My name is Nick and I am currently doing my PhD in physiology with an emphasis in muscle physiology. Welcome to my exercise science blog. Unlike a lot of fitness blogs out there, this one is unique because it is backed by true science. You will find only articles that have been peer reviewed and published in top tier science journals on this blog. For the fast easy read, just read the bold type. If you have any questions do not hesitate to ask me. I am at your disposition for any advice in exercise or just basic physiology. This is not a progress blog to benefit myself but rather to share some of my knowledge and expertise with you that I have gained over my years dedicating my career to exercise science. If I do not know the answer, I will do my best to search through the journals to find it for you. Although I am in biomedical research, I am not a licensed medical professional so please consult a physician before entering any exercise or nutrition program.
Have a 5K coming up or a race in a track meet? Would you like to improve your time in the event (wow, it sounds like I’m trying to sell something)? Well, a group from Denmark just published a paper with an interesting endurance training method to help you reach your new time goal. This one is for the runners and I assure you I’m not selling anything but exercise.
Introduction: It is known that people who are already trained need to intensify their training protocols to continue to improve. Training at maximal or near maximal intensities creates the muscular adaptations necessary for these improvements. A popular method to do this is introducing 30 second sprint intervals into your training coupled with a short recovery period. Normally, this is repeated 4-5 times. However, it is uncertain whether training using just 10 second near maximal sprints has the same effect as the 30 second intervals. In addition, it is unclear whether training at this high of an intensity can affect the health profile of people who are previously trained. Therefore, the 10-20-30 training concept is introduced and tested to see whether or not it can lead to endurance performance, increases in cardiovascular fitness, as well as health.
Methods: Eighteen moderately trained individuals (12 males and 6 females) were divided into 2 groups, the 10-20-30 group or a control group. For a period of 7-weeks, the 10-20-30 group trained with this method whereas the control group continued with their normal weekly training sessions (2-4 times per week, 27km and 137min total). The 10-20-30 training concept consists of 3-4 x 5 min running interspersed with 2 min of rest. During the 5 min running period, a person would run 1 min of an interval divided into 30, 20, and 10 seconds at an intensity related to <30%, <60%, and >90-100% of maximal intensity. They performed this 3 times per week with a volume of 14 km per week. To test differences in the training methods, the groups performed a 1500m race, a 5-K run, and a running test to exhaustion.
Results (after 7 weeks):
The 10-20-30 group improved performance by 6% in the 1500m and 4% in the 5-K run with no difference in the control group.
The 10-20-30 group increased their VO2max (maximal oxygen uptake) by 4% with no changes in the control group.
The 10-20-30 group lowered their total cholesterol and LDL cholesterol with no changes in the control group.
The 10-20-30 group’s systolic blood pressure was lower with no changes in the control group.
Discussion: After a 7-week period, the 10-20-30 training method, lead to an increase in VO2max of 4% and decreased times on the 1500m by 21 seconds and on the 5-K by 48 seconds. In regards to health, this training concept also decreased LDL cholesterol as well as resting systolic blood pressure. This all occurred even though the volume of training reduced by 54%. One explanation for this by the authors is that high cardiac stress (the max effort 10 second sprints) coupled with a reduction in training volume is sufficient enough to increase VO2max because the group that did the 10-20-30 spent approximately 40% of training time spent above 90% of maximal heart rate whereas the control group spent 0% of training at this level. For health parameters, the authors also state that the 5 mmHg decrease in systolic blood pressure is of clinically significant because a decrease such as this can reduce the risk of cardiovascular death by 10-15%.
Practicality: If you were wondering approximate running speeds in case you want to try this out on the treadmill, the 10 second intervals were at speeds >20 km/h, the 20 second intervals were between 10-14 km/h, and the 30 second intervals were <10 km/h. For those still having trouble understanding the 10-20-30 principle I will give an example: You would run a warm-up of 5 min at a very low intensity, following this you would begin the 5 minutes interval which is divided into 10-20-30 seconds for each minute. You run <10 km/h for 30 seconds then right away increase the speed to 10-14 km/h for 20 seconds then again immediately increase the speed to >20 km/h (or as fast as you can run for 10 seconds). After repeating this another 4 (to make 5 minutes) times you would then have a recovery period of 2 min at a low intensity before repeating the 5 minute intervals 2 or 3 more times. For those who have tight time schedules, this is practical because all of these improvements with this technique can be accomplished in just 30 minutes. The authors also state that 10-20-30 is also applicable for anyone who is sedentary up to elite running levels.
Taking ice baths post-exercise seems to be the most popular method of reducing delayed onset muscle soreness for novice and elite athletes. This method, known scientifically as cryotherapy, is growing to be more popular than traditional ones such as massage, stretching, or taking non-steroidal anti-inflammatory drugs (NSAIDs). The most popular forms of cryotherapy are cycling 1 min in ice water (5 degrees Celsius) followed by 1 minute out for a total of three times or a longer duration of 15 minutes at 15 degrees Celsius. Now that you have the background, I’ve went out and found an enormous extensive review on the subject to make clear whether or not this technique is useful or useless at combating muscle soreness and aiding recovery.
The scientific claims: You know that you treat sprains, strains, or any swelling in the body with ice. The mechanisms for why cryotherapy works are similar; reduce pain, swelling, and inflammation. There is also vasoconstriction (decreasing the diameter of the blood vessel) which stimulates blood flow and nutrient and waste transfer as well as decrease in nerve transmission speed, which could alter the threshold of pain receptors.
The studies used: The review included 17 small trials (published from 1998-2009) of 366 participants. No restrictions were placed on age (16-29), gender female, or type of level of exercise. Also, no restrictions were placed on duration or frequency of immersions or depth of immersion. The studies were all of small sample size (20 participants or less) except for one that used 54.
The exercises used: All exercise used were designed to produce delayed onset muscle soreness (DOMS) under laboratory controlled conditions. Repetitions for resistance exercise ranged from 50-100 of eccentric or alternative concentric and eccentric contractions. The other studies used running or cycling in single bout efforts (for the bike) or steady state efforts. Few actually included team sport exercise (basketball and soccer).
The cryotherapy used: The most common for the studies was 10-15 degrees Celsius with an average immersion of 12.6 minutes. This was employed in almost all of the studies immediately after exercise. The different methods of cold-water immersion were compared to nothing/rest (the most common), cold-water immersion vs. contrast immersion (switching between hot and cold), cold-water immersion vs. warm water, and cold-water immersion vs. active recovery.
Enough with the technicalities. Let’s go to the results.
Cold-water immersion vs. nothing: In terms of muscle soreness, there is no significant difference immediately between the two conditions but at 24, 49, 72, 96 hours later the cold-immersion group reported a significantly lower amount of muscle soreness than the group that just rested. This effect seems to be more prevalent after running based exercises than resistance exercises but the authors not that due to the various types of exercises that were performed between all the studies, plus the sample sizes being small, it is difficult to find whether or not this is truly significant. There were no significant differences in strength, power, functional performance, swelling, or biomarkers of muscle damage.
Cold-water immersion vs. contrast immersion: In terms of muscle soreness, there was no significant differences between the groups. Also, there was no significant differences in strength, power, functional performance (time to fatigue), swelling, range of movement, or biomarkers of muscle damage.
Cold-water immersion vs. warm-water immersion: There was significant lower levels of muscle soreness reported only for the cold-water immersion group at time-point 96 hours with no differences in strength, power, functional performance, swelling, or biomarkers of muscle damage.
Cold-water immersion vs. active recovery: There are no significant differences in reports of muscle soreness, strength, power, functional performance, swelling, or biomarkers of muscle damage.
Discussion/Conclusions: Cold-water immersion did significantly reduce muscle soreness at time points 24, 48, 72, and 96 hours post-exercise. However, it is important to note that these were all subjective reporting (self-reports) and the authors state it is hard to draw true conclusions from the data due to poor methodological quality. There were high risks of bias due to the fact that blinding was performed poorly as well as concealment of group assignments (only 1 study did this effectively). There were also large differences in the types of exercises used and subjects were a mix between trained and untrained. The effectiveness very well may rely on the specificity of the exercise performed as well as the athletic level of the individual.
My input: Did you know that in the 1920s, cyclists in the Tour de France would smoke during the race because they believed that smoking opened up the blood vessels and oxygen transport machinery of the lungs? Ridiculous, right? I’m not saying ice-baths are as crazy as this, but are they truly beneficial to aid recovery in the muscle? I’m not so sure. From the most basic laws of chemistry, we know that when something is heated up the molecules in it move faster and when something is cooled down the molecules in it slow down. If you are exposing your muscles to cold, all of the molecular processes will slow down. You need enzymes (which function effectively at specific temperatures) and proteins moving post-exercise to begin the repair process and signal inflammation, and if you’ve read my previous posts on muscle hypertrophy, you know inflammation is necessary. It is the same reasoning to avoid NSAIDs in hopes of reducing muscle soreness. For this reason, I’m always heading for the exact opposite after training, a hot shower. The reason I do this is not only to continue normal biochemical processes in the muscle but also to incorporate the activation of what are called heat shock proteins. Heat shock proteins are proteins in the body that respond to stress or elevated temperatures. They function as chaperones for other proteins by aiding them to conform to a certain shape and stabilize proteins that are not shaped properly. Basically, they can clean up the mess inside of the muscle cell and help with repair. This is another reason why I’m not on the ice-bath bandwagon. You might feel that it has helped you before in the past and it possibly could have helped, but I just want to let you know there is no scientific evidence supporting it. The studies are low quality studies. If you truly want a good study on this, take a group of at least 35 people, train their legs or their arms simultaneously with the same protocol and put one limb in the ice and one limb not in the ice or in warm water, take muscle biopsies, and see the differences between the conditions (Anyone want to take this on as a nice Master’s or PhD project? I’ll be glad to give advice for it). To my knowledge this has not been done and this would be the best way to see if cold-immersion truly helps. Although there was some evidence in a decrease in self-reported muscle soreness, I’m still not convinced and higher quality studies are necessary before I’ll be convinced.
You’ve heard the debate before, you know you have. High intensity interval training (HIT) versus continued steady state running. Which is better? A new article has been published showing that when it comes to the two, they may in fact be more similar than we initially thought.
Introduction: When we talk about adaptations to endurance training, we’re talking about muscle mitochondria. These adaptations are thought to be turned on by increases in molecular responses from the onset of contraction (e.g. increases in the AMP/ATP ratio, calcium levels, reactive oxygen species, lactate, reduced glycogen availability, etc). All of these lead to activation of proteins called kinases which phosphorylate targets such as transcription factors or transcriptional coactivators. Okay, I know, too much science. It’s gross for you. Basically, what this means is that these signals increase markers responsible for allowing the mitochondria to adapt to the endurance training and subsequently, you become a better athlete. However, it is uncertain if there is an optimal exercise stimulus to create these adaptations. Therefore, the aim of this study was to see the whether or not the signals of these molecular responses after an acute bout of either HIT or continuous running increase greater for one mode of exercise or the other. The primary hypothesis is that HIT will increase these signals responsible for adaptation to a greater level than that of continuous running.
Methods: The study recruited 10 recreationally active males who underwent both the HIT and the continued running protocol. For those unfamiliar with HIT, the protocol was 3-min running at 90% of one’s maximal oxygen uptake followed by a recovery period of 3-min at 50% maximal oxygen uptake (this was repeated 6 times). The group in the continued running ran the entire time at 70% maximal oxygen uptake. Muscle biopsies were taken pre-exercise, post-exercise, and 3 hours after exercise.
Results: Muscle glycogen decreased by 30% in both groups but there was no difference between HIT and continuous running (CONT). There were increases in all of the molecular markers of mitochondrial content (AMPK, p38MAPK, PGC-1a) in both HIT and CONT but again, no differences between the two modes.
Discussion/Conclusion: This is the first study to demonstrate that both HIT and continuous running induce comparable responses of molecular markers in muscle. The authors state that this could be due to both protocols being relatively intense since there is only a difference of 20% maximal oxygen uptake between the two groups. Another first-time discovery of this study was an increase in stress proteins in response to HIT training indicating a stress response on the body (although this was not significant).
My input: The main power of this study is that the even though the 2 groups performed different types of endurance training, the researchers matched the groups to perform the same intensity, duration, and work performed. Without doing that, it would have been very difficult for them to conclude that HIT and continuous running show similar molecular responses. It bothers me that the intervals were not the usual ones prescribed for exercise protocols in studies (4-6 times of 30 seconds all out cycling/sprinting). My only critique comes with the time. When matching for time, the HIT group exercised for 18 min of sprinting and 18 min of recovery plus a warm up and cool down period totaling 50 min. The continuous running group did 50 minutes without a warm up and cool down. If they took the biopsies after the sprints were finished and not after a cool down, they may have seen responses similar to what they hypothesized. It is also worth mentioning that this study is short-term and it is not yet known the responses to long-term endurance training of this variety. Other than that, this is the first study to show that following a short bout of endurance exercise, there are similar responses in the mitochondrial of muscle between both HIT and continuous running. It seems that for now, both are sufficient in making you a better athlete.
Great, great, great video. John Hawley is a big time name in exercise metabolism research as well as a good friend of our lab. He came to visit us a few months back on a tour of speaking throughout Europe. I got to spend two days with him and I must tell you I gained a month’s worth of knowledge in those two days. If you’re an endurance athlete, you need to watch this.
I’ve been spending a lot of time finishing a manuscript for publication and the head of our lab put me on a new project so that is why I haven’t been posting much. There are some good articles saved in my drafts right now that I’ll post later this week. For now, take some time out of your day, enjoy this video, and most importantly, learn something that will help you with your fitness endeavors.
I received a question about heart rate prescription and how to use it to benefit runners. Basically, how does heart rate work when prescribing exercise?
Let’s go into exercise prescription 101 (and this is perfect because this is something you can use in yourself to set your HR zone, very practical).
The method I use is heart rate reserve, aka the Karvonen method which can be done in three easy steps:
Subtract resting HR from maximal HR to obtain the heart rate reserve (HRR)
Take 60-80% of the HRR
Add each HRR value to resting HR to obtain the target heart rate range
For instance, the person that asked me the question is 21 years old and I do not know her maximal HR but I can estimate it using a crude equation (which I hate) of 220-age. Therefore her maximal HR is 199 beats per min (bpm). Now on to the example with three simple steps:
Assuming her resting HR is around 60 bpm and her maximal is 199 bpm, her HRR is 139.
60% x 139 bpm = 83 bpm and 80% x 139 bpm = 111 bpm
83 bpm + 60 bpm = 143 bpm and 111 bpm + 60 bpm = 171 bpm. Therefore, her target heart rate zone is 143 bpm to 172 bpm.
This is why purchasing a heart rate monitor is a great investment for those interested in running. If you need some help with this don’t hesitate to message me on here.
This one is for the runners, age 16 to 21 and 28 (who writes a title like that?), or for those that like blood (Twilight and True Blood fans, maybe)
Introduction: Hemoglobin is responsible for the transport of oxygen to muscle which is toted as the rate limiting factor of maximal oxygen uptake (VO2 max). It is well known that adult top endurance athletes have higher levels of body weight-related HBmass compared with either nonendurance athletes or untrained persons. However, it is not known whether this can be attributed to genetics or years of training.
Purpose: "To compare absolute and relative levels of HBmass and RCV in adolescent and adult top endurance athletes at different age categories (junior, U23, and elite) with age-matched controls to compare plasama and blood volume (PV and BV) between the aforementioned groups, and, finally, to compare aerobic capacity (VO2max) between the groups."
Results: HBmass was lower in the athletes age 16 group than in older athletes age 21 and 28. There were no differences in HBmass between the older athlete groups or control groups. Athletes age 16 had lower BV than athletes age 21 and 28. Athletes age 16 had lower relative VO2max than athletes age 21 and 28.
Conclusion:"HBmass increases with endurance training between ages 16 and 21 years old but the potential to increase further past this point is limited. There is an assumed genetic predisposition that could play an important role for high HBmass in elite athletes."
My input: Sure it is easy to play the genetic game and assume this is the sole reason for an athletes success but I feel that is not the case in this situation. There were some discrepancies in this study, one being that some of the athletes were not in season during the testing. As the authors state, a longitudinal study of following the same athlete from age 16 to age 21 would be more practical to see if there truly is a difference in hemoglobin rather than age-matching sedentary individuals with athletes. For now, there seems to be a “set” amount of hemoglobin that a person has when they have reached their twenties.
The term free radicals refers to substances that bring about cell damage, ageing, and even cancers. As you know, antioxidants are defense mechanisms against these deleterious events. Free radical production is known to be greater during exercise; hence, supplementation with these antioxidants. However, scientists are starting to discover this could be erroneous, and that for normal physiological functioning in the cells, there needs to be a balance between the free radicals and antioxidants.
Free radicals refer to reactive oxygen species (ROS) and nitrogen species (RNS). These are highly reactive in the body due to an unpaired valence electron (remember drawing your dots around your periodic elements in chemistry class?). The following are the five main radicals found in muscle fibers:
Superoxide - formed in the mitochondria and cytosol
Hydrogen peroxide - can be formed from superoxide via an enzyme.
Hydroxl radical - which is formed when the previous two radicals react with metal ions such as iron or copper.
Nitric Oxide (still want to take those pre-workout “pump” supplements?) - formed by the amino acid L-arginine reacting with the enzyme nitric oxide synthase
Peroxy nitrite - formed in the cytosol when Superoxide reacts with Nitric Oxide
These are all linked with the mitochondrial transport chain activity (responsible for creating ATP for energy) and this is the primary reason they increase during exercise. When created, they wreak havoc on cell membranes, proteins, DNA, and even the ability of the muscle to contract (this one is due to Nitric Oxide. Like I said, do you still want to take your BSN NO-Xplode?)
Although you may think these are your enemies, scientists are starting to suggest that these radicals are necessary for proper exercise adaptations responsible for mitochondrial genesis and capillarization, muscle atrophy, glucose transport ability, increase in blood flow, and the cellular repair processes.
Antioxidants scavenge these free radicals and convert them into unreactive substances. They contain two classes: endogenous and exogenous (those that are consumed ie. Vitamins A, C, E). So let’s get to the negative effects of supplementing with antioxidants:
One group reported significantly greater oxidative damage following half and full Ironman triathalons in athletes who took antioxidants suppelements than in those who did not.
Other groups report interference of oral antioxidant vitamin C on exercise-induced signalling and dependent events such as the expression of an enzyme responsible for mitochondrial volume as well as improvements in insulin sensitivity.
Another group reports that supplementing with vitamin C & E prevented exercise-induced vasodilation by blocking nitric oxide release (okay, maybe you do want to take your “pump” supplement).
Mean improvements in oxygen uptake was 2 times greater and improvements in endurance capacity 7 times greater in humans who received a placebo rather than vitamin C daily via increases in peripheral adaptations to exercise.
Vitamins E & C also have negative effects on muscle recovery from eccentric weight training by delaying the recovery process.
The authors conclude that more research is necessary to better understand dosage, timing, and settings necessary for antioxidant supplementation. Clearly, there needs to be a balance between free radicals and antioxidants. Now, free radicals are not so bad as you thought, n’est-ce pas (that’s French)?
Introduction: Research suggests that the combination of increased body temperature and dehydration leads to decreased cardiac functionality during exercise. The main factor leading to this is a decline in cardiac stroke volume (SV), that is the volume of blood pumped through the left ventricle of the heart during one beat. Exercises physiology 101 tells us stroke volume is the difference between the end diastolic volume (EDV) (period when the ventricle relaxes and fills) and the end systolic volume (ESV) (period when the ventricle contracts and pushes blood throughout the entire body). Therefore, the researchers wished to elucidate the effect of dehydration on left ventricular volume and mechanics at rest and during exercise (bouts of cycling in the heat)
Hypothesis: dehydration would reduce left ventricular mechanics at rest and during exercise.
Results: Dehydration caused a reduction in EDV, ESV, and SV during exercise.
Conclusion: The decline in SV is clearly due to a decrease in left ventricular filling of approximately 20ml. The factor attributed to this is a lower venous return which adds to the EDV in the stroke volume equation (SV = EDV - ESV) as well as a reduced time for the ventricle to fill with blood.
My input:The take home message is simple here, runners and cyclists, drink your water!
Introduction: Adaptations from exercise in skeletal muscle is thought to be induced by the creation of reactive oxygen species (ROS). One such process in the muscle is via an increase in mitochondrial content and density which are the main adapatations that occur in muscle after endurance exercise training. Genes and transcription factors that govern these adaptations include PGC-1alpha, NRF-1&2, Tfam, cytochrome C and it’s enzyme (COX IV) (protein that controls oxidative phosphorylation), and citrate synthase. Antioxidant supplementation (vitamins E, C, and coenzyme-Q10) blocks ROS. Thus, they may block the main cell signaling processes invovled in skeletal muscle adaptations to exercise training.
Results: Antioxidant supplementation in both exercise and sedentary groups reduced the expression of:
PGC-1alpha mRNA & protein
COX IV protein
citrate synthase activity
There was no significant interaction effects between exercise and antioxidants.
Conclusion: Prolonged antioxidant supplementation could potentially impair the endogenous metabolic and redox status (ROS creation) of skeletal muscle in sedentary people and prevent some of the beneficial adaptations to exercise training.
My input: One of the major setbacks of this study is that it was performed in rats and not humans. Other than that, the study design is very well done. As the authors noted, this is long-term antioxidant supplementation of 14 weeks which is necessary for Vitamin E (the antioxidant that they used) to even enter skeletal muscle. In fact, they cite another study that shows that the other popular antioxidant supplement, Vitamin C, is poorly taken up in skeletal muscle. Therefore, it may be to your advantage to not include supplementation with Vitamin E due to its diminishing effects on mitochondrial markers necessary for adaptation to endurance training. Escpecially if you are a beginniner to endurance training.
Background: Typically, there are two ways to increase the amount of intramyocellular lipids (IMCL) that the muscle uses during exercise. One is training in the fasted state and the other is administering a high fat diet (HFD). Another possible way is to train with little ingestion of carbohydrates and thus, low carbohydrate availability during exerise. Therefore, the primary aim of this study was to investigate the effects of edurance training in the fasted state versus training with carbohydrate intake before training sessions on IMCL utilization during a period of a HFD.
Conclusion: the current study clearly demonstrates that the administration of a hypercaloric HFD elevates IMCL content and increases the contribution of IMCL to energy provision in endurance exercise. This effect is not altered by exercise training, independent of whether the training is consistently performed in the fasted state or in the fed state. Interestingly, a fat-rich diet elicits significant IMCL utilization during exercise in type IIa fibers, which otherwise do not exhibit exercise-induced IMCL breakdown in young healthy male volunteers.
My input: The study went into a lot of molecular aspects of how the muscle changed the capacity to use lipids over glyocogen for energy. However, for the scope of this blog, I will not go into the enzymes and other factors they investigated. What I can say though that their methods are sound and it is unique in that the groups also utillized IMCL in Type 2a muscle fibers which are primarily more glycolytic (they use more glycogen) than Type 1 endurance fibers.
Practicality: Perhaps the future of endurance performance will lead athletes to “fat load” as well as carb load for a race. With the given HFD that the scientists administered to the subjects, there clearly is an increase in IMCL content used during exercise over glycogen which has the potential to fuel longer performances in endurance events. While I do not recommend training in the fasted state for races, I think it would be possible to keep this method for those just doing aerobic activity for weight loss purposes. For endurance athletes, feel free to continue ingesting carbohydrates before your events since this study showed that even with the ingestion of carbohydrates, the subjects utilized lipids for fuel. The diet here lasted for 6 weeks but potentially for race purposes could be cut in half to ensure the muscle has the necessary IMCL stores needed to perform at your opitmal level.