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.
Questions?
The most consistent overall finding in endurance and strength-trained athletes who have OTS is a decrease in the maximal lactate concentration while submaximal values are unaffected or only slightly reduced. Glutamine levels are often toted as another possible marker to indicate excessive training stress. However, several problems exist with biochemical testing of overtraining:
Lactate differences can be subtle and depend on the type of exercise test used.
No lactate changes are reported in strength athletes.
Glutamine may decrease with excessive training but low levels are not a consistent finding in OTS.
At first, scientists tried to measure the testosterone/cortisol ratio as a marker of overtraining. This is not possible because this ratio only indicates the actual physiological strain of training. Furthermore, during rest days in endurance-trained athletes, 24 hour cortisol secretion is normal and even comparable to levels of sedentary individuals. Problems exist with hormonal testing as well:
Many factors other than exercise affect blood hormone concentrations such as stress or food intake.
In females, it depends also on the menstrual cycle.
Different hormones are released depending on the modes of training (endurance vs. resistance).
It is noted that there is no definitive way to identify overtraining syndrome (OTS). The only way a coach can do so is by eliminating all other factors that could be causing these symptoms. Once all of the other factors are eliminated, one can then diagnose OTS. The only clear sign is a decrease in performance during competition or training.Currently, there are no simple diagnostic tests to diagnose overtraining and the theories regarding what triggers it are speculative at best.
Taking into account the overlap and still unclear guidelines of overreaching/overtraining, I will now list for you some of the statistics on the prevalence of OTS.
One survey listed a rate of approximately 10% in collegiate swimmers and other endurance athletes.
For elite runners, 60% of females and 64% of males indicated experiencing OTS with numbers being 33% in non-elite adult runners
A recent longitudinal study reported a rate of 29% in age-group swimmers
91% of US collegiate swimmers that reported OTS a first time went on to experience it a second time or more.
To assess OTS, several studies have listed it as being the sum of multiple life stressors, such as training, sleep deprivation, environmental stress, work pressure, and interpersonal problems. Scientists are still looking for a biomaker (in the blood) to measure and determine the existence of OTS.
We know that there must be a balance between appropriate training stress and adequate recovery. Otherwise, this leads to what exercise scientists define as overreaching. Overreaching is an accumulation of training and/or non-training stress resulting in short-term decreases in that capability to perform with or without related physiological and psychological signs and symptoms of maladaptation. Restoration of performance capacity could take several days to several weeks. The difference between this and overtraining is that overtraining is long-term,in which restoration of performance capacity can take several weeks or months. We are looking at solely a time difference between the two.
An example of an athlete who is overreaching would be one that goes to a training camp. The intensity level of the camp is normally very vigorous, which would lead to a temporary decline in performance accompanied later by overall improvement of performance. This can also be noted as functional overreaching. When it gets to the extent of not helping the athlete improve their performance capacity, it then can be described as non-functional overreaching because it leads to stagnation or decreases in performance which will require several weeks or even months to recover.
Overtraining syndrome is considered a syndrome because it takes in to account not just exercise as the main factor but also inadequate nutrition, illness, psychosocial stressors, and sleep disorders.
Below is an example of the difference stages of training and how they relate to overreaching and/or overtraining.
For training to be successful, it must involve an overload on the body but also avoid the negative outcomes of this overload. For the upcoming month up until I leave for the 2013 ACSM conference in Indianapolis (holla atcha boy if you’re going), I will outline for you the mutual American and European “consensus statement” on the Prevention, Diagnosis, and Treatment of Overtraining Syndrome. This will consist of the following sections:
Definitions
Diagnosis
Prevalence
Assessment of overtraining
Biochemistry
Performance testing
Psychology
Physiology
Immune system response
Conclusions
I hope to make clear for you the true scientific evidence on how to diagnosis overtraining and what actually is happening molecularly in the body to bring about these symptoms. If you are a performance coach hoping to better your athletes or someone who wishes to have all the myths surrounding overtraining debunked I promise you the next several posts will be good reads. Until then, all the best!
A fresh article was published in the New England Journal of Medicine yesterday that looks at the most common myths, presumptions, and facts about obesity. What really makes this paper intriguing is that the authors used internet searches to find these. Since some of you might not have assess to the full text, or not have the time to read the entire article, I’ll highlight some of them for you below.
The myths (the authors define myths as “beliefs held true despite substantial evidence refuting them”)
Small sustained changes in energy intake or expenditure will produce more substantial long-term weight changes.
Setting realistic goals for weight loss is important; otherwise, people will become frustrated and likely lose less weight.
Slower gradual weight loss is better than large rapid weight loss in regards to long-term outcomes.
PE classes in school play an important role in reducing or preventing childhood obesity.
A bout of sexual activity burns 100-300 kcal for each participant. (The authors state the actual numbers are more like 14-21 kcal considering the average sexual experience lasts 6 minutes, ouch).
The presumptions (the authors define presumptions as “unproved yet commonly espoused propositions”)
Eating breakfast each day as opposed to skipping it is protective against obesity.
Eating more fruits and vegetables will result in weight loss or less weight gain, regardless of any other behavioral or environmental modifications.
Weight cycling (yo-yo dieting), is associated with increased mortality.
Snacking contributes to weight gain and obesity.
An individual’s environment (parks, recreational playgrounds, etc.) influence the incidence and prevalence of obesity.
THE FACTS (“sufficient evidence to be considered empirically proved”)
This one is for the night-eaters. The ones who find themselves diving into some snacks before bed. You know who you are. Did you know they actually consider this a syndrome though?
Introduction: Night eating syndrome is classified as a delay in the circadian timing for food intake which can alter metabolism and eventually lead to obesity. This syndrome is diagnosed as ingesting a quarter of your total energy for the day after an evening meal up to three times per week. The aim of this study was to see how two weeks of snacking either during the day or at night, without changing meal frequency, would alter energy metabolism in lean young women.
Methods: 13 lean healthy women were recruited with 7 of them being randomly assigned to the snacking during the day group (10:00am) and the other 6 to the snacking at night group (11:00pm). After the two weeks, their energy expenditure and substrate utilization were measured in a whole-room respiratory chamber for one day. The snack consisted of merely 200kcal. Breakfast, lunch, and dinner were given at 9:00am, 2:00pm, and 7:00pm for each group during the two weeks.
Results:
During the afternoon, the group that snacked at night had a significantly higher RQ (using more carbohydrates instead of lipids for energy) and significantly lower fat oxidation. There was a small decrease in 24-hour fat oxidation with the group that snacked at night but this was not statistically significant. LDL cholesterol levels significantly increased as well in the group that snacked at night.
My input: A major strength of this study was the strict control of meal frequency during the two weeks. However, the groups were small and likely underpowered when it came to statistical significance, particularly with the slight decrease in 24-hour fat oxidation which could have been significant had they recruited more volunteers. Regardless, this study shows the importance of nutrient timing and how eating at specific hours of the day can alter our metabolism due to the hormones naturally controlled by circadian rhythms at those hours. It is a necessity for the nutritional science field to step away from calories in versus calories out and start looking more towards nutrient timing at different hours of the day under different conditions (rest versus pre/post-exercise).
Exercising in a dehydrated state can hurt performance. That really is nothing new. However, what is not known is how dehydration can effect substrates being used by the muscle during exercise, particularly in women. So, this one is for you ladies.
Introduction: Did you know that a 2% loss in body mass because of dehydration can elevate HR, core temperature, and the osmolarity of blood plasma? Did you also know that it is said that women thermoregulate less effectively because of a higher core temperature during the same exercise load as men? In fact, females usually experience a quicker rise in core temperature during exercise. Depending on core temperature during exercise, the body can switch between using muscle glycogen or fat. Therefore, you could say that depending on hydration status (which effects core temperature) the body will switch between these two fuel sources as well. But which one? The hypothesis in this study states that women will rely more heavily on whole body carbohydrate oxidation as well as the breakdown of glycogen from muscle during dehydrated exercise.
Methods: Nine women underwent cycling at 65% VO2peak for 120 min. Some received fluids during the exercise and the others did not. It is important to note that before the exercise trial, both groups were properly hydrated. Thus, this study is just examining the consequences of not drinking water during prolonged endurance exercise.
Results: One way to measure whether or not you are using carbohydrates or fat during exercise is by a method called indirect calorimetry, which can provide you with a RER. RER, as I’ve described before, is the respiratory exchange ratio. A RER of 1 means you are using primarily carbohydrates and a RER closer to 0.75 means you are using primarily fat. With that said, the RER of the dehydrated group was significantly higher than the hydrated group, meaning that they were using more carbohydrates during exercise. Likewise, carbohydrate oxidation and total body carbohydrate oxidation was higher in the dehydrated group whereas fat oxidation was lower. The dehydrated group had a significantly higher core temperature and heart rate as well.
Discussion: At this point you would probably like to know why being dehydrated makes the body rely more on carbohydrates rather than fat. There currently is no answer to that; however, the authors suggest three theories behind it.
An augmented nervous system response from the adrenal glands leading to activation of an enzyme that uses glycogen.
Low energy levels that are sensed in cells
Higher intramuscular temperature (which appears to be the primary mechanism)
My input: It is now being understood a little more why dehydration causes performance deficits. Clearly, if you are going to tap into your muscle glycogen faster, you will not be able to perform as long as if you were using primarily fat, which is very energy rich. Still, more needs to be done to understand the exact mechanism for the switch.
Maximize your muscle protein synthesis after weight training, bros. I’ll highlight for you a recent review, which the scientist nerds can read entirely for free here, from Dr. Stuart M. Phillips. I encourage you to take the time to read this one.
Introuction: When scientists talk about muscle protein synthesis they are referring to accruing muscle proteins in an overall net positive balance. That is to say, taking the most basic form of proteins, amino acids, and eventually creating structural muscle (aka hypertrophy). Normally, this is done by adding to already existing contractile machinery of the muscle cells. Researchers suggest that muscle protein synthesis (MPS for now on) is controlled by certain factors including dose, food source, and timing. Let’s see what Dr. Phillips has to say about each of these areas.
“The anabolic window” -Timing
It’s like the holy grail of muscle growth for bros. ”You can’t miss the window or you ruined the entire workout.” Well, that’s a bit exaggerated. Phillips states that, “It is now unequivocal that immediate post-exercise amino acid provision is an effective nutrition based strategy to enhance MPS above rates observed with exercise alone.”Early post-exercise ingestion of amino acids or protein comes from studies that showed that exercise induced increases in rates of MPS are greatest right after exercise; approximately 100-150% above basal rates. However, it may not be that big of a deal if you miss this window. If you look at the figure below, the increase in MPS is in fact greater after exercise but can remain elevated for up to 48 hours. Phillips suggests that consuming protein during these later times as well can be just as beneficial as ingesting protein directly after exercise.
More importantly, Philips discusses the importance of actual exercise intensity and how it relates to muscle failure. This is in lines with a study I touched upon in the past. Looking at yet again another figure below, you can see that groups that take resistance exercise to failure, regardless if they’re using heavy load and low volume, or a light load and high volume had an enhanced amino acid sensitivity to muscle protein synthesis. Let me say that again, IRREGARDLESS OF HOW MUCH WEIGHT YOU USE, as long as you are taking the muscle to failure, you will increase your rates of muscle protein synthesis more than loads not till failure.
Protein source
Let it be noted that whey, egg albumin, soy, casein, and beef have all been shown scientifically to be able to stimulate MPS. However, the Philips group has shown in the past that whey and milk can increase MPS greater than soy products following resistance exercise (this could be due to differences in amino acid profiles and/or digestion kinetics). Why is whey fast-digesting and casein slow-digesting? Every one knows that or will tell you that but do they even have an explanation why? Phillips drops a knowledge bomb with one sentence, “Whey protein is acid soluble and is associated with a very rapid, large, but transient increase in postprandial amino acid availability, while casein coagulates and precipitates when exposed to stomach acid and the resultant dairy curd is slowly released from the stomach resulting in a much more moderate but sustained rise in plasma amino acids.” I love knowledge bombs.
Dose
It is still accepted that in young healthy individuals, approximately 20-25g (which corresponds to approximately 8-10g of essential amino acids) of a rapid digesting protein source (whey or milk) can help maximize stimulation of MPS after resistance exercise.
Weight training and some form of aerobic in the same session. Does it hurt or help?
Introduction: Exercise scientists use the term concurrent exercise when referring to resistance training and aerobic exercise being performed in the same session. These two modes of exercise are different in regards to skeletal muscle profiles and therefore may not be compatible with one another on the cellular level. This is noted as an “interference effect” between the different signals occurring in the muscle. The purpose of this study was to see the effects of a short bout of aerobic exercise on the molecular responses that are supposed to control exercise-specific muscle adaptations to resistance exercise.
Methods: The subjects (9 men) underwent one-legged aerobic exercise in the morning followed by four sets of resistance exercise six hours later. One leg received both aerobic and resistance exercise while the other volunteer’s leg served as a control and only received resistance exercise. Standardized meals were given the day before and the day of to each person and muscle biopsies were taken.
Results: The leg that underwent both aerobic and resistance exercise decreased in muscle glycogen more than the leg that just did resistance (makes sense). A well-known marker of mitochondrial biogenesis was higher in the leg that underwent both training modes. Another marker or muscle size regulation (myostatin) was significantly lower in both the resistance trained leg and in the leg that underwent both modes. Finally, a marker of protein synthesis was higher in the leg that underwent aerobic plus resistance training than the other leg.
Discussion/conclusion: From this study, the authors conclude that concurrent exercise may in fact enhance the skeletal muscle anabolic environment although it is important to note that these differences between legs were modest. An interesting finding is that the well-known marker of mitochondrial biogenesis which is usually increased from endurance training also increased from the resistance trained leg as well. Myostatin inhibits muscle hypertrophy and the finding that both legs decreased myostatin levels shows that both training modes could be effective at increasing muscle mass (although both legs did resistance and this very well may be the main reason for that). In conclusion, the authors state that both exercise types can be scheduled on the same day without compromising important molecular signals in the muscle.
My input: I’ve written about this previously on my blog. This study has similar results to the other in that they conclude resistance training after aerobic training may in fact enhance muscle machinery and subsequently help with performance. Although, the two studies are truly hard to compare due to the fact that this current one waited 7 hours later to do the resistance training, while the previous one I wrote about hit the weights immediately after. A great strength of this study was using one leg for aerobic and resistance exercise and using the person’s other leg as the control that just received resistance exercise. As far as a doing weights after cardio on the same day in the gym, there seems to be no immediate inference effect but this can not yet be extrapolated to more long-term sessions.
“Yo, you gotta take your casein before bed so you stay anabolic. Steady flow of amino acids while I sleep.” How many times have you heard that? How many people have showed you a study validating it? Finally, one exists.
Introduction: It is hypothesized that ingesting protein before sleep could be beneficial to increase plasma amino acid availability, stimulate skeletal muscle protein synthesis and increase whole-body protein balance during sleep. Thus, this group took 16 recreationally active young men and after a single bout of resistance training gave them either casein protein or a placebo before bed. This is the first study to look at the effect of ingesting casein protein immediately before sleep and subsequently seeing how it effects protein synthesis and protein balance overnight.
Methods: All subjects received a standard meal the evening before the test and a standardized diet throughout the experimental day. Tracers were implemented in this study which allows for measurements of certain molecule in the blood. A tracer is a molecular that contains radioactive isotopes that can be measured by machines to see the overall flux of the molecule throughout the body. In this study, the researchers traced radioactive amino acids (it’s safe because they are stable isotopes, trust me)throughout the night following the exercise protocol. The protocol consisted of leg extensions and leg press and was performed three hours before bed.
Results: After ingestion of protein before sleep, the total essential amino acid concentrations in the plasma increased rapidly and stayed higher throughout the night as compared to the placebo group. For the tracer, the amount of protein available from the plasma-derived amino acids was 50% higher in the protein ingestion group at time 7.5hrs after sleep compared to the placebo. Finally, whole-body protein synthesis rates were higher in the protein group versus the placebo group.
Discussion: It is evident that the casein protein was in fact digested and absorbed normally throughout the night because the tracer used in this case came directly from the casein protein shake. Not only did they observe and increase in whole-body protein synthesis with the blood plasma samples, but the group also showed an increase in synthetic rate by taking muscle biopsies as well. Of course this could not be confirmed throughout the night but only before bed otherwise the person would not be able to sleep when the biopsy was being performed. Also, it is important to keep in mind that this is an acute (one-time) bout of resistance training and not chronic (long-term).
Conclusion:
Casein protein at bedtime is effectively digested and absorbed which would lead to an increase in available amino acids from blood plasma overnight
Casein protein at bedtime stimulates muscle protein synthesis rates which would increase overnight protein balance.
My input: This study highlights the practicality and necessity of using tracers. Without labeling the amino acid in the casein drink, it would be difficult to tell whether or not the amino acids in the plasma are coming from inside the body (endogenous) or what was ingested (exogenous). The authors clearly show in the figures that the rise in the amino acids come from the isotope labelled casein source that they provided. Now for the first time, you can all finally tell your friends it is a good idea to supplement with casein before bed because science suggested it.
