It is no secret that exercise is very important for optimal health. But many people still do not see the connection and it seems to be a low priority for them when it comes to managing their health. However, I realize that many people truly do not understand how important it really is, even from the perspective of glycolytic pathway, so I want to take the time to summarize it here. Exercise is known to stimulate glycogenolysis, especially when it is conducted first thing in the morning after an overnight fast. In fact, I often tell my clients to do their exercise fasted when they want to optimize weight loss. But how does it work?
Before I review that, I want to do a quick summary of biochemistry.
In our muscles, glycogen supplies glucose-6-phosphate for ATP synthesis in the glycolytic pathway. Any enzyme known as glycogen phosphorylase in the muscle is stimulated during exercise by the increase of AMP and by phosphorylation. The phosphorylation is stimulated by calcium released during contraction and by epinephrine, the fight or flight hormone, as well as hypoglycemia during stressful situations or exercise where there is an immediate need for glucose. It is important to understand that liver glycogen stores are principally for the support of blood glucose during fasting or extreme need such as exercise, and the degradative and biosynthetic pathways are regulated principally by changes in the insulin/glucagon ratio and by blood glucose levels. The key point to remember is that muscle glycogenolysis is regulated principally by AMP, which signals a lack of ATP, and by Ca2+ released during contraction. Epinephrine, which is released in response to exercise and other stress situations, also activates skeletal muscle glycogenolysis.
Let’s take a practical look at what happens when someone begins to contract their muscles during exercise. If someone were to immediately begin running as fast as possible, the following cascade would take place.
- Within 3 seconds, muscle cells exhaust stored ATP.
- As exercise continues, this ATP must be regenerated, so the ATP–PCr system kicks in to shoulder most of the load. This lasts for about 10 seconds. And because time is required for ATP to be regenerated, you start to slow down a bit.
- As exercise continues and the ATP–PCr stores are depleted, the glycolytic system will begin to provide most of the energy transfer for ATP regeneration. This lasts for about 90 to 120 seconds or so, depending on the intensity of the exercise. Since the glycolytic system generates ATP more slowly than the ATP–PCr system, again, you have to slow down a bit more.
- If exercise continues beyond this time frame, the oxidative system will start to provide most of the energy transfer for ATP regeneration. And again, because the oxidative systems are slower than the anaerobic systems, the pace must slow again. In fact, if the pace is slow enough, the exercise can last for quite a long time.
There are two main types of exercise: anaerobic exercise and aerobic exercise. Anaerobic exercise is defined as higher-intensity, shorter-duration (less than 2 minutes) activity, whereas aerobic exercise occurs when the exercise is longer than 2 minutes in which the oxidative system must kick in to provide the remaining energy for ATP regeneration. As our initial energy stores can only supply energy for about three seconds, our ATP must be regenerated in large amounts, and quickly, to support this type of exercise.
Short-burst activities such as the following:
- The golf swing
- Field events (shot put, discuss)
- The tennis swing
- The 100-meter sprint
- The baseball swing
Oxidative energy transfer takes place in the mitochondria of our cells and utilizes a combination of muscle glycogen, intramuscular fatty acids, free fatty acids, and amino acids. As the oxidative processes utilize breakdown products from both glycolysis (glucose through to pyruvate) and beta oxidation (fatty acids through to acetyl-coA), energy transfer occurs at a slower rate. However, what this system lacks in speed, it makes up for in ATP regeneration. As a result, oxidative metabolism can support activities including the following:
- 800-meter run
- 2000-meter rowing
- 1500-meter skating
- Cross-country skiing
- Long-distance swimming
Indeed, any activity done at a high intensity for longer than two minutes derives a large percentage of its energy transfer from the oxidative system. There is a “switchover point” at which an activity moves from anaerobic to aerobic, as seen in this interesting comparison.
- 200-meter run: 29% aerobic; 71% anaerobic
- 400-meter run: 43% aerobic; 57% anaerobic
- 800-meter run: 66% aerobic: 34% anaerobic
- 1500-meter run: 84% aerobic; 16% anaerobic
The primary muscle fiber types that contribute to aerobic exercise are the oxidative type I and type IIA fibers. As aerobic exercise is heavily oxygen dependent, training adaptations occur in order to support oxygen transport and delivery in these fibers. Specifically, aerobic exercise can increase the number and size of the blood vessels. This occurs through increased capillarization. Specifically, with aerobic training, there is a greater number of capillaries per unit of muscle. This allows for enhanced delivery of oxygen (fuel) to muscle cells, enhanced removal of CO2 and waste products, and the transfer of heat away from the muscle. In addition to enhanced oxygen delivery, there is an increase in the size and number of mitochondria along with greater myoglobin content within cells. While the greater capillarization leads to more oxygen transport, the greater myoglobin leads to increased muscle oxygen uptake, and the larger and more numerous mitochondria allow for greater oxygen use. Of course, in addition to these adaptations, the enzymes involved with aerobic energy transfer will adapt as well.
Let’s talk a bit about oxygen and the adaptations that occur with regular exercise.
After a full exercise session, or even after a single interval within an entire exercise session, the oxygen deficit that’s accumulated must be paid back. This means that after you’ve stopped exercising and the amount of mechanical work you’re doing is no different than you’d be doing at rest, you still continue to consume more oxygen. This period of increased oxygen consumption and energy demand has been called the period of oxygen debt or EPOC (excess post-exercise oxygen consumption). In essence, after exercise, the amount of oxygen consumed can be elevated for minutes to hours. This is due to the fact that the body must:
- a) metabolize additional nutrients,
- b) replenish the energy stores that have been used up, and
- c) reload the depleted oxygen stores in the muscle and blood.
In addition to these recovery-type activities, the following also contribute to the EPOC:
- Elevated post-exercise body temperature
- Increased activity of the heart and respiratory muscles
- Elevated levels of metabolism-boosting hormones
- Increased conversion of energy transfer products such as lactate into other substrates
- Increased protein synthesis
- Recovery of muscles stressed and damaged with the activity
It is important to note, however, that the energy systems do not work independently from one another. During various types of exercise, from aerobic to anaerobic, all three energy systems are activated. However, the extent to which they are activated, and the amount of ATP they regenerate relative to the total ATP regeneration required, determines the description of the activity. For example, during short-burst activity, the ATP–PCr system is most important. When immediate and explosive movement is desired, the brain initiates the contraction with a signal that’s passed along the nerves to the muscles. The muscles then contract, using ATP and depleting these immediate energy stores within a second or two. In order for the muscles to continue to contract, the resulting ADP and P must be regenerated to ATP.
Adaptations to Exercise.
In response to regular exercise training, whether anaerobic or aerobic, certain changes occur in the muscle. These changes improve the body’s ability to respond to similar exercise challenges in the future. Each of these processes is regulated by protein synthetic mechanisms initiated within our genetic material (our DNA). Cellular communication through hormones is intimately involved in this process. The hormone insulin, in the presence of adequate nutrient availability, encourages the stimulation of protein synthesis and a positive nitrogen balance. Insulin availability is greatest during well-fed conditions and during periods of energy surplus. Protein and amino acid intake is key here as protein-containing meals stimulate a positive protein status. In addition, hormones like testosterone and growth hormone have a stimulatory effect on muscle adaptation.
On the other hand, the counter-regulatory hormones such as glucagon, catecholamines, and glucocorticoids have a contradictory effect, promoting protein breakdown and a negative nitrogen balance. These hormones are released in large numbers during periods of fasting or energy deficit
Protein synthesis and exercise adaptation are also affected by:
- The amount of mRNA in our cells
- Ribosomal number
- Ribosomal activity
- Amino acid availability
- The hormonal environment
- Our native genetic code
Interestingly, even the process of recovering and adapting to our exercise training demands is metabolically costly. As proteins are degraded and amino acids re-synthesized into proteins, this process of protein turnover builds more functionally adapted enzymes, contractile units, etc. And this process accounts for between 10% and 25% of resting energy expenditure. Therefore, as you can see, not only does exercise increase total daily energy expenditure during the activity, it also increases post-exercise expenditure through two mechanisms. Energy expenditure is increased due to both the oxygen debt being paid back and to the increased protein turnover and synthesis just described.
Adaptations of anerobic exercise such as weight training and sprint training:
- muscle fibers both increase in size and in myofibrillar number
- mitochondrial size and number
- increases in myoglobin number
- increases in intracellular storage capacity and availability (such as stored glycogen)
- increases in intracellular glycogen storage can also contribute to muscle hypertrophy
- In addition to changes in muscle cross-sectional area, anaerobic exercise can enhance the activity of ATP–PCr system enzymes (creatine kinase, myokinase) and the glycolytic system enzymes (glycogen phosphorylase, phosphofructokinase).
These changes help to increase the rate of energy transfer within the muscle, allowing for more rapid responses to energy demands in the future.
Adaptations to aerobic exercise such as jogging, steady state cardio or swimming:
Please note, this type of lower-intensity, longer-duration activity primarily influences muscle quality (as opposed to muscle size).
- Enhancement of oxidative or mitochondrial enzyme activity
- Increase in intramuscular glycogen and triglyceride content
- Increase in blood volume due to increase uptake and delivery of aerobic activity- due to increase in red blood cell content and the oxygen-carry capacity of the body.
- Capillary density of trained muscles increases- meaning there will be a great number of capillaries per muscle fiber
- With this lengthened border between blood vessels and muscle fibers, oxygen delivery, carbon dioxide removal, waste removal, fuel delivery to muscle, and the transfer of heat are all amplified.
- Beyond this, the myoglobin content of skeletal muscles will increase, improving oxygen delivery across muscle cells
- Finally, the number and size of mitochondria are increased with aerobic activity of high enough intensity. This promotes greater oxygen utilization through the process of pyruvate, fatty acid, and ketone utilization through the Krebs cycle and electron transport chain
Additional benefits of both aerobic and anaerobic exercise training include:
- The attenuation of sympathetic nervous system activity.In essence, “stress” to the body with exercise is minimized over time, and therefore greater workloads are required to promote the same amount of adaptation.
- Greater insulin sensitivity.With exercise training, the body responds to carbohydrate intake with less insulin release, allowing insulin to act in carbohydrate update and protein synthesis without preventing fat loss/stimulating fat gain.
- Improved fatty acid uptake and transport.Another positive response to exercise training is that fats can be more easily mobilized from adipose tissue, transported, taken up, and broken down.
- Less lactate produced per intensity.At every intensity, less lactate will be produced. This is due to greater aerobic production of ATP at every intensity, lower catecholamine response, reduced carbohydrate metabolism, and changes in the isoenzymes of lactate dehydrogenase to forms that favor the conversion of lactate to pyruvate.
- More lactate removed per unit of intensity.At every intensity, more lactate will be removed. Increased rates of lactate removal are due to increased blood flow to the liver and enhanced uptake of lactate by cardiac and skeletal muscles.
- Better lactate tolerance.With training at the highest intensities, the body can better deal with high acid conditions and high levels of lactate. This means higher intensities can be achieved and sustained for short periods of time.
sympathetic nervous system: One division of the autonomic nervous system that is always active and provides sympathetic tone. Its activity increases during times of bodily stress.
So, what qualifies as “intense exercise”? Resistance training (strength training), interval training(through activities such as running, climbing, cycling, and rowing), circuit training, rope jumping, running hills, squat thrusts, plyometrics, explosive medicine ball work, explosive kettlebell exercises, and strongman activities are all high-intensity activities.
Basically, high-intensity activity includes any physically demanding task that:
- a) incorporates many muscle groups, and
- b) is done near your maximum heart rate.
The high-intensity activities listed above require a maximum of muscle activity, which leads to high amounts of cellular stress and the need for muscle adaptation. It’s this muscle stress and adaptation that brings about the maximum number of benefits, including increased protein turnover, muscle preservation and building, a high energy cost, and even cardiovascular benefits.
However, as important as exercise is to this process, nutrition is equally critical.
Firstly, nutritional status can impact energy transfer. Therefore, a good nutrition program will help facilitate top performance of each of the energy systems: ATP–PCr, glycolysis, and oxidative phosphorylation. Both macronutrients and micronutrients are important here.
A sub-optimal nutritional intake can reduce enzyme efficiency (due to deficiencies of co-enzymes and co-factors) and lead to substrate deficiencies. And this means poor exercise performance and fewer calories burned both at rest and during exercise. So much for the metabolic and muscle preserving and building benefits of exercise. In addition, with an inadequate intake of dietary protein and fat, amino acid availability and the ratio of anabolic to catabolic hormones can be compromised. This can lead to an inability to build and preserve muscle mass, even in the face of a solid exercise program.
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Having worked in the fitness industry for over 15 years and helping people with their weight loss goals, I always wondered what role exercise had on inflammation and aging. In obesity, various mechanisms are thought to contribute to a low- grade inflammation within the fat tissue affecting the development of several secondary diseases of aging such as metabolic syndrome, insulin resistance (IR), diabetes, arterial hypertension, and autoimmune diseases (Schmidt et al., 2015). Most importantly, exercise is demonstrating to help modulate the inflammatory processes associated with aging (inflammaging). Two to four- fold elevations in circulating levels of pro-inflammatory cytokines such as IL-6, TNF-a, and acute phase proteins such as CRP and serum amyloid A (SAA) are typical in the elderly when compared to the young, in the absence of chronic disease. Significant declines in immune function with aging promote inflammation, which can increase the prevalence of conditions associated with “inflammaging” such as hypertension, CV disease, and neurodegeneration. Aging is also associated in increases in circulating levels of reactive oxygen specie (ROS), decline in antioxidant capacity and increase in oxidative stress (Woods, Wilund, Martin, & Kistler, 2012). “While transient inflammation is necessary for recovery from injury and infection, it has been hypothesized that the excessive inflammation in aging may also be caused by an exaggerated acute-phase response that may be a cause or consequence of a delayed recovery from an insult that promotes inflammation” (Woods et al., 2012). This is often seen in failure to completely resolve an immune response or can often been seen in an exaggerated immune response and impaired clearance of the immune mediators.
Exercise has a strong influence on the levels of pro-inflammatory cytokines (Gleeson et al., 2011). In fact there is a strong relationship to BMI that may indicate that the decrease in inflammatory molecules may be related to decrease in visceral fat. Additionally, physical activity may further mitigate inflammation by improving endothelial function, increasing insulin sensitivity, enhancing liver health and increasing blood vessel growth and blood flow.
Various mechanisms are involved in exercise’s role in lowering inflammation, some of them are listed below:
- Reduction in visceral mass-as mentioned early, a reduction in visceral mass has an indirect effect of being able to decrease inflammation, since accumulation of fat in the omentum, liver and muscles, as well as the expansion of adipose tissue, results in enhanced production of certain inflammatory mediators. Therefore loss of visceral fat can result in reduction in inflammation (Gleeson et al., 2011).
- Release of IL-6 from working muscles-A fall in muscle glycogen content with exercise signals the muscles to secrete IL-6 (a pro-inflammatory cytokine), which stays high during the duration of exercise. However, this also initiates a rise in anti-inflammatory cytokines IL-10 and IL-1RA to minimize the effects on the tissue. Also, it was interesting that you really need 2.5 hours or more of strenuous exercise to get a significant elevation of IL-6, which may partially explain why marathon runners may have suppressed immune systems (Gleeson et al., 2011).
- Increased levels of cortisol and adrenaline-IL-6 stimulates the release of cortisol, which is smaller doses, can have anti-inflammatory effects. It should be pointed out that too much cortisol secretion from the adrenal glands can create a chronic state of inflammation as well, so this could also be a dose dependent phenomenon (Gleeson et al., 2011).
- Reduction in oxidative stress-Regular exercise can reduce oxidative stress by up-regulating endogenous anti-oxidant defense systems, mitigating the damage from overproduction of oxidants such as nitric oxide, peroxynitrate and hydroxyl radicals during aging (Woods et al., 2012
- Resistance training can reduce TNF–a-Muscle protein synthesis was inversely related to TNF-a as demonstrated in the effects of TNF-a genes after 3 months of resistnace training (Woods et al., 2012).
- Vagus nerve stimulation– Stimulation of the parasympathetic nervous system via the vagus nerve can inhibit pro-inflammatory cytokine production and protects against systemic inflammation (Woods et al., 2012). “hey referred to this pathway as the “cholinergic anti-inflammatory pathway,” and described it as a central homeostatic mechanism by which the sympathetic division of the autonomic nervous system stimulates the inflammatory response through the release of epinephrine and norepinephrine, while the parasympathetic nervous system works reciprocally to suppress this release of proinflammatory cytokine” (Woods et al., 2012). This is often evidenced by a decrease in heart rate recovery (HRR) and heart rate variability (HRV) since one of the primary functions of the vagus nerve is to control heart rate (Woods et al., 2012).
- Activation of HPA-axis– Exercise can activate the HPA axis and sympathetic nervous system. This can be due to cortisol’s potent anti-inflammatory effects and catecholamines that can inhibit pro-inflammatory cytokines (Woods et al., 2012)..
“In summary, exercise training is known to have beneficial effects across a broad spectrum of organ systems and its anti-inflammatory actions are complicated by the intricate interplay among organs and cytokines” (Woods et al., 2012). Exercise prescriptions are definitely a necessary element in any protocol that involves optimizing health, reducing inflammation and slowing down inflammatory diseases of stress and aging such what this patient is experiencing.
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Gleeson, M., Bishop, N. C., Stensel, D. J., Lindley, M. R., Mastana, S. S., & Nimmo, M. A. (2011). The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nat Rev Immunol, 11(9), 607-615. doi:10.1038/nri3041
Part 2 of 2: Inflammation and Exercise: friend or foe? (2011, August 25). Retrieved 2018, May 2 from https://inscientioveritas.org/inflammation-and-exercise/ (Links to an external site.) (Links to an external site.)
Schmidt, F. M., Weschenfelder, J., Sander, C., Minkwitz, J., Thormann, J., Chittka, T., . . . Himmerich, H. (2015). Inflammatory cytokines in general and central obesity and modulating effects of physical activity. PLoS ONE, 10(3), e0121971. doi:10.1371/journal.pone.0121971
Woods, J. A., Wilund, K. R., Martin, S. A., & Kistler, B. M. (2012). Exercise, inflammation and aging. Aging Dis, 3(1), 130-140.
As a fitness instructor, I can really relate to this module. I have been teaching fitness for over 10 years, and have taught all levels of classes from basic cardio classes, HIIT, indoor cycle, and strength classes. In fact, my favorite class I teach is metabolic conditioning, that consists of both higher impact cardio intervals and full body weight training. Due to my extensive experience in the fitness industry, I am a bit biased and believe that all modes of exercise are important for brain health. This includes traditional cardio, interval training and weight training.
Exercise is a promising strategy for combating cognitive decline. According to a study by Nagamatsu et al (2012), both aerobic training and resistance training enhance cognitive performance and functional plasticity in healthy community-dwelling seniors and those with mild cognitive impairment (Nagamatsu, Handy, Hsu, Voss, & Liu-Ambrose, 2012). According to Lucas et al (2015), regular exercise promotes angiogenesis, neurogenesis and synaptic plasticity. This can translate into more “efficient cerebral perfusion and metabolism, neural and vascular adaptation that contribute to the maintenance of cognitive function” (Lucas, Cotter, Brassard, & Bailey, 2015). Exercise affects all the factors and interactions involved in the regulation of cerebrovascular health, such as brain and metabolic neuronal activity, blood pressure, partial pressure of arterial carbon dioxide, cardiac output and sympathetic nervous activity (Lucas et al., 2015). “The increase in vascular NO bioavailability is considered as a key factor in the maintenance of cerebrovascular function and optimal regulation of CBF (cerebral blood flow)” (Lucas et al., 2015). Exercise can help memory and thinking both directly and indirectly. For example, according to Herting et. al (2016), higher-fit children show better performance on tasks of executive functions, such as attention, compared to low-fit children (Herting, Keenan, & Nagel, 2016) The benefits of exercise come from its ability to reduce insulin resistance, reduce inflammation and stimulate the release of growth factors, which can affect the health of brain cells, the growth of new blood vessels in the brain and angiogenesis of new brain cells (Godman, 2014). Indirectly, exercise can improve mood, sleep, reduce stress and anxiety, all contributors of poor brain health which can lead to cognitive impairment. “Many studies have suggested that the parts of the brain that control thinking and memory (the prefrontal cortex and medial temporal cortex) have greater volume in people who exercise versus people who don’t” (Godman, 2014).
Is it more valuable to the brain to do traditional “cardio” work versus resistance training, and why?
According to Nokia, aerobic exercise can enhance adult hippocampal neurogenesis (AHN). “Adult hippocampal neurogenesis (AHN) is a continuous process through which cells proliferate in the subgranular zone of the dentate gyrus, mature into granule cells and, ultimately, become incorporated into hippocampal neuronal networks “ (Nokia et al., 2016). The increase in AHC is considered to be mediated by an upregulation of BDNF and IGF-1. Compared to a sedentary lifestyle, aerobic exercise had the greatest effect on AHN, whereas HIIT has less effect and there was no effect from resistance training (Nokia et al., 2016). However, there are other changes in the brain promoted by exercise, and that includes changes in the hippocampus and also adult neurogenesis in the subventricular zone, as well as the hypothalamus (Nokia et al., 2016). This suggests the neurogenic effects of exercise occur throughout the brain. According to Herting et. al (2016), aerobic exercise also can lead to better cognition and greater gray matter density in regions responsible for cognitive function, leading to greater thickness and volumes in frontal and parietal regions (Herting et al., 2016).
Even though aerobic exercise promotes the most AHN, this does not mean that resistance training is not beneficial for the brain. In fact, a study published in 2012 indicates that resistance training promotes cognitive and functional brain plasticity with people who are already diagnosed with mild cognitive impairment or at risk for dementia. In the 6 month RCT trial by Nagamatsu et. al, six months of twice-weekly resistance training improved selective attention/conflict resolution, associative memory, and regional patterns of functional brain plasticity (Nagamatsu et al., 2012). This provides some evidence that resistance training can benefit multiple areas of in those already at risk for dementia. Aerobic training demonstrated improved selective attention/cognitive resolution in older women with mild cognitive impairment, whereas the resistance training improved associative memory performance, “co-occuring with positive functional changes in hemodynamic activity in regions involved in the memorization of associations” (Nagamatsu et al., 2012).
If you were to design the ultimate brain-based exercise program what would it look like?
An ideal program would consist of both aerobic and resistance exercise in a combinational format. In fact, an article published in 2018 by Northey et al indicates that exercise that is combined with resistance and cardio can boost brain power of people over 50. This study consisted of a large meta-analysis which includes a large number of studies without imposing a limit on publication date or exercise mode. “This study confirms previous suggestions that resistance training may play an important role in improving cognitive function in older adults” (Northey, Cherbuin, Pumpa, Smee, & Rattray, 2018). Although this does not show that resistance training is better than other modes of exercise, it does suggest that this type of training has particularly pronounced effects on these domains of cognitive function. In addition, this review also demonstrated that multicomponent training (cardio and weights combined) can benefit cognitive function in people over age 50. “Our meta-analysis provides positive evidence for the prescription of both aerobic and resistance training (ie, multicomponent training), in accordance with exercise recommendations, for this age group to specifically improve cognitive functions” (Northey et al., 2018). This confirms what I have suspected and seen anecdotally myself in my classes: combinational classes that utilize both cardio and weights seem to be the most effective on all fronts of health, and that includes cognitive health as well.
There are many types of exercise protocols/prescriptions. The one that I use often is called Metabolic Training. It consists of steady state cardio (typically in aerobic or dance format) with some weight training in either Tabata or some type of timed format. I typically use Rest-Based Training (RBT), which has become popular through one of my mentors Jade Teta. His philosophy is to “push till you can’t, rest till you can”. According to Teta (2017):
RBT is a system that makes rest, not work, the primary goal of the workout. It allows participants to take a rest for as long as necessary. Rest actually becomes a tool for increasing intensity, because exercisers can strategically use it to work harder than they could without rest. It also provides a buffer against overexertion, making even high-intensity workouts safe. In RBT, the protocol adapts to the individual rather than forcing the individual to adjust to it.
The ability for the participant to self-regulate gives them autonomy and more likely to develop and maintain innate motivation (Teta, 2017). “When exercisers have control over when to rest and for how long, work volume can increase while safety is maintained” (Teta, 2017). RBT gives the participant full control of their intensity and gives them ownership to the exercise so that “not only work harder but also become more aware of their physiology and more engaged in their programs” (Teta, 2017). I like this, since half the battle I encounter is keeping my clients motivated and committed to their exercise routine. No matter how effective the prescription is, if it is not maintained, benefits are diminished greatly.
I also like to use a format called “Tabata”. In Tabata, we work hard for 20s and rest for 10 seconds, and continue that pattern for a total of 8 rounds. I mix up strength training with cardio training within a Tabata circuit. It comes out to 4 minutes per set. I often superset two different exercises, often times one strength and one cardio, so they are only doing 4 sets instead of 8. The possibilities with Tabata are endless and we have a lot of fun with it! There are other protocols used by trainers as well, but I have found that the higher duration intervals are not perceived as enjoyable as the lower duration. “Protocols with 120s high-intensity intervals are rated as being less enjoyable than protocols with 30s or 60s high-intensity intervals” (Heisz et al., 2016). According to Heiz, this reduced enjoyment of the more strenuous protocols may be related to the individual’s ability to complete the exercise, or their competence. I have found the Tabata to elicit the most favorable feeling of competence with my participants, especially when the intensities were higher. “Alternatively, the accumulated fatigue or physical stress from chronically performing a strenuous exercise may actually increase negative feelings and reduce enjoyment for the exercise over time” (Heisz et al., 2016). I have taught to all different fitness levels. In my morning gym classes, I typically have younger moms and retired folks attending. The class I teach in my neighborhood clubhouse consists of an age group of 50-60, and they also love Tabata and metabolic conditioning. The duration of the exercise never exceeds 30 minutes, although I have even recommended 15-minute metabolic training when time is constrained.
I have to mention that care must be taken to address the individual variation to exercise training. “Although aerobic exercise is, on average, beneficial for health, its effects vary between individuals, presumably as a result of considerable genetic variance” (Nokia et al., 2016). For some, aerobic training provides substantial gain in maximal aerobic capacity (V˙ O2 max) and metabolic health, whereas for others the same amount of training results in little or even negative change. In fact, there are individual differences in the BDNF gene that has been shown to mediate the effect of exercise and brain cognition and how exercise affects brain and behavior (Herting et al., 2016). “The secretion and intracellular trafficking of BDNF is altered by a common functional single nucleotide polymorphism (SNP) within the BDNF gene, known as the val66met” (Herting et al., 2016). In fact, AHN is highest in animals born with a tendency for a higher response to exercise training and that engage in a large amount of voluntary aerobic activity.
Here is a sample weekly workout program for brain health for someone who responds well to the types of training selected (keeping in mind each individual’s prescription will vary based on their genetics):
Sunday-rest and recovery (gentle walk, yoga, tai chi)
Monday- 20-30 minutes Metabolic Training
Tuesday-rest and recovery
Wendesday-20-30 minutes rest and recovery (gentle walk, yoga, tai chi)
Thursday-30-45 minute steady state cardio (optional)
Friday- 15-30 minutes Metabolic Training
Saturday-choose from Metabolic Conditioning or steady state cardio or rest and recovery (based on biofeedback from the training days earlier in the week)
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BMJ (n.d.) Aerobic and Resistance exercise combo can boost brain power of over 50’s. Retrieved (2018, October 8) from https://www.bmj.com/company/newsroom/aerobic-and-resistance-exercise-combo-can-boost-brain-power-of-over-50s/
Boutcher, S. H. (2011). High-intensity intermittent exercise and fat loss. J Obes, 2011, 868305. doi:10.1155/2011/868305
Foster, C., Farland, C. V., Guidotti, F., Harbin, M., Roberts, B., Schuette, J., . . . Porcari, J. P. (2015). The Effects of High Intensity Interval Training vs Steady State Training on Aerobic and Anaerobic Capacity. J Sports Sci Med, 14(4), 747-755.
Herting, M. M., Keenan, M. F., & Nagel, B. J. (2016). Aerobic Fitness Linked to Cortical Brain Development in Adolescent Males: Preliminary Findings Suggest a Possible Role of BDNF Genotype. Front Hum Neurosci, 10, 327. doi:10.3389/fnhum.2016.00327
Lucas, S. J., Cotter, J. D., Brassard, P., & Bailey, D. M. (2015). High-intensity interval exercise and cerebrovascular health: curiosity, cause, and consequence. J Cereb Blood Flow Metab, 35(6), 902-911. doi:10.1038/jcbfm.2015.49
Nagamatsu, L. S., Handy, T. C., Hsu, C. L., Voss, M., & Liu-Ambrose, T. (2012). Resistance training promotes cognitive and functional brain plasticity in seniors with probable mild cognitive impairment. Arch Intern Med, 172(8), 666-668. doi:10.1001/archinternmed.2012.379
Nokia, M. S., Lensu, S., Ahtiainen, J. P., Johansson, P. P., Koch, L. G., Britton, S. L., & Kainulainen, H. (2016). Physical exercise increases adult hippocampal neurogenesis in male rats provided it is aerobic and sustained. J Physiol, 594(7), 1855-1873. doi:10.1113/jp271552
Northey, J. M., Cherbuin, N., Pumpa, K. L., Smee, D. J., & Rattray, B. (2018). Exercise interventions for cognitive function in adults older than 50: a systematic review with meta-analysis. Br J Sports Med, 52(3), 154-160. doi:10.1136/bjsports-2016-096587
Teta, J. (2011). Rest-Based Training. Retrieved (2018, October 8) from http://www.ideafit.com/fitness-library/rest-based-training
As many of you know, I am a fitness instructor with over 15 years of teaching experience in group fitness and personal training. I am launching an app that includes a series of exercise videos targeted for increasing fat free body mass and reducing body fat. Recently I have started to incorporate high intensity interval training (HIIT) into my classes. An interesting observation I have made is that the interval style training seems to contribute to greater feelings of competence and adherence. My participants feel successful, accomplished and always return for more! This type of response I have seen in all my classes, but particularly in the interval style classes. However, I have noticed there is a sweet spot within ratio of intensity and duration. If the class is too hard or too long, the dropout rate is greater. For example I have experimented with HIIT classes that are 75 minutes and I notice about 25% will leave the class within the first 45 minutes. I have found that 20-30 minutes and a rate of perceived exertion not to exceed 8 or 9 during the intervals drives the most positive response from my participants of all age groups. For this review, I conducted some research to see if there is any data to demonstrate that interval training improves competence and perceived adherence to support or refute my own personal experience. These are very important variables that will support practitioners in making their future exercise prescriptions.
We are all told we must exercise because it has important health benefits. Unfortunately, few adults meet the weekly guidelines of 150+ minutes of moderate –intensity or 75+ minutes of vigorous-intensity aerobic physical activity, and 2+ days of resistance exercises.(Heinrich, Patel, O’Neal, & Heinrich, 2014) For weight loss, the minimum requirements double. The good news is that high intensity interval training (HIIT) provides fitness and health improvements in less time per week than current guidelines. (Heinrich et al., 2014) There are two main methods of exercise that I have worked with in my career as a trainer: continuous training (CT) and high-intensity interval training (HIIT). The main difference between these two modalities of training is that CT is characterized by a lower-intensity (sub-maximal) effort for a longer duration, whereas HITT is characterized by repeated bouts of short duration at higher intensities above lactate threshold. “Compared to CT, HIIT induces similar-to-greater improvements in fitness and cardiovascular function but in a shorter amount of time.”(Heisz, Tejada, Paolucci, & Muir, 2016) There are many types of HIIT protocols. The one that I use often is called Tabata. In Tabata, we work hard for 20s and rest for 10 seconds, and continue that pattern for a total of 8 rounds. It comes out to 4 minutes per set. I often superset two different exercises, sometimes one strength and one cardio, so they are only doing 4 sets instead of 8. The possibilities with Tabata are endless and we have a lot of fun with it! The video I am posting is an example of a strength only Tabata. There are other protocols used by trainers as well, but I have found that the higher duration intervals are not perceived as enjoyable as the lower duration. “Protocols with 120s high-intensity intervals are rated as being less enjoyable than protocols with 30s or 60s high-intensity intervals.”(Heisz et al., 2016) According to Heiz, this reduced enjoyment of the more strenuous protocols may be related to the individual’s ability to complete the exercise, or their competence. I have found the Tabata to elicit the most favorable feeling of competence with my participants, especially when the intensities were higher. “Alternatively, the accumulated fatigue or physical stress from chronically performing a strenuous exercise may actually increase negative feelings and reduce enjoyment for the exercise over time.”(Heisz et al., 2016)
Another benefit to the HIIT I have found is the shorter time commitment being favorable among my participants. This also contributes to the differences in enjoyment for HIIT compared to CT even though the HIIT is more physically strenuous. My participants have often told me, “I know that the exercise session is shorter so I am able to push harder mentally knowing that is will end soon!” The great thing I have noticed that even with the shorter duration, the physiological benefits I have observed have been comparable or even better than the longer duration CT. According to Heiz et al (2016):
Even with the shorter time commitment, HIT induced similar physiological adaptations as indicated by pre-to-post change on maximal aerobic fitness test for both VO2 peak and PPO. Together, these results support the growing evidence that HIT is similarly effective but more time-efficient at improving aerobic fitness compared to more traditional moderate forms of continuous exercise.
According to Heinrich et al, although the intensity requirement for HIIT may be intimidating, the reduced time requirement may be appealing to many adults, showing potential for higher rates of adherence.(Heinrich et al., 2014) Interestingly, there is also mention that combining aerobic and resistance training may result in greater weight and fat loss and fitness improvement than each modality alone. This is exactly the way I teach my classes and it has been received very favorably thus far among my participants!
Perceived pleasure, according to Oliveira et al, has been reported to be an important contributor to exercise adherence. (Oliveira, Slama, Deslandes, Furtado, & Santos, 2013) There are mixed results according to the literature I read in regards the HIIT and perceived pleasure. In a few studies, I read that HIIT is correlated to a great enjoyment of exercise, but other studies show if the intensity is too high or difficult to complete it can lead to a higher dropout rate and a lower perceived competence and adherence. In one study it was observed that changes in exercise enjoyment were predicted by increases in workload, suggesting that strength adaptions may be important for promoting exercise enjoyment. (Heisz et al., 2016) I have encountered this as well with my beginners. I have to start them slowly and gradually build up the intensity over time. If the intensity is too hard at first, they drop out. “For sedentary individuals, a key barrier to starting an exercise program is the preconceived notion that exercising is not enjoyable and failing to find enjoyment from exercise can make it more difficult to adhere to an exercise program over time.”(Heisz et al., 2016) According to a 6 week study conducted by Heisz et al., “across the six weeks of training, increases in workload predicted increases in enjoyment.”(Heisz et al., 2016) Typically it takes my participants about 4 weeks of consistent training with gradual builds in intensity for the pleasure to stick. If my participants continue with me past this point, the enjoyment of the exercise seems to outweigh the discomfort, and I typically see an increase in adherence. This seems consistent with the data from the 6 week study conducted by Heisz et al.
Not everyone shares my enthusiasm for HIIT, however. One study discusses that sprint interval training as being inappropriate for a largely sedentary population. “An inactive population is unlikely to engage in sprint interval training (SIT) due to poor aﬀective responses, low self-eﬃcacy and motivation, and increased challenges to self-regulation.”(Robertson-Wilson, Eys, & Hazell, 2017). According to Robertson-Wilson et. al, one of the key concerns with HITT/ SIT is negative affective responses with faced with arduous physical activity of this nature. It appears that differences in the methodological procedures may explain the divergent results. The studies that utilized longer work sessions with inadequate recovery were the ones that demonstrated negative affective responses during the HITT sessions.
Under these conditions, over 50% of the participants were unable to finish the HIIT session. Although it was not the focus of this study, this is an important fact because self-efficacy may be negatively influenced in cases of participant dropout. It is possible that HIIT sessions with longer recovery periods would provide better affective responses than the HIIT sessions used in the present study.(Oliveira et al., 2013)
The rule of thumb I use when designing my classes is when the work portion is longer (greater than 45s), then the intensity is lower and the rest is longer. But when the work portion is shorter (as in Tabata), the intensity is higher and the rest is shorter. When I stick to these basic rules, I noticed the most adherence and satisfaction among my participants. According to Oliveria et. al, the affective response seems to have been influenced by the magnitude of the stimulus intensity and by the predominant metabolic pathway engaged by the exercise. “It is possible that other HIIT configurations with greater recovery periods could result in positive affective responses, and this hypothesis should be tested in future studies.”(Oliveira et al., 2013) I have personally tested this informally in my classes and have found this to be true.
As a final note, another area I have found quite intriguing are the psychological components involved exercise. Oliveira et al. have conducted numerous studies in regards to intrinsic and extrinsic motivation, and they discuss the opponent process theory and its involvement in the enjoyment of exercise. According to Oliveira et al.(2013):
The opponent process theory, postulates that after every affective perception (pleasant or unpleasant), an opponent process occurs. Thus, according to this theory, a feeling of pleasure can occur after an aversive stimulus or stress, which can activate the reward system and can then lead to a repetition of that stimulus. The increased production of neuromodulatory substances such as anandamide, dopamine, serotonin and endorphins may be associated with decreased anxiety and increased pleasure after intervals of intense stimulation. However, this hypothesis was not objectively investigated, and it is not well known whether individuals choose to continue to engage in physical activities based on perceptions experienced during or after exercise. Future studies should investigate this issue.
In conclusion, I think any exercise is better than no exercise. However in order for exercise to be effective, it must be consistent. In order for participants to be motivated to continue exercising, the workout should be enjoyable, achievable, and effective. I have found that HIIT training meets all these requirements. The classes I teach are short (no more than 30 minutes), achievable ( the intensity I select is appropriate for my participants) and effective (my participants report increases in strength, flexibility, fat free body mass and decreases in body fat). These variables thus make the HIIT classes I teach enjoyable. Because my participants enjoy my classes, they feel competent and come back for more! I have been known to have a pretty strong following, and I think these simple guidelines I use contribute greatly to my success as a fitness instructor.
Heinrich, K. M., Patel, P. M., O’Neal, J. L., & Heinrich, B. S. (2014). High-intensity compared to moderate-intensity training for exercise initiation, enjoyment, adherence, and intentions: an intervention study. BMC Public Health, 14, 789. doi:10.1186/1471-2458-14-789
Heisz, J. J., Tejada, M. G., Paolucci, E. M., & Muir, C. (2016). Enjoyment for High-Intensity Interval Exercise Increases during the First Six Weeks of Training: Implications for Promoting Exercise Adherence in Sedentary Adults. PLoS ONE, 11(12), e0168534. doi:10.1371/journal.pone.0168534
Oliveira, B. R., Slama, F. A., Deslandes, A. C., Furtado, E. S., & Santos, T. M. (2013). Continuous and high-intensity interval training: which promotes higher pleasure? PLoS ONE, 8(11), e79965. doi:10.1371/journal.pone.0079965
Robertson-Wilson, J., Eys, M., & Hazell, T. J. (2017). Commentary: Why sprint interval training is inappropriate for a largely sedentary population. Front Psychol, 8, 1603. doi:10.3389/fpsyg.2017.01603
I am very interested in alternative therapies that can be used either stand alone or in conjunction with conventional therapies like chemotherapy. I found a paper in regards to AHCC that looked promising, but unfortunately has not reached mainstream. Many immune enhancers are natural compounds that have proved to be nontoxic for humans and with great potential for anticancer activity (Yin, Fujii, & Walshe, 2010). ACHH is active hexose correlated compound (AHCC), an extract prepared from mycelia of the basidiomycete mushroom Lentinula edodes. 74% of AHCC is oligosaccharides containing about 20% of the -1, 4-glucan type. It has received special attention in the past few years by its reported benefits. AHCC is commercially used as a nutritional supplement and contains a mixture of polysaccharides, amino acids, and minerals (Yin et al., 2010). Results of this particular study suggest that AHCC can enhance CD4 and CD8 T cell immune responses in healthy persons via increasing production of cytokines IFN-gamma and TNF-alpha from T cells. It has also been found that the effects of AHCC are more evident in hosts with the impaired immune function. The study measured the frequency of IFN-gamma and TNF-a producing CD4 and CD8 T cells in adults over age 50 before and after taking AHCC. The results were pretty interesting. AHCC was provided as 500-mg capsules. Total daily dose was 3 g (3 capsules twice daily). The production of the cytokines was measured at 30 and 60 days after AHCC intake and 30 days after the last dose. Interestingly, the frequency of CD4 T cell subsets producing the cytokines was higher at 30 and 60 days. Even after 30 days of discontinuing the AHCC, the frequency of CD4 T cells producing the combination of IFN-gamma and TNF-a at visit 4 was still higher compared to baseline levels. This implies that the effect of AHCC on CD4 T cells could last for several weeks even after this compound is discontinued (Yin et al., 2010)
Two published peer-reviewed human clinical studies (on 269 and 40 subjects respectively) evaluating advanced liver cancer showed extended survival, lower recurrence and improved quality of life among patients taking AHCC. Several other studies demonstrated the ability of AHCC to significantly increase NK cell activity in immune compromised patients. “Given the abundance of preliminary positive results across different infections, AHCC supplementation demonstrates valuable and clinically-relevant potential as an immune-enhancing compound” (Pescatore, n.d.). Finally, AHCC boasts a strong safety profile supported by a Phase I study conducted at Harvard, a 20-year history of use in Japan, its adoption by over 700 clinics and use by an estimated 70,000 people worldwide (including 20,000 in the U.S.). Thus, there is a strong case to be made for adding AHCC to a daily supplement regimen to support the body’s immune system, not only during the apparent times of increased infectious threat such as the flu season, but also all year long.
How can this help the population with bladder issues?
Theoretically, AHCC should be able to boost your natural immune system to defend you against pathogens that cause UTI’s. Both human and animal studies have pointed to AHCC’s ability to enhance the activity of natural killer cells (“NK cells”). These cells provide a crucial first defense for the body, launching a rapid attack while the other cells of the immune system are still mobilizing. AHCC has been the subject of several studies, which investigated its potential as a countermeasure to various infectious diseases, methicillin-resistant Staphylococcus aureus (MRSA) and several other opportunistic infections (Klebsiella pneumoniae, Candida albicans and Pseudomonas aeruginosa.) Looking at “opportunistic” or hospital-acquired infections, the effects of AHCC supplementation on the resistance to Klebsiella pneumoniae (principally associated with bacterial pneumonia and urinary tract infections) was studied in both infected and stress induced mice. Again, the AHCC-supplemented mice demonstrated increased survival, increased mean time until death, decreased susceptibility to infection and increased bacterial clearance from the blood.
Here is a link for the product on Amazon: https://amzn.to/2uaEVYN
Pescatore, F. (n.d.) AHCC a Powerful Aid in Fighting Viruses and Infections
Yin, Z., Fujii, H., & Walshe, T. (2010). Effects of active hexose correlated compound on frequency of CD4+ and CD8+ T cells producing interferon-gamma and/or tumor necrosis factor-alpha in healthy adults. Hum Immunol, 71(12), 1187-1190. doi:10.1016/j.humimm.2010.08.006
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The areas I am going to focus on are Inflammation and the Immune System, Leaky Gut and Pain Management.
What is CBD anyway?
Believe it or not, your body produces endocannabinoids. The endocannabinoid receptors (ECS) are the biggest receptors in your body, and they exist in all higher life forms. The ECS has emerged as one of the key regulatory mechanisms in the brain controlling multiple events such as mood, pain perception, learning and memory among others. “It is also thought to provide a neuroprotective role during traumatic brain injury (TBI) and may be part of the brain’s natural compensatory repair mechanism during neurodegeneration.” (Kendall & Yudowski, 2016) We have two main receptors, CBD1 and CBD2. The CBD1 receptors are found primarily in the central nervous system, and CBD2 is found in immune cells. According to Gyires and Zadori, modulating the activity of the endocannabinoid system (ECS), which comprises CB1 and CB2 receptors, the endocannabinoids and their synthetic and metabolizing enzymes, may have therapeutic potential in numerous diseases including obesity/metabolic syndrome, diabetes, neuro- degenerative, inflammatory, cardiovascular and psychiatric disorders, liver and skin diseases, pain, cachexia, cancer, as well as chemotherapy-induced nausea/vomiting. ((Gyires & Zadori, 2016)
CBD1: Central cannabinoid receptors
“TheCB1 receptor is one of the most abundant G protein-coupled receptors (GPCRs) in the CNS and is found in particularly high levels in the neocortex, hippocampus, basal ganglia, cerebellum and brainstem.”(Kendall & Yudowski, 2016). The CBD-1 receptor binds the THC to mediate most of the CNS effects of it. CB1 receptors also act on 2-aracodonalglycerol (2 AG), which is found in breast milk and CNS as well as annandamines (AD) which is considered the “bliss molecule”. CBD1 receptors are restricted to presynaptic sites, which could indicate a possible role in local modulation of gene and protein expression after chronic receptor activation. CB1 receptors are indicated in many disorders that impact the CNS including several neurodegenerative disorders such as Huntington’s disease (HD), multiple sclerosis (MS) and Alzheimer’s disease (AD).” It’s expression is heterogeneous within the nervous system and is mainly responsible for cannabinoid psychoactive properties.”(McCoy, 2016)
CBD2: peripheral cannabinoid receptors
“The CB2 receptor exhibits a more defined pattern of expression in the brain than CB1 receptors, and is found predominantly in cells and tissues of the immune system.”(Kendall & Yudowski, 2016). They too act on 2AG and AD like CB1. However, in the CNS, CB2 receptor expression is associated with inflammation, particularly in the brain. “Unlike CB1 receptor-mediated cell activation, signal transduction through the CB2 receptor lacks psychotropic effect making it an attractive target for immunotherapy.”(McCoy, 2016)
A word about THC:
The cannabis plant contains more than 60 different active synthetic ligands for CBC1/2 with THC being the major psychoactive molecule among them. At the molecular level, THC acts as a partial agonist (promoter) of the CBD1 receptor. However, THC is not really required for the therapeutic mechanisms of CB1/CB2. Therefore in most over-the-counter products, such as Prime My Body CBD oil, the THC is <0.02%. Depending on the chemistry of the product and the bioavailability of the CBD’s, the THC is not required in high levels for the absorption of CBD.
A summary of what CBD does in your body:
Here is a summary of what CBD can do in your body. Keep in mind, exogenous CBD modulates the receptors; it does not attach directly on them or block them. It can pull up your own endogenous cannabinoid production and molecularly, it can modify gene transcription and stabilize neuroinflammation. For example, it can stabilize over-active glutamate receptors and stabilize activated microglia cells in the brain. In essence, CBD changes the way we create things in our brain. Other benefits of CBD include:
- Turning up genes like glutathione and superoxide dismutase
- Protein repair
- Turning down genes that are pro-inflammatory
- Lowering brain inflammation
CBD, INFLAMMATION AND IMMUNE SYSTEM
A fundamental characteristic of the immune system is the ability to distinguish friend and foe…..self and non-self-molecules or antigens. Inflammation is the innate immune response against infectious agents, and the inflammatory response promotes initiation of an adaptive immune response by antigen-specific T and B cells. When the immune system encounters a pathogen, innate immune cells recognize the pathogen via Toll-like receptors and other pattern-recognition receptors to trigger an inflammatory response. “Innate immune cells are an important source of endocannabinoids, and these cells synthesize and metabolize endocannabinoids.”(McCoy, 2016)
For many years, one puzzling aspect of innate immunity has been autoimmune conditions, which are due to inflammatory responses in the absence of an infection that contribute to tissue damage. Important innate immune cells express cannabinoid receptors, and cannabinoids influence their immune functions. For example cannabinoid studies involving toll-like receptors have concentrated in bacterial LPS responses via TLR4 as a classic model for inflammation. “For the most part, exogenous and endogenous cannabinoids interfere with proinflammatory cytokine and nitric oxide production by LPS or LPS stimulated monocytes, macrophages, microglia and macrophage cell lines in culture.”(McCoy, 2016) LPS is released from bacteria cells which are implicated in adrenal and HPA axis in individuals who have chronic bacterial infection. CBD oil can increase CB1 and CB2 receptor expression on peripheral blood monocytes, and “exogenous cannabinoids may alter the endocannabinoid system leading to greater suppression of the LPS response.”(McCoy, 2016) All this means is that using exogenous sources of CBD, such as found in CBD oil, can be used therapeutically to modulate inflammation and subsequent endocrine disruption caused by bacteria and modulate the immune system, which can be helpful in treating autoimmune diseases.
GASTROINTESTINAL ACTIONS OF CANNABINOIDS
There is evidence that activation or inhibition of peripheral and central cannabinoid receptors may influence the function of the GI tract. The existence of a functional endocannabinoid in the gut has been established – as CB1 and CB2 receptors are found in colonic tissue (Coutts and Izzo, 2004). The cannabinoid receptors, the endocannabinoids AEA and 2-AG, and proteins responsible for their synthesis and degradation are widely distributed in the GI tract and several data suggest that their expressions are substantially altered during inflammatory processes. (Gyires & Zadori, 2016) According to (DiPatrizio, 2016):
Evidence also suggests that dysregulation of the endocannabinoid system might play a role in intestinal disorders, including inﬂammatory bowel disease, irritable bowel syndrome, as well as obesity. There is evidence that the dyregulation can be expressed epigenetically. For example, single-nucleotide polymorphisms in genes for constituents of the endocannabinoid system—including fatty acid amide hydrolase (FAAH), the degradative enzyme for the endocannabinoid, anandamide, and cannabinoid type1receptor(CB1R)—are associated with increased colonic transport and irritable bowel syndrome.
In one study done on rats in 2016, it was seen that the released of non-cholinergic excitatory neurotransmitters may be regulated by CB1 receptors. CB1 and CB2 receptors and enzymes in regulating endocannabinoids can be modulated to protect the gastric mucosa against erosions, mucosal lesions and inflammation. “Activation of cannabinoid receptors by exogenous or endogenous ligands has been shown to decrease the formation of different types of experimental gastric ulcers.”(Gyires & Zadori, 2016) Acid secretion that occurs during NSAID-induced mucosal damage can also be inhibited via the CB1 receptors.
Another area that CBD’s are showing activation of the cannabinoid receptors in the gut that can suppress many of the inflammatory bowel related symptoms, such as diarrhea and visceral hypersensitivity. This is showing promise in modulating disease such as Chron’s disease and ulcerative colitis, both which are complex diseases involving altered intestinal flora that can induce mucosal disruption and result in penetration of luminal antigens into the gut wall. (Gyires & Zadori, 2016)
Below are some areas where there is a large body of evidence that cannabinoids exert on the GI Tract.
- Inhibition of inflammation. CBD can have both immunomodulatory and immunosuppressive effects. These effects are primarily mediated by CB2 receptors localized on macrophages and lymphocytes, but some studies underline the importance of CB1 receptors as well. Due to the complex anti-inflammatory action, cannabinoids can efficiently inhibit the development of colitis, as well as reduce the already established inflammation.
- Modulation of intestinal barrier functions-Epithelial damage and breach of the intestinal barrier are important factors in intestinal diseases and “leaky gut”, which allow bacterial products and other antigens to cross the epithelium and enter the lamina propria, resulting in inflammation and tissue damage. Restoration of the barrier function is an important approach in treating individuals with gut-related conditions. Although the data from various in vitro and in vivo studies are mixed, the anti-inflammatory properties of the cannabinoids can indirectly modify their action on intestinal permeability and improve barrier function. Alhamoruni, Larvin, and O’Sullivan (2012) looked specifically at the role cannabinoids had on intestinal permeability. T hey concluded that “locally produced endocannabinoids, acting via CB1 receptors play a role in mediating changes in permeability with inflammation, and that phytocannabinoids have therapeutic potential for reversing the disordered intestinal permeability associated with inflammation.” Alhamoruni, Larvin, and O’Sullivan’s (2012) study provides the suggestion that THC and/or CBD can/may (depending on your state) have a therapeutic role in healing IP and their research also provided evidence of a prophylactic role.
- Motility and Secretion-Beside their potent anti-inflammatory property and modulatory effect on intestinal epithelial permeability, cannabinoids also inhibit gastrointestinal motility and secretion, which both may alleviate diarrhea, a common clinical manifestation of IBD. They also have been shown to alleviate visceral hypersensitivity and abdominal pain. (Gyires & Zadori, 2016) Preclinical data suggest that cannabinoids may serve as useful tools for alleviating visceral hypersensitivity and relieving abdominal pain in IBD, and this assumption is supported by preliminary clinical studies, in which IBD-patients treated with cannabis reported a statistically significant pain reduction.
- Gut Microbiome-Several studies suggest the possibility of interactions between the endocannabinoid receptors and gut bacteria. Collectively, these studies underscore the ability for CB1R activation to control endothelial barrier integrity and provide novel evidence for interactions between the endocannabinoid system, gut microbiota, and possibly adiposity.
CBD AND CHRONIC PAIN
Chronic pain represents an emerging public health issue of massive proportions, particularly in view of aging populations in industrialized nations (Russo, 2008). Associated facts and figures are alarming: Responses to an ABC News poll in 2005 in the USA indicated that 19% of adults (38 million) have chronic pain. I am sure those numbers are even higher now. According to Russo, clinicians face difficulties managing intractable patients afflicted with cancer-associated pain, neuropathic pain, and central pain states (e.g., pain associated with multiple sclerosis) that are often inadequately treated with available opiates, antidepressants and anticonvulsant drugs. Therefore, the integration of cannabinoid medicines to the pharmacopoeia offers a novel approach to pain management. I wanted to summarize some of my findings on this topic in regards to pain management. When I searched on PubMed, there were many articles on this topic, so clearly there is quite a bit of research being conducted, but I decided to choose two of them that I felt was most appropriate.
Interesting their functions have been termed “relax, eat, sleep, forget, protect” (Russo, 2008). It demonstrates the ability to mediate the suppression of pain and inflammatory processes (Russo, 2008). Interestingly, a deficiency in endocannabinoid has been found in people suffering from conditions such as migraines, fibromyalgia and intestinal conditions such as IBS.
Below are some areas I bulleted that was particularly of interest in regards to ECS and pain management:
- Cannabinoids proved to be 10-fold more potent than morphine in wide dynamic range neurons mediating pain, through widespread action in areas of the thalamus (Russo, 2008).
- The ECS is active peripherally, where CBD1 stimulation reduces pain, inflammation, and hyperalgesia (Russo, 2008).
- Cannabinoid agonists produce many effects beyond those mediated directly on receptors, including anti-inflammatory effects and interactions with various other neurotransmitter systems (Russo, 2008).
- THC can increase serotonin. It affects widespread serotonergic systems, including its ability to decrease 5-hydroxytryptamine (5-HT) release from platelets, increasing its cerebral production and decreasing synaptosomal uptake (Russo, 2008).
- Cannabinoids pre-synaptically inhibit glutamate release. “The glutamatergic system is integral to development and maintenance of neuropathic pain, and is responsible for generating secondary and tertiary hyperalgesia in migraine and fibromyalgia via NMDA mechanisms” (Russo, 2008)
- THC produces 30%–40% reduction in NMDA responses, making THC a neuroprotective antioxidant (Russo, 2008).
- THC has been shown to stimulate beta-endorphin production by interacting with the endorphin/enkephalin system (Russo, 2008).
- Cannabidiol, inhibits glutamate neurotoxicity, and displays antioxidant activity greater than ascorbic acid (vitamin C) or tocopherol (vitamin E) (Russo, 2008).
- CBD is able to inhibit tumor necrosis factor-alpha (TNF-α) , as seen in a rodent model of rheumatoid arthritis (Russo, 2008).
- Cannabinoids suppress inflammatory and neuropathic pain by targeting a3 glycine receptors (Xiong et al., 2012)
- THC has twenty times the anti-inflammatory potency of aspirin and twice that of hydrocortisone. In contrast to all nonsteroidal anti-inflammatory drugs (NSAIDs), demonstrates no cyclo-oxygenase (COX) inhibition at physiological concentrations. “At a time when great concern is accruing in relation to NSAIDs in relation to COX-1 inhibition (gastrointestinal ulcers and bleeding) and COX-2 inhibition (myocardial infarction and cerebrovascular accidents), CBD, like THC, inhibits neither enzyme at pharmacologically relevant doses” (Russo, 2008).
Based on some of these facts from a small source of literature, I think there are opportunities for further research in the use of CBD supplements to determine if it can be used to complement any therapeutic healing protocol. I believe it has really helped me in many ways.
Alhamoruni, A., Wright, K., Larvin, M., & O’Sullivan, S. (2012). Cannabinoids mediate opposing effects on inflammation-induced intestinal permeability. British Journal of Pharmacology, 165(8), 2598–2610. http://doi.org/10.1111/j.1476-5381.2011.01589.x (Links to an external site.)
Coutts, A. A., & Izzo, A. A. (2004). The gastrointestinal pharmacology of cannabinoids: An update. Current Opinion in Pharmacology, 4(6), 572–579. https://doi.org/10.1016/j.coph.2004.05.007
DiPatrizio, N. V. (2016). Endocannabinoids in the Gut. Cannabis Cannabinoid Res, 1(1), 67-77. doi:10.1089/can.2016.0001
Gyires, K., & Zadori, Z. S. (2016). Role of Cannabinoids in Gastrointestinal Mucosal Defense and Inflammation. Curr Neuropharmacol, 14(8), 935-951.
Kendall, D. A., & Yudowski, G. A. (2016). Cannabinoid Receptors in the Central Nervous System: Their Signaling and Roles in Disease. Front Cell Neurosci, 10, 294. doi:10.3389/fncel.2016.00294
McCoy, K. L. (2016). Interaction between Cannabinoid System and Toll-Like Receptors Controls Inflammation. Mediators Inflamm, 2016, 5831315. doi:10.1155/2016/5831315
Russo, E. B. (2008). Cannabinoids in the management of difficult to treat pain. Ther Clin Risk Manag, 4(1), 245-259.
Xiong, W., Cui, T., Cheng, K., Yang, F., Chen, S. R., Willenbring, D., . . . Zhang, L. (2012). Cannabinoids suppress inflammatory and neuropathic pain by targeting alpha3 glycine receptors. J Exp Med, 209(6), 1121-1134. doi:10.1084/jem.20120242