and rapid pulse (tachycardia). DVT could be impossible to detect without an MRI, ultrasound, blood test, and/or venography.
- Neoplasm. Definition: a new and abnormal growth of tissue in some part of the body, especially as a characteristic of cancer. A search led to indications that growths could appear throughout the lower leg, in or adjacent to bones, muscles, and tendons. The University of Rochester (n.d.) divided the possibilities into four groups: benign and malignant, appearing in bones or soft tissue. Generally speaking, those possibilities occurred in young people; appeared in specific (not necessarily relevant) locations (e.g., thigh); involved a mass (e.g., lump) or swelling; grew aggressively; and/or resulted in consistent pain, a fracture or other bone dysfunction, or otherwise became obtrusive.
- Infections. Sources indicated that this bone infection could originate in an open injury to the bone, an infection elsewhere in the body (e.g., pneumonia, urinary tract), or a chronic open wound or soft tissue infection. In adults, osteomyelitis was found most often in the vertebrae and pelvis. Risk factors included old age, intravenous drug use, sickle cell disease, weakened immune systems, hemodialysis, and diabetes. Symptoms could include pain, tenderness, swelling, or warmth in the infected area; fever, nausea, or general discomfort or ill feeling; limping; and (in the case of open sores) draining of pus through the skin.
- Myopathy. Wikipedia said that a myopathy was “a disease of the muscle in which the muscle fibers do not function properly.” Symptoms included muscle weakness, cramps, and stiffness. Myopathies could be caused by, or related to, a variety of inherited or acquired conditions and diseases (e.g., endocrine, inflammatory, infectious, metabolic, mitochondrial, drug-induced). Medscape (Bethel, 2016) said that symptoms of a myopathy could include muscle weakness, malaise or fatigue, dark-colored urine, fever, and/or scaly areas at joints, among others. As an example of one such myopathy, Medscape (Kedlaya, 2015) said that muscle cramping was one symptom of hypothyroidism.
- Dystonia. Cutsforth-Gregory et al. (2016) described an uncontrolled muscle contraction causing abnormal postures that occurred, rarely, in distance runners and others who regularly engage in cycling, elliptical training, and other repetitive lower-body exercise. Most frequently, in the 20 cases they examined (mostly aged 40-70), the disorder manifested in an unwanted, persistent bending of the foot inward or downward (i.e., toes pointed). In most cases, as one would expect, this symptom eventually impaired the ability to walk.
- Complex regional pain syndrome. The National Institute of Neurological Disorders and Stroke published a Complex Regional Pain Syndrome (CRPS) Fact Sheet. This webpage described CRPS as a pain condition, lasting more than six months, usually arising after an injury, usually affecting just one limb, resulting in prolonged, severe pain (often described as a burning or pins-and-needles sensation) and changes in skin color, temperature, and/or swelling. Often, there would also be high sensitivity, such that normal contact with the skin would be very painful. The peak age for CRPS was 40. It was rare in children under 10 and in the elderly.
In most of the foregoing diagnoses, my situation simply did not seem to match with the causes and/or symptoms just described. Among other things, I did not seem to have an infection, a tumor-like mass, swelling, weakness, cancer, venous plaque, or prior trauma; my pain was not constant, but rather was related directly to the act of running; I didn’t have the sick feeling of a loss of body integrity that I had noticed with previous bone breaks; the pain was not in the expected place (i.e., in my calf), but was instead said to appear in other places (e.g., shin, ankle, thigh, behind the knee); the pain did not consistently arise at a relatively consistent point during exercise (e.g., after a few minutes of running); and/or I was not the right age. There did seem to be at least a possibility that a few of these diagnoses might apply to me, but the connection seemed weak enough that I was inclined to exhaust other possibilities first.
Tendinopathy
For my purposes, it was relatively easy to dismiss most of the foregoing possible diagnoses. But a few others called for a closer look, starting with tendinopathy.
MedlinePlus (2016) and Wikipedia explained that both ligaments and tendons were fibrous tissues, made mostly of collagen, that tied certain body parts together. The difference was that a ligament would connect one bone to another bone. For example, the anterior cruciate ligament (ACL) connected upper and lower leg bones at the knee. By contrast, a tendon would connect a muscle to a bone or to some other structure (e.g., the eyeball). The tissue connecting bone to tendon or ligament was called the enthesis (plural entheses). Researchers observed that some tendons could stretch; for example, the Achilles tendon seemed to add a springlike energy to the stride. To the extent that tendons were able to provide elasticity needed for various motions, it appeared that muscles were spared from having to stretch; apparently this helped them to generate more force.
Wikipedia said, “As of 2016 [tendinopathy] is poorly understood . . . there are several competing models, none of which had been fully validated or falsified.” Under the “tendinopathy” umbrella term, the Cleveland Clinic (2016) distinguished tendinitis, involving “an acutely inflamed swollen tendon that doesn’t have microscopic tendon damage,” from tendinosis, which involved “a chronically damaged tendon with disorganized fibers and a hard, thickened, scarred and rubbery appearance.” In tendinitis, the focus was on inflammation; in tendinosis, it was on degeneration.
Bass (2012) said that tendinitis typically resulted from heavy or sudden overload, while tendinosis was a matter of chronic overuse. She said that, typically, the tendon was twice as strong as its associated muscle; therefore, injury to the tendon (rather than to the muscle) would suggest that the tendon must have been greatly weakened. In her argument, tendinitis tended to be secondary to tendinosis. The practical difference was that treatment for tendinitis would merely seek to reduce inflammation over a period of up to six weeks, while tendinosis rehabilitation would take three to nine months.
Tendon rupture (also called tendon tear) could apparently occur without prior tendinopathy. A search led to various indications (by e.g., Wikipedia, eMedicine) that this would most commonly occur during sports activity, especially when attempting explosive acceleration (e.g., pushing off, jumping), but could also result from direct trauma, from other atypical motions (e.g., twisting, jerking, stumbling, falling), from simply using the tendon after a long period of inactivity, and also from certain medications (notably quinolones) and illnesses (e.g., arthritis, diabetes).
This image from Radsource (Bodor, 2016) showed a cross-section of the two largest muscles of the calf — the gastrocnemius and the soleus — and their tendons (in white), with particular focus on the broad, flat kind of tendon known as an aponeurosis:
According to O’Rahilly et al. (2008), “gastrocnemius” (commonly shortened to “gastroc”) is a combination of the Latin terms gaster (“belly”) and kneme (“leg”), while soleus is the Latin word for a type of flat sandal. As shown here, a single tendonlike feature starts out as the anterior (i.e., front) gastroc aponeurosis, goes down to become a part of the posterior (i.e., rear) soleus aponeurosis, and ends as the Achilles tendon.
My searches for tendinopathy related to these features yielded some discussions of gastrocnemius tendinopathy, and many pages on Achilles tendinopathy, but virtually nothing on soleus tendinopathy. It appeared that “gastrocnemius tendinopathy” referred to problems with the tendons at the upper end of the gastroc, and that “Achilles tendiopathy” referred to problems with the (Achilles) tendon at the lower ends of both the gastroc and the soleus. It seemed that most references to the soleus tendon were atypical if not confused references to the lower (i.e., Achilles) tendon. If the tendon at the upper end of the soleus rarely had problems, presumably that was because stress on the soleus would be absorbed or mitigated by the Achilles, the gastroc, and the soleus itself, leaving the (upper) soleus tendon mostly unscathed.
My pain was not behind the knee. That ruled out the gastroc tendons. For problems with the Achilles, a search led to articles by MedlinePlus (2016) and the Cleveland Clinic (2017) indicating that causes could include sudden increase in activity (e.g., running notably longer distances); sports that have quick starts and stops; bad footwear; running too often, or on hard surfaces, or uphill, or on uneven ground; tight calf muscles; flat arches; heel spurs; and not warming up before exercise. Symptoms could include swelling or pain in the back of the heel, limited range of motion in the ankle, lower leg weakness or pain, stiffness especially in morning, bad pain the day after exercising, and pain when climbing stairs or going uphill.
Sources generally seemed to agree that Achilles tendon problems would tend to be manifested below the calf muscles. That was one reason why I ruled it out in my case: my pain was squarely in the calf muscles, much closer to the knee than to the ankle. As with the soleus tendon, it seemed the upper Achilles and particularly the aponeuroses were generally not problematic.
I also ruled out the Achilles because some of the symptoms seemed directly opposed to what I was experiencing. I noticed, in particular, that running uphill was the one kind of running that never resulted in serious calf pain. If anything, running uphill felt like therapy: it often seemed to reduce calf tightness or soreness. Also, I did not have pain when climbing stairs; the pain was never worse the next day; and I did not have “a slow progression of pain” (AOFAS, n.d.).
Chronic Exertional Compartment Syndrome (CECS)
Compartment syndrome was mentioned by many, and favored by several, of the sources I reviewed (e.g., Parker, 1996; PerformancePlace, n.d.). The general idea was that calf pain was due to the expansion of a muscle during exercise, as the muscle filled with blood, to the point that the limited size of the “compartment” containing that muscle would interfere with normal muscle functioning. According to Tucker (2010), “Muscle volume can increase up to 20% of its resting size during exercise.”
As shown by this diagram from AAOS (2009), there were four muscle compartments in the lower leg: anterior (i.e., up front, by the shin), lateral (on the outer front side of the leg), deep posterior (in the vertical center of the leg, immediately behind the bones), and superficial posterior (at the rear of the leg). Compartment walls consisted of “fascia,” which WebMD (2016) described as “[s]trong webs of connective tissue.” Duke University School of Medicine indicated that the large muscles of the lower leg (notably, the gastrocnemius and the soleus) were in the superficial posterior compartment.
Acute vs. Chronic CS
Compartment syndrome (CS) could be either acute or chronic. Medscape (Rasul, 2017) said that acute CS would typically follow a traumatic event, especially a fracture. Somewhat like crush syndrome, the trauma would impair blood flow through the muscles in a compartment. Often, this impairment would be limb- and even life-threatening. The standard response to acute CS would be a fasciotomy (i.e., relieving pressure by cutting the fascia that formed the affected compartments). In a study of 36 patients who underwent acute compartment fasciotomies, Heemskerk and Kitslaar (2003, p. 747) found that 45% of patients recovered from surgery with good limb function, 27.5% kept their leg with reduced function, 12.5% underwent amputation, and 15% died.
Chronic (i.e., ongoing) CS was similar to acute compartment syndrome, in the sense that it would entail constriction of blood flow, but the constriction was not so extreme; hence, chronic CS was not a matter of emergency medicine. Chronic CS would commonly result from exercise, and was thus often referred to as chronic exertional compartment syndrome (CECS). WebMD (2016) elaborated:
[B]lood or . . . [fluid] may accumulate in the compartment. The tough walls of fascia cannot easily expand, and compartment pressure rises, preventing adequate blood flow to tissues inside the compartment. . . .
[C]hronic compartment syndrome develops over days or weeks. Also called exertional compartment syndrome, it may be caused by regular, vigorous exercise. The lower leg, buttock, or thigh is usually involved. . . .
Symptoms of chronic compartment syndrome . . . include worsening aching or cramping in the affected muscle (buttock, thigh, or lower leg) within a half-hour of starting exercise. Symptoms usually go away with rest, and muscle function remains normal. Exertional compartment syndrome can feel like shin splints and be confused with that condition.
Tucker (2010) cited fascial defect as an alternate, related diagnosis. The concept here was that there could be a hole or weak spot in the fascia, allowing muscle to bulge through and resulting in nerve compression. But I, myself, did not have the pain radiating to the foot that Tucker said would typify that malady.
Prevalence of Superficial Posterior CECS
CECS appeared to be fairly rare. Orlin et al. (2016) contended that “a large proportion of those presenting with muscular pain actually have [chronic compartment syndrome].” Yet this conclusion was possible only through relaxation of the diagnostic standard; none of their study participants’ legs had compartment pressures meeting the conventional standard. As Orlin et al. acknowledged, the symptoms for patients without markedly elevated compartment pressure could be “very mild.”
During a period of eight years (2003-2010 inclusive) when an estimated four million Americans served in the U.S. military (see Pew Research Center, 2011; the average number of Americans in uniform at any specific point was apparently about 1.4 million), Waterman et al. (2013) found a total of only 611 service members who underwent fasciotomies for chronic CS in any lower leg compartment. Elsewhere, acknowledging that military service members constituted “an idealized subset at risk” of CECS, Waterman et al. (2013) found an incidence rate of about one case of CECS per 2,000 person-years.
Among the few who did suffer from CECS, only a small fraction involved the posterior compartments. A glance at the AAOS diagram (above) showed why: the anterior compartment was especially small and tightly bound. Various sources (e.g., Gross et al., 2015; Duke Medicine) considered CECS rare to nonexistent in the superficial posterior compartment, where the big calf muscles were.
For that matter, CECS hardly seemed to occur in the deep posterior compartment. Over a 3.5-year effort to sign up study participants at the second-largest medical center in a region comprised of nearly three-quarters of a million inhabitants, Winkes et al. (2016) diagnosed only 91 individuals with deep posterior CECS (dp-CECS). In a study of 36 patients with CECS, Edmundsson et al. (2009) found only four who appeared to have compression in both the deep posterior compartment and the anterior compartment; none with compression only in the deep posterior compartment; and none (or perhaps one — the account is unclear) with compression in the superficial posterior compartment. Among the 611 U.S. military CECS patients identified by Waterman et al. (2013), only 19.4% of fasciotomies involved an unspecified (but apparently the deep) posterior compartment, along with the anterior compartments, and only 2.2% involved a posterior compartment without an anterior compartment.
Fasciotomy Outcomes
I ran a search to learn more about fasciotomy outcomes. Starting with articles already cited (above), I saw that, among Waterman’s et al. (2013) 611 U.S. military CECS patients, many experienced less-than-ideal post-fasciotomy outcomes: for 45%, CECS symptoms recurred; 28% were unable to return to full duty; 16% had surgical complications; 6% underwent surgical revision (i.e., one or more additional surgeries to reduce scar tissue or otherwise clean up undesirable aspects of the previous surgery); 17% were ultimately referred for medical discharge from the military due to continuing CECS rendering continued service infeasible; and only 14% experienced complete recovery.
In an article published about the same time as (and not citing) the work of Waterman et al. (2013), Winkes et al. (2013) contended that prior research was of poor quality, for purposes of determining the effectiveness of fasciotomy for deep posterior CECS (dp-CECS). Winkes et al. acknowledged that the previous literature concluded that “outcome for dp_CECS is traditionally considered unpredictable.” For example, Edmundsson et al. (2009) found that, of 57 legs on which fasciotomies were performed, only 41 (72%) yielded outcomes that could be considered good or excellent.
In evaluating prior studies, Winkes et al. (2013) were willing to consider only seven (26%) of 27 prior papers; they excluded Edmundsson’s research from consideration on grounds that it was not specifically oriented toward dp-CECS and did not state postoperative outcomes with sufficient clarity. I appreciated that, for legitimate reasons, one could select criteria that would exclude most prior research. Aweid et al. (2012, p. 356) agreed that “the quality of [prior] studies was generally not high.” Nonetheless, it seemed glib to claim, as Winkes et al. did (p. 5), that “Surgery for most types of CECS . . . is successful” when Edmundsson et al. reported that, post-surgery, one-third of patients still had pain during exercise.
In subsequent work, Winkes et al. (2016) performed fasciotomies and studied outcomes for 44 athletes diagnosed with dp_CECS. Winkes et al. (p. 1) claimed that, “Based on their outcome, 76% of [those] patients would opt for surgery again.” But given the alleged precision of this team’s work, I was disappointed to see that the details of this post-operative survey were not provided. It seemed fair to wonder whether the outcomes had been in any sense skewed, intentionally or otherwise, given the admission (p. 2) that Winkes himself had performed more than 500 fasciotomies, including these 44. Bias is a widely recognized and significant risk in most varieties of research (e.g., Pannucci & Wilkins, 2010). It would be expected that many people in such a position would interpret evidence in ways supportive of their own choices.
Winkes et al. (2016, p. 5) said that, as of May 2015, 37 of the 44 patients had been out of surgery for more than a year (median = 26 months), and at that point were asked about four topics: their surgical complications, time to full recovery, time to return to sports, and residual symptoms. Two of the 44 did not respond to contact attempts. It was not clear why Winkes et al. did not wait to administer these questionnaires to the remaining five patients, nor why three others were not included. Of the 34 whose long-term reports were used, only 12% reported excellent results. Another 35% reported good results, and 24% reported moderate results, leaving 18% reporting only fair results and 12% reporting poor results (total = 101%; presumably rounding error). Only 29% returned to their preinjury level of sports activity; 47% were able to exercise only at a lower level, and 23% ceased to be engaged in sports. Wilkes et al. did not explain how questions about those four different topics (e.g., surgical complications) were combined to produce those simple percentages, nor why patients would be asked for a subjective evaluation of, say, their time to full recovery, instead of specifying a number of months. Winkes et al. (p. 4) arbitrarily decided that patients who did not rate the results of their fasciotomies as either excellent or good — specifically, those who rated the results as only moderate — would nonetheless be considered part of “the success group.” Lavery et al. (2017) did not share that enthusiasm. Even then, such a claim implicitly acknowledged that fasciotomy was a failure for at least 30% of these carefully selected patients.
Packer et al. (2013) compared outcomes for 71 fasciotomy patients against those of 27 patients given nonsurgical treatment. The former reported higher success (81% vs. 41%) and satisfaction (81% vs. 56%). Contrary to some reports, the measured pressure within the targeted compartment did not correspond to the degree of operative success. What did matter was choice of compartment and age of patient: failure rates were 0% for fasciotomies limited to the anterior compartment, but 31% for fasciotomies on both the anterior and lateral compartments; and satisfaction rates were 89% for high school-age patients, 94% for college patients, but only 66% for post-college patients.
Pasic et al. (2015) reported results from fasciotomies on 46 patients. The authors found that 11% of patients required a revision fasciotomy. In long-term follow-up (average = 55 months), 78% reported being satisfied or very satisfied with the results of the surgery. Patients also provided high ratings regarding their ability to return to sport and to pre-surgery activity levels generally; 76% reported that their expectations were met; 87% said that, with the benefit of hindsight, they would choose the surgery; and 91% said they would recommend it to others. Unlike some other studies, Pasic et al. found that dp-CECS patients were just as satisfied as the those without dp-CECS. The authors credited this to the use of a surgeon experienced with this procedure. But there was one odd thing in the Pasic et al. (2015) report: an indication that, among those 46 patients, with a total of 80 legs having one or more affected compartments, there were 42 legs with superficial posterior CS. I had encountered no other study suggesting that more than half of studied patients experienced sp-CECS. I noticed, too, that Pasic et al. (p. 710) claimed that exactly the same number (i.e., 42) also had dp-CECS. Likewise, Pasic et al. said that 80 legs had anterior CECS, and also 80 legs had lateral CECS. The article did not seem to explain these numbers.
Reading these research articles, I felt myself drawn somewhat to the medicine man hypothesis: what he believes may not be as important as how good he is at it. Having become personally acquainted with the possibility of a poor surgeon, I was willing to contemplate that maybe fasciotomy was a delicate matter, involving deep meddling into one of the most important things you will ever own, and maybe the Army was just not the best place for that sort of thing. As Lavery et al. (2017) put it,
Historically, deep posterior fasciotomy has resulted in consistently poorer surgical results than anterior and lateral release, with success rates reported from 30% to 65%. . . . The reason for less predictable outcomes after the surgical treatment of deep posterior CECS is unclear. Causes may be attributed to improper diagnosis, treatment, or both. . . . [T]he clinical presentation of deep posterior CECS can be vague, often consisting of nonspecific pain or cramping. The extensive differential diagnosis combined with an often nebulous presentation, lack of physical findings, and unreliable objective diagnostic testing results in the increased potential for misdiagnosis or unrecognized concomitant pathology. There is also a lack of consistency among surgical techniques . . . . [I]t is clear that posterior fasciotomy presents a more challenging surgical dissection than anterior and lateral releases.
Perhaps it wasn’t surprising that even these supposed wizards of the process seemed to be turning out rather alarming failure rates. This was not like getting a tooth filled. Those who have witnessed plastic surgery gone wrong may share my sense that some might want to consider alternative approaches (e.g., Isner-Horobeti et al., 2013).
Ruling Out CECS for Me
In the first draft of this post, I came rather quickly to the conclusion that I probably didn’t have CECS. But when I revisited the matter, I decided that this was the point at which I should explore the calf’s structures in more detail. It also seemed, upon review, that before proceeding in other directions, I should have a good sense of how strongly I was going to resist CECS as a possible diagnosis. The foregoing exploration made me pretty firmly inclined to explore other possibilities first. That inclination was consistent with Tucker’s (2010) advice to consider other diagnoses because detection of compartmental pressure buildup would require invasive measures. I was even more doubtful of the CECS concept after reviewing Tucker’s indication that (at least as of 2010) experts disagreed as to what was actually happening in CECS.
Some of the arguments against CECS have already come up. For one thing, CECS often felt like shin splints because 95% of cases of CECS involved the small forward (i.e., anterior and lateral) compartments of the lower leg (Tucker, 2010). Even when the pressure was in the deep posterior compartment, the pain was evidently most noticeable up front. Winkes et al. (2013, p. 7) characterized medial tibial stress syndrome (MTSS) as “the greatest mimicker of dp-CECS” because “a substantial portion of patients with dp-CECS do demonstrate signs associated with MTSS such as distal tibial bone tenderness.”
In other words, it seemed that, even within the minority of a minority that had CECS in the deep posterior compartment, very few would have calf pain without also having shin or other anterior pain. Since I did not have shin pain, this seemed to be an argument against a diagnosis of dp-CECS in my case. Superficial posterior (i.e., sp-CECS) seemed to be virtually nonexistent, for a logical reason. When you exercise your calves, they get bigger. The soleus and gastroc are not locked into a compartment; they are able to expand outwards. No doubt smaller muscles in other compartments could develop too, but they would tend to result in pain up front, and I wasn’t having that. Besides, I was getting this pain early on, when my muscles were relatively undeveloped, after taking time off from running. If anything, I felt that the calf problem diminished as my legs became more conditioned.
And then there was the fact that I was an older runner. According to the Mayo Clinic (2017), CECS was most common in people under 30. At my age, the problem was not that muscles were swelling out beyond the city limits; it was that muscle would tend to shrink. As far as I could tell, this was a case of surplus storage room, where my leg compartments and I were waiting and hoping that those muscles would come back and take up residence once again. Compression? Probably not.
Another classic sign of CECS, according to Lavery et al. (2017): “Symptoms occur after a predictable duration and intensity of exercise.” Bonasia et al. (2015) and the Mayo Clinic (2016) said the symptoms would start, each time, after about the same time, distance, or intensity of exertion, and would subside within 10-20 minutes after stopping. Mine was not a gradually increasing pain or discomfort. It actually had two parts. There was an enduring ache that might come and go at various times during a run; and then there was a sharp pain that could come on quite suddenly, at any point during a run (although especially when I was first starting out, especially if I did not take a warmup walk or bike ride first), and could also go away very quickly, almost as soon as I stopped running.
Those sources also said that the symptoms in question could include aching, burning, cramping, tightness, numbness, tingling, or weakness (e.g., “floppy foot”). That made sense, if the problem did involve a cutoff of blood to the muscles. But as noted in connection with other possible diagnoses (above), I did not have most of those symptoms, and the symptoms I did have were not spread across an entire posterior compartment. I would find no pain, swelling, or discoloration if I probed with a firm finger anywhere in my calf, except in the one specific spot where I felt the dull ache or the sharp pain.
Historical Review of Muscle Injury Grading
I started this post with a belief that I had a muscle problem. I went through a number of other possibilities, involving other leg components (e.g., bones, tendons, compartments), to make sure I wasn’t overlooking something. I hadn’t gotten into those alternative diagnoses in great detail, so it was still possible I had missed the real explanation, but now at least I could have some confidence that the muscle focus made sense.
In looking at those other possible diagnoses, I had been pretty much on my own. I had found several lists of things that could cause calf pain, but there was no real structure or organization to those lists; they were just haphazard collections, most of which mentioned some but not all of the things that appeared on other lists. It was actually kind of crazy that people had been having problems with legs for as long as there had been people, and yet it seemed nobody had sat down and come up with an organized plan or flow chart that would take you through the options.
Now that I was in a position to focus on muscle problems, I sympathized with Hamilton et al. (2014) when they bemoaned “the lack of a uniform approach to the categorisation and grading of muscle injuries.” But here, at least, people had tried to come up with an organized system. Hamilton et al. offered a brief review of efforts, especially during the past half-century, to classify muscle injuries and to grade their severity. Having seen so many different alleged classifications of injury, it seemed advisable to try to understand what Hamilton et al. were saying.
Based on a substantial historical literature review, Hamilton et al. (2014) Supplementary Table One offered a remarkable chronology of attempts to classify and grade muscle injury, from Marsh (1896) to Pollock et al. (2014). I was particularly interested in that list because Hamilton et al. included what appeared to be the key classificatory terms used by those sources. For example, Heald (1931) was the first listed source to use the word “strain” to describe a kind of muscle injury. I was particularly interested in that word because I wanted to verify that it was a synonym of a muscle “pull” or “tear,” as WebMD (2016) and Wikipedia indicated. Generally, the listed sources did seem to treat muscle pull, strain, and tear as synonymous. As I was about to see (below), the Munich Consensus Statement (Mueller-Wohlfahrt et al., 2012) recommended not using “strain,” because that term “is used with a high degree of variability between practitioners,” preferring “tear” instead.
From that literature review, Hamilton et al. (2014) posited a Clinical Era (roughly 1900-1980) in which clinicians indirectly evaluated the degree of muscle damage according to symptoms. For example, Featherstone’s (1957) Sports Injuries: Their Prevention and Treatment (pp. 31-34) used the knee to illustrate the desired clinical method: start by taking a history of what has been happening; examine for visible signs (e.g., swelling, bruises); identify what is painful by probing and by having the patient move it; conduct diagnostic tests (e.g., “spring” the knee by bending it slightly in ways it was not meant to go, so as to stretch the suspected ligaments); and examine the “voluntary, passive, and resisted movement” of related muscles (e.g., quads).
Whatever the merits of such procedures, Hamilton et al. (2014) said that, during the Clinical Era, there was virtually no research linking the clinician’s observations to specific outcomes — and yet “historical (clinical) grading systems of muscle injury . . . have been recycled in various modified forms and continue to appear in the literature.” As an example, Hamilton et al. cited Maquirriain et al. (2007, p. 844, Table 1), who used a pain-based clinical grading system for strains of the rectus abdominis muscle proposed by Lehman (1988). The point appeared to be that nobody had established that pain levels had anything to do with how long it would take to recover, or how satisfactory the recovery would be.
Altogether, in a quick look at Hamilton et al. (2014) Supplementary Table One, aside from very simple distinctions (e.g., minor vs. severe), I counted a total of 28 different schemes by which to divide muscle injuries into (typically, three or four) grades, types, or degrees of injury. In that light, it was not surprising that I had encountered a bewildering assortment of muscle injury gradations in various webpages.
Hamilton et al. (2014) suggested that the Clinical Era was followed by the Imaging Era of the 1980s and 1990s, when ultrasound and MRI imaging facilitated direct viewing of muscle injury; but here, again, researchers generally failed to link such observations with actual outcomes. Hamilton et al. cited the exception of Pomeranz and Heidt (1993), who studied the correlation of injury size to progress during rehabilitation.
Finally, according to Hamilton et al. (2014), for present purposes the medical world entered the Modern Era (circa 2000-present), characterized by three key features:
- Accumulation of evidence demonstrating the extent to which various injury symptoms (i.e., the patient’s subjective experience, e.g., pain) and signs (i.e., outwardly observable indications, e.g., MRI imagery) were useful for predicting outcomes.
- Use of continuous variables. The focus here seemed to be on precision. If you have an MRI that can determine that one injury is 1.2 centimeters long and another is 2.4 centimeters long, you might be able to demonstrate that, say, an injury twice as large can require three times as long to heal. In addition, precise measurement eliminates the gray areas that can arise when, for instance, an injury is right on the boundary between so-called Grade 2 and Grade 3 injuries.
- Hamilton et al. said, “The past 5 years have seen a range of publications touting ‘new’ muscle injury classification and grading systems,” but only two provided supportive clinical data. Of those two, Hamilton et al. were particularly interested in the Munich Consensus Statement (MCS): they described it as the first time, in more than 100 years of muscle injury grading, when large amounts of data were being used to test a system of classifying and grading muscle injuries.
Hamilton et al. (2014) concluded,
To date, there remains minimal pathological or prognostic validity to the majority of classification and grading systems utilised. . . . [I]t seems unlikely that any categorical grading of muscle injury severity will accurately predict an individual’s healing time. . . . [I]t is time to recognise the complexity of muscle injury.
In short, Hamilton et al. conveyed, to me, the impression that it could make sense to classify types of muscle injuries, but that simplistic and discrete muscle injury gradings were better replaced with continuous and nuanced analyses. As I was about to see, this impression would prove inconsistent with Hamilton’s later suggestions.
Differential Diagnosis via the Munich Consensus Statement
Since at least 2012, several authors (notably Hamilton, Valle, and Tol) have been prominent in the evaluation of proposed muscle injury classification systems. As just noted, Hamilton et al. (2014) considered the Munich Consensus Statement (MCS) (Mueller-Wohlfahrt et al., 2012) a step in the right direction. As described by Mueller-Wohlfahrt et al. (2013), the MCS arose from responses to questionnaires completed by 19 English-speaking scientists and team doctors of national and first-division professional sports teams, as evaluated by 14 sports medicine experts from a number of Western countries.
Context of the MCS
Recently, Valle et al. (2017) proposed an MLG-R system with the potential to rectify several problems that Tol et al. (2012) identified in the MCS. The letters in the name of this system referred to Mechanism of injury, Location of injury, Grading of severity, and (number of) Re-injuries. While Hamilton et al. (2017) did not evaluate this MLG-R system, they did convey several features of the MLG-R system that, to me, appeared problematic:
- As its authors acknowledged, the MLG-R system so far had been developed only for use with hamstrings: it remained “only a theoretical model” that would require “[s]ubsequent studies . . . [and probable] modification . . . to include other muscle groups and validate its content.” There was no guarantee that its content would, in fact, be validated.
- Hamilton et al. (2017) criticized existing systems (including the MCS) for failing to provide an effective prediction of when an injured athlete could return to play (RTP); and yet, in the end (for understandable reasons), the MLG-R writeup likewise offered only a hope that the MLG-R system would assist in RTP decisions.
- While the MLG-R authors contended that their system offered “easy clinical application” for physiotherapists and trainers, the words of Hamilton et al. (2017) seemed to apply here as well: after the MCS, proposed classification systems had become “increasingly complex.” This was true particularly of the proposed injury severity grading. For instance, the MLG-R described a grade 3 injury in terms that would be “easy” only for trainers fluent in MRI-speak:
Any quantifiable gap between fibers in craniocaudal or axial planes. Hyperintense focal defect with partial retraction of muscle fibers ± intermuscular hemorrhage. The gap between fibers at the injury’s maximal area in an axial plane of the affected muscle belly should be documented. The exact % CSA should be documented as a sub-index to the grade.
- The MLG-R system seemed to achieve a degree of simplicity primarily by dispensing with concepts that could help the clinician to zero in on the most likely diagnosis. As illustrated in my own case (below), these included the distinction between structural and non-structural disorders, and the possibility of neuromuscular disorders.
Among the muscle injury classification systems that had been developed to a relatively complete degree, Hamilton et al. (2017, Table 2) seemed to indicate that the MCS (Mueller-Wohlfahrt et al., 2012) offered the best available guidance, for purposes of achieving a practical, relatively simple differential diagnosis. (See also Grassi et al., 2016.) Indeed, rather than replace the MCS, it seemed that the MLG-R might complement it. The MCS offered someone like me some assistance in guessing how I might best proceed in my own self-treatment, as an alternative to the presently nonexistent option of sports medicine for less-than-wealthy residents in certain American jurisdictions.
MCS Top Levels: Direct vs. Indirect, Functional vs. Structural
As just described, I concluded that the Munich Consensus Statement (MCS) (Mueller-Wohlfahrt et al., 2012) offered helpful guidance for a runner seeking the guidance of leading clinicians on the question of what might be wrong with his calf.
Table 2 of the MCS started with the question of whether the injury was direct or indirect. For this purpose, “direct” meant either a contusion (most commonly a bruise) or a laceration (i.e., a cut or tear, from the surface of the leg down into the muscle). The MCS said direct injuries would be caused by external rather than internal forces — by, for example, a blow from an opponent’s knee or, for runners, a fall or a collision.
Plainly, the calf attacks I was experiencing were indirect injuries. In that case, the MCS offered a choice between functional and structural. Structural muscle injuries consisted of total or partial muscle tears. WebMD (2016) explained that symptoms of muscle or tendon strain — or tearing, to use the term preferred by the MCS — could include swelling, bruising, or discoloration; pain at rest; pain when using the related muscle or joint; weakness of the muscle or tendons; and/or inability to use the muscle.
Most of those symptoms did not apply to me. At times, I did have pain or inability when trying to use the specific muscle for running. In those instances, there might have been some tearing. But that wasn’t a core, consistent aspect of the problem. Therefore, I suspected that the calf attack was an indirect (not direct), functional (not structural) muscle disorder. MCS Table 3 said that MRI and ultrasound would see problems in direct muscle injuries, and also in the structural kinds of indirect injuries (i.e., muscle tears), but would not show anything (other than possibly finding some fluid buildup) for functional muscle disorders. That was the case for me: at one point, early on, I went for an ultrasound and a series of physical therapy sessions, but the therapy seemed ineffectual and the ultrasound showed nothing.
MCS Type 1 (Overexertion) and 2 (Neuromuscular) Disorders
Within the sphere of indirect, functional muscle disorders, MCS Table 2 (Mueller-Wohlfahrt et al., 2012) offered a choice: my muscle disorder was either Type 1 (overexertion) or Type 2 (neuromuscular). MCS Table 3 divided each of those into two subtypes. I started with a look at subtypes 1A and 1B.
Subtype 1A involved fatigue-induced muscle disorder. This appeared to be the simple and common muscle soreness and/or tightness that would occur during or shortly after strenuous activity, resulting in “dull, diffuse, tolerable pain.” Subtype 1B involved delayed-onset muscle soreness (DOMS), arising 24-48 hours after the activity ended. This, too, was familiar: it was the fatigue-induced soreness that a person might experience when s/he participates enthusiastically in some sporting activity, for the first time in a long time, and then awakens the next morning to discover sore muscles s/he didn’t even know s/he had. I had experienced both of these, but neither captured what was unusual and most problematic about the calf attack.
That left me with Type 2 disorders. These were described as “neuromuscular” because they involved not only the sore muscle, but also nerves related to it.
Ordinarily, it seemed, “neuromuscular disorder” would mean a serious disease. Among the many (often incurable) examples listed by MedlinePlus (2017) and Johns Hopkins (n.d.), I saw multiple sclerosis, Parkinson’s disease, and myasthenia gravis. But those were surely not the kinds of maladies intended by the MCS article (Mueller-Wohlfahrt et al., 2012), when it indicated that its concept of Type 2 disorders would be related to specific muscles. This was, after all, an article whose title referred to “muscle injuries in sport.” I inferred that, when the article spoke of neuromuscular disorders, it meant a type of problem that could be fixed or at least ameliorated, sufficient to allow the patient to return to some level of sporting activity.
In the MCS article’s subtype 2A neuromuscular disorders, the nerves in question were those of the spine, not of the calf. The spine could be implicated because, according to that article,
[T]heoretically any pathology relating to the lumbar spine, the lumbosacral nerve roots or plexus, or the sciatic nerve could result in hamstring or calf pain. . . . Thus, it is important that assessment . . . should include a thorough biomechanical evaluation, especially that of the lumbar spine, pelvis and sacrum.
Medscape (Shortell, 2017) said that spinal issues related to the lower leg could include pseudoclaudication, lumbar disc disease, and spinal stenosis. The MCS article said, “[B]ack injuries are very common in elite athletes.” I looked at the article they cited in support of that view. That article (Ong et al., 2003) examined 31 athletes treated for lower back pain and/or sciatica during the Sydney 2000 Olympic Games. Notably, that article said 21 of those 31 athletes were from track and field. In my brief glance, the article did not seem to specify how many of those might have been runners, but presumably some were: running was quite commonly associated with lower back pain.
The concept appeared to be that I might be able to probe deep into the calf muscle and identify the injured spot, and yet the actual (or at least primary) problem would be found in the spine. I could not absolutely rule that out. But, to my knowledge, I did not have back problems. Thus, before looking for spooky action at a distance of several feet away from the sort spot, it seemed advisable to make sure I had exhausted the remaining and, to my mind, more likely alternative.
The remaining alternative was subtype 2B. MCS Table 3 said that subtype 2B consisted of neuromuscular functional disorder related, not to the spine, but rather to the nerves in the calf itself. What I found particularly relevant, in Table 3, was that they said a subtype 2B disorder would involve “gradually increasing muscle firmness and tension,” along with “[c]ramp-like pain” extending across the entire muscle. That did describe part of what I was experiencing. They also said, “Therapeutic stretching leads to relief,” but in my experience that was not particularly true. Stretching the tight calf did not feel bad — it felt like something that it might be helping — but I had not yet found a form of stretching that seemed to have any significant effect on that tightness.
Understanding the Calf Muscles
At this point, I had exhausted the categories of disorder shown in Tables 2 and 3 in the MCS article (Mueller-Wohlfahrt et al., 2012). I had a clues that perhaps nerves in the calf were responsible for my symptoms, but I was not sure what to do with that. It seemed I would need to learn more about the operation of calf nerves and muscles. I started with the muscles.
Overcontraction in Antagonistic Muscle Pairs
The MCS article provided a useful starting point, for purposes of investigating learning more about MCS subtype 2B injuries. Specifically, I was interested in that article’s cryptic reference to muscle overcontraction:
Dysfunction of . . . neuromuscular control mechanisms can result in significant impairment of normal muscle tone and can cause neuromuscular muscle disorders, when inhibition of antagonistic muscles is disturbed and agonistic muscles overcontract to compensate this.
To understand that statement, I had to understand agonistic and antagonistic muscles. Wikipedia explained that the agonist muscle would be the one causing movement. In a dumbbell curl, for example, the elbow flexor muscle group (including the biceps) was the agonist: those muscles would curl the wrist back toward the shoulder. Meanwhile, the elbow extensor muscle (i.e., the triceps) was the antagonist. Antagonist muscles would also be active during a dumbbell curl, providing opposing force to help control the movement, and also returning the arm to its original (extended) position after the curl. Together, the flexor and extensor muscles (i.e., biceps and triceps) formed an antagonistic muscle pair.
Hence, the MCS quote seemed to be describing a dysfunctional situation in which the nerves would fail to restrain the antagonist muscle properly. It would be like driving while pressing both the gas pedal and the brake: the two would fight against each other in an inefficient and potentially destructive manner. Specifically, the antagonist muscle would not be properly inhibited — it would oppose the agonist muscle too strongly — and that would require the agonist muscle to overcontract (i.e., to work too hard) in order to complete the desired motion. In the dumbbell curl example, the triceps would impose excessive resistance, and the biceps would therefore have to work harder.
That might not seem like a bad thing in the case of a dumbbell curl. It might make the biceps stronger. But you’re not doing five thousand bicep curls within a single hour. If this was happening every time I took a step, at a rate of more than 1,400 steps per mile, it would be no surprise if the calf muscles started to degrade — resulting, as the quote says, in “significant impairment of normal muscle tone.” It seemed that, paradoxically, further exercise could actually make the affected muscle weaker, as its antagonist gradually wore it down.
In the upper leg, Elias et al. (2003) said, the hamstring muscles were agonists, and the quadriceps (quads) muscles were antagonists. The hamstring (on the back of the leg) would pull, to power a runner’s step. The quads would also pull slightly, to control the angle of hamstring pull during the step. Then, to return the leg to its original extended position, the quads would pull, and the hamstrings would help to control the angle. The quads and the hamstrings were on opposite sides of the leg, so it did seem reasonable that one would have to loosen up when the other tightened.
The quads and hamstrings would pull both the upper and lower sections of the leg. This was possible because, while those muscles were located on the upper leg, they (with their associated tendons) were long: they ran from above the hip joint to below the knee joint. So they were involved with bending at the hip as well as the knee.
The situation was somewhat similar for at least one of the largest calf muscles. As shown in this Duke Medicine image, the gastroc ran down from its two heads, above the back of the knee, to form the Achilles (calcaneal) tendon, which was attached to the back of the heel bone. Thus, just as the upper-leg muscles were involved in bending at both knee and hip, the gastroc was involved in bending at both knee and ankle.
The soleus was not like these other upper- and lower-leg muscles. For one thing, it was not on the opposite side from the gastroc, and thus did not operate as its antagonist. Also, according to Gray’s Anatomy for Students (Drake et al., 2009, p. 589), the soleus did not span the knee joint, but rather was anchored to the top ends of the lower leg bones, and thus did not play a role in knee bending. At its lower end, the soleus joined the gastroc in forming the Achilles tendon. Perhaps for that reason, as evidenced in numerous sources, some anatomists viewed the gastroc and soleus as forming, in effect, a single muscle, referred to as the “gastrocnemius-soleus complex” or (with the plantaris muscle) the “triceps surae” (e.g., Wikipedia). Or perhaps one could call it simply the gastroleus. One would not want to overstate the unity of these two, however; they were not simply identical or parallel. For instance, Suzuki et al. (2014) found that straightening the leg and pointing the toes would entail increased activity by the soleus but decreased activity by the gastroc.
Plantaris Tendon and Tennis Leg
The Duke Medicine image (above) shows the plantaris tendon. I looked into that briefly, while the image was fresh. Wikipedia said the plantaris (not found in an estimated 7-20% of the population, according to other sources) was a long, thin tendon with a relatively short (~4″) muscle, running from above the knee down to the heel.
The New York Daily News (Maharam, 2014) characterized the plantaris as “one of evolution’s leftovers,” a muscle whose former function of helping to point the toes has been taken over by other calf muscles. Maharam linked the plantaris with “tennis leg,” a frequent malady of aging (40+) athletes who get a sudden, sharp pain in the calf, akin to getting “shot with a BB gun” or, in other accounts, being kicked or hearing a “pop” in the calf. What causes rupture of the plantaris is, as one would expect, a motion that stretches it as much as possible: the leg is locked straight at the knee, and the foot flexes upward toward the shin.
Burdett (2006) said that “tennis leg” is a general term that could also refer to strain to the soleus, or to the medial (i.e., inner) head of the gastroc. (Note: in the Duke Medicine image (above), those are two right legs, not a right and a left. InnerBody offered a useful interactive graphic to clarify.) While Maharam (2014) said that the two ends of a ruptured plantaris would “shrivel up and go away — in a couple of weeks with a little physical therapy and warm water soaks,” Burdett remarked that gastroc and soleus injuries would generally be more severe, would take longer to heal, and could require splinting and dedicated rehabilitation.
Well. If Burdett was right, that would be one more way in which Indiana University screwed me, and it could explain why the calf pain that commenced during a run there in 2007 never went away: instead of getting the kind of proactive, sports-aware treatment (e.g., a doctor; an MRI) that a PhD student buying student healthcare at a Big Ten university might expect, I got inconclusive ultrasound and massage from a therapist. It was nice, as far as it went, but it didn’t help at the time and, as I say, the problem was still here. In Burdett’s (2006) words,
Plantaris tendon rupture and medial head of the gastrocnemius muscle rupture may also occur together, in which case MRI would demonstrate edema of the medial head of the gastrocnemius muscle, fluid between the soleus and medial gastrocnemius muscles, and a visible torn plantaris tendon. Visualization of the torn plantaris tendon is important, since fluid between the soleus muscle and medial gastrocnemius muscle is non-specific, and can be seen with plantaris tendon rupture, medial gastrocnemius muscle injury, or a ruptured popliteal cyst. The differential diagnosis of calf pain includes the more serious clinical entities of deep venous thrombosis (DVT) and compartment syndrome.
I mean, during the present writeup, when I saw the description of DVT (above), I did not have clinical grounds or medical opinion to tell me why I did not have it; I only had the fact that I wasn’t dead yet. There certainly had been times, in the intervening decade, when I would and possibly could have gotten an MRI scan, if I had thought it was anything more than just a generic sore calf. Now that I was aware that a calf injury could be life-threatening, of course, I did not have health insurance. If I did have DVT, then apparently it was another one of those things that I would just have to deal with.
In an article Burdett cited, Delgado et al. (2002) examined 141 patients diagnosed with “tennis leg,” using MRI scans, and evaluated the legs of four cadavers, to study the involvement of the gastroc and the plantaris tendon in that diagnosis. The authors concluded that plantaris tendon rupture was responsible for only 1.4% of cases, and partial soleus rupture was responsible for less than 1%. By far the dominant diagnoses were rupture of the medial head of the gastroc (67%), fluid collection between the soleus and medial gastroc aponeuroses (21%), and DVT (15%). In response to that last finding, the authors recommended routine examination of leg veins to rule out DVT in cases of tennis leg.
More recently, Spang et al. (2016, p. 1315) summarized literature finding that a small percentage (4-10%) of athletes sustained a plantaris injury each year, of which one-quarter were ruptures and the rest were tendinopathy; that running and jumping were the primary causes; and that ruptures require only a short period of rest before returning to full activity. Harwin and Richardson (2017) said that, even for gastroc rupture, surgery would only be indicated for tennis leg only when associated with compartment syndrome.
Tennis Leg and the Musculotendinous Junction
As I read various accounts of tennis leg, it was not always entirely clear which part of the calf they were talking about. This uncertainty or confusion was perhaps epitomized in a report by Nsitem (2013). That report said, “Muscle injuries in the calf are a relatively common clinical condition, and are also termed ‘tennis leg’ in general because of the prevalence in that sport.” Nsitem focused particularly on “the musculotendinous junction of the medial head of the gastrocnemius, and . . . the medial belly of the gastrocnemius just above the musculotendinous junction.”
As its name suggested, the musculotendinous junction was simply the place of connection between a muscle and its tendon (Oxford Reference). If Nsitem hadn’t referred to the gastroc “above” that junction, it might not be clear whether she was talking about the gastroc’s upper (proximal) or lower (distal) musculotendinous junction. But with that hint, it seemed plain that she was talking about the point where the gastroc transitioned into the Achilles tendon, as shown in this diagram (from an article focused on Achilles tendon injury) provided by Singapore Osteopathy:
It was confusing, though, when Nsitem said that she had measured the man’s calf swelling at a point just four inches below the kneecap. That’s about as high as you could go, to measure the calf, if the person was sitting. The answer seemed to be that his pain extended throughout “the entire medial gastrocnemius muscle.”
It seemed clear, in particular, that I was not experiencing so-called “tennis leg.” For instance, reported a classic case in which the injury to the medial head of the gastroc was measured at a distance of about four inches below the kneecap — well above the sensitive zone in my case. Similarly, De Cree (2015, p. 3) described a case of tennis leg in which “the entire upper and mid-portion of the right calf was found painful, tight and cramped up, with significant diffuse swelling, muscle weakness, and loss of range of motion.” (See also Bergman, 2013.)
Gastrocnemius Location and Functioning
I had concluded that the gastroc and/or soleus were not antagonistic to each other. But this was not to say that they had no antagonists. To identify their possible opponents, it seemed I would have to learn something about what those two muscles did. (In this exploration, by the way, it was interesting to glance at progress in developing mechanical models of human running.) Key terms here included dorsiflexion (i.e., bringing the toes closer to the shin, as when walking on one’s heels) and its opposite, plantarflexion (as in pointing one’s toes) — so named because the front side of the leg was its dorsal side, and the back side of the leg was its plantar side.
Starting at the top, the gastroc had two heads, medial and lateral. I had seen one or two non-expert sources describe those two heads as separate muscles. However characterized, there was the question of how they differed in function. My impression was that, as with other antagonistic muscle groups, they would have the capacity to pull the joint in slightly different directions — a little to the left, a little to the right — in concert with allied and opposing muscle groups.
As a knee flexor, in lay terms the gastroc was allied (i.e., synergistic) with the hamstrings and antagonistic to the quads (Wellness Digest, n.d.). This would suggest that the gastroc could be strained if the hamstrings were failing to counteract the quads sufficiently, either because the hamstrings were too weak or because the quads were too strong. Such reasoning, if correct, could raise a question of whether running — by itself, or in connection with general (e.g., otherwise sedentary) lifestyle factors — could result in imbalanced muscle development. Hypothetically, imbalance could be prevented if I had been spending the same proportion of my time running, walking, jumping, skipping, cycling, wrestling, and otherwise using a variety of leg muscles, as an adult, as I had spent when I was a kid. There was, in other words, a question of how much cross-training would be needed to restore balance, in the case of someone who spent hours running each week.
Again, that was all hypothetical. I could perhaps explore its relevance to me, personally, by investing some time in hamstring-strengthening exercises. But that sounded like a lot of work, I had no particular reason to think my hamstrings were atrophied, and there were other possibilities that, at this point, seemed likely to be closer to the mark.
If I quit running for a while and then resumed, I would usually have occasional minor aches and faint twinges around the knee. I assumed that was because the muscles and tendons and ligaments were all getting back in shape and learning to work together again. The aches and pains tended to go away after a while. Not to make too much of that, but my first guess would be that the knee and its attendant muscles were mostly doing OK.
I was not having much calf pain at this writing. But from memory and from the bit of pain that persisted, it seemed to me that my calf pain occurred along a line, perhaps the length of my index finger, starting in the center of the calf, or maybe a bit lower, and running down past the bottom of the gastroc bulge. I did not have the extremely clear muscle definition that I had seen in some pictures of calves, so I could not verify the conclusion visually, but it seemed probable that I was not having pain in either head of the gastroc. I was inclined to say, rather, that the location and the depth of the pain tended to rule out the gastroc, consistent with this great image from The Daily Bandha, incidentally showing the lesser calf muscles (right-hand image) anterior to the Achilles:
I was also inclined to doubt the gastroc was the primary issue after reading what Medscape (Saglimbeni, 2016) said about gastroc strain. He said gastroc pain, bruising, and swelling could radiate to the knee or ankle; there could be tenderness across the entire gastroc, but especially at the medial head, along with moderate to severe pain when dorsiflexing the ankle or resisting plantarflexion. This was largely not a good description of my sore calf experiences.
Wikipedia said the gastroc functioned not only to bend the knee, but also to pull on the heel — that is, to plantarflex the ankle — and, as such, was at risk of being torn by a severe dorsiflexion. Medscape (Saglimbeni, 2016) said injury was most common when the gastroc tried to contract while the leg was extended and the foot was dorsiflexed. In other words, all other things being equal, the gastroc would tend to be more stretched and at risk when I was running uphill. This, too, was pretty much the opposite of what I experienced. Running uphill, when the ankle was most strongly dorsiflexed, was the one kind of running that had never produced my calf pain. As mentioned earlier, running uphill was therapeutic: it seemed to reduce what I was coming to consider my Phase 1 tightness, and also to prevent my Phase 2 sharp pain. It seemed, then, that my pain probably did not arise from stretching an overly tight gastroc.
There was another factor to take into account: muscle type. Wikipedia distinguished skeletal muscle, of the kind appearing in the leg, from the smooth muscle found in various organs (e.g., trachea, arteries, digestive tract). According to Neunhäuserer et al. (2011), skeletal muscle fibers were of two types: Type I, also called “slow twitch,” and Type II, also called “fast twitch.” (There were two subtypes of fast-twitch fibers.) According to Scientific American (Greenemeier, 2012), “The fast-twitch fibers contract many times faster and with more force than the slow-twitch ones do, but they also fatigue more quickly.” It was reasonable to believe, and Runner’s World (Magill, 2010) did believe, that one’s body would use fast-twitch fibers for the shortest and most intense workouts, but would switch to using more slow-twitch fibers as the focus switched from speed to stamina.
That was interesting because of the longstanding awareness that the gastroc and the soleus tended to contain different percentages of fast- and slow-twitch fibers. Edgerton et al. (1974, p. 261) studied cadavers and found that, in people who had died of various illnesses (mean age 59), the gastroc was typically divided, about 50-50, between fast- and slow-twitch fibers, while the soleus was about 70% slow-twitch. More recently, as summarized by Clippinger (2007, pp. 39-40), researchers had found that the two muscles could vary considerably from Edgerton’s percentages. It appeared that genetics and training were responsible for observations that elite sprinter gastrocs contained as much as 73% fast-twitch fibers, while in some cases (e.g., distance runners) the slow-twitch percentages could range to, and beyond, 70% for the gastroc and 85% for the soleus.
It seemed this information might help to explain some calf pains. It was conceivable, for instance, that an emphasis on the long, relatively slow slog of distance running could yield an imbalance favoring slow-twitch fibers. This could matter if the remaining fast-twitch fibers were not sufficient to handle the stress of propelling a body rapidly, when speed was needed. Some of my sharp calf pains had occurred when I had attempted longer strides, and I had assumed that was just because I was stretching. And maybe it was; but maybe fast-twitch fibers were better at stretching, and maybe I needed a certain number of them to avoid straining the rest. The theory here would be that walking tended to reduce calf aches because walking put less emphasis on fast-twitch fibers.
Not that I wanted to overstate how much was actually known about the functioning of these muscles and their fibers, nor to oversimplify what did truly seem to be understood. For instance, Lenhart et al. (2014) grappled with the seemingly straightforward question of what the gastroc and soleus did while a person walked, and found that both muscles affected flex angles in everything from ankle to hip, and also that their functioning varied at different parts of the stride.
In short, while it seemed I might have arrived at a partial explanation of my situation, I felt there was surely more to it than this. My spreadsheet demonstrated, among other things, that my calf aches had started before I began running distances longer than three miles — though now it seemed three miles was probably long enough to count as distance (i.e., soleus-heavy) running, for these purposes. I had never done much sprinting; perhaps I should have been doing more.
Soleus Functioning
Unlike the gastroc, the soleus was not involved in bending the knee; but like the gastroc, it was involved in ankle plantarflexion. Wikipedia seemed to say that, by plantarflexing (i.e., keeping the front of the foot pressed against the ground), the soleus was vital for the act of standing.
Possibly both the soleus and the gastroc would prefer running uphill, as mentioned above, because the angle of the roadway would make it easier for them to do the job of plantarflexing. This suggested that it might be a struggle, relatively speaking, for these muscles to keep the front of the foot pushing against the ground with the requisite pressure when I was running on a level surface — not to mention running downhill, which in my experience was a prime source of calf attacks.
Several years after my first calf attack, I switched from heel striking to midfoot landing, and also switched from standard running shoes to a minimalist shoe, in a bid to reduce heel and arch soreness. I believed but was not certain these measures helped.
As just indicated, the soleus consisted predominantly of slow-twitch muscle fibers — 60% to 100%, according to Wikipedia — and was thus more oriented toward toward standing, walking, and distance running rather than sprinting. Presumably the soleus would have shared in an overemphasis upon slow-twitch muscle fibers, as described above.
According to Wikipedia, “The gastrocnemius muscle is prone to spasms, which are painful, involuntary contractions of the muscle that may last several minutes.”
Wikipedia said the soleus had two primary functions: plantarflexion and pumping blood.
Lenhart et al. (2014) found that, during walking, the gastroc functioned …
Non-Antagonistic Muscle Overcontraction
The MCS quote (above) referred to muscle overcontraction involving antagonistic muscles. But it was also possible for muscles to overcontract even when there were no opposing muscles. For instance, addressing the problem of “muscles responsible for excessive destructive forces” in dentistry, Rao et al. (2011) described the use of Botox (i.e., botulinum toxin) to counteract “muscular over-contraction” in the upper lip; others likewise described bruxism (i.e., tooth-grinding) as a matter of muscle overcontraction. Thus, it seemed that the gastroc and/or soleus could overcontract despite the absence of …
Overcontraction Due to Spasm
An agonist-antagonist pairing was not necessary, in order for a muscle to overcontract. For example, Schultz (2015) said, “Spasticity is a factor in over-contraction of muscles. A spasm is an uncontrolled muscle contraction.” MedlinePlus (2016) similarly equated spasticity with the condition of having muscle spasms. Other sources were more inclined to distinguish spasm from spasticity. For instance, Wikipedia said, “Spasticity mostly occurs in disorders of the central nervous system.” WebMD (2017) cited cerebral palsy, traumatic brain injury, stroke, multiple sclerosis, and spinal cord injury as common causes of spasticity.
As with the possibility of spinal pathology (above), it seemed unlikely that my calf pains were due to brain problems. I didn’t have any such diagnosis (e.g., stroke), and I also saw that my calf problems arose directly from my running. It seemed, in other words, that spasms (or, if you prefer, spasticity) was relevant only on the local level, involving spasms within one or more calf muscles due to some aspect of running activity.
According to WebMD (2017), muscle spasms could cause muscle cramps. But WebMD (n.d.) also said cramps had many other possible causes, including muscle overuse, shortage of minerals (e.g., potassium, magnesium, calcium), dehydration, use of certain medications (e.g., antipsychotics, statins), and unhealthy postures (e.g., sitting, lying, or standing for a long time, or in an awkward position).
or the various conservative approaches listed by Tucker (2010), such as using arch supports, icing the soreness, or not running on hard surfaces. Unfortunately, according to Wuellner et al. (2017), such techniques are “generally ineffective in controlling symptoms if the patient continues to engage in the inciting activity.”
Gross et al. (2015) offered the reasonable suggestion that compression of different compartments could have divergent, externally visible symptoms. Compression of the anterior compartment could result in weak ankle dorsiflexion – also soleus …
For years, I thought it was just a pulled muscle. And that first time, maybe that’s what it was. I had noticed that my right calf was tight, during a three-mile run; and then later that day, walking to my car after a meeting, I jumped over a flowerbed and came down feeling like my leg had been stabbed. I had a sharp pain that left me limping.
Eventually, though, I realized that this problem was not behaving like a simple muscle injury. It would come back when I had not done anything particularly strenuous; sometimes it would disappear the next day, and I could resume running (which would be unlikely if I had actually torn something); and yet, on the other hand, I could take months off, and it would be back almost immediately when I did start again.
I did learn, the hard way, that this was not one of those pains you could just run through. It was not something that would gradually die out. This was the kind of pain that, if I kept running — if I could even stand to keep running — it would only get worse, and the recovery would be longer.
Calf attacks rarely kept me from other forms of exercise. There were a few instances when, in the first minutes (or, rarely, hours) after the injury, I would barely be able to use the leg; but for the most part, I was free to bike, walk, or swim, starting almost immediately. The pain was highly specific to running. It also seemed that sometimes, when I felt the calf stiffening and feared an attack was imminent, I could prevent an attack by switching from midfoot to heel strike, or by reducing stride length or speed.
Note: I was not sure that I was having only one kind of calf problem. It just seemed advisable to focus on calf attacks as the most painful and crippling problem I was experiencing. It seemed that some of the following material would also be useful for purposes of understanding and responding to other kinds of calf problems as well.
The reader may notice that my own story changed somewhat, as I worked through the information provided in this post. That happened because I was not experiencing any calf pain at this particular moment, and thus had to rely on my notes and recollections. As I got more into the subject and had to focus more carefully on the sore calf experience, I was reminded that there were at least two different phases in the progression to the kind of injury that would prevent me from running.
As I say, there were times when I was able to resume running more quickly than a tear would warrant, and there were also times, in the middle of a run, when a shift of pace, posture, stride length, or strike would reduce or even eliminate a growing feeling of calf tightness presaging an attack.
For most of these years, I would have said that MCS Type 1 was the most likely candidate. It seemed that I would get calf attacks just when I was starting to get into shape again. I saw it as a situation where the calf muscle was growing strong once more; I thought maybe I was overdoing the training in my eagerness to get back on the road.
For me, not all aspects of subtype 2B were precisely on target; but as I thought about it, subtype 2B did seem to apply to the early phase of my calf attacks. I did have the sharp pain noted above; but before I experienced that sharp pain, I usually had a general feeling that my calf muscle was knotted or tight.
I might start with that tightness, or it might come on during a run. If it got too intense, I knew that the sharp pain might arrive at any moment. At that point, I would attempt mitigation. That could mean slowing my pace, shortening my stride, or switching from midfoot to heel landing. Sometimes those would reduce the knotting; sometimes the dull ache would get worse, and I would start walking; sometimes the sharp pain would
This part was a little confusing. I noticed that I could have minor sharp calf pains from just standing up from my desk, even when the calf had not otherwise been sore; and I also noticed that calf tightness could appear, grow stronger or weaker, and disappear entirely during the course of a run. Moreover, during a run, the calf attack could come on very quickly after the feeling of tightness first appeared.
Of course, it would help to have a clear understanding of the problem before attempting a solution.
The concept I was developing, at this point, was that the calf attack could consist of two phases. First, in the usual situation, there was the neuromuscular cramping; and if that became severe, it could result in a structural injury (i.e., a pulled or torn calf). Or perhaps the end product would not be an actual tear: after all, my ultrasound had shown no physical damage, even when the pain had been sharp. Maybe it was just that the cramping would switch into an aggravated mode, where continued running was painful because the muscle was too tight to use. I think I had always stopped running immediately, when I got to the point of sharp pain, because at that point injury seemed imminent. Maybe I had always stopped before that cramping could result in an actual tear.
In addition to the gastroc and the soleus, the calf had several minor muscles. It was possible that one of them was responsible. But I doubted it. If I was correct — if this was a problem of the gastroc and/or the soleus — the foregoing remarks suggest that I was probably not experiencing overcontraction due to agonist-antagonist muscle imbalance.
Updates
In normal times, when there had not been any recent calf trauma, I found that I was able to run down longish hills without a problem if, before attempting that, I began with a warmup walk and then an initial run on a largely level or uphill track, each extending more than a mile.
Although the Mayo Clinic (2022) said that a young runner could recover in six to eight weeks, but that an over-50 runner might require 12+ weeks, that was not my experience. Presumably their error was due to the assumption that the runner to whom they were responding was certain that he had experienced an actual “torn” muscle, as he said, when instead it might have been merely the intense cramping described above. I found that sometimes I could actually resume running within the same run. For example, on one run, I had the acute calf pain; I walked for a mile or two; then I ran mostly on uphills and walked the rest, during the remainder of that outing.
During a period of several years ending in late September 2023, I had only the sort of experience described in the previous paragraph: cramps that were sharply painful during the run, but that would go away within a few days or maybe a week if I made sure to warm up well and didn’t push it. But in late September 2023, I had a sharper attack. This one was actually not associated with a downhill run of any significance: I had just crossed a bridge, but it was only very slightly downhill. Despite a few longer warmup walks and then a week or two of doing nothing but walking, it didn’t go away. In this case, I noticed two associations: I had just stopped taking magnesium supplements (just the ordinary, cheap Walmart “Spring Valley” brand) a week earlier, and I drank a moderate amount of alcohol (which I didn’t do much anymore) within about 24 hours earlier. I resumed the magnesium supplements and, with gradual increases in walking and running, I resumed my usual three-mile runs in late October, about a month after the initial attack. At least within the first week, at this writing, it appeared that the magnesium had made a difference: the attacks had not resumed.
Running & Biking 