I had two favorite aspects of this course. The first was being able to compare the same topics that I learned last term in Comparative Animal Physiology to how they are affected by exercise. Since the same general physiology topics were covered in both classes, I had a general understanding of the material, but it was interesting to see how the topics changed when exercise was thrown into the mix instead of comparing the similarities and differences of the topics in various animals. The exercise component was without a doubt more interesting.

The second would be how different forms of training impact the body differently. For example, how the body adapts to strength training much faster than endurance training, and how the muscle fibers can switch over to accommodate for the new activity. How muscles adapt to exercise was fascinating – how they use the spindle fibers to detect mechanical stretch, detect the calcium levels which vary with muscle activation, how free radicals affect recovery, and the AMP/ATP ratio. Going off of the idea of how muscles adapt to training, how quickly they react to detraining was not only interesting, but also a little worrisome. The fact that you could spend months or years running trying to get your endurance up, and then you take two weeks off, maybe because of an injury or because you were on vacation, and your VO2max would decrease by 8%.. and then 20% after 84 days. It’s weird to think about that in a short period of time, there could be significant physiological changes going on in your body (i.e. rapid loss of plasma volume leading to the decrease in stroke volume, switching of the fibers back to type IIx, decrease in mitochondria). That just doesn’t seem right.

Overall, my favorite part of the course was learning about how all the systems change and adapt to work together to maintain homeostasis when you decide to go for a run and how those changes can improve your overall health in the long run.

Sorry – I read the prompt wrong and thought it was supposed to be a recent journal article. So here is my news article response!

New research coming out of the University of Otago is suggesting that high-intensity exercise may restore heart function in people with type 2 diabetes. In the study, they found that 3 months of high-intensity interval training improved heart function in adults with type 2 diabetes. This makes sense based on what we learned in class, as exercise increases cardiovascular ability to pump more blood to the tissues that need it, and it reduces the presence of free radicals, which can be linked to heart attacks/heart damage following a heart attack. The consistent increase in cardiac output leads to athletes having a higher stroke volume at a higher VO2max, as well as a higher end-diastolic volume and more ventricular filling.

Usually, studies involving diabetics do not focus on how to improve their heart health, so this was an important study. Since increasing aerobic capacity through exercise is one of the best prevention techniques for heart disease, and exercise is a major treatment plan for diabetics, this study made a lot of sense. The goal was to have the subjects spend 10 minutes doing vigorous activity during a 25 minute exercise period. Originally, they were worried that the high-intensity exercise would be too much for the diabetic heart, but no one died in the study so I guess it was okay? They never clarified what parameters they used to ensure safety or how they made sure their hearts could handle it, which is a little concerning.

The overall results showed that type 2 diabetics are capable of comparable increases in aerobic capacity as their non-diabetic counterparts and that high-intensity exercise is capable of reversing some of the changes in heart function that precede diabetic heart disease.

Based on this study, and all studies related to type 2 diabetes, it seems like it is in the best interest of these individuals to find a personal trainer and make sure their body stays healthy. The article from Science Daily can be found below:

https://www.sciencedaily.com/releases/2019/05/190524094318.htm

Hopefully it’s fair to use an article for both this blog post and my presentation…

So this study looked at how patients believed their recovery went who underwent surgery to treat a proximal hamstring avulsion and those who had non-surgical treatment. For the purpose of this study, a proximal hamstring avulsion was defined to be “when at least one of three tendons were avulsed from their origin on the ischial tuberosity.” Treatment was determined based on age (younger more likely to get surgery), comorbidity (the presence of two chronic diseases or conditions in the patient), activity level of the patient (the more active patients got surgery), MRI findings (more severe injury received surgery), and clinical findings (if the patient was unable to extend their hip in the prone position, they received surgery).

Surgery consisted of reinserting the common proximal hamstring tendon into the footprint. Following surgery, the patients rehabbed. The non-surgically treated group were referred to a physiotherapist and used the same rehab protocol as the surgical group.

The experimental group consisted of 47 patients, 33 of which had surgery and 14 of which did not (would the results be skewed due to the imbalance of subjects?), who had a mean age of 51 years old. Following their treatment, whether it was surgical or non-surgical, the authors of the study followed up with them 3.9 years later (oddly specific time but okay). The experimental test consisted of a Lower Extremity Functional Scale to determine the range of motion following the injury, and questions from the Proximal Injury Questionnaire (more subjective measurement). The study made sure to account for the severity of the original injury, by looking at the MRI following the injury.

The only result that was significant was that the MRI from the surgically treated group had a larger proportion of tendons retracted more than 2cm (probably why they required surgery…). The Lower Extremity Function Scale resulted in a score of 74 (SD+/-12) for the surgical group and 72 (SD+/-16) for the non-surgical group. However, they looked at their average time of exercise following treatment, and the surgical group reported that they exercised more often and for longer durations than their counterparts. That being said, 94% of the surgical group considered themselves high-performance amateur athletes, and 74% of the non-surgical group did. Do we think this is because they were a more physically active group prior to the injury (which is why their injury required surgery?) or could it be because they experience less pain while exercising?

Overall, the study concluded that there was no significant difference in recovery between surgically treated and non-surgically treated groups. That being said, if you ever have a proximal hamstring avulsion, you should probably think twice about going into the OR since the risk doesn’t provide you with any statistically significant reward.

Some questions I had while reading the article. Both of the tests they used to determine functionality after injury were subjective (which was very clear). Is there any way to do an objective study? Any test to determine if the range of motion is impaired following recovery, or if maybe the non-surgically treated patients fatigue sooner than the surgically treated group? How would this study differ if it was done in younger individuals who have a quicker recovery time? What about the elderly – is surgery less common since the risk of complications is greater? Is the PT program they designed for rehabilitation really equivalent for both groups or should they have created an alternative PT program for the non-surgically treated group to target specific areas for recovery (seeing as though their tendons were never surgically reattached)?

The link to the article is below if you are interested:

https://bmjopensem.bmj.com/content/5/1/e000511

The main question I plan to explore for my presentation is as follows: does exercising through an injury improve recovery time or does it result in permanent damage? For example, it’s possible to live with a torn meniscus, but they suggest getting it repaired if you plan to continue playing sports or plan to live a more physically intensive life. Going off of this example, if you do not get it repaired but live a more physically intensive life anyway, just treating the pain, will the surrounding tissues compensate for the torn meniscus making it possible to have an active lifestyle, or will ‘playing through the pain’ result in permanent knee damage?

I’m interested in this topic because I never took the necessary steps to repair my hip and I am still suffering from the consequences of this. During my research, I hope to determine whether the pain I feel is from not getting it repaired at all, never rehabbing it properly following the initial injury, or if I decide to get it fixed at some point, have I done irreversible damage to my joint?

As of now, the main questions I hope to answer are as follows: Is it helpful or hurtful to exercise while injured? What type of exercise is best (i.e. moderate intensity, low intensity, strength training, etc.)? Is exercising through an injury the foundation of physical therapy (i.e. is it beneficial to exercise through an injury as long as you are doing the correct exercises, the correct way)? What are the pros and cons of playing through the pain and never actually treating the injury? How does exercising while injured affect the recovery time? What are the benefits of physical therapy over surgical intervention? And the overarching question of how exercising through the pain may impact future overall health?

Since the majority of the class seems to have been an athlete at some point in their lives, I’m 98% certain that we have all gone back out on the field when we knew we were injured. There seems to be a mentality of powering through the pain so you don’t let your team down, but I don’t think many of us thought about the possible repercussions at the time.

So far, it seems like if you should exercise and the type/intensity of exercise depends entirely on the type/severity of the injury (which makes sense). However, for many injuries, it is suggested to swap whatever activity you were doing when you were injured, with a very modified version of the same activity to encourage the body to repair these areas without causing more damage. That being said, one of the main subtitles of the article was “Don’t Work Through the Pain” so I guess that answers that question (another article said if it hurts, even a little, stop doing it). As of now, it appears the only injury where you should really force an exercise would be a spinal cord injury, as exercise is “useful in facilitating elongation and/or synaptic activity of regenerating axons and plasticity of spinal neurons below the level of injury” [1]. Exercise was again suggested (albeit delayed) following a traumatic brain injury, as it can upregulate brain-derived neurotrophic factor involved in synaptic function, which enhances recovery [2].

[1] https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/nyas.12052

[2]https://www.sciencedirect.com/science/article/abs/pii/S0306452204000764

There is an ongoing debate attempting to determine whether lactic acid buildup during exercise is an advantage that improves performance or a disadvantage that results in muscle fatigue occurring sooner. While there is evidence to support both sides of the argument, the data supporting lactic acid accumulation being a disadvantage during muscle activity is more compelling.

A brief intro into what lactate is and why it is produced in the first place: lactate metabolism is necessary to produce the required energy to continue exercising, but its role in the production of hydrogen ions depresses muscle function. So while the lactate is being produced to satisfy high energy demands, it must be cleared from the muscles and sent to the liver to be metabolized (or sent to the muscles to be used as an energy source) if the activity is to continue. In general, adrenaline causes a decrease in the clearance of lactate and fast twitch fibers produce the most lactate [1].

The first crucial data supporting lactic acid’s role in muscle fatigue is that when the lactate concentration of the blood is elevated, there is a reduction in overall performance. These studies take into account the potential fatigue factor by exercising one part of the body to increase the lactate levels, and then while the blood had these increased levels, they exercise another part of the body until fatigue. It has been done over and over again, with all the studies producing the same results: increased blood lactate levels promote muscle fatigue. The performance reduction was associated with a lower release of lactate, a lower muscle pH, and a greater potassium release. These factors work together to result in a potassium buildup in the muscle interstitium, which leads to fatigue [2].

Another study that has been done to test the effects of lactate on muscle fatigue involved incubating the muscle in lactic acid. These studies have found that when the muscles are incubated in lactic acid, force development is reduced and fatigue is achieved faster. The studies also found that lactate mostly affects the function of the muscle membrane and that the effect of lactate can be linked back to the pH-induced changes, such as the potassium balance [2].

Lactate does not just affect the pH balance and potassium concentrations. It also has been found to affect the intracellular calcium, which is responsible for muscle activation. The lactate affects the sarcoplasmic reticulum’s calcium release channels, affecting calcium’s ability to bind to the troponin, providing a binding site on the actin filament for the myosin head to bind to, causing a muscle contraction. Since this process is inhibited, muscle contraction is limited [2].

Lactic acid is not necessarily what is causing the fatigue. Lactic acid is dissociated into lactate anions and hydrogen ions under normal internal body conditions, so it is the lactate anions and hydrogen ions that are accumulating in the muscle, not ‘lactic acid’. It is believed that the hydrogen ion accumulation is what truly influences muscle fatigue, as opposed to the lactate anions. Studies support the earlier claims that the decline in exercise performance is due to the decrease in sarcoplasmic reticulum function, increase in hydrogen ions, and inhibiting the calcium, which inhibits the myofibrillar ATPase thereby inhibiting the maximal shortening velocity [1].

When these factors work together (the potassium accumulation, low pH, the calcium release channels), muscle fatigue is inevitable. So while lactate may not directly cause fatigue, it induces enough changes within the normal pathways to affect the process and cause fatigue.

(FYI: Based on the articles I found during my research, I am more on the lactate is advantageous bandwagon.)

References:

[1] Aldeam Facey, Rachael Irving, and Lowell Dilworth, “Overview of Lactate Metabolismand the Implications for Athletes.” American Journal of Sports Science and Medicine 1, no. 3 (2013): 42-46.

[2] Point:Counterpoint, “Lactic acid accumulation is an advantage/disadvantage during muscle activity.” Journal of Applied Physiology, 100 (2006): 1410-1414.

1. My favorite athletic accomplishment is probably going to sound like an odd one, as it is quite bittersweet. Starting in freshman year, I was on my high school’s lacrosse team. Lacrosse was not big in my town and our team was still in the developmental phases, as were many of the surrounding schools. During the third game of my sophomore year, we were playing our rival team. I went for a ground ball and was hip-checked by a girl who had originally played on her school’s men’s team (since there was no women’s team at that point). I felt my hip pop out when I hit the ground, but I was angry at this point, so I kept playing. I played the rest of the season, making sure to always ice my hip before and after playing. The trainer told me it was bursitis so he didn’t bench me. Flash forward to senior year of college, and I can no longer run without limping for the next two days. Turns out it wasn’t bursitis – I had torn my labrum and in the process of favoring my right leg, I destroyed my left hip. So while the story does not have a happy ending, the entire process taught me how much my body can endure if I refuse to quit, but also the consequences of ignoring my limitations.
2. Biology has never been my strongest subject, but I am interested in seeing how the cellular processes work together during seemingly simple everyday activities such as going for a run. I have always taken the biological processes for granted while focusing on the bigger picture, but I believe understanding the inner workings of the body will give me a greater appreciation for these simple everyday activities. I got a glimpse of this in Animal Physiology last term, but I want to dive deeper into understanding the differences between slow twitch and fast twitch muscle fibers and how these differences contribute to the overall functionality of the muscles to produce cohesive movements. I now recognize that it is crucial to look at all aspects of the system individually to understand how we live our day to day lives.
3. The previous upper-level courses that I’ve taken that would contribute the most would be Orthopedic Biomechanics, Mechanobiology, and Animal Physiology. Orthopedic Biomechanics would be helpful, as we learned about all the bones of the body and how they all experience loading in different ways from the various forces applied during both activity and when you are stationary. Mechanobiology (as much as we’ve done this term) seems to continue on this topic, focusing on how different types of bones respond to forces. Animal Physiology focused on how the various systems within the body respond to different conditions. By combining what I have learned in these various classes and what we will learn in this class, I hope to have a complete understanding of how the major systems within the human body work together to maintain homeostasis.