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.

Using NIRS to non-invasively monitor muscle oxygenation during exercise

Skeletal muscles are the basis of all movement in the human body, and athletes work years to train their muscles to be powerful yet efficient. Even if a single muscle could allow a person to lift a car, it would not be very useful if the muscle could no longer create forceful contraction again for several hours. The muscle also must be efficient in the use of oxygen, ions, and other substrates that allow for contraction to be able to quickly recover and be prepared for repeated contraction. Muscle oxygenation is particularly important for both endurance and power of a muscle because it is necessary to produce ATP to power muscle cells to contract. Heart rate and blood oxygen delivery are helpful for getting an idea of an athlete’s efficiency, but they do not tell the whole story for the muscle. At the muscle, the balance between delivery and consumption of oxygen explains its efficiency [1]. To measure muscle oxygen saturation, a technique called near-infrared spectroscopy (NIRS) is used to get real time data to inform athletes of the state of their muscles during training. This is a powerful tool for maximizing athletic gains in muscles from training and to see the state of the muscle over time and after rest.

Early NIRS instrumentation was contained to the lab, but recently portable versions have become more common, which is very important for its use in both the medical and research fields. In medicine, NIR has been used for study of septic shock, free tissue transfer, real-time tissue perfusion during surgery, cancer nanotechnology, and peripheral arterial disease.  For this post, the use of NIR in exercise will be highlighted. In exercise, NIRS is a great tool because it is a non-invasive method that can be applied locally to muscles or tissues of interest and provide real time data during exercise. NIRS is highly sensitive to changes in muscle tissue oxygenation [2, 3, 4], and it reflects the balance between oxygen delivery and utilization, unlike measurements of arterial or venous blood samples which have been used previously and are minimally invasive [2]. NIRS works by measuring the percentage of oxygenated hemoglobin to total hemoglobin (oxygenated and deoxygenated hemoglobin) to give muscle oxygenation. Hemoglobin is the main oxygen carrying protein in the blood and can carry 4 oxygen molecules (O2). Oxygenated and deoxygenated hemoglobin scatter NIR light (600-1000 nm) differently, so their relative concentrations can be found from their molecular absorption coefficients. To do this, three to four different wave lengths of light will be used to determine the concentrations of each based on the change in molecular absorption coefficients at different wavelengths (Fig 1). NIR light must be used as it: 1) passes through skin, bone, and most biological tissue, and 2) is the appropriate wavelength where the small amount of absorption that occurs is predominately from hemoglobin (Fig 2) [5].  As the muscle performs work, the muscle oxygenation will decrease as a function of the work and the training of the muscle.

Fig. 1: Molecular Absorption Coefficient Profiles for Oxygenated and Deoxygenated Hemoglobin [5]

Fig 2: Light Absorption by Wavelength [5]

 

 

 

 

 

 

 

 

 

 

A patent on google patent claims to leverage this technology in a wearable article of clothing for athletes to be able to measure muscle oxygenation real-time (Fig 3) [6]. The patent claims to be a method and apparatus for assessing tissue oxygenation saturation through two main claims that summarize to: a portable apparatus that is a wearable article capable of measuring oxygenation saturation of at least one of a skin dermis layer, adipose layer, or muscular fascial layer of a user during physical activity using at least one near-infrared spectroscopy probe including at least one near-infrared light source and at least one photodetector. In short, the patent is a claim on a portable, wearable NIRS device for tissue oxygenation levels. NIRS has been a research method for decades, so the novel part of this patent lies in the incorporation of this technology into a wearable article of clothing.

Fig 3: Figure from patent illustrating wearable shirt, shorts, and socks using NIRS

Fig4: Figures from patent showing example data of muscle oxygenation average during constant rate running at different grades (top) and real time data from medial gastrocnemius muscle during weighted exercise and unweighted control (bottom)

This patent pertains primarily to the measurement of tissue during exercise (Fig 4). This could be of use for athletes during training to be able to compare what levels of exercise cause certain levels of muscle oxygen saturation loss. For example, highly trained athletes often train at high altitude to reduce oxygen in the air so that their body adapts to becoming more efficient with oxygen usage. This prompts higher performance when returning to normal oxygen levels. Using NIRS could allow them to find a training regime that caused the same hypoxia in muscle without traveling to higher altitude (they will still miss out on some of the pulmonary and cardio vascular advantages that training at altitude can produce). This may also be helpful in rehabilitation as the change in muscle oxygenation is an indicator that the muscle is being used and can inform physical therapists if the patient is engaging the correct muscles during rehab. Additionally, the device may also have merit in the medical realm for monitor muscle oxygenation in patients with chronic heart failure, peripheral vascular disease, chronic obstructive pulmonary disease, and varying muscle diseases [3, 4].

  1. Patent title: Method and apparatus for assessing tissue oxygenation saturation
  2. Patent number: US20170273609A1
  3. Patent filing date: 2017-03-22
  4. Patent issue date: Patent Pending
  5. How long it took for this patent to issue: TBD
  6. Inventor(s): Luke G. Gutwein, Clinton D. Bahler, Anthony S. Kaleth
  7. Assignee (if applicable): Indiana University Research and Technology Corp
  8. U.S. classification: A61B5/0075
  9. How many claims: 20

References and Further Reading

[1] BSX Athletics https://support.bsxinsight.com/hc/en-us/articles/204468695-What-is-muscle-oxygenation-

[2] Bhambhani, Y. N. (2004). Muscle Oxygenation Trends During Dynamic Exercise Measured by Near Infrared Spectroscopy. Can. J. Appl. Physiol., 29(4), 504–523.

[3] Hamaoka, T., Mccully, K. K., Quarisma, V., Yamamoto, K., & Chance, B. (2007). Near-infrared spectroscopy / imaging for monitoring muscle oxygenation and oxidative metabolism. Jounal of Biomedical Optics, 12(6), 1–16. http://doi.org/10.1117/1.2805437

[4] Boushel, R., & Piantadosi, C. A. (2000). Near-infrared spectroscopy for monitoring muscle oxygenation. Acta Physiol Scand, 168, 615–622. http://doi.org/10.1046/j.1365-201x.2000.00713.x

[5] Shimadzu Commercial Website https://www.ssi.shimadzu.com/products/imaging/labnirs-principle-of-operation.html

[6] Patent https://patents.google.com/patent/US20170273609A1/en?oq=US20170273609A1

[7] Ferrari, M., Muthalib, Makii, & Quarisma, V. (2011). The use of near-infrared spectroscopy in understanding skeletal muscle physiology : Phil. Trans. R. Soc. A, 369, 4577–4590. http://doi.org/10.1098/rsta.2011.0230 

[8] Artinis Commercial Site https://www.artinis.com/portamon#portamon-software

Patent Blog Post: Fitbit’s Wearable Heart Rate Monitor

Perhaps you’ve been barraged by emails from Fitbit that try and get you to buy one of their products during one of their many sales. Perhaps you’re a trendy techie and have a wearable in the form of a Galaxy or Apple Watch. Or perhaps you’re simply the owner of a smartphone made within the past few years. All these technologies have heart rate monitoring built into them from the get-go, and it is increasingly hard to get away from gadgets that don’t have some form of heart monitoring. With how ubiquitous the technology has gotten, I would like to look today at one of the patents put forward by Fitbit, one of the more popular brands when it comes to wearable fitness trackers. For this post, I’ll be using the information put forward by Google Patents, seen here.

One of the many figures in the patent, detailing the backside of the wearable.

The patent is simply titled as, “Wearable heart rate monitor,” and has a patent number of US8945017B2. It was originally filed on June 3rd, 2014, and was then approved on February 3rd, 2015. This makes the time to issue a little under a year, which is quite fast for an electronics product. The two inventors credited in the patent are Subramaniam Venkatraman and Shelten Gee Jao Yuen. Looking at the other patents associated with them, Venkatraman seems to have worked on more navigational devices, while Jao Yuen has worked on several other gyroscope-related projects. The assignee is, of course, Fitbit Inc. themselves. Officially, one of the classifications of the patent is, “signal processing specially adapted for physiological signals or for diagnostic purposes for noise prevention, reduction or removal.” This one patent has 30 different claims to its name.

Of the 30 different claims in the patent, many of them tie into 2 main claims. The first is that the wearable heart monitor has a way to efficiently, accurately, and quickly determine the heart rate of the user. The second is to ensure that the wearable is capable of compiling the heart rate monitor’s data, including the heart rate data. This patent is aimed at both casual and advanced fitness enthusiasts, as the data gleaned from the wearable is handy to track. Runners, in particular, would find this tempting as it also mentions step tracking and other forms of movement.

The heart rate monitor works by using a waveform sensor, which reads signals at the surface of the skin. These signals are sent to the rest of the device, where the data is processed. The raw data from the sensor is rough and has a lot of noise from several factors, including movement and moisture. To remove the noise, the data has to be passed through several filters. From that data, a heart rate can be determined, and then presented to the user. Unlike the monitors of prior ages, this heart rate monitor would not rely upon disposable components, instead simply being able to be used multiple times by wearing it. In addition, the heart rate tracker would track more than just heart rate, including details about steps.

References:

Venkatraman, S., & Yuen, S. G. J. (2014). Wearable heart rate monitor. Retrieved from https://patents.google.com/patent/US8945017B2/en

How it Works: Pedometers

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

Epigenetic Muscle Memory

What comes to mind when I hear the term muscle memory is the typical example being able to ride a bike with ease even if you haven’t ridden one in a long time.  This time of memory is neurologic and comes from repetition of motor tasks. It primarily involves the dorsolateral premotor cortex and cerebellum.[1] However, there is a different kind of muscle memory that a recent study just discovered a lot about.[2] This muscle memory is referring to epigenetic changes to the DNA of human skeletal muscle.

Epigenetics is changes that affect gene expression without altering the DNA sequence but instead turn on and off specific genes. Three ways that genes can be silenced are DNA methylation, histone modifications, and RNA-associated silencing.[3] DNA methylation is what plays a key role in muscle memory and is a major part of the study.  It is a chemical process of adding a methyl group onto DNA that only occurs where cytosine and guanine nucleotides are next to each other and the guanine is linked to a phosphate.[2] This is referred to as a CpG site.

This study used 8 healthy males with no previous training. They went through three phases: loading, unloading, and reloading. Whole-body DEXA and vastus lateralis muscle biopsies were taken at baseline and at the end of each phase. Over 850,000 CpG sites were investigated. Many genes where found to be hypomethylated and showed increased gene expression. This epigenetic memory of earlier muscle growth means that at a later time there can be a greater response to exercise and more muscle growth.

 

As a person who has encountered many injuries and been forced to take multiple weeks off from the gym, it is comforting to know that despite the loss in strength that occurs during the time off my muscles will hold this memory and be more capable of regaining it.

One possible major implication of this study is a change in bans due to performance enhancing supplements, as this could mean the effects may be much longer lasting. Should people caught using them ever get to return to their sport knowing this? More research needs to be done on this specifically before real decisions can be made on this but it is definitely a future path for this research

 

References and further readings

[1] Robb T. How to play like a pro: The neuroscience of muscle memory. Oxford Neurological Society. http://neurologicalsociety.org/play-like-pro-neuroscience-muscle-memory/. Published 2016. Accessed March 14, 2018.

[2] Seaborne RA, Strauss J, Cocks M, et al. Human Skeletal Muscle Possesses an Epigenetic Memory of Hypertrophy. Sci Rep. 2018;8(1):1898. doi:10.1038/s41598-018-20287-3.

[3] Simmons, D. (2008) Epigenetic influence and disease. Nature Education 1(1):6

[4] Improving your Muscle Memory – Making Good Technique Automatic. National Federation of State High School Associations. https://www.nfhs.org/articles/improving-your-muscle-memory-making-good-technique-automatic/. Published 2014. Accessed March 14, 2018.

[5] Sharples AP, Stewart CE, Seaborne RA. Does skeletal muscle have an “epi”-memory? The role of epigenetics in nutritional programming, metabolic disease, aging and exercise. Aging Cell. 2016;15(4):603-616. doi:10.1111/acel.12486.

Calories Counted on Exercise Equipment

HIIT: Is it all it’s hyped up to be?

By Andrew Taylor and Kathleen Wright

 Figure 1.  Women participate in a HIIT class.

How many of us have said we would go to the gym, only to realize later that we don’t have the time? High-intensity interval training (HIIT) classes have increased in popularity over the last few years, partly because the sessions are shorter than traditional workouts. HIIT workouts alternate short (20 or 30 second) intervals of maximum exertion with periods of rest or low-intensity exercises. Elite athletes might take part in HIIT to improve their aerobic energy metabolism and performance. If you have ever played a demanding sport, you have probably been subjected to HIIT during the game or practice. The recent obsession with HIIT raises the question: is it just a fad, or will it stick around as an effective means of exercise?

HIIT can be defined as brief exercise that generates a VO2peak, or 90% of the maximum VO2 potential, commonly followed by a relaxation period. This study utilized the Wingate test: participants repeated 30 seconds all-out maximal cycling on a specialized ergometer, with 4 minutes of recovery in between, for a total of 2 to 3 minutes of intense exercise. The authors focused on specific markers in skeletal muscle metabolic control; they determined an increase in skeletal muscle oxidative capacity after 2 weeks of HIIT. They also found that changes in carbohydrate metabolism (Figure 2) were comparable to adaptations from endurance training. Although exercise performance improved, there was no measurable change in participants’ VO2peak after 2 weeks of HIIT. However, this study did not fully investigate how HIIT affects the cardiovascular and respiratory systems, or metabolic control in other organs.

 

Figure 2. Results depict the glycogen content, or resting carbohydrate dry weight, found in skeletal muscle during rest and 20 minutes after exercise, both before and after 2 weeks of HIIT.

 

Additional HIIT data concerning VO2peak and citrate synthase activity support the previous claim that HIIT provides similar benefits to endurance training. This review recognizes that Wingate-based training may not be tolerable for everyone, and instead tested low-volume HIIT. The authors found that their model was time-efficient and effective in producing cardiovascular and skeletal muscle adaptations. They reference the results of similar studies, saying that HIIT is superior to moderate-intensity continuous training (MICT)  in increasing cardiorespiratory fitness and endothelial function. However, researchers still don’t know what intensity or training volume is required to be effective.

A study concerning overweight and obese adults found that HIIT had similar results to MICT, in terms of body composition measures, but HIIT required less training time. They concluded that HIIT may be a time-efficient way to manage weight. Meanwhile, this systematic review determined that MICT and HIIT provide similar benefits for body fat reduction, but HIIT was no more time-efficient than MICT.

The data from these studies indicate that HIIT is comparable to MICT, similar to the difference between traditional and functional workouts, as described previously in this postHigh intensity workouts can be very demanding, as seen with the Wingate test, and may not be suitable for all individuals. HIIT should not be substituted for specialized athletic training, but can be beneficial for athletes who need to quickly use their bodily carbohydrates. Many HIIT studies are short-term, like the first study we mentioned, and further research needs to be conducted to determine the long-term effects of HIIT on cardiovascular and respiratory systems. Although HIIT attracts people with the allure of getting fit fast, there isn’t enough data currently to support that HIIT is actually more time-efficient than endurance training.

Questions to Consider:

Should HIIT workouts be recommended for the average person?

Why could an increase in glycogen dry weight be considered important for exercise?

How could your current workout routine benefit from HIIT?

What athletes do you feel would benefit most from HIIT?

Recommended Further Reading- Works Cited

  1. Figure 1. HiiT_40-20_6108. Attribution: Cathe Friedrich. https://www.flickr.com/photos/cathefriedrich/albums/72157622565339997 [CC BY-NC-ND 2.0 (https://creativecommons.org/licenses/by-nc-nd/2.0/)]
  2. Gibala, M. J., & McGee, S. L. (2008). Metabolic adaptations to short-term high-intensity interval training: A little pain for a lot of gain? Exercise and Sport Sciences Reviews, 36(2), 58-63. 10.1097/JES.0b013e318168ec1f
  3. Gibala, M. J., Little, J. P., MacDonald, M. J., & Hawley, J. A. (2012). Physiological adaptations to low-volume, high-intensity interval training in health and disease. The Journal of Physiology, 590(5), 1077-1084. 10.1113/jphysiol.2011.224725
  4. Wewege, M., van den Berg, R., Ward, R. E., & Keech, A. (2017). The effects of high-intensity interval training vs. moderate-intensity continuous training on body composition in overweight and obese adults: A systematic review and meta-analysis. Obesity Reviews, 18(6), 635-646. 10.1111/obr.12532
  5. Keating, S. E., Johnson, N. A., Mielke, G. I., & Coombes, J. S. (2017). A systematic review and meta-analysis of interval training versus moderate intensity continuous training on body adiposity. Obesity Reviews, 18, 943-964. 10.1111/obr.12536

How it Works: Direct Calorimetry