How Garmin Watch Heart Rate Monitors Work

Using a GPS watch has become the norm in distance running. These watches provide users with information regarding distance traveled, pace, and even maps of the route taken. Newer watches also include heart rate monitors, providing users with greater information about their fitness. The popular watch brand, Garmin, has a patented heart rate monitor [1] used in their watches, seen in Figure 1 below. 

Figure 1. Back of Garmin watch with heart rate monitor device (labeled “610”) [1].

The heart rate monitor in Garmin watches monitors cardiac signals via the user’s wrist. The main claims of this invention are as follows:

  • The device consists of an emitter, receiver, inertial sensor, and time-variant sensor. The processor determines frequency associated with the motion signal, transforms the signal from PPG into the frequency domain, identifies the cardiac component of the PPG signal, configures a time-variant filter, and calculates the time between cardiac component cycles.
  • The device emits a light signal and receives an input of the light’s reflection, which eventually allows for the isolation of the cardiac component of signal.
  • The cardiac component of signal allows for heart rate to be determined.
  • The time between successive cycles gives insight into heart rate variability, stress, recovery time, VO2 max, and/or sleep quality.
  • The device contains an interface that displays determined information to the user.

This device would be of interest to any Garmin watch user, especially those interested in heart rate during exercise. This watch, primarily used by runners, tells the user their heart rate and therefore how fast their heart is pumping blood through the body at any given time during exercise. This gives insight into the user’s fitness and exertion levels and ensures the user is in desired heart rate zones while training. Knowing how heart rate changes personally affect the user can also give insight into dehydration, stress, and needed recovery. Using this device over an extended period of time allows for users to see improvements in heart rate due to exercise.

How Does it Work?

The heart rate monitor in Garmin watches directs light from a light-emitting diode (LED) to the skin of the user. The reflection of the light is received by a photodiode, which sends a light intensity signal to the processor. The processor generates a photoplethysmogram (PPG) signal – containing cardiac, motion (determined by an inertial sensor, which senses movement of the device), and respiratory components – based on the intensity of the reflected light.

To isolate the cardiac component of the PPG signal, time-variant filters are used to remove non-cardiac components. The PPG signal can initially be filtered with a bandpass filter that only passes signals within the range of possible cardiac component frequencies. This bandwidth can be adjusted by the processor to account for lesser or greater expected cardiac frequencies based on changes in the environment. For example, if the user begins running, the processor senses rapid motion change and the bandwidth will increase since heart rate is expected to rise.

To determine which other signals to remove within the passband, the processor first identifies one or more frequencies associated with the motion signal via the inertial sensor. The processor then transforms the PPG signal into the frequency domain. Comparing the identified motion signal frequencies with the transformed PPG signal allows for the cardiac component of the signal to be determined within the frequency domain. Then, based on the identified cardiac component, the processor is able to determine filter coefficients for the cardiac component which are configured into the time-variant filter. When the PPG signal is transformed back into the time domain and filtered through this time-variant filter, the motion component is removed from the PPG signal. This results in a time domain PPG signal without the motion component, making it easier to identify the cardiac component of the PPG signal in the time domain. See Figure 2 below for a flowchart describing this filtering process.

Figure 2. Flowchart describing the process of isolating heart rate from PPG signal [1].

The processor does not need to identify frequencies of the motion signal for every time point. It identifies these frequencies within the PPG signal for an initial time period, configures a filter to remove these frequencies, then uses the same filter to filter the motion signal from subsequent time periods of the PPG signal.

The device is also capable of storing memory. This allows for the device to create a model of expected cardiac component frequencies from previously determined data. Based on the model, the processor can then determine the probability of any given frequency within the PPG signal to be a frequency of the cardiac component.

Heartbeat and respiratory patterns are cyclical over a short period of time while motion data and noise can be cyclical or irregular for any length of time. Over a longer period of time, cardiac and respiratory signals can potentially have non-cyclical patterns (e.g. increasing heart rate during an exercise session). This allows for the variability in cardiac parameters to be determined. Analyzing variability in heart rate allows for estimates of parameters of stress, recovery time, VO2 max, and sleep quality.

 

This patent cites numerous references of inventions this device incorporates or improves upon. This device improves on a previous wrist-watch heart rate monitor (patent 2009/0048526), which was developed as an alternative to wearing a chest strap heart rate monitor. The Garmin device is different from this wrist-watch as this device does not include any inertial sensors. Therefore the Garmin device is able to better remove noise from motion [2]. Another exercise device by Samsung Electronics (patent US 7,867,142 B2) uses heart rate data to inform users about changes in their exercise speed by playing a sound. While the Garmin device does not play a sound, it uses the heart rate data to extrapolate information about stress, recovery time, VO2max, and sleep quality, which is likely to be of greater value to the user [3].

The following lists basic information regarding the Garmin heart rate monitor patent:

  1. Patent title: Heart Rate Monitor With Time Varying Linear Filtering
  2. Patent number: US 9,801,587 B2
  3. Patent filing date: Oct. 18, 2016
  4. Patent issue date: Oct. 31, 2017
  5. How long it took for this patent to issue: 1 year, 13 days
  6. Inventors: Paul R. MacDonald, Christopher J. Kulach
  7. Assignee: Garmin Switzerland GmbH
  8. U.S. classification: CPC: A61B 5/02416 (20130101); A61B 5/1112 (20130101); A61B 5/1118 (20130101); A61B 5/7285 (20130101); A61B 5/721 (20130101); A61B 5/02405 (20130101); A61B 5/02427 (20130101); A61B 5/02438 (20130101); A61B 5/0833 (20130101); A61B 5/486 (20130101); A61B 5/4815 (20130101); A61B 5/681 (20130101); A61B 5/725 (20130101); A61B 5/7278 (20130101); A61B 5/165 (20130101); A61B 2562/0219 (20130101)
  9. How many claims: 29 claims

 

References:

[1] P. R. MacDonald and C. J. Kulach, “Heart Rate Monitor With Time Varying Linear Filtering.” U.S. Patent 9,801,587 B2, issued October 31, 2017.

[2] R. M. Aarts and M. Ouwerkerk, “Apparatus for Monitoring A Person’s Heart Rate And/Or Heart Variation; Wrist-Watch Comprising The Same.” U.S. Patent 2009/0048526 A1, issued February 19, 2009.

[3] S. K. Kim, J. S. Hwang, and K. H. Kim, “Method and Apparatus for Managing Exercise State of User.” U.S. Patent 7.867,142 B2, issued January 11, 2011.

Enough (N)SAID about Ibuprofen & Soreness

If I’m being honest here, it’s been a while since I’ve had a solid gym routine. But this semester I’ve been going pretty regularly, and let me tell you, I’ve felt the burn. My muscles have felt pretty sore in the 2-3 days following my workouts, so I’ve had to turn to ibuprofen a few times to relieve the pain. But even after taking ibuprofen in the morning, I’ve felt sore again by the end of the day. This got me thinking: how effective is ibuprofen at reducing muscle soreness?

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly served over-the-counter at pharmacies. Some common forms you may recognize include aspirin and ibuprofen (Motrin, Advil). NSAIDs are taken for many reasons; they reduce pain and inflammation, lower fevers, and reduce clotting action.[1,2] The typical dosage for adults who are looking to reduce mild-moderate pain is 400 mg every 4-6 hours. For adults who have pain caused by osteoarthritis, the typical prescribed dose is 1200 mg.[3] However, despite their pain reducing use, NSAIDs could yield negative side effects such as increased risk in developing nausea, stomach pains, or an ulcer.[1]

The mechanism of NSAIDs when it comes to reducing pain and inflammation is known and understood. After intense workouts, prostaglandins are produced by muscle cells. They aid in the healing process of muscle, but this often leads to inflammation, pain, and fever. Enzymes called cyclooxygenases (COX-1, COX-2) produce the prostaglandins that promote inflammation, pain, and fever. The goal of NSAIDs is to inhibit COX-1 and COX-2 from producing prostaglandins, thus decreasing the pain. However, the COX-1 enzyme is responsible for creating prostaglandins that protect the stomach lining and support platelet aggregation, so the inhibition of the enzyme is what could lead to stomach ulcers and the promotion of bleeding.[1,2,4] The science behind NSAIDs seems promising, but clinical research may prove otherwise.

Athletes commonly take NSAIDs after performing physical activity because they claim the drugs reduce pain and decrease recovery time. But here is the issue: only very few studies have been able to support this claim. Some studies have reported results that do indicate a beneficial effect, by stating NSAIDs used prophylactically mitigate exercise-induced inflammation, circulating creatine kinase levels, and muscle soreness.[5] On the other hand, these claims made by athletes lack scientific support. NSAIDs are known to treat inflammation, but many histological studies have proven that most overuse injuries are caused by tissue degeneration and not inflammation. Also, NSAIDs temporarily “mask” the pain caused by tissue degeneration or soreness. This does not ensure that muscles or tissues are actively getting healthier; it only hides the pain from the athlete. [5] Clearly, there are many different opinions about the use of NSAIDs, specifically ibuprofen, in the sports medicine field. Let’s take a look at what the “research says” about it. 

A study at the University of Saskatchewan was conducted to determine the effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training. Participants (12 males, 6 females) trained their left and right biceps for six weeks, alternating arms on each day. The training program called for concentric curls at 70% of RM and eccentric curls at 100% of 1 RM. Every day after their training, they either received a 400 mg dose of ibuprofen or a placebo. On training days, each participant was asked to rate their soreness on a scale from 0-9. For both the placebo and ibuprofen, the participants reported soreness during the first week and that soreness decreased throughout the program to the point where participants felt no soreness in either arm during the final week. The researchers concluded that ibuprofen was not effective in reducing perceived soreness during the training. However, the researchers do not reflect on the limitations of their own study.  They had a small and uneven sample size when it came to gender and there could have been discrepancies and residual effects that came along with taking ibuprofen inconsistently. Additionally, they seemed pretty convinced by their findings, but maybe the dose they chose was not strong enough to show any reduction in soreness in a long term study.[6]

On the other hand, another study drew opposite conclusions. Researchers in Greece conducted a study to determine the effects of ibuprofen on delayed onset muscle soreness (DOMS) and muscular performance. Participants (14 men, 5 women) who have not done strength training in the last 6 months performed eccentric leg curls at 100% RM. Nine (9) subjects were given a 400 mg dose of ibuprofen every 8 hours for 48 hours after exercise, while the remaining 10 subjects received a placebo. The subjects rated their amount of soreness on a scale of 1-10 prior to exercising, 24 hours after exercising and 48 hours after exercising.  The results showed that muscle soreness was significantly lower for the ibuprofen group at both 24 hours and 48 hours after exercising. Similar to the previous study, the researchers did not evaluate the limitations of their study. The number of participants and number of each gender were low and uneven, respectively. Also, the soreness results were not discussed much in the conclusion of the paper. The researchers did not support why the soreness decreased with scientific evidence, which is what they did for the other the parameters they were testing for.[7]

Clearly, both studies came to different conclusions. However, both studies were conducted for different amounts of time, contained different exercises, and with subjects of different athletic abilities. There have been plenty of studies conducted to determine how effective ibuprofen is at reducing soreness, but each study contradicts the next. 

Overall, many studies show that ibuprofen is a short term solution to hiding muscle soreness, but it may not be effective long term. Though, I’m still going to keep on using it to treat my soreness.

Questions to consider:

  • Do you take NSAIDs to reduce your soreness after working out? How effective do you find them to be?
  • Do you think there’s a better way to measure soreness and how ibuprofen affects our muscles?
  • Do you think the length of the study has any correlation with the effectiveness of ibuprofen?

Sources: 

  1. (n.d.) Nonsteroidal Anti-inflammatory Drugs (NSAIDs). Retrieved from  https://www.medicinenet.com/nonsteroidal_antiinflammatory_drugs/article.htm#what_are_nsaids_and_how_do_they_work
  2. Tscholl, M., et al (2016). A sensible approach to the use of NSAIDs in sports medicine . Swiss Sports & Exercise Medicine , 65(2), 15–20.
  3. (n.d.) Ibuprofen (Oral Route). Retrieved from https://www.mayoclinic.org/drugs-supplements/ibuprofen-oral-route/proper-use/drg-20070602 
  4. (n.d.) What Are NSAIDs? Retrieve from https://orthoinfo.aaos.org/en/treatment/what-are-nsaids/
  5. Stuart J. Warden (2010) Prophylactic Use of NSAIDs by Athletes: A Risk/Benefit Assessment, The Physician and Sportsmedicine, 38:1, 132-138, DOI: 10.3810/ psm.2010.04.1770
  6. Krentz , J. (2008). The effects of ibuprofen on muscle hypertrophy, strength, and soreness during resistance training. Applied Physiology Nutrition and Metabolism , 33(3), 470–475. doi: 10.1139/H08-019

Dry Needling: Is it Worth the Pain?

Arriving at a physical therapy appointment to have a needle stuck deep into the body’s muscles only to leave hobbling and sorer than before doesn’t seem like an effective method for rehabilitation. However, the post-treatment benefits have made dry needling one of the many techniques individuals are using to treat and prevent injury from exercise.

What is Dry Needling?

While wet needling uses hollow needles to inject corticosteroids into muscle [7], dry needling (DN) consists of inserting a fine needle, similar to those used in acupuncture, deep into the muscle without injections. The needle is then twisted and moved around the area without being fully removed from the skin. The needling itself can be uncomfortable, feeling like a pinch, cramp, or deep prick, and can result in local soreness post-treatment. Physical therapists seek to insert the needle into a myofascial trigger point (MTrP) to relieve myofascial pain syndrome (MPS), the most common muscle pain disorder seen in clinical practice [1]. In exercise science, MTrPs are defined as “hyperirritable local point(s) located in taut bands of skeletal muscle or fascia which when compressed causes local tenderness and referred pain” [10]. Potentially caused by muscle overuse [2], this pain is commonly described as having a knot in a muscle and creates localized tenderness, pain to deep touch, and restricted movement [1].

The video above shows a physical therapist performing the dry needling technique on various muscles. Created by Dynamic Physical Therapy, Covington, LA (2013).

Dry needling is used as a rehabilitation technique to decrease the pain MTrPs can cause. The “fast-in and fast-out needle technique” applies high pressure stimulation to the MTrP, often causing a twitch response. These twitch responses are the result of a spinal reflex generated by the activation of nociceptors and mechanoreceptors. These receptors respond to the painful mechanical irritation and stretch the needle causes within the muscle [1]. When this occurs, a single motor unit fires and a visible, isolated contraction – the “twitch” – can be seen. These twitch responses can occur local to the needle or within muscles on the opposite side of the body. This phenomenon has led researchers to believe that the pain associated with MTrPs is due to central nervous system (CNS) changes [1]. 

How is Dry Needling Portrayed in Healthcare?

Healthcare providers, such as MedStar National Rehabilitation Network and ChristianaCare, have been advocates for dry needling. They mention DN is “an effective physical therapy modality…in the treatment of orthopedic injuries” [5] and that it can even be used for preventing pain and injury [4]. There have been many personal accounts of the wonders of dry needling in recovery from nagging injuries. AshleyJane Kneeland, who struggles with muscular pain due to lupus, fibromyalgia, and postural orthostatic tachycardia syndrome, cites DN treatment as relief for her painful spasms and headaches, as well as providing general relaxation [6]. But how effective is dry needling, really? Is there science to back up these claims?

What Does the Science Say?

Elizabeth A. Tough and co-authors performed a meta-analysis in 2009 of seven studies assessing the effectiveness of DN in managing MTrP pain. This study provides an update for the systematic review by Cummings and White, which found no evidence suggesting injections through wet needling generate a better response than dry needling [3]. One study found by Tough et al. suggests DN is more effective in treating MTrP pain than undergoing no treatment, two studies produced contradictory results when comparing DN in MTrPs to DN elsewhere, and four studies showed DN is more effective than other non-penetrating forms of treatment (placebo controls). However, when combining these studies for a sample size of n=134, no statistical significance was found between DN and placebo treatments. 

While the authors conclude the overall direction of past studies trend towards showing that DN is effective in treating MTrP and MPS [10], there is no significant evidence yet. The lack of statistical significance could be due to low consistency in study design for studies included in the meta-analysis, as each employed varying mechanisms for needle placement, depth, and treatment frequencies, along with there being an overall small sample size. Therefore, further studies are required to significantly conclude that DN is effective in MTrP rehabilitation.

Ortega-Cebrian et al. recognized the limitations in previous studies and thus sought to create a significant evaluation of the ability of DN to decrease pain and improve functional movements. The authors use a myometer (MyotonPro, [8]) and surface electromyography (sEMG) to assess the mechanical properties of muscle in subjects (n=20 M) with quadricep muscle tension and pain [9]. 

The MyotonPro allows researchers to quantify muscle tone and stiffness. While no standards exist for describing these parameters with respect to changes after rehabilitation techniques, researchers found the device to be reliable through inter-rater reliability (comparing values of the MyotonPro to another rater). Pain was assessed by subjects using the Visual Analogue Scale (VAS) and a goniometer was used to measure small range of motion (ROM) improvements. DN was performed by one of two experienced therapists until twitch responses ceased [9].

Authors report that DN resulted in statistically significant pain reduction and an increase in flexion ROM. However, the ROM was very small and could be within the range of measurement error of the goniometer. Also, the p-values reported in-text for these parameters do not match the corresponding table which presents a question of the reliability of author reporting. All sEMG parameters, except for decreased vastus lateralis activity, were not significantly changed by DN, as well as all MyotonPro parameters, besides a decrease in vastus medialis decrement (muscle elasticity) and resistance. In a power analysis performed after the study, authors report needing 198 subjects for statistically significant results – much higher than the 20 subjects used [9]. Therefore this study continues the uncertainty in the benefits of DN, but does present significant subject-reported pain reduction.

Is it Worth the Pain?

So is dry needling worth the pain? After being put to the test through experimental studies, there is no clear evidence that dry needling is more beneficial than alternative rehabilitation methods such as wet needling, placebo needling, or acupuncture [9]. However, while the mechanisms of changes in muscles with trigger points due to dry needling are unknown, subjects do report pain reduction. Dry needling should be taken on a case-by-case basis since current knowledge of widespread benefits is limited. Essentially, if dry needling treatment alleviates pain more than other rehabilitation methods and the pain of the procedure is bearable, why not give it a try?

 

Questions to Consider:

  • Would you be willing to try dry needling regardless of uncertainties in the literature?
  • Do you believe it is a problem that healthcare providers claim dry needling is effective despite a lack of conclusive evidence?
  • What should future studies do to ensure significant results?

 

References:

[1] Audette, J. F., Wang, F., & Smith, H. (2004). Bilateral Activation of Motor Unit Potentials with Unilateral Needle Stimulation of Active Myofascial Trigger Points. American Journal of Physical Medicine & Rehabilitation, 83(5), 368–374. doi: 10.1097/01.phm.0000118037.61143.7c. 

[2] Bron, C., & Dommerholt, J. D. (2012). Etiology of Myofascial Trigger Points. Current Pain and Headache Reports, 16(5), 439–444. doi: 10.1007/s11916-012-0289-4. 

[3] Cummings, T., & White, A. R. (2001). Needling therapies in the management of myofascial trigger point pain: A systematic review. Archives of Physical Medicine and Rehabilitation, 82(7), 986–992. doi: 10.1053/apmr.2001.24023. 

[4] Dry Needling®. (n.d.). Retrieved from https://christianacare.org/services/rehabilitation/physicaltherapy/dryneedling/

[5] Dry Needling. (n.d.). Retrieved from https://www.medstarnrh.org/our-services/specialty-services/services/dry-needling/

 [6] Dry Needling: The Most Painful Thing I’ve Ever Loved. (2015, March 25). Retrieved from https://www.everydayhealth.com/columns/my-health-story/dry-needling-most-painful-thing-ever-loved/

[7] Dunning, J., Butts, R., Mourad, F., Young, I., Flannagan, S., & Perreault, T. (2014). Dry needling: a literature review with implications for clinical practice guidelines. Physical Therapy Reviews, 19(4), 252–265. doi: 10.1179/108331913×13844245102034. 

[8] Muscle Tone, Stiffness, Elasticity measurement device. (n.d.). Retrieved from 

 [9] Ortega-Cebrian, S., Luchini, N., & Whiteley, R. (2016). Dry needling: Effects on activation and passive mechanical properties of the quadriceps, pain and range during late stage rehabilitation of ACL reconstructed patients. Physical Therapy in Sport, 21, 57–62. doi: 10.1016/j.ptsp.2016.02.001. 

[10] Tough, E. A., White, A. R., Cummings, T. M., Richards, S. H., & Campbell, J. L. (2009). Acupuncture and dry needling in the management of myofascial trigger point pain: A systematic review and meta-analysis of randomised controlled trials. European Journal of Pain, 13(1), 3–10. doi: 10.1016/j.ejpain.2008.02.006.

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.