She was the goddess of water in Greek mythology. Both Zeus and Poseidon loved her and did their best to win her hand in marriage until Prometheus warned them of a prophecy that her son would become greater than his father. She married a mortal king instead, and dropped their son into the river Styx to make him immortal – holding him by the heel of his foot.
I had exercised patience regarding the time required to recover from a dislodged peroneal tendon, but when the swelling subsided and I could no longer move the tendon around with my finger there was still a hard bump on the back of my heel. Even relatively easy exercise made it sore. It was time to visit the doctor.
My husband and I sat quietly while the doctor examined my heel. As he left to order the x-ray he mumbled something about a pump-bump. My husband immediately took to his phone and by the time the good doctor returned he had discovered everything there was to know about Haglund’s Heel.
Dr. Haglund was a friend of Dr. Roentgen, the inventor of the x-ray. Haglund began researching the boney anatomy of humans for his dear friend, and came up with a fairly common deviation of the heel bone, which became known as Haglund’s Heel (also Hagulund’s Syndrome or Deformity).
This deviation is associated with decreased range of motion of the ankle and increasing age, typically hitting women in their 40s, 50s, and 60s after years of wearing high heel shoes. Jumping, running and navigating stairs can exacerbate the condition making inflammation and heel pain worse. It develops gradually, but we usually take notice when the tendon becomes inflamed. In many cases, especially with runners, Haglund’s Heel evolves into Achilles tendinitis.
Insertional Achilles Tendinitis is a common overuse injury among athletes causing stiffness in the heel especially in the morning, pain along the tendon that increases with activity and possibly swelling. A bone spur gradually develops around the tendon that can cause irritation (bone tends to generate new bone in an attempt to heal itself), and eventually the tendon may calcify and harden.
Note: Insertional Achilles tendinitis affects the back of the heel where the Achilles tendon inserts into the heel bone. Non-insertional Achilles Tendinitis causes pain in the lower calf, where the Achilles tendon and calf muscle meet.
Male and female athletes alike can develop insertional Achilles tendinitis with or without the underlying Haglund’s Heel, but in many cases Haglund’s Heel will trigger or evolve into insertional Achilles tendinitis.
Whyithurts: When a healthy tendon experiences an increased load, it responds by increasing its stiffness to handle the greater demand as it also increases the production of collagen cells. Researchers propose that this non-inflammatory cell response is an attempt by the tendon to increase the cross-sectional area to better handle the load. This short-term adaptation is reversible if the load is diminished or the tendon has a chance to rest before the next stress is applied. Over time a healthy tendon adapts to the stress by growing larger and stronger. An overused or diseased tendon does not recover from the stress and the injury progressively worsens.
Tendinitis is inflammation of the tendon (the suffix “itis” indicates inflammation), in this case of the Achilles. The condition lasts about six weeks although most practitioners view tendinitis as the first in a continuum of tendon injuries that subsequently increase in severity (you’ll also see it spelled tendonitis). If you feel pain in your heel, this is the time to take action.
Tendinosis is a non-inflammatory degeneration of a tendon that can include changes to its structure or composition. These changes often result from repetitive micro-traumas or failure of the tissue to heal and will likely require several months of treatment.
The suffix “pathy” is derived from Greek and indicates a disease or disorder. Tendinopathy is the term also applied to a chronic condition that fails to heal. For example, a runner who has suffered a hamstring tendon rupture that does not heal properly may be diagnosed with tendinopathy.
Insertional Achilles Tendinopathy is inflammation, and later, degeneration of the tendon fibers that insert on the back of the heel bone. Since the Achilles tendon connects the calf’s gastrocnemius and soleus muscles to the calcaneus, or heel bone, by the time you’ve reached the Achilles tendinopathy stage you will likely also notice reduced strength in the calf muscles.
Treatment: The Achilles’ tendon is exposed to greater amounts of strain in the dorsiflexed or upward position where the forward section of the tendon is exposed to low loads. Researchers suggest the lack of stress on this forward aspect of the tendon may cause that section to weaken and eventually fail. The treatment goal of insertional Achilles tendinitis is to strengthen the forward-most aspect of the tendon, which is accomplished through a series of eccentric exercises.
TheAlfredsonProtocol: The story goes that Hakan Alfredson, an orthopedic surgeon and professor of sports medicine in Sweden, developed Achilles tendon problems in the mid-1990s. When his boss refused his request for surgery because the injury was not yet advanced enough, Dr. Alfredson attempted to deliberately aggravate the injury with a series of exercises. Instead of getting worse, however, his injury disappeared.
These exercises, now known as the “Alfredson protocol” are considered the most effective first line of treatment for Achilles tendinopathy. The eccentric movements are designed to physically stimulate the cells in the tendon as they move relative to each other, causing the cells to initiate a tissue repair process.
Stand on your toes at the edge of a step (holding onto something for balance). Slowly lower the injured foot until the heel drops below the edge of the step. Return to the starting position (on your toes) by using the non-injured foot. The injured foot should never be used to raise onto your toes.
Perform 2 sets of 20 reps with the knee straight, which strengthens the gastrocnemius muscle, and another 2 sets of 20 with the knee bent to strengthen the soleus muscle. Repeat the exercises twice daily for 12 weeks. If the effort become too easy, add weight to increase the load.
(The original protocol called for 3 sets of 15 reps with the knee straight and another 3 sets with the knee bent for a total of 180 reps daily.)
Note: as with everything science, there is a corresponding study that found no difference when performing the heel drop using a straight knee only, and performing the exercise from both the straight and bent knee position.
Another study published last year involves a 3-prong approach combining the eccentric exercises mentioned above with compression band therapy, or CBT, and Lacrosse Ball Management (basically massaging the tendon using a lacrosse ball).
LBM: Once daily apply firm but comfortable pressure with the lacrosse ball while rotating the ball over the tendon.
I’ve followed the exercise and massage protocol for 4 weeks (although I will admit that I have performed the flossing motion without the band). After not running one step for several months (because it hurt), I ran three times last week with no pain during or after the run. My results have been similar to the results achieved by the test subject at this same interval in the study. At the study’s nine month follow-up, the test subject was exercising up to nine hours each week with no pain. It would be premature for me to claim victory over this injury, but I am cautiously optimistic.
This post reviews generic muscle characteristics and how they relate to runners, including muscle contractions, muscle/tendon/ligament injuries and treatment, muscle cramps and remedies, lactate, strength vs mass, slow vs fast, muscle fuel, endurance and loss, flexibility vs inflexibility, stretching and fatigue.
In a future post, we’ll look at how specific training methodologies affect each of these areas for short-, medium- and long-distance runners.
Key points from this post:
Muscle is a result of three factors that overlap: physiological strength (muscle size and responses to training), neurological strength (how strong or weak the brain’s signal telling the muscle to contract), and mechanical strength (the muscle’s force, leverage, joint capabilities).
The most common muscle injuries occur during eccentric loading and usually involve muscles that cross two joints, although the hip abductor muscles are also commonly affected even though they only cross the hip joint.
A stretched tendon can cause muscle spasms, but will typically resolve on its own. Ligament injuries can destabilize the associated joint and require many months, and sometimes surgery, to heal.
Eccentric training, such as downhill running, is the most effective in strengthening muscle and connective tissues, is effective for increasing flexibility, and can increase hip and joint range-of-motion, but is also known for causing muscle soreness (DOMS). Muscle rapidly adapts to the damage caused by eccentric training, however, and protects from the future damage of long distances.
Although the brain is responsible for creating strength (i.e., muscle recruitment), increased size or muscle mass (muscle hypertrophy) happens within the muscle. Following a period of inactivity, it is initially the brain’s ability to excite the muscle that declines in correlation with the muscle’s decrease in strength, rather than a physiological change in muscle size.
Our diets provide three sources of fuel: carbs, fat and protein. The body always uses a combination of carbohydrates and fat for fuel depending on the intensity of exercise. Low intensities use more fat, but by the time you’re gasping for air the proportions have flipped to mostly carbs.
Carb-free diets have become a popular way of encouraging fat burning, but there are trade-offs with this approach.
Lactate is an important source of energy, and is produced in muscles even at rest. The use of lactate as fuel varies with how well a person’s endurance muscle fibers are trained aerobically. Highly trained athletes use lactate more efficiently, which prevents it from accumulating to high levels in the muscle.
Protein is used as an energy source if calories are insufficient, although with sufficient calories, protein contributes only minimally to the total amount of energy used by working muscles.
In addition to strengthening teeth and bone, calcium also helps with muscle contraction. If a person’s diet provides too little calcium or too much phosphorus, their body siphons calcium out of teeth and bones and stops providing it to the muscles.
Exercise-induced muscle cramps have long been misunderstood to be caused by ”dehydration” and “electrolyte depletion” (water-salt imbalance). Muscle injury or muscle damage, resulting from fatiguing exercise causes a reflex ‘‘spasm’’, resulting in a sustained involuntary contraction, or cramp. Stretching is the most effective way to resolve cramps.
We break down and rebuild 1 to 2 percent of our muscle each day, meaning that you completely rebuild yourself every two to three months. The research shows you literally are what you just ate.
Studies show adults ages 50 and up with low muscle strength were more than twice as likely to die in follow-up periods of studies than those with normal muscle strength. Having low muscle mass (vs strength) didn’t seem to matter as much. The best outcomes of all were those adults who met the aerobic and strength-training guidelines: at least 150 minutes of moderate exercise or 75 minutes of vigorous exercise per week and performing a “strength-promoting exercise” at least twice a week.
When running frequency increases past 4 days a week or the intensity of endurance exercise increases above 80% VO2max, endurance exercise prevents the increase in muscle mass and strength typically associated with strength training.
Being inflexible creates greater elastic energy in the stretch shortening cycle. In fact, as much as 40-50% of the energy needed for distance running can be obtained from the elastic ability of skeletal muscle. Being less flexible is not as valuable for sprinters.
Static stretches before running caused a decrease in running distance, increased ground contact time during a 1-mile uphill run, increased muscle activation, and resulted in an approximately 8% decrease in performance.
In women, the variables related with muscle mass are generally 60-75% of the exercise physiology values recorded in men. When measured in terms of strength per square centimeter, however, the female muscle can achieve the same force of contraction as that of a male.
There are THREE TYPES OF MUSCLE in the body: 1) Smooth, involuntary muscles, 2) Cardiac heart muscle, and 3) Skeletal, or voluntary muscles that move the body, arms and legs. This post will focus on Skeletal muscle.
Muscle is a result of THREE FACTORS THAT OVERLAP: physiological strength (muscle size and responses to training), neurological strength (how strong or weak the brain’s signal telling the muscle to contract), and mechanical strength (the muscle’s force, leverage, joint capabilities).
Muscle tissue has THREE CHARACTERISTICS THAT GOVERN EXERCISE:
Contractility – Ability to shorten
Extensibility – Ability to stretch without damage
Elasticity – Ability to return to original shape after extension
The fundamental behavior of skeletal muscle is shortening, which produces joint motion and allows the body to move. Skeletal muscles attach to bones via tendons and often appear in antagonistic pairs, so that when one muscle contracts, the other lengthens.
THREE TYPES OF MUSCLE CONTRACTIONS:
Concentric contractions: muscle shortens, or contracts, pulling on the bone causing the joint to move. A reciprocal muscle on the other side of the joint contracts and shortens to return the joint to its original position. Muscles don’t push joints, they only shorten and pull.
Eccentric contractions: muscle shortens and lengthens at the same time, resulting in a resisting force to decelerate the lengthening movement. By opposing the downward force, a joint is safely repositioned and tissue is protected. Examples of eccentric contractions include walking down stairs, running downhill, lowering weights, and the downward motion of squats, push ups or pull ups.
Note: Eccentric training is effective for increasing flexibility, can increase hip and joint range-of-motion, and has been used as a form of training for several pathological conditions such as Parkinson disease (Dibble et al. 2006), and older cancer survivors (LaStayo et al. 2010),
The last form of muscle contraction is an isometric contraction where the muscle is activated but is held at a constant length rather than lengthened or shortened – there is no movement.
WHY IT HURTS
Muscle injuries commonly occur during eccentric loading of the muscle; that is, when the muscle is contracting while it is also elongating. Muscles that cross two joints, such as the hamstrings (the hip and knee joints), the calf (the knee and ankle joints), and the quadriceps (the hip and knee joints) are the most susceptible to injury. The hip abductor muscles are also commonly affected, though they only cross the hip joint. (Click here to discover more information about specific muscle injuries in other anatomy of a runner posts.)
Although exercises that involve eccentric contractions are the most effective in strengthening muscle, they are also the cause of muscle soreness. All forms of vigorous exercise can become painful, but only eccentric exercise causes delayed onset muscles soreness (DOMS). Muscles are very adaptable to eccentric exercises, however, and rapidly adapt to the damage, resulting in less muscle stiffness or soreness during a second bout of eccentric exercise.
When muscle is initially injured, significant inflammation and swelling occurs. Following the inflammatory phase, muscle begins to heal by regenerating muscle fibers from stem cells that live around the area of injury. However, a significant amount of scar tissue also forms where the muscle was injured. Over time, this scar tissue remodels, but the muscle never fully regenerates. This is thought to make injured muscle more prone to subsequent injury. Other factors that can predispose an athlete to injury include older age, less flexibility, lack of strength in the muscle, and fatigue.
Muscle (and tendon) injuries can be categorized into three grades ranging from mild damage to individual muscle fibers (less than 5%), causing minimal loss of strength and motion, to a complete rupture of the muscle or tendon.
Treatment and Recovery
The majority of acute muscle injuries are partial thickness tears. These can usually be treated successfully with rest, ice, compression, elevation (also known as RICE), and nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. This will be done for the first week, followed by progressive functional physical therapy, as needed. A return to full activity is usually possible when you are pain free, and when full range of motion and full strength is restored.
Recovery can be 2-3 weeks for Grade 1 injuries, or 2-3 months for Grade 2. The most severe injuries may require surgery to reattach damaged muscle and tendon. The resulting scar tissue of each injury makes athletes more susceptible to subsequent injuries at the same location.
In a study that examined professional football players with severe hamstring tears with palpable defects, an intramuscular cortisone injection led to a return to full activity time of 7.6 days, and 85% of the players did not miss a single game. However, the use of cortisone injections in the recreational athlete should be reserved for chronic or lingering injuries since there is a chance of weakening the remaining muscle and increasing the severity of the injury.
Several new therapies are in the investigational phase, including platelet-rich plasma (or PRP) which requires blood to be drawn and then spun in a centrifuge to concentrate the platelets and injected into the site of the injury. These platelets contain several growth factors that may stimulate healing and muscle regeneration, and limit the amount of scar tissue that forms. There are currently no reliable scientific studies that show if this therapy works. Antihypertensive medications have been shown to reduce scar tissue formation and improve healing in experimental models.
Tendon & Ligament Injuries
Tendons connect muscle to bone and ligaments connect bones to other bones. Tendons allow muscles to move bones, whereas ligaments stabilize joints. When tendons and ligaments are stretched beyond their basic capacity, they become damaged. For tendons, this can result in tendonitis, which occurs when the tendon becomes torn. This damage causes the tissue of the tendon to inflame while it heals; as a result, tendonitis causes swelling and soreness, as well as temporary loss of muscle function. Ligament injuries weaken the joint and threaten its integrity. A common ligament injury among athletes involves the ACL, or the anterior cruciate ligament in a person’s knee.
A stretched tendon can cause muscle spasms, but will typically resolve on its own. Ligament injuries can destabilize the associated joint and require many months, and sometimes surgery, to heal.
Tendonitis is inflammation of the tendon (the suffix “itis” indicates inflammation). Achilles tendonitis tends to be an acute (or quick-onset) condition lasting 6 weeks or less, although some view this diagnosis as the first in a continuum of tendon injuries that subsequently increase in severity.
Tendinosis is a non-inflammatory degeneration of the tendon which typically occurs from long-term overuse of the tendon leading to weakening of the tendon fibers. Unlike tendonitis, which can often be successfully treated within several weeks, tendinosis can take several months to treat.
Paratenonitis is inflammation of the tissue surrounding the tendon, which may thicken and adhere to the tendon. This diagnosis is controversial, as some practitioners do not believe paratenonitis is a separate condition from tendonitis.
Tendinopathy: The suffix “pathy” is derived from Greek and indicates a disease or disorder, in this case of a tendon. The term is also applied to a chronic condition that fails to heal. For example, a runner who has suffered a hamstring tendon rupture that does not heal properly may be diagnosed with tendinopathy.
SLOW VS FAST
Every muscle contains some combination of three basic types of fibers or motor units: slow twitch, intermediate, and fast twitch.
Slow-twitch fibers (Type I or Red Muscle) – are smaller, develop force slowly, maintain contractions longer, and have higher aerobic capacity that is well suited to long-distance/marathon oriented running. Red fibers are easier to target with exercise. For example, any repetitive, weight-bearing action above your accustomed-level intensity produces red muscle adaptations such as growth and increased endurance.
Fast-twitch fibers (Type IIx or White Muscle) – are larger, capable of developing greater forces, contract faster and have greater anaerobic capacity – better for sprinting or <400m races). White muscle specializes in high-intensity actions lasting fewer than 30 seconds and responds well to heavy resistance training and ballistic exercise such as fast, yet controlled, weightlifting, or plyometric training.
Intermediate fibers (Type IIa) – intermediate in size, speed, power, and susceptibility to fatigue such as those needed for prolonged fast running; the kind demanded for 800m and 1500m races.
Not all runners inherently have the same percentage of each type of muscle fiber. Elite distance runners have high percentages of slow-twitch and intermediate fibers, and as expected, sprinters have more fast-twitch. Since genetics determine our individual percentages, you may find you are more successful in sports that complement your specific muscle configuration. Finding your muscle type can be as simple as defining your preferences: Do you prefer long interval and tempo training (slow-twitch) or short, fast workouts (fast-twitch)? Despite genetic disposition, it has been suggested that training can cause type II fibers to take on the properties of slow-twitch type I fibers. (Specific training considerations will be covered in a future post.)
Muscles are recruited by the brain according to the Size Principle. Muscles with fewer slow-twitch muscle fibers are recruited first and, as more force is demanded by an activity, progressively larger, fast-twitch units are recruited. As the intensity of exercise increases in any muscle, the contribution of fast fibers also increases.
Top athletes in explosive sports like Olympic weightlifting or the high jump appear to have the ability to recruit nearly all of their motor units in a simultaneous or synchronous fashion. In contrast, the firing pattern of endurance athletes becomes more asynchronous. During continuous muscle contractions, some units are firing while others recover.
Initially we might maintain the desired pace/duration with no involvement from fast motor units. As these slow units become fatigued, however, the brain will recruit more motor units in an attempt to maintain pace. Recruiting these additional motor units brings in the fast, but easily fatiguable units. This explains why fatigue is accelerated at the end of a long or intense run.
Lactate is an important source of energy, and is produced in muscles even at rest – something that has been previously misunderstood. Lactate is sent to the brain and heart for fuel, or to active and inactive muscles for energy.
During exercise, we breathe faster to supply more oxygen to working muscles which also clears excess lactate. If exercise intensity increases beyond our ability to supply required oxygen, the muscles continue energy production, but in an anaerobic condition (without oxygen). The muscles produce energy in this anaerobic condition for only one to three minutes, during which time lactate can accumulate to high levels.
The potential for lactate accumulation varies by muscle type with fast-twitch muscles having the highest potential because of their maximum oxygen delivery requirements. “Producer” cells make lactate which is used by “consumer” cells. In muscle tissue, for example, the white, or “fast twitch,” muscle cells convert glycogen and glucose into lactate and excrete it as fuel for neighboring red, or “slow twitch,” muscle cells. Type II muscle fibers are highly glycolytic (they use lots of glucose) which results in the production of high amounts of lactate.
We’ve always associated these high levels of lactate with the burning sensation of muscle fatigue that ultimately causes us to stop exercise – a process that is thought to prevent muscle damage – although lactate may not actually be the cause of the burn. (Continuing research indicates muscle fatigue may be caused by other factors.) Lactate production is a strain response; it’s there to compensate for the metabolic stress of high intensity exercise. The deep breaths we take post-exercise helps clear excess lactate from muscles and restores balance.
The use of lactate as fuel within the muscle varies with how well a person’s endurance muscle fibers are trained aerobically. Highly trained athletes use lactate more efficiently as energy preventing it from accumulating to high levels. Conditioning in sports is all about getting the body to produce a larger mitochondrial reticulum in cells to use the lactate and thus perform better.
The muscles of untrained athletes, and also bodybuilders, produce energy without oxygen; a condition that produces high lactate levels in the muscles. At the same time, muscles begin to fatigue and the muscles feel “heavy”. This is considered an anaerobic training process (without oxygen) as compared to marathon training, for example, which is an aerobic (with oxygen) process.
Endurance training changes the metabolism of muscles by stimulating the production of a protein, PGC-1a. Trained mice that developed a high PGC-1a maintained their performance levels, and their lactate levels remained low despite a high training load. Endurance training programs, such as for the marathon, reduces the formation of lactate, while the remaining lactate in the muscle is converted and used immediately as energy substrate.
The energy drink, Cytomax, is based on research that indicates lactate is the body’s primary fuel. The combination of lactate, glucose, and fructose takes advantage of the different ways the body uses fuel: lactate can get into the blood twice as fast as glucose – peaking in just 15 compared to 30 minutes after drinking. Most sports drinks contain only glucose and fructose. (This reference is not an endorsement of the Cytomax product.)
1) High lactate levels are also seen in the blood during illness or after injury, such as severe head trauma, and are a key part of the body’s repair process. Lactate is now being used to help control blood sugar after injury, to treat inflammation and swelling, for resuscitation in pancreatitis, hepatitis and dengue infection, to fuel the heart after myocardial infarction and to manage sepsis.
2) Disturbances in lactate metabolism are common in obese and diabetic patients. The stimulation of PGC-1α achieved by endurance exercise means endurance training can be an effective approach to improve the metabolism of these groups, and could help prevent the resulting damage and progressive physical limitations caused by metabolic diseases.
POST EXERCISE OXYGEN DEBT
After exercise has stopped, extra oxygen is required to metabolize lactic acid and to replace (“pay back”) any oxygen that has been borrowed from other parts of the body. This debt is paid by labored breathing that continues after exercise has stopped. Highly trained athletes are capable of greater muscular activity without increasing their lactic acid production and have lower oxygen debts, which is why they do not become short of breath as readily as untrained individuals. Eventually, muscle glycogen must also be restored. Restoration of muscle glycogen is accomplished through diet and may take several days, depending on the intensity of exercise.
EXERCISE INDUCED MUSCLE CRAMPS (EAMC)
There are two theories about the origin of EAMC. The older one is the “dehydration” and “electrolyte depletion” theory (water-salt balance), while the more recent one is the “altered neuromuscular control” theory, or a sustained, involuntary muscle contraction brought on by muscle fatigue. In 1904, muscle spasms (cramps) were reported for the first time in two men at the Episcopal Hospital and were presented as a new disorder due to exposure to intense heat, which gave us the term “heat cramps”. Except, we’ve since learned that EAMC occurs in hot conditions, moderate to cool temperatures and in extreme cold. Also, multiple studies of endurance athletes, marathoners and triathletes have shown no evidence of low salt levels or electrolyte imbalances after cramping during a race (Schwellnus et al, 2004; Sulzer et al, 2005; Schwellnus et al, 2007).
One of the first studies showing that fatiguing muscle can develop cramping in normal healthy subjects during exercise was reported in 1957, but it wasn’t until 1997 that muscle fatigue was credited as the predecessor to EAMC. Click here to read the technical details behind this theory (Part III of a 5-part series on the history of EAMC studies) or here to read the full study.
A previous history of EAMC and a positive family history of cramping are also considered risk factors for EAMC. Muscle injury or muscle damage, resulting from fatiguing exercise, are thought to cause a reflex ‘‘spasm’’, and thereby result in a sustained involuntary contraction, or cramp.
Prevention & Recovery
Prevention of EAMC primarily is use of dietary supplements and kinesio taping, massage therapy, corrective exercises that will lead to the improvement of the function of a particular group of muscles or the biomechanics of the organism itself, although stretching exercises are said to be the most effective. Post-isometric relaxation techniques, plyometric or eccentric muscle strengthening programs have also proven effective. Mustard and pickle juice are listed as the nutritional form of EAMC prevention.
Note: non-exercise related cramps include rest cramps (also known as nocturnal cramps). These may be more prevalent in older adults, but can occur at any age. Rest cramps are started by making a development that abbreviates the muscle; for example, pointing the toe downward while lying in bed, which shortens/abbreviates the calf muscle, resulting in cramping of the muscle. Rest cramps can also occur in other areas, such as the arches of the feet or abdominal muscles.
STRENGTH VS MASS
Strength: People generate more strength if they can recruit and fire 50,000 muscle fibers than if they can only recruit 25,000 fibers. Muscle recruitment is controlled by the brain, and initial improvements are achieved because the brain gets more efficient at communicating with the muscles, using more of them, and using them more efficiently. In fact, muscle recruitment is the mechanism that allows us to gain strength before our muscles even increase in size. It is only through practice, or training, that the brain improves muscle recruitment.
Mass: Although the brain is responsible for creating strength (i.e., muscle recruitment), increased size or muscle mass (muscle hypertrophy) happens within the muscle. Microscopic damage (microtears) occurs in the muscle fiber during strengthening activities, which stimulates the body’s repair response to repair the damage. This repair response causes the muscle fibres to enlarge or swell, ultimately increasing their volume and size. Once running frequency increases past 4 days a week or the intensity of endurance exercise increases above 80% VO2max, however, endurance exercise prevents the increase in muscle mass and strength that typically occurs with strength training.
Note: Even with the greater muscle mass typically found in short distance runners, a sprinter cannot win a marathon. A sprinter’s specially-trained and strengthened muscles will fatigue faster than the endurance-trained muscles of a long distance runner. The research group of Prof. Christoph Handschin of the Biozentrum, University of Basel, shows that during endurance exercise the protein PGC-1α shifts the metabolic profile in the muscle.
The three basic fuel options are carbohydrate, fat and protein.
Fat is the preferred fuel for light-intensity to moderate-intensity exercise, such as slow running or hiking, cycling, and recreational swimming. However, the body always uses a combination of carbohydrates and fat depending on the intensity of exercise. Low intensities use more fat, but by the time you’re gasping for air, the proportions have flipped to mostly carbs.
Endurance (low-intensity) training teaches the body to preserve glucose and utilize more fat as fuel, but you’ll burn the same fat-carb mix at any given relative intensity. One study found that marathoners running a 2:45 pace relied on 97 percent carbohydrate fuel, while slowing to a 3:45 pace reduced the carb mix to 68 percent.
It is now believed that lactate is produced in healthy, well-oxygenated muscle and is preferentially used for energy throughout the body. In fact, about 30 percent of all glucose we use during exercise is derived from lactate “recycling” to glucose.
Carbohydrate-free diets have become popular in recent years to encourage the body to burn predominantly fat as fuel. Studies show it takes several weeks for the body to adjust to a mostly carb-free diet and that any benefits in terms of performance are mixed. In exchange for their enhanced ability to burn fat, a study of cyclists seemed to lose their ability to harness quick-burning carbohydrate for short sprints resulting in “a severe restriction on the ability of subjects to do anaerobic work.”
The conclusion among researchers is that high-fat (carb-free) diets don’t just ramp up fat burning; they actually throttle carbohydrate usage by decreasing the activity of a key enzyme called pyruvate dehydrogenase. This may or may not matter depending on your running goals. Fat burning is ideal for long distances that never require speed. Racing, on the other hand, may be enhanced by having carbohydrates in reserve for that end spurt, or for more intensive training sessions.
Protein is used as an energy source if calories are insufficient, although with sufficient calories, protein contributes only minimally to the total amount of energy used by working muscles. When a person begins a moderate endurance exercise program, they initially lose more protein than they ingest. This corrects itself within 2–3 weeks without dietary intervention. To increase muscle size and increase strength, however, athletes must ingest more protein than is lost. On the other hand, ingesting too much protein can result in dehydration, loss of urinary calcium, and will put stress on the kidneys and liver.
Luc van Loon, Professor at Maastricht University in the Netherlands, and his colleagues developed a technique to track protein as it progressed from a person’s mouth to their biceps in the hours following a meal. Just over 50 percent of the protein made it into the subjects’ circulation within five hours (the remaining protein was presumably taken up by tissues in the gut or not absorbed.) During the same period, 11 percent of the ingested protein was incorporated into new muscle. Literally, you are what you just ate. Overall, van Loon points out, we break down and rebuild 1 to 2 percent of our muscle each day, meaning that you completely rebuild yourself every two to three months.
Calcium is predominantly used by the body to strengthen teeth and bones, but also helps with muscle contraction. If a person’s diet provides too little calcium or too much phosphorus, their body siphons calcium out of teeth and bones and stops providing it to the muscles. Cola based soft drinks and some junk foods are high in phosphorous, unduly increasing the body’s need for calcium.
Fun Fact: studies in the 1960s found that people who retained more of their own teeth tended to have more muscle.
Our ability to engage in physical activity for long periods of time is thanks to efficient energy production in the mitochondria—the small “powerhouses” of our muscles. Endurance training increases the number of mitochondria and their structure, and the more we have, the longer we can exert ourselves. Endurance athletes have more than twice as many mitochondria that generate about 25% more energy as non-athletes.
During a two-week period following inactivity, it is the brain’s ability to excite the muscle that declines in correlation with the muscle’s decrease in strength, rather than a physiological change in muscle size. Getting older is another factor that causes changes within the muscle since muscles are less sensitive to protein signaling as we age. Studies show adults ages 50 and up with low muscle strength were more than twice as likely to die in follow-up periods of studies than those with normal muscle strength. Having low muscle mass (vs strength) didn’t seem to matter as much.
A similar study of 80,000 adults found those doing any strength training were 23% less likely to die and 31% less likely to die of cancer. The best outcomes of all – a 29% reduction in mortality risk – were those adults who met the aerobic and strength-training guidelines (at least 150 minutes of moderate exercise or 75 minutes of vigorous exercise per week and performing a “strength-promoting exercise” at least twice a week).
Note: A recent study led by researchers at Keele University has shown for the first time that periods of skeletal muscle growth are ‘remembered’ by the genes in the muscle, helping them to grow larger later in life.
Long-term observations of runners have shown improvements in running economy when the athletes are less flexible – being inflexible creates greater elastic energy in the stretch shortening cycle. In fact, as much as 40-50% of the energy needed for distance running can be obtained from the elastic ability of skeletal muscle. One of the reasons plyometric and resistance training improves running economy is due to an increase in muscle stiffness. Imagine a ball bouncing off a wall – if it gets softer, it bounces off more slowly, whereas a stiff ball returns quickly (golf ball vs squash ball, for example).
Being less flexible does not appear to be as advantageous in shorter distances, sprinting, or the long jump. A sprinter (i.e., events <800 m), for example, requires a greater range of motion at the hip that benefits from more flexibility as compared with a long-distance runner (i.e., events >800 m).
The sit and reach test is a common measure of flexibility, and specifically measures the flexibility of the lower back and hamstring muscles.
Researchers have sought to determine whether acute bouts of static stretching before exercise would affect running economy. (Static stretches hold a stretched or elongated position for 15 seconds or more.) Findings show runners who performed these stretches before running caused a decrease in running distance, increased ground contact time during a 1-mile uphill run, increased muscle activation, and resulted in an approximately 8% decrease in performance.
Stretching, considered an exercise, also fatigued the muscle resulting in more muscular recruitment to perform a given task. Considering that one of the adaptations to endurance training is asynchronous recruitment of the musculature, having to recruit more muscle fibers per given intensity would be counterproductive to performance for distance running.
Static stretching is helpful to increase range of motion or improve flexibility and is a useful component of an overall training program depending on your sport (i.e., for sprinters and short distance runners). If you feel a need to stretch before running, dynamic stretches use controlled movements that can make muscles more limber while also activating major muscle groups.
Fatigue was defined in a previous post as peripheral (within the muscles) or central (within the brain and spinal cord). Although fatigue produces the belief that our resources are limited, exercise generally ceases before all the muscle fibers have been activated. In fact, just 35-50% of active muscle mass is recruited during prolonged exercise. Read more here.
Limited studies show that women appear to be more resistant to fatigue than men during long efforts. A study that was published in the journal Medicine and Science in Sports and Exercise measured fatiguability of subjects completing an isometric arm contraction. Women were able to perform the task until failure almost three times longer than men, 23.5 minutes versus 8.5.
One difference between the sexes is that women have a greater number of fatigue-resistant fibers (Type I) while men have more faster-contracting fibers. Secondly, men have larger muscles that demand more blood, which makes their hearts work harder. Female endurance athletes also have a metabolic edge in moderate-intensity aerobic exercise by deriving more of their energy from fat as compared with males. In women, the variables related with muscle mass are generally 60-75% of the exercise physiology values recorded in men. When measured in terms of strength per square centimeter, however, the female muscle can achieve the same force of contraction as that of a male.
Note: Muscle fatigue is usually resolved within hours, while muscle damage can impair force generation for up to 7 days.
THE TRAINING EFFECT
Skeletal muscle has three basic performance parameters that describe its function: 1) Movement production (speed), 2) Force production (strength), and 3) Endurance. Increasing muscular strength will increase muscular power, which is the product of force (strength) and speed.
Athletic performance is ultimately limited by the amount of force and power that can be produced and sustained. The theories behind the various components of a running training program will be discussed in the next anatomy of a runner post.
American College of Sports Medicine position stand. Progression models in resistance training for healthy adults. Keele University. “Study proves ‘muscle memory’ exists at a DNA level.” ScienceDaily. ScienceDaily, 30 January 2018.