Kinesio Tape : Does it Really Work?

Most individuals, athletes or not, have experienced a musculoskeletal injury due to the overuse of a specific tissue or muscle. These overuse injuries can slow down an individual either in the workout routines or daily life. While not all injuries react the same way, many overuse injury areas are known to build up lymphatic fluid causing swelling and pain. The swelling and pain come from the accumulated lymphatic fluid putting increased pressure on the injured muscle or tissue.

 

Taping using Kinesio Tape (KT) has become a very popular proposed treatment and recovery aid over the past couple of years. KT became popular after the 2008 Beijing Olympic games, where beach volleyball player Kerri Walsh Jennings caught the attention of many spectators for wearing multi colored tape strips on her shoulder. KT is believed to lift the skin from the underlying layers of fascia, or bands or connective tissue. The lifting of the skin from the fascia results in a greater movement of lymphatic fluid, which transports white blood cells throughout the body and removes bacteria, waste products, and cellular debris. When the tape is correctly used it may also be able to provide support to the surrounding muscles and help to ensure that the muscle does not over extend or over contract [1].

                                                           

Figure 1. Athlete wearing Kinesio Tape.

 

Research suggests show that the tape will allow increased oxygen to the injured muscle and decreased inflammation. A 2012 study tested the effects of KT on blood flow in the gastrocnemius muscle and whether or not the way KT is applied changes the outcome on the muscle performance. In this study 61 healthy active individuals with no recent leg injuries were assigned to either treatment KT, sham KT, or a control group. Before taping a blood flow, circumference, and water displacement was taken for the gastrocnemius muscle. The individuals were then taped, and each measurement was taken again 24 hours and 72 hours after being taped. The results of this study showed no significant differences in the blood flow to the muscle using KT. There was also no change in the muscle’s performance based on the application technique of the tape [1].

 

From five previous systematic reviews, a new systematic review had been created to evaluate whether or not KT was more effective than no treatment or a placebo treatment, for people with musculoskeletal conditions, on pain levels, disability, and quality of life. Several different studies had been performed that looked at the pain levels on a scale from (0-10) for performing different activities while wearing either KT or another form of tape. These studies are prone too potential bias from the users and small sample sizes. Many of the referenced studies only shared certain of the results or were considered significant but of low quality [2].

 

Within a study done on subjects who had been diagnosed with rotator cuff tendonitis/impingement similar results were found as in the studies before. The only difference in this study was that they took self-reported measurement for range of motion along with pain. While the taping was ineffective compared to sham tape in long term, the KT provide immediate in pain free abduction range of motion. Once again, this study was limited to a. young population and it lacked a control group for comparison [3].

 

Although studies show that KT is ineffective in aiding injury rehabilitation, it is. Still used often by many groups of people. Since KT is relatively safe there is no reason why it cannot be used. Whether or not KT acts as a placebo or works I ways that are yet to be understood, it has worked for a large population of people for many years in helping to get past injuries for exercise and daily life.

 

Questions to Consider

 

Have you ever used Kinesio Tape? If so, did it help alleviate pain or support movements?

 

KT placebo effect or valid injury rehabilitation aid?

 

Do you think KT will last as an injury aid?

 

References

 

[1] Hannah L. Stedge, Ryan M. Kroskie, and Carrie L. Docherty. (2012). Kinesio Taping and the Circulation and Endurance Ratio of the. Gastrocnemius Muscle. Journal of Athletic Training, 47(6), 635-642.

 

[2] Patricia do Carmo Silva Parreira, Luciola da Cunha Menezes Costa, etc. (2014). Current evidence does not support the use of Kinesio Taping in clinical practice: a systematic review. Journal of Physiotherapy, 60(1), 31-39.

 

[3] Mark D. Thelen, James A. Dauber,  Paul D. Stonemen. (2008).Journal of Orthopaedic & Sports Physical Therapy,38(7), 389-395.

 

[4] “WHAT’S THE DEAL WITH THE TAPE? Benefits of Kinesiology Theraputic (KT)Tape-Small Tool Delivers Big Impact.” Fischer Institute, 16 Oct. 2017, fischerinstitute.com/benefits-kinesiology-therapeutic-tape/.

 

I wanna rock and roll (out my myofascial tissue)!

Anyone who has partaken in any physical activity, whether it is a sport, exercise routine, or just simple around the house chores that require a little more muscle power than normal, has experienced muscle soreness or discomfort.  Generally, when muscles are pushed passed what they are used to (i.e. new exercising routines, increased weight, eccentric exercises) the muscle fibers undergo damage and the body’s response is to add muscle fibers and/or to increase the size of muscle fibers to help increase muscle strength. When talking about sore muscles, it is generally thought the soreness comes from the physical effects of muscle tearing, repairing, and growing from a workout. There is, however, one part of the muscle that plays a role in not only soreness, but also range of motion (flexibility), and muscle performance that not many people know needs special attention: the myofascial tissue.

Figure 1: Skeletal muscle structure through different layers of the muscle. Myofascial tissue lies over the epimysium connective tissue which coats the muscle bundle. The epimysium, perimysium, and endomysium are specialized versions of myofascial tissue.

Different forms of fascia can be found all over the body, from encasing organs, to blood vessels and nerves, to muscle.  Fascial tissue that specifically covers muscle, or myofascial tissue, is a thin, white/transparent connective tissue that covers muscle, bundles, muscle fibers, and the muscle as a whole.  If you have ever picked off the thin white stuff covering parts of a chicken breast while preparing it for dinner, you tore off the myofascial tissue layer. Myofascial tissue is an extremely flexible and strong material, which is made up of elastin fibers, for stretch, and collagen fibers, for strength, that are embedded in a gelatinous ground substance, which reduces friction between the muscle fibers and promotes ease of motion [1]. Considered a “deep fascia,” myofascial tissue is made up of a more compacted weave than other fascia found throughout the body and can modify itself depending on the forces placed on it.   (Figure 2).  Because of this, if there is “trauma” or “injury” to the tissue, it can become out of alignment and

Figure 2: 3D visualization of myofascial tissue (white web like structure) and fascia tissue between the skin and muscle (yellow web like structure). Myofascial tissue can be related to a cotton candy structure that is extremely complex and strong. Retrieved from https://www.myofascialrelease.com/about/definition.aspx

cause trigger or dysfunctional points. These points, most commonly referred to as knots, is when the fibers that make up the tissue gets stuck together, loses its elasticity, and becomes taught [2]. Polly de Mille, R.N., C.S.C.S., director of performance services at the Hospital for Special Surgery in New York City explains in an interview for SELF that it is very similar to getting ice cream in silky smooth hair.  When there are “knots” in the muscle fascia, it limits range of motion, and can trigger immune responses which can ultimately lead to pain and discomfort (cytokines have been shown to cause pain and soreness) [3,4].

 

 

Now, what is the best way to heal and prevent muscles from experiencing these knots and discomfort? When talking about getting rid of knots in your body, a massage should be the first thing that comes to mind.  The “hurts so good” mentality of deep massaging muscles to where the patient feels pain and then relief afterwards is a popular desire, though not for everyone. Applying pressure and different forces to the tissue through a massage, or foam roller which we will talk about in a little bit, while moving around the fascia helps to separate and relax the tissue and muscle, allowing it to go back to its natural state.  Effects also include an increase in blood flow, which should help muscles get the proper nutrients to repair. Massaging also releases “feel good” brain chemicals, like endorphins, which basically inhibit pain receptors and overall makes you feel better. A study conducted by Mal-Soon Shin and Yun-Hee Sung induced muscle fatigue on 21 young males and treated 11 of them to massages afterwards while recording surface muscle activation and position of their medial gastrocnemius muscle.  According to their study, massaging increases muscle activation and strength due to a change of structural properties. However, in their discussion, they mention that not all messages are effective, which seems to be a common issue in the argument of whether foam rollers, or self myofascial release in general, works or not [5].

Massages are so great because when another person is working out your muscles, they are not only more accurate in pinpointing the location, but they can also apply more force (remember: collagen is EXTREMELY strong in ratio to its size. Proportionally, it is stronger than steel!).  As great as they are, unless someone at home is a masseuse, it can be costly. Self myofascial release techniques, such as foam rolling, have taken over the exercise world and are now regularly used. Foam rolling is when the user applies pressure to “trigger point” or sore spot before or after a workout by using their body weight to roll against a foam cylinder. Though it feels good, does it actually work?

Research has proven that foam rolling is great for warming up muscles and increasing range of motion and flexibility, but the verdict is still out on decreasing muscle soreness.  Though the mechanism behind foam rolling is not exactly known, there is great evidence that it does work on some type of level, whether it is physical or just simply mental. In a systematic literature review of research on using a foam roller before and after workouts, Scott W. Cheatham identified different scientific articles that were critically appraised with trusted conclusions.  From these articles, he identified five studies on the effects of foam rolling and range of motion before exercising. All of these studies resulted with an increase in stretching or range in motion in test subjects [6]. It is common knowledge to stretch before a workout or game to help “warm up” the muscles so that they’re are more flexible, which helps prevent injury and soreness. It is also speculated that rolling out could create a friction that literally heats up the fascia and muscle, making it more flexible and the typical “loose” feeling [2].  After a workout, however, there is a preconception that rolling out will help with delayed onset muscle soreness and pain in general. In this literature review, Cheatham identifies two different journals that conclude that foam rolling does reduce pain, but since the mechanism behind it is still unknown, how much can we trust? In the same SELF article as mentioned previously, Lewis J. Macgregor, Ph.D., an exercise physiologist and lead author of the University of Stirling confirms foam rolling does help increase blood flow, which in turn promotes muscle recovery, but foam rolling does not actually help with myofascial release. Since the collagen in the fascia is so strong, it is argued using your body weight to roll out is not enough. Instead, the pressure of rolling stimulates nerve receptors, which sends the same “hurts so good” feeling to your brain that is then perceived as loosening up the muscle, when really it is not happening.

Overall, foam rolling and myofascial release is an effective way to warm up your muscles and stretch them out before a workout and to help stimulate more blood flow post workout, just don’t get your hopes up about avoiding soreness! Increasing range of motion and flexibility before a workout is a great step to ease muscle soreness, but foam rolling alone is not the answer.  The verdict is still out on the mechanism behind the effects of myofascial release on a cellular level, but hey, if it feels good, why not!

 

If you’re interested, here is a video of foam rolling techniques because like anything, it’s not effective if you don’t do it properly.

https://www.youtube.com/watch?v=WCj1dvTwOF0

 

Questions to consider:

Is it worth it to foam roll or stretch in general before physical activity?

Is myofascial release something to think about daily and not just dealing with exercising?

Do you think foam rolling has a placebo effect or is it both systems (nervous and skeletomuscular) working together?

Do you think foam rolling is just another exercising fad?

Would adding heat be beneficial? Or a waste of time?

 

Sources:

  1. Shah, S., & Bhalara, A. (2012). Myofascial Release. International Journal of Health Sciences and Research,2(2), 69-77.
  2. Fetters, K. A. (2018, July 21). Here’s What Foam Rolling Is Actually Doing When It Hurts So Good. Retrieved April 12, 2019, from https://www.self.com/story/what-foam-rolling-is-actually-doing-when-it-hurts-so-good
  3. Grosman-Rimon, L., Parkinson, W., Upadhye, S., Clarke, H., Katz, J., Flannery, J., … Kumbhare, D. (2016). Circulating biomarkers in acute myofascial pain: A case-control study. Medicine, 95(37), e4650. doi:10.1097/MD.0000000000004650
  4. Zhang, J. M., & An, J. (2007). Cytokines, inflammation, and pain. International anesthesiology clinics, 45(2), 27–37. doi:10.1097/AIA.0b013e318034194e
  5. Shin, M., & Sung, Y. (2015). Effects of Massage on Muscular Strength and Proprioception After Exercise-Induced Muscle Damage. Journal of Strength and Conditioning Research,29(8), 2255-2260. doi:10.1519/jsc.0000000000000688
  6. Cheatham, S. W., Kolber, M. J., Cain, M., & Lee, M. (2015). THE EFFECTS OF SELF-MYOFASCIAL RELEASE USING A FOAM ROLL OR ROLLER MASSAGER ON JOINT RANGE OF MOTION, MUSCLE RECOVERY, AND PERFORMANCE: A SYSTEMATIC REVIEW. International journal of sports physical therapy, 10(6), 827–838.

7 Minutes of Sweating: Taking the HIIT

One of the most commonly stated New Year’s Resolutions is losing some extra pounds, starting a jogging routine, or otherwise getting physically fit. It is a very noble goal with good intentions, but many people who make this resolution for the new year end up breaking this promise to themselves. Chief among the reasons for quitting is the lack of time during the day. Between work, school, family, friends, and other obligations, it can be hard to set aside one or two hours to do a full traditional workout routine. But what if there were a way to get some exercise in regardless? What if you could work out for as little as 7 minutes, and get the same results as if you worked the full hour? As long as you follow a specific type of workout, this dream could be a reality. Enter: High-intensity interval training.

Figure 1: A Warrior Training instructor, leading her class.

By Any Other Name:

High-intensity interval training (HIIT) takes many different forms and names: Tabata Training, Sprint Interval Training, 7 Minute Workouts, and Warrior Training are all different forms of HIIT. The core idea behind HIIT is that athletes who take part of these programs work at maximum exertion for a short period of time before taking a short break. According to the guidelines put forth in the ACSM’s Health & Fitness Journal [2], working at a maximal output for short bursts of time causes you to generate close to 90% of your VO2 Max (also known as a VO2 Peak) over the course of the exercise. These guidelines, which have formed the basis of the 7 Minute Workout, pen the program as a time-efficient way to get similar efforts to other workouts that last longer, by trading time for increased effort. But how true is this claim? Can you really get the same workout you would in an hour in the span of 7 minutes, simply by working at maximal output? This is the question, one that I hope to answer.

Insulin Activity:

One study [3] focused on the potential for Sprint Interval Training (SIT) to be used for promoting insulin sensitivity, as well as other indicators for increased cardiometabolic health. In this study, they took 27 sedentary men with similar age, weight, and VO2 Peak. These men were divided into three groups and were given different workout routines: one was SIT, one was a traditional moderate-intensity continuous training (MICT), and the last did not train at all as a control. The SIT group would do high intensity, 10-minute sessions, while the MICT group would do more moderate bouts over 50 minutes sessions. Over the span of 12 weeks, these men worked out and got measurements of their results. They concluded that SIT was comparable to MICT, with regards to improving VO2 Peak, insulin sensitivity, and skeletal muscle adaptations. The study does not, however, make any mention of weight loss, though that is due to it being outside of their scope.

Figure 2: VO2 Peaks of the different groups in the study before, in the middle of, and after the full study.

New Year’s Resolution Buster:

In regards to body fat, one review [4], though dismayed at the effort required to adhere to the HIIT program, found it to be a preferable alternative to MICT. In that review, not only did they find many of the same adaptations from the study above, they found that many studies point out increased levels of skeletal muscle fat oxidation using HIIT. Another study [5] found that HIIT, while better than sedentary activity, was not significantly better than MICT, and may even be slightly worse. Still another study review [6] suggests that HIIT and MICT have similar benefits, with the only difference between the two being time.

One term that gets thrown out a lot during discussions is EPOC or Excess Post-Exercise Oxygen Consumption. Long name aside, it is a process that your body undergoes after exercising in order to bring the body back to a normal state. In this recovery state, the body uses more energy and calories compared to your resting rate as it tries to help heal and build your muscles. This gets thrown around especially in regards to HIIT, as some review articles [6] report that HIIT can lead to increased levels of EPOC, compared to MICT. This sounds like a decisive point in HIIT’s favor, as calorie burn is often the biggest signifier of hard work for starting athletes. But the actual amount of calories that are burned as a result of EPOC, according to this review [7] might not be very substantial in the first place.

The Bottom Line:

Armed with all of this information, what can we say about HIIT? As a form of exercise, it seems to be a perfectly valid way of working out. Whether it is better or worse than traditional duration exercises is up for debate, but HIIT is at least around as good as MICT. Both MICT and HIIT cause similar increases in VO2 Max and other adaptations such as increased insulin sensitivity. Neither method has been shown to be significantly better at burning calories, either.

That being said, one common theme appears across several studies is how harsh the workout is. In almost every single review study involving HIIT, the discussion often concedes that HIIT is very intense and that not everyone will be able to maintain the level of exertion requested by HIIT. With this, I can say that HIIT will not be replacing MICT. Ultimately, the question of whether to do MICT or HIIT comes down to personal preference. If you don’t have time during your day and are willing to really sweat it out for a short amount of time, then HIIT is a good alternative choice. If you do have time during the day and don’t want to work out to near your maximal output, then stick with a more traditional workout may be the right thing for you.

Questions To Consider:
  • Given a choice between working out using the HIIT method or the traditional MICT method, which would you choose?
  • Would you recommend HIIT to a beginner athlete?
  • What about someone more grounded in their routine? Would you ask them to give it a shot?
  • Looking through a calories-down lens, would you focus on HIIT?
  • If you are working out using the traditional MICT method, would you integrate some HIIT workouts in there as well?
  • Given the short time investment, would you work out using HIIT 7 days a week?

[1]: Figure 1: Warrior Trained Fitness offers service members, families’ group workout. https://www.nellis.af.mil/News/Article/665186/warrior-trained-fitness-offers-service-members-families-group-workout/.

[2]: Klika B, Jordan C. HIGH-INTENSITY CIRCUIT TRAINING USING BODY WEIGHT. ACSMs Health Fit J. 2015;17(3):8-13. doi:10.1249/fit.0b013e31828cb1e8

[3]: Skelly LE, Martin BJ, Gibala MJ, Gillen JB, MacInnis MJ, Tarnopolsky MA. Twelve Weeks of Sprint Interval Training Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment. Sandbakk Ø, ed. PLoS One. 2016;11(4):e0154075. doi:10.1371/journal.pone.0154075

[4]: Boutcher SH. High-intensity intermittent exercise and fat loss. J Obes. 2011;2011:868305. doi:10.1155/2011/868305

[5]: Keating SE, Johnson NA, Mielke GI, Coombes JS. A systematic review and meta-analysis of interval training versus moderate-intensity continuous training on body adiposity. Obes Rev. 2017;18(8):943-964. doi:10.1111/obr.12536

[6]: Børsheim E, Bahr R. Effect of Exercise Intensity, Duration and Mode on Post-Exercise Oxygen Consumption. Sport Med. 2003;33(14):1037-1060. doi:10.2165/00007256-200333140-00002

[7]: Laforgia J, Withers RT, Gore CJ. Effects of exercise intensity and duration on the excess post-exercise oxygen consumption. J Sports Sci. 2006;24(12):1247-1264. doi:10.1080/02640410600552064

Delayed Onset Muscle Soreness: What We Know and What We Don’t (Emphasis on Don’t)

Ever get that feeling two days after a tough run, or a ride that you knew was just a few miles too long, or your first leg day in months (come on, we’re all guilty of that), where you begin to question whether you will ever walk the same again? Walking down the stairs feels like torture, and your quads feel like they get angrier at you with every step you take? Muscle soreness, more specifically delayed onset muscle soreness (DOMS) is common in athletes of all levels of expertise. It occurs after performing a training activity that is unfamiliar. This could be activities than an athlete has not performed in a few months, activities they’ve never performed before, or even simply an intensity level or duration of exercise that they don’t normally reach, despite performing that exercise regularly. These unfamiliar activities, also known as eccentric training, are known to induce severe muscle soreness characterized by increasing intensity of symptoms beginning as late as 24-48 hours after exercise and lasting for days. The underlying physiological mechanism causing DOMS is still unknown and highly disputed, but at least six hypothesized theories for this mechanism have been proposed: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation, and enzyme efflux theories [1]. Currently, there exist therapies that have been experimentally shown to decrease DOMS prevalence, including various hydrotherapies [2] and foam rolling [3], but more effective preventative therapies could probably be developed if the underlying physiological mechanism was identified. In order to better understand this phenomenon and the unfortunate encounters I’m sure we’ve all had with it, we are going to look into some of those proposed mechanisms and try to get some insight on how it works (or doesn’t).

Lactic acid is easy to blame for exercise-related muscle pain because of its high production rates during exercise and its perceived role in muscle fatigue and soreness (which is often highly exaggerated). While lactic acid is a common byproduct of exercise, its role in the development of DOMS is likely insignificant. A study performed in 1983 measuring blood lactic acid concentration before and during two different 45-minute treadmill exercises, one on a level surface and one at a 10% decline, found that DOMS was not prevalent in level-surface runners, even though lactic acid concentration was significantly increased. Conversely, downhill runners saw no significant increases in lactic acid concentrations but experienced significant DOMS [4]. There was clearly no relationship between presence of lactic acid and development of DOMS, and the two in fact appeared to be mutually exclusive, so let’s move on to another of the previously mentioned theories.

The inflammation theory initially seems to have a bit more validity, as the similarities between the acute inflammation response, a response to various types of injury including muscle damage, and DOMS are striking. Both phenomena can be characterized by pain, swelling, and loss of function at the area of interest. The time lines seem to match up as well, as both have been reported to increase in severity for about 48 hours and show signs of healing at 72 hours. The issue with this theory though, is the lack of physiological evidence, which is arguably the most important kind. Studies investigating the relationship between DOMS onset and inflammatory biomarkers, like white blood cells and neutrophils, have often failed to find significant results, leading us to believe that inflammation does not cause DOMS [5]. Another drawback of the inflammation theory is the ineffectiveness of anti-inflammatory drugs in preventing DOMS-related pain. A study done using an anti-inflammatory drug and placebo on athletes undergoing eccentric bicycle exercise found no changes in subjective soreness between drug and placebo groups, suggesting that inflammation is not the source of DOMS pain [6]. We won’t completely remove inflammation from the picture though, as it may play more of a role than it appears.

While inflammation itself is likely not the cause of DOMS pain, inflammatory-related processes may not be completely innocent. Bradykinin, an inflammatory mediator, is believed to play a role in DOMS after a study done in 2010 by Murase et al [7]. This study used a previously established rat model of DOMS to show that injecting a B2 (but not B1) bradykinin receptor antagonist 30 minutes before exercise completely prevented DOMS in those rats. The antagonistic effects of the drug used, HOE 140, only last about an hour in the body, and they found that when injecting it 30 minutes after exercise, it had no effect in preventing DOMS. The results can be seen below.

This suggests that bradykinin released during exercise plays a direct role in the development of DOMS, and that preventing that bradykinin from interacting with the B2 receptor prevents DOMS. The role of bradykinin and the B2 receptor in the development of DOMS is not well understood, but it seems like a step in the right direction to me.

There is too much research out there on DOMS to cover in one lowly blog post. I wanted to debunk the lactic acid theory as lactic acid is often a scapegoat for exercise-related pain that is likely sourced elsewhere. While inflammation and DOMS have many similarities that may lead some to believe that there is a causal relationship there, that is also likely not the case. However, there is definitely evidence of some sort of relationship between the two. Further research into the physiological pathway that leads to DOMS is definitely needed to make any conclusive statements on the issue, and the bradykinin B2 receptor pathway is probably a good place to start. But until then, you’re just going to have to suck it up next time you feel like your quads will never work again two days after your new leg routine. Many have been there and survived before. You will too.

 

Questions to consider:

What distinguishes DOMS from standard muscle soreness?

Think about any times you may have experienced DOMS- what were you doing and why do you think it led to DOMS?

How could you determine the presence of DOMS in animal models when it cannot be subjectively reported? (Hint: check reference 7 for ideas)

How could preventative therapies for DOMS promote better health and wellness?

 

References:

[1] Cheung, K., Hume, P. A., & Maxwell, L. (February 01, 2003). Delayed Onset Muscle Soreness: Treatment Strategies and Performance Factors. Sports Medicine, 33, 2, 145-164.

[2] Vaile, J., Halson, S., Gill, N., & Dawson, B. (March 01, 2008). Effect of hydrotherapy on the signs and symptoms of delayed onset muscle soreness. European Journal of Applied Physiology, 102, 4, 447-455.

[3] Pearcey, G. E., Bradbury-Squires, D. J., Kawamoto, J. E., Drinkwater, E. J., Behm, D. G., & Button, D. C. (January 01, 2015). Foam rolling for delayed-onset muscle soreness and recovery of dynamic performance measures. Journal of Athletic Training, 50, 1, 5-13.

[4] Schwane, J. A., Watrous, B. G., Johnson, S. R., & Armstrong, R. B. (January 01, 1983). Is Lactic Acid Related to Delayed-Onset Muscle Soreness?. The Physician and Sportsmedicine, 11, 3, 124-31.

[5] Smith, L. L. (January 01, 1991). Acute inflammation: the underlying mechanism in delayed onset muscle soreness?. Medicine and Science in Sports and Exercise, 23, 5, 542-51.

[6] Kuipers, H., Keizer, H. A., Verstappen, F. T., & Costill, D. L. (January 01, 1985). Influence of a prostaglandin-inhibiting drug on muscle soreness after eccentric work. International Journal of Sports Medicine, 6, 6, 336-9.

[7] Murase, S., Terazawa, E., Queme, F., Ota, H., Matsuda, T., Hirate, K., Kozaki, Y., … Mizumura, K. (January 01, 2010). Bradykinin and nerve growth factor play pivotal roles in muscular mechanical hyperalgesia after exercise (delayed-onset muscle soreness). The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 30, 10, 3752-61.

A Closer Look At: Cupping

Among Olympic athletes you may have noticed something different in recent years – spots. Big red spots. Elite athletes from a variety of different sports have been spotted with – well- spots. But where are these markings coming from?

Michael Phelps, Alex Naddour, and Natalie Coughlin are a few of many athletes who have utilized cupping, an ancient therapeutic technique that has given them their spots.

Michael Phelps, male US swimmer, 2016 Rio Olympics

Cupping is a practice used in traditional medicine in which suction is created using a glass, bamboo, plastic, or ceramic cup. Negative pressure is generated within the cup and used to lift the skin and surrounding tissues. There are over ten different types of cupping therapy, each utilized to treat a variety of ailments. Most broadly cupping can be categorized in to wet cupping, where incisions are made on an indiviudal prior to applying negative pressure via cup, and dry cupping, where no incisions are made. However, treatments can be further classified by their power of suction, method of suction, and material inside the cup [1].

Since 3500 BC cupping has been practiced across several cultures. The earliest references to cupping therapy are found in the Ebers Papyrus, one of the oldest and most important medical papyri of ancient Egypt dating back 1550 BC. However, this form of therapy has not just been exclusively used by the Egyptians, rather it has been used across many cultures for thousands of years. In ancient Macedonia, cupping therapy was used to treat diseases and health disorders. Ancient Arab practitioners utilized cupping therapy to treat hypertension, polycythemia, headache and migraine, and drug intoxication. Hippocrates advocated cupping therapy as a treatment for many ailments in his treatise Guide to Clinical Treatment. Greek and Roman practitioners regularly used wet and dry cupping to treat a variety of diseases. To this day, Cupping therapy acts as one of the cornerstones of traditional Chinese medicine [2].

Today, athletes utilize cupping to decrease recovery time between training sessions, improve range of motion, alleviate inflammation, and reduce pain [3,4,5].

Research suggests that cupping may alleviate pain in individuals. A 2012 pilot study was conducted to assess the effects of a single wet cupping session on pain. Fifty individuals suffering from non-specific chronic neck pain were selected to receive a single wet cupping therapy session. Relative pain levels were measured through participant questioners and mechanical sensory and pain threshold values. Measures taken directly before therapy sessions and three days after treatment and were compared to assess changes in pain levels. Participants reported a statistically significant reduction in pain three days after treatment; however, because measures in reduction of pain are directly correlated with patient reporting, findings may be based on placebo effect or patient bias making it difficult to draw significant conclusions from this study [6].

Several systematic reviews (SR) assessing the impact of cupping on pain relief suggest there may be a positive correlation between the treatment and pain reduction. Several published randomized clinical trials including cupping interventions have been associated with a reduction in pain; however, these studies are limited by size and potential bias, and share a poor study design. Many studies are limited in longevity, participant sample size, and lack of a sufficient placebo for cupping therapy making it difficult to draw significant conclusions regarding the impact of cupping on pain relief [7,8,9,10].

Little is known about the mechanism of action of cupping. Several theories look to explain the pain relief experienced by individuals, including the following two:

  • The Pain Gate Theory: Chronic pain is influenced by altering pain signaling at the nociceptor level. Through stimulating pain via cupping, the frequency of nociceptor impulses will be increased, leading to the closure of pain gates and inevitably pain reduction.
  • Diffuse Noxious Inhibitory Controls: “Cupping therapy may produce an analgesic effect via nerves that are sensitive to mechanical stimulation. This mechanism is similar to acupuncture in that it activates A∂ and C nerve fibers which are linked to the DNICs system, a pain modulation pathway which has been described as ‘pain inhibits pain’ phenomenon”[9]

The potential mechanisms by which cupping may alleviate pain are not well understood, and certainly require validation by scientific studies. However, in addition to participant pain relief, reported effects of cupping also include increased blood flow to the skin [11] and a reduction in inflammation [12]. These physiological impacts may also influence pain relief experienced in clinical trial participants; however, further research is required to draw any conclusions about the mechanisms by which cupping works to potentially reduce pain.

Although it is difficult to draw significant conclusions relating cupping therapy with pain relief, research study participants, athletes, and thousands of other people claim cupping has helped reduce their pain. Cupping has been practiced for over 5000 years across a number of cultures and has alleviated the pain of many. It’s long history of helping indiviudals enduring pain and illness gives it promise as an effective treatment method. Bottom line- whether it directly facilitates pain relief or acts as a placebo – cupping has helped alleviate pain for thousands of years and can be beneficial.

Questions to consider

  • Cupping therapy – placebo or effective? Does it matter?
  • Measures of patient pain have been qualitative in many clinical trials, is an effective way to evaluate the impact of treatment? Are there any other ways to measure pain that may be more effective?
  • Recently cupping has become more commonly seen in popular culture – featured in films such as The Karate Kid and The Gua Sha Treatment and publicly displaced on the bodies of Olympic athletes: what impact does the integration of this traditional treatment in popular culture have on public perception?

References

[1] Aboushanab, T.S., AlSanad, S. (2018). Cupping Therapy: An Overview from a Modern Medicine Perspective. Journal of Acupuncture and Meridian Studies, 11(3), 83-87.

[2] Qureshi, N. A., Ali, G. I., Abushanab, T. S., El-Olemy, A. T., Alqaed, M. S., El-Subai, I. S., & Al-Bedah, A. M. (2017). History of cupping ( Hijama ): A narrative review of literature. Journal of Integrative Medicine,15(3), 172-181. doi:10.1016/s2095-4964(17)60339-x

[3]How Cupping Therapy Benefits Athletes. (2018, August 31). Retrieved from https://www.communityacupuncture.org/2018/05/01/how-cupping-therapy-benefits-athletes

[4] Is cupping therapy effective among athletes?. (2018, January 13). Retrieved from https://medicalxpress.com/news/2018-02-cupping-therapy-effective-athletes.html

[5] What is Cupping Therapy? (Or Why Do Athletes Have Red Spots?). (2019, January 29). Retrieved from https://wellnessmama.com/129773/cupping-therapy/

[6] Lauche, R., Cramer, H.,Hohmann, C., Choi, K.E., Rampp, T., Saha, F.J, Musial, F., Langhorst, J., Dobos, G. (2011). The Effect of Traditional Cupping on Pain and Mechanical Thresholds in Patients with Chronic Nonspecific Neck Pain: A Randomised Controlled Pilot Study. Evidence-Based Complementary and Alternative Medicine, 2012. doi:10.1155/2012/429718

[7] Kim, J.I., Lee, M.S., Lee, D.H., Boddy, K, Ernst, E. (2011) Cupping for Treating Pain: A Systematic Review. Evidence-Based Complementary and Alternative Medicine, 2012.

[8] Kwon, Y.D., Cho, H.J. (2007). Systematic Review of Cupping Including Bloodclotting Therapy for Musculoskeletal Diseases in Korea. Korean Journal of Oriental Physiology and Pathology, 21(3), 789-793.

[9]Al-Bedah, A.M.N., Ibrahim, S.E., Qureshi, N.A., Aboushanab, T.A., Ali, G.I.M., El-Olemy, A.T., Khalil, A.A.H, Khalil, M.K.M., Alqaed, M.S. (2018). The medical perspective of cupping therapy: Effects and mechanisms of action. Journal of Traditional and Complement Medicine, 1-8.

[10] Mehta, P., Dhapte, V. (2015) Cupping therapy: A prudent remedy for a plethora of medical ailments. Journal of Traditional and Complementary Medicine, 5(3), 127-134. 

[11] Liu, W., Piao, S.A., Meng, X.W., Wei, L.H. (2013). Effects of cupping on blood flow under skin of back in healthy human. World Journal of Acupuncture, 23(3), 50-52.

[12] Lin, M.L., Lin, C.W., Hsieh, Y.A., Wu, H.C.,Shih, Y.S., Su, C.T., Chiu, I.T., Wu, J.H. (2014). Evaluating the effectiveness of low level laser and cupping on low back pain by checking the plasma cortisol level. 2014 IEEE International Symposium on Bioelectronics and Bioinformatics.

Is chronic stretching actually beneficial?

Jackie Haffey and Matt Ballman

 

Have you ever wondered why stretching was always emphasized so heavily in gym classes growing up? Stretching is something that has been coupled with exercise all of our lives. Growing up we are taught to stretch before and after exercise in order to help prevent injury, promote recovery, and enhance your overall performance, but does it actually work? There are professional athletes out there who undergo strict training regimens that involve lots of stretching, but still manage to have career altering injuries like tearing their ACL. There are many athletes who are out there that are very talented but almost never stretch before or after a workout. On the flipside, there are many professional athletes out there that vow that stretching helps them extend their careers and improve recovery. In the NBA, yoga has become a common practice among players doing all that they can in order to help their bodies sustain their elite level of play and handle the rigors of playing in an 82 game season. Arguably the best player of all time Lebron James practices yoga regularly [6]. He even attributes it to helping him extend his career and play at a high level for as long as he has [6]. So does stretching actually help people perform better or avoid injury or is it all just a myth?

Figure1. Passive hamstring stretches

For a long time, stretching was highly recommended with little evidence to support it. Now studies are showing that acute stretching before exercise can actually be harmful as discussed in the previous blog post, “Holding Your Stretch is Holding You Back”.  So what is evidence saying about chronic stretching?When discussing effects of chronic stretching, it is referring to long term effects of consistent stretching. People normally associate this with increasing flexibility, or joint range of motion (ROM). The American College of Sports Medicine (ACSM) has recommendations for maintaining flexibility. A study was done in 2010 to support the ACSMs advice specifically for hip flexion [5]. There was a significant improvement in ROM for all stretching groups and a decrease for the control group [5]. The paper did mention its own limitation in only studying one muscle group, saying its findings should not be generalized to any muscles in the body. Another limitation was that the participants could not start a new or increase intensity of an existing exercise program during the study [5]. This may have allowed the collected data to have less noise but it may not accurately translate to real world scenarios as many athletes aim to increase workout intensity or switch up their workout programs. So with the knowledge that chronic stretching can increase ROM, how does it affect performance?

Table 1. Data from the 2007 study showing the improvements of the stretching group.

Table 2. Data from a study on D3 athletes showing no difference between stretching and control groups.

 

A study completed in 2007 had the goal of determining the effects of chronic stretching on specific exercise performances. Performed on relatively inactive people, the study lasted eight weeks long and tested whether stretching had an impact on power, strength, and endurance in the lower body by using various exercises according to each fitness category [1]. The, “stretching,” or experimental group showed significant improvement in all categories whereas the control group showed no improvements [1]. On the contrary there was a study completed on hamstring performance in female D3 athletes [4]. Six weeks long, this study found there to be no significant difference in power performance in either the stretching and control groups [4]. So maybe stretching just has an effect on sedentary individuals?

Another aspect of stretching that is renowned is its ability to decrease the body’s risk of injury. A study completed on patients with chronic neck pain had subjects undergo 6 weeks of stretching and/or global posture reeducation twice a week during that time [2]. After the study was completed it was found that both the stretching and posture reeducation groups had significant reduction in pain [2]. However, this study also lacked a control group so it is hard to tell whether the reduction in pain was at the result of a placebo effect. On the opposite end, a large scale literature search evaluated over 90 different studies trying to determine whether there was sufficient evidence that stretching does indeed reduce the risk of injury [3]. After reviewing a large amount of literature it was found that it cannot be determined whether stretching reduces the risk of injury [3]. In fact, it found it is more than likely to not have anything to do with injury risk because stretching depends on different characteristics of muscles than characteristics that rely on eccentric movement which is often the movement where non-contact injuries occur [3].

After reviewing the above literature and evaluating research that studied chronic stretching it really cannot be determined whether chronic stretching is essential in order to maintain performance and prevent injury. All of the studies observed either could not find data to support the fact that stretching indeed plays a pivotal role in exercise or the study was to limited in its structure to provide accurate results. The biggest problem was how the term, “chronic,” is defined. The longest study that we found was only 12 weeks long which can hardly represent professional athletes who have been stretching throughout their entire lives. Without longer studies it’s hard to determine anything about chronic stretching because there’s simply not enough data out there. Although stretching cannot be supported with factual scientific data it is hard to argue that it can’t hurt to stretch after exercise. With successful athletes swearing by its benefits why could it hurt to spend a little time after you exercise to stretch out? Even if it’s just for peace of mind stretching does have at least some benefit after all.

 

Questions to Consider:

In what populations is it most important to determine the effects of stretching?

Since most current studies are on the lower extremities, should studies been done on the effect of stretching the upper extremities ?

What would be your personal definition of chronic? Do you think 6 or 8 or 12 weeks studies count towards data for the effects of chronic stretching?

 

References and Further Readings:

  1. Kokkonen ’ J, Nelson AG, Eldredge C, et al. Chronic Static Stretching Improves Exercise Performance Chronic Static Stretching Improves Exercise. Performance Med Sci Sport Exerc. 2007;39(10):1825-1831. doi:10.1249/mss.0b013e3181238a2b.
  2. Aure OF, Hoel Nilsen J, Vasseljen O. Manual Therapy and Exercise Therapy in Patients With Chronic Low Back Pain. Spine (Phila Pa 1976). 2003;28(6):525-531. doi:10.1097/01.BRS.0000049921.04200.A6.
  3. Shrier I. Stretching before exercise does not reduce the risk of local muscle injury: a critical review of the clinical and basic science literature. Clin J Sport Med. 1999;9(4):221-227. https://www.colorado.edu/intphys/iphy3700/shrierCritRev.pdf. Accessed May 7, 2018.
  4. Bazett-Jones DM, Gibson MH, McBride JM. Sprint and Vertical Jump Performances Are Not Affected by Six Weeks of Static Hamstring Stretching. J Strength Cond Res. 2008;22(1):25-31. doi:10.1519/JSC.0b013e31815f99a4.
  5. Sainz de Baranda P, Ayala F. Chronic Flexibility Improvement After 12 Week of Stretching Program Utilizing the ACSM Recommendations: Hamstring Flexibility. Int J Sports Med. 2010;31(6):389-396. doi:10.1055/s-0030-1249082.
  6. Toland S. The Rise of Yoga in the NBA and Other Pro Sports | SI.com. Sports Illustrated. https://www.si.com/edge/2014/06/27/rise-yoga-nba-and-other-pro-sports. Published 2014. Accessed May 7, 2018.

DOMS: Why do your muscles hurt days after exercise?

Chris Hernandez and Christian Poindexter

Soreness is a typical and often expected side effect of any moderate level of physical activity or exercise.  However, contrary to popular belief, there are many different types of soreness which are a result of separate things. For example, the soreness that many people experience during or immediately after exercise is known as acute soreness. Acute soreness typically develops within a couple of minutes of the muscle contraction and dissipates within anywhere from a few minutes to several hours after the contractions have ended[1].  It is widely accepted that this soreness is a result of the accumulation of chemical byproducts, tissue edema, or muscle fatigue.  Delayed Onset Muscle Soreness (DOMS) typically develops between 12-24 hours after muscle contractions end, with peak ‘soreness’ being experienced 24-72 hours after the exercise is over[1].  Exercises typically associated with DOMS include strength training exercise, jogging, walking down hills, jumping, and step aerobics. Apart from soreness, people suffering from DOMS also experience swelling in their sore limbs, stiffness of adjacent joints, tenderness to the touch, and temporary reduction of strength in affected muscle[1].  Unlike with acute soreness, there are several competing theories on the cause of DOMS, none of which have been ultimately proven to be the predominant cause.  

One of the first and most touted theories was the Lactic Acid Theory.  This was based on the concept that the muscles continue to produce and accumulate lactic acid even after the exercise is abated.  The accumulation of this lactic acid is thought to cause the noxious stimulus associated with soreness[2].  The paper we are using, “Delayed Onset Muscle Soreness: Treatment Strategies and Performance Factors”, cited a study done by French researchers regarding misconceptions about lactic acid, and more specifically lactate[3].   This study goes on to explain that during the recovery phase post-contraction, accumulated lactate gets oxidized by lactate dehydrogenase (LDH) into pyruvate.  This pyruvate is either oxidized in the mitochondria where it contributes to the resynthesis of ATP, or it is transported in the blood to be used or disposed of elsewhere in the body[3].  It has been observed that for test subjects whose lactate levels were monitored for 72 hours before, during, and after exercise, their lactic acid levels returned to pre-exercise levels within 1 hour of the cessation of exercise[2].  Since DOMS does not set in for 24-48 hours, it is very unlikely that lactic acid accumulation is the cause of the pain and other symptoms associated with this disease.  

These researchers did note some conditions however that were noted to affect the lactate levels of those participating in the study.  For example, a participant with a diet rich or low in carbohydrate concentrations can cause lactate levels to decrease or increase respectively[3]. Further, participants who had undergone strenuous exercise the day before are likely to show signs of glycogenic depletion, which could cause them to have irregular lactate levels[3]. Further, the type of exercise performed was also shown to have an effect on not only lactate levels but also on the time frame required for levels to return to normal[3].  To improve this study and potentially get better results it would be best to make sure that all test subjects were undergoing the same exercise regimens.  It would also be beneficial if the amount of carbohydrates (based on body weight) was held standard, and that they all experienced 48 hours of rest before data collection[3].  However, even given these potential weaknesses, given that the lactate levels return to below normal within an hour of exercise cessation, it can be said with reasonable certainty that lactic acid is not the cause of DOMS[2,3].

A more current and well-supported theory is the Muscle Damage theory, which is based on the disruption of the contractile component of muscle tissue after eccentric exercise. Type II fibers have the narrowest z-lines and are particularly susceptible to this type of disruption. Nociceptors located in the muscle connective tissue and in the surrounding tissues are stimulated, which leads to the sensation of pain that we know as DOMS. In practice, muscle soluble enzymes can be used as an indicator of z-line disruption and sarcolemma damage. Creatine Kinase (CK) is used as one of these muscle permeability indicators; any disruption of the z-lines and damage to the sarcolemma will enable the diffusion of  CK into the interstitial fluid, where it can be measured.

To test the connection between eccentric exercise and changes in CK, this study[4] used five healthy adults and had them walk on a treadmill for an hour at a 13-degree incline to test the effect of concentric exercise, and then a 13-degree decline five weeks later to test eccentric exercise. Venous blood samples were taken pre-test and every 24 hours until CK levels had returned to pre-exercise levels. Following downhill walking, all subjects reported muscle pain and tenderness in the calves and glutei muscles, which developed several hours post-exercise and was maximal between 1-2 days after. The severity of pain differed between subjects, but following uphill walking none reported any pain or tenderness. Both concentric and eccentric exercises showed increases in CK levels, but eccentric work showed much greater levels and peaked after 4-7 post exercise, as shown in figures 1-2.

Newham, et al. conclude that rises in CK levels are a result of eccentric work, and suggests that the extent to which muscle is lengthened and the level of habituation to eccentric work play a role in the enzyme response, and thereby in DOMS. However, they acknowledge that there is only a correlation between CK levels and DOMS and not necessarily a causation. Additionally, the sample size they used is small which could lead to inaccurate data.

There are many theories of the cause of DOMS, and none can fully explain the phenomenon. A combination of models has also been proposed[5], drawing aspects from various theories. Of the two theories we examined, the muscle damage theory was the most conclusive, showing a relationship between plasma CK levels and DOMS. Additional studies will be necessary to determine whether the muscle damage theory, another theory or possibly a combination of multiple can best explain the symptoms of DOMS.

 

Questions to Consider:

  1. Which types of exercise would help to prevent DOMS?
  2. How would you better design an experiment to correlate DOMS with enzyme activity?
  3. Can we conclusively rule out lactic acid as an explanation?

 

References/Further Reading:

[1] American College of Sports Medicine. Delayed Onset Muscle Soreness. Delayed Onset Muscle Soreness, American College of Sports Medicine, 2011, www.acsm.org/docs/brochures/delayed-onset-muscle-soreness-(doms).pdf.

[2] Schwane JA, Hatrous BG, Johnson SR, et al. Is lactic acid 63. Hasson SM, Wible CL, Reich M, et al. Dexamethasone related to delayed-onset muscle soreness? Phys Sports Med phoresis: effect on delayed muscle soreness and muscle function 1983; 11 (3): 124-7, 130-1

[3]Léger , L., Cazorla , G., Petibois , C. & Bosquet , L. (2001). Lactate and exercise: myths and realities. Staps , n o 54, (1), 63-76. doi: 10.3917 / sta.054.0063.

[4]Newham, D. J., Jones, D. A., & Edwards, R. H. T. (January 01, 1986). Plasma creatine kinase changes after eccentric and concentric contractions. Muscle & Nerve, 9, 1, 59-63.

[5]Cheung, K., Hume, P. A., & Maxwell, L. (2003). Delayed Onset Muscle Soreness. Sports Medicine,33(2), 145-164. doi:10.2165/00007256-200333020-00005

[6]Armstrong, R. B. (January 01, 1990). Initial events in exercise-induced muscular injury. Medicine and Science in Sports and Exercise, 22, 4, 429-35.

Wheying the Benefits of BCAAs in Exercise

Andrew Reynolds and David Appleby

After hitting the gym, playing sports, or even going for a run, many athletes turn to protein and amino acid (AA) supplements to enhance muscle recovery and growth. Multiple studies suggest that individuals who regularly exercise or partake in high intensity training require more dietary protein and AAs than sedentary individuals. This additional protein not only allows the human body to repair itself, but is also required for everyday metabolic activities and immune function. Of the twenty amino acids that comprise muscle protein, nine are considered essential amino acids. These essential AAs are not able to be produced by the body on its own, and therefore must be ingested through one’s diet. While it is possible to obtain the necessary protein and nutrients through a regular balanced diet, evidence shows that supplementation before and after exercise may prove advantageous. Among the most popular and cost efficient are powdered proteins, found most commonly in the form of whey and casein. Whey protein, often referred to as “fast” protein, has been shown to elicit a sudden, rapid increase of plasma amino acids following ingestion, providing immediate delivery to the body. Casein, however, is known as “slow” protein and induces a rather progressive and prolonged increase in plasma amino acids. While the digestion of these different proteins has been found to mediate protein metabolism and synthesis after exercise, it is debated whether the use of branched-chain amino acids (BCAAs) augments these processes on its own.

 

The branched-chain amino acids make up approximately one third of skeletal muscle protein in the body, and account for three of the nine essential AAs. Of the three BCAAs are leucine, isoleucine, and valine, which have laid the foundation for a multi-million dollar industry of nutritional supplements. Distributors of BCAA supplements rave of their anabolic capabilities and claim of their role in muscle recovery when taken post-exercise, particularly in regard to leucine. Leucine has been said to not only act as a precursor for muscle protein synthesis, but also a regulator of intracellular signaling pathways involved in the process of protein synthesis. A few studies have reported that the ingestion of BCAAs increases protein balance either by decreasing the rate of breakdown, increasing the rate of synthesis, or a combination of both. Additionally, it was observed that pairing leucine supplements with carbohydrates and protein before and after workouts led to a heightened level of protein synthesis in the body when compared to trials where leucine was not present. However, the credibility and repeatability of the research behind these claims is unclear, and has been rebutted by other scientific studies.

In this study assessing BCAAs and muscle protein synthesis in humans, the idea that BCAAs alone are capable of promoting muscle anabolism is questioned. This claim has been put forward for more than 35 years, but has been chiefly recorded in rat and other animal studies, with almost no studies being conducted regarding the response to oral consumption. The study involves a detailed literature search, and evaluates the theoretical and empirical data used to make these initial claims regarding BCAAs. It discusses how skeletal muscle in humans comprises a much larger portion of total body mass than in rats and therefore leads to several differences in the way muscle protein synthesis is regulated. Another problem with these previous studies is that they often use the “flooding dose” technique, which involves the administration of an amino acid tracer over a very short time period, therefore neglecting any possibility of sustained effects. With that being said, many of the results found in past experiments employ methods that make the extrapolation of the data to humans unfitting and reduce the physiological significance. In addition, this study displayed how only two studies were conducted analyzing the intravenous effects of BCAAs in humans, noting in both that BCAAs decreased both muscle protein synthesis and protein breakdown. However, the rate of the catabolic processes that broke down muscle protein exceeded the rate of protein synthesis in both cases during BCAA infusion. Due to these findings, the researchers refuted the claim that consumption of dietary BCAAs initiates anabolic activity and increases muscle protein synthesis.

Overall, it is evident that additional attention to diet and supplementation is essential for athletes and individuals who regularly exercise in order to promote the growth and repair of muscles, and to maintain a healthy body. While use of protein powders in the role of muscle protein synthesis has been backed by extensive scientific research, it is still unclear of the extent to which BCAAs are capable of carrying out these same processes on their own. More studies need to be conducted in human subjects observing the activity and metabolism of proteins when dietary BCAAs are ingested to better determine the effectiveness of their use. Many factors come into play when assessing the best supplements to take in regards to exercise, including intake quantity, timing of ingestion, and interaction effects. After observing the conflicting research claims, the use of BCAAs alone may not yield noticeable results, but seems to have little to no risk involved in taking them. Many trainers and workout regimens advise the combination of protein supplements and BCAAs to maximize benefits, but the scientific research is still lacking.

Questions to Consider

  1. What would happen if an individual took more protein supplements/BCAAs than the body needed?
  2. How could studies be better designed to assess the role of BCAAs in humans?

Further Suggested Reading

[1] https://www.ncbi.nlm.nih.gov/pubmed/20048505

[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5568273/

[3] https://www.ncbi.nlm.nih.gov/pubmed/16365096/

[4] https://jissn.biomedcentral.com/articles/10.1186/1550-2783-4-8

[5] http://healthyeating.sfgate.com/primary-role-protein-diet-3403.html

Can Altitude Masks Improve Athletes Efficiency in Utilizing Oxygen and Increase Athletic Performance?

Eric Bartholomew and Joe Yovanovich

Altitude training has been shown to give athletes a competitive edge by increasing VO2 max, endurance performance, and lung function. The “live high-train low” method as been adopted as one of the most beneficial training methods. By athletes living high and training low, they get the benefits of altitude acclimatization which increases their performance on sea level. As the human body reaches altitude of around 2,100 m, the saturation of oxyhemoglobin decreases significantly. However, a long-term adaptation of living at high altitude is that your body starts to accomodate for the lack of oxygen. By exposing the body to hypoxic conditions, the body will increase its red blood cell (RBC) production as close to 30-50%. This increase in RBCs, increases the oxygen carrying capacity as sea level which will lead to a higher VO2 max, and an increase in athletic performance.  An easy and accessible way to simulate altitude training is through the use of altitude training masks.  

Elevation Training Mask

Many products have been put on the market in order to simulate high altitude training while training at sea level. One of these products is the “Elevation Training Mask” (ETM). The ETM covers both the nose and mouth, using different sized opening and fluxed valves in order to increase resistance of respiration in hopes of increasing VO2 max and lung function. The resistance system in the masks allows the user to stimulate altitude ranges from 914m to 5486m. But in order to truly stimulate a hypoxic state, the masks would have to be able to decrease the partial pressure of oxygen, questioning if ETMs can truly simulate high altitude training and help with overall performance.

In this study, they tested to see the effects of wearing the ETM on endurance performance variable to conclude if ETMs can act as altitude simulators. Using two groups (a control and those using masks), twenty five subjects completed two, 30 minute, high-intensity workouts per week for 6 weeks. Before and after the 6 week training period, VO2max, ventilatory threshold (VT), peak power output (PPO), respiratory compensation threshold (RCT) and maximal heart rate (MHR) were measured in all subjects. The results are shown in Table 1.

Table 1: Changes in Performance Variables

There was significant improvement in VO2max and PPO in both the control and mask groups. Only the mask group had significant differences in VT, Power Output (PO) at VT, RCT and PO at RCT but improvements in VT and PO at VT did not reach statistical significance (VT p=0.06, PO at VT p=0.170). This study was a well executed study, including  pilot testing and constant monitoring of each subject. A limitation of this study is that the subjects volunteered to participate in the study who claimed they were moderately trained. However, the mask and control groups were similar in age, height, weight and BMI at the start of the study.  This decreased the amount of variability in the study. Also, the 6 week training period was titrated based on subjects RPE. RPE is a very subjective way to measure intensity and is not always seen to be the most accurate. This however would not skew results significantly. With all this in mind, it is safe to say that the conclusions made from this article are valid. From this study, we can conclude that wearing an EMT during high-intensity workouts does not appear to act as a simulator of altitude, but more like a respiratory muscle training (RMT) device.

 

The next study, completed at Lindenwood University is a follow up to the previous study to try and determine if the EMT functions as a RMT device. The study was comprised of 20 recruited resistance-trained men to track the acute effects of the EMT in regards to resistance exercise and maximal effort sprint performances, as well as overall metabolic stress. Baseline testing was completed 3-7 days before the subjects experimental results were obtained. These tests were used to determine the subjects body composition and to assess their 5-repetition maximum (5RM) for bench press and back squat after they were appropriately familiarized with the equipment (bench press, squat rack and non-motorized treadmill). Two trials for all subjects were completed on non-consecutive days with and without the mask (EMT and No Mask (NM) conditions, respectively). The subjects were to complete a bench press and back squat (using weight based off their individual 5RM), as well as a 25-second all out sprint test. Velocity of the bars for the bench and squat tests were determined using a linear position transducer (accuracy correlation coefficient of 0.97). Blood samples were collected to determine blood lactate and oxygen saturation was determined using a finger pulse oximeter.  ANOVA was used for statistical analysis to compare the EMT and NM conditions. Peak velocity of the bench press and back squat were significantly greater in the NM trial (both p = 0.04 < 0.05). Blood lactate was higher in the NM condition for the bench press and sprint test (p < 0.001). Using a 5-point Likert scale to the subjects self-selected their energy, fatigue, alertness and focus for both conditions. The EMT surprisingly did not differ significantly from the NM condition. It should also be noted that 3 subjects were unable to complete the protocols using the EMT masks due to extreme discomfort and their results were omitted from the study. Contrary to the original hypothesis, the EMT condition did not significantly decrease the amount of bench and squat repetitions completed to failure. It was confusing, however, that the blood lactate was found to be higher for the NM condition. It would be expected, since the mask’s purpose is to restrict the user’s access to oxygen, that the EMT group’s blood lactate would be higher since less oxygen would lead to more anaerobic respiration and therefore more lactate. The researchers attribute this phenomenon to less fast twitch fibers being recruited, which explains why the velocity for the bench and squat were lower for the EMT condition. They also admit that more studies need to be completed before that claim can be made.

Overall, this study was well controlled. All subjects diets were monitored carefully before all testing, and all results were obtained in a relatively consistent manner. However, using a 5-Point Likert scale opens the study up to subjective bias, especially since the subjects were not blinded to the different test conditions (they were consciously aware of wearing the mask). Also, the long-term aim of this study seems to be a little unclear. They mentioned in the introduction they wanted to see if the masks could serve as a RMT device, but only measured the acute responses. The effects of the EMT on respiratory muscle function would probably not be seen after weeks or even months after training. All in all, the study yielded few significant results to support that EMTs can acutely affect respiration at an anaerobic capacity.

Both studies were able to conclude that the EMTs did not completely mimic an environment of higher elevation. As mentioned previously, this probably has to do with the EMT’s inability to alter the partial pressure of oxygen. The first study had indicated that the mask served more as an RMT device, rather than a simulator of altitude. The second study, however, did not obtain results to support this claim. Elevation masks are a relatively new technology, and more extensive studies will need to take place before any conclusive claims can be made. Studies in the future, should probably follow the first’s with studying the effects long-term, rather than one time use. Additional studies lasting weeks or even months will be able to determine if EMTs have any long lasting effects on aerobic capacity and respiratory muscle function with training.

Questions to Consider

  1. How can Elevation Masks be designed differently to alter the partial pressure of oxygen?
  2. Do EMTs have any negative effects on the brain (oxygen deprivation, ect.)?
  3. What effects to EMTs have on the different portions of the respiration system (i.e. lungs, gas exchange, ect.)?

 

References/Further Reading

[1] Porcari, John P., et al. “Effect of Wearing the Elevation Training Mask on Aerobic Capacity, Lung Function, and Hematological Variables” Journal of Sports Medicine and Science, Online, 15(2): 379-386, 2016. 

[2] Jagim, AR, Dominy, TA, Camic, CL, Wright, G, Doberstein, S, Jones, MT, and Oliver, JM. “Acute effects of the elevation training mask on strength performance in recreational weightlifters”. Journal of Strength and Conditioning Research, Online, 32(2): 482-489, 2018.

[3] Elevation Training Mask

[4] Do Elevation Masks Work?

[5] Effects of Simulated Altitude on Maximal Oxygen Uptake and Inspiratory Fitness