VIAGRA: THE LATEST RESEARCH ON EXERCISE PERFORMANCE

http://musculardevelopment.com/articles/chemical-enhancement/3703-viagra-the-latest-research-on-exercise-performance.html#.VFeTM4ehYW0


Written by Thomas Fahey

Viagra has moved from the bedroom to the locker room. The buzz on the street was that Yankee superstar Roger Clemens had a bottle of Viagra disguised as vitamin pills stashed in his locker. Last May, Italian cyclist Andrea Moletta was removed from the Giro d'Italia after police found a cache of Viagra and syringes in his car. Not surprisingly, the tabloids had a field day following these incidents and charged that legions of athletes in baseball, football, bodybuilding and Olympic sports took Viagra to boost endurance and physical performance. The World Anti-Doping Association (WADA) considered banning Viagra before the Beijing Olympics, but backed off because it had no evidence that the drug provided a competitive advantage.

What do firm erections have to do with sports like bodybuilding? Viagra improves blood flow control. Muscles need plenty of blood to remove wastes and deliver energy, oxygen, and hormones. Increased blood flow could speed the delivery of key amino acids to the muscles, which would promote muscle protein synthesis and growth. It seems reasonable that Viagra could boost performance and that bodybuilders might take it.

A Stanford University study by Ann Friedlander and colleagues published in 2006 triggered the Viagra craze among athletes. The researchers found that Viagra improved cardiovascular capacity during exercise on a stationary bike at a simulated altitude of 12,710 feet but not at sea level. Viagra increased cardiac output (blood pumped by the heart per minute), stroke volume (blood pumped by the heart per heartbeat), and oxygen saturation (percent of red blood cells carrying oxygen). Cycling performance at altitude improved by 15 percent. The drug increased exercise capacity by reducing blood pressure in the lungs, which increases at high altitude. Not all subjects benefited from the drug— there were responders and non-responders. Other researchers confirmed the Stanford results and also showed that Viagra improved exercise capacity in people suffering from lung disease and heart failure.

Bodybuilding is an incredibly difficult sport that requires years of backbreaking work to achieve success. Most athletes will do whatever it takes to increase muscle mass and win contests. It’s understandable that they take Viagra: it’s not on any banned substances list; it’s readily available; it has few side effects; and it might provide a significant edge. The fact that it only worked in some people above 12,000 feet altitude and didn’t work at sea level was somehow lost in the shuffle.

Why Viagra Might Be an Effective Bodybuilding Drug

 Viagra (sildenafil) is one of three FDA-approved, erection-promoting drugs called PDE-5 inhibitors that also include tadalafil (Cialis) and vardenafil (Levitra). They work by inhibiting the PDE-5 enzyme, which then increases the concentration of a chemical called nitric oxide that promotes blood flow to the penis and other tissues throughout the body. Blood vessels, smooth muscle, skeletal muscle, blood platelets, and lung tissue contain this and similar PDE enzymes. In addition to promoting erections, PDE-5 inhibitors decrease systemic blood pressure, lung blood pressure, lung resistance, and promote coronary (heart) blood flow. Long-term use improves endothelial function, which is critical to blood flow control.

 The drugs reduce stress in pressure-overloaded hearts, which is important for bodybuilders because large increases in muscle tension restrict blood flow to working muscles. Increasing muscle blood flow during training could increase muscle strength, size, and fitness, while reducing stress on the heart. They also improve lung blood flow and boost quality of life in patients suffering from lung disease.  These drugs have promising pulmonary and cardiovascular applications that go beyond firm erections.

To date, no study has found that Viagra improves exercise performance in athletes at sea level. The drug is helpful in people with blood pressure limitations that interfere with oxygen transport to the tissues. For example, lung blood pressure increases substantially in some people at altitude, which makes it difficult to move oxygen from the air into the bloodstream. Viagra reduces lung blood pressure, which enhances oxygen consumption and the capacity to exercise.

A small percentage of elite endurance athletes have a performance imbalance between the heart and lungs. Their powerful hearts exceed breathing capacity, which causes a mismatch between the pulmonary and cardiovascular systems. Viagra might increase lung function to match their superior heart capacity, which could give them a significant competitive advantage. However, other athletes might benefit as well.

Physical inactivity, diets high in saturated and trans-fats and simple sugars, and reduced muscle mass impair the ability of insulin receptors to regulate carbohydrates, amino acids (building blocks of proteins) and fats. Insulin sensitivity affects the health of the endothelium, the cells that line the blood vessels. These cells release nitric oxide (NO) that opens blood vessels in tissues throughout the body. Long-term use of Viagra has training-like effects on the endothelium, which increases its capacity to release NO. While the Viagra-induced improvements in blood flow control might be greater in men suffering from poor metabolic health, they might also promote blood flow in the muscles and nervous systems in bodybuilders and physically fit adults. Viagra doesn’t appear to increase endurance performance following short-term use, but it might have long-term benefits in well-trained athletes.

Long-term use of Viagra might also benefit metabolic capacity by enhancing blood sugar control and increasing testosterone levels. Scientists from Vanderbilt University School of Medicine found that the drug helped restore energy balance and boosted insulin metabolism in mice fed high-fat diets (compared to a placebo). The animals showed lower blood sugar and insulin levels and improved blood sugar regulation after a high-carbohydrate meal. They also lost bodyweight and fat mass during the 12-week study. In humans, long-term use of Viagra increased the production of the blood vessel controlling chemical nitric oxide, which has strong links to insulin metabolism.

 Viagra boosts testosterone, which is a critical hormone for increasing muscle mass, strength, and aggressiveness— all critical for athletes. Testosterone is linked to sexual arousal and performance. Middle-aged men who take testosterone supplements improve sex drive, capacity for erections, self-confidence, and aggressiveness. Italian researchers found that total and free testosterone levels increased by 50 percent in men treated for erectile dysfunction with Cialis or Viagra. It’s not clear whether these drugs increased testosterone directly or if they increased it indirectly through increased sexual activity. Frequency of sexual intercourse was greatest in men who took Cialis (a longer-acting PDE-5 inhibitor), which makes it the preferred drug for men in stable relationships. Men who had the most sex also had the highest testosterone levels.

Factors affecting testosterone include psychological health, diet, exercise, and sexual activity. Men who have a lot of sex are happier, more confident, and have better-functioning sex organs than men who don’t. The sex organs— like your muscles— function best when you use them, so Viagra might give them a boost. We don’t know if Viagra increases testosterone levels in healthy, fit bodybuilders.

Long-term use of Viagra might also increase muscle strength, power, and size by triggering biochemical pathways that increase protein synthesis and prevent protein breakdown in muscle cells. As discussed, Viagra increases nitric oxide (NO) release by the blood vessels. NO helps turn on protein synthesis in muscles, particularly when the fibers are under tension or stretch. NO also triggers the formation of satellite cells that add mass to the muscle fibers. To date, no study has shown that Viagra and similar drugs have steroid-like effects in athletes, but we can infer from biochemical studies that they might.

 Viagra is on WADA’s Radar

WADA first took notice of Viagra following the Stanford University study and reports that the drug was given to greyhounds to improve running performance. They were concerned that Viagra might improve performance at lower altitudes and provide a competitive advantage at venues such as Denver, Mexico City, or areas hosting the Winter Olympics. The margin of victory is often a matter of seconds in endurance events in cycling and cross-country skiing, so a drug that provides even a small advantage could be very significant.

WADA is currently funding a series of studies at Marywood University in Scranton, Pennsylvania and at the University of Miami, to determine the effects of Viagra on exercise capacity and performance at sea level, moderate altitudes, and in polluted environments. They also want to know if the drug has different effects in men and women. The results of these studies will determine whether Viagra ends up on the banned substances list.

 Will Viagra Make You a Superstar?

 Viagra can help make you a sexual Olympian, provided that you have game, good hygiene, and a reasonably firm body. It definitely won’t get you a spot on the Yankee’s roster or the Olympic team if you don’t have the talent. To date, no study has found that Viagra improves exercise capacity at sea level. However, long-term use of the drug might promote muscle protein synthesis and improve metabolic fitness enough to have a small effect on endurance or strength. Viagra and similar drugs have side effects; so don’t use them without following the advice of a physician. We need many more studies before we can adequately assess the effects of these drugs on exercise capacity and athletic performance.

References:

            Ayala, J. E., et al. Chronic treatment with sildenafil improves energy balance and insulin action in high fat-fed conscious mice. Diabetes, 56: 1025-1033, 2007.

            Betters, J. L., J. H. Long, K. S. Howe, R. W. Braith, Q. A. Soltow, V. A. Lira, and D. S. Criswell. Nitric oxide reverses prednisolone-induced inactivation of muscle satellite cells. Muscle Nerve, 37: 203-209, 2008.

            Di Luigi, L., et al. The long-acting phosphodiesterase inhibitor tadalafil does not influence athletes' VO2max, aerobic, and anaerobic thresholds in normoxia. Int J Sports Med. 29:110-115, 2008.

Faoro, V., et al. Effects of sildenafil on exercise capacity in hypoxic normal subjects. High Alt Med Biol, 8:155-163, 2007.

            Ghofrani, H. A., et al. Sildenafil increased exercise capacity during hypoxia at low altitudes and at Mount Everest base camp: A randomized, double-blind, placebo-controlled crossover trial. Ann Intern Med, 141:169-177, 2004.

            Hsu, A. R., K. E. Barnholt, N. K. Grundmann, J. H. Lin, S. W. McCallum, and A. L. Friedlander. Sildenafil improves cardiac output and exercise performance during acute hypoxia, but not normoxia. J Appl Physiol, 100:2031-2040, 2006.

            Jackson, G. Hemodynamic and exercise effects of phosphodiesterase 5 inhibitors. Am J Cardiol, 96:32M-36M, 2005.

            Lewis, G. D. et al. Sildenafil improves exercise capacity and quality of life in patients with systolic heart failure and secondary pulmonary hypertension. Circulation, 116:1555-1562, 2007.

            Perimenis, P. Sildenafil for the treatment of altitude-induced hypoxaemia. Expert Opin Pharmacother, 6:835-837, 2005.

            Ricart, A., et al. Effects of sildenafil on the human response to acute hypoxia and exercise. High Alt Med Biol,6:43-49, 2005.

            Rubin, L. J. and R. Naeije. Sildenafil for enhanced performance at high altitude? Ann Intern Med, 141:233-235, 2004.

            Siepmann, M., R. Rauh, O. Dill, M. W. Agelink, and M. Mueck-Weymann. The effects of sildenafil on heart rate variability in healthy subjects. J Cardiovasc Pharmacol, 50:598-600, 2007.

            Snyder, E. M., T. P. Olson, B. D. Johnson, and R. P. Frantz. Influence of sildenafil on lung diffusion during exposure to acute hypoxia at rest and during exercise in healthy humans. Eur J Appl Physiol, 2008.

            Spring, R. M., et al. Sildenafil for pulmonary hypertension: Dose-dependent improvement in exercise performance. Pulm Pharmacol Ther, 21: 516-521, 2008.

            Tatsumi, R., et al. Satellite cell activation in stretched skeletal muscle and the role of nitric oxide and hepatocyte growth factor. Am J Physiol Cell Physiol, 290:C1487-1494, 2006.

            Wozniak, A. C. and J. E. Anderson. Nitric oxide-dependence of satellite stem cell activation and quiescence on normal skeletal muscle fibers. Dev Dyn, 236:240-250, 2007.

            Wozniak, A. C. and J. E. Anderson. The dynamics of the nitric oxide release-transient from stretched muscle cells. Int J Biochem Cell Biol, 41:625-631, 2009.

Testosterone and the Heart— A New Era?

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If you are a man, at some point in your life you are likely to be a candidate for hormone replacement therapy. As we age, our testosterone levels decline, and with them often a number of physical and psychological characteristics. It has long been understood that low testosterone levels can be linked to reduced libido, sexual dysfunction, diminished energy, and a reduced overall sense of well-being. For these reasons, replacement therapy with testosterone drugs is a strong and steadily growing area of medicine for aging men.

Beyond these basic facts, testosterone remains a controversial drug. Its abuse is linked to changes in the body that may increase the likelihood of cardiovascular disease, and partly because of this, the potential benefits and risks of testosterone replacement therapy have long been the subject of much debate. Is this therapy actually safe?

In recent years, evidence has been surfacing that testosterone replacement may actually reduce cardiovascular disease risk. Usually isolated in scope, these papers concern many favorable changes in cardiovascular health markers, such as the management of triglycerides and cholesterol. I believe I’ve discussed some of these papers in this column before. Hopefully, a paper published in the Journal of Andrology will further this discussion a great deal.

This 37-page report entitled “The Dark Side of Testosterone Deficiency” is the third in a series of papers covering the potential benefits of hormone replacement therapy in men.¹ It specifically reviews the mounting evidence in favor of the use of testosterone for reducing heart disease risk, addressing the most detailed and relevant studies on the subject. This is the most extensive paper on testosterone therapy and heart disease to date, and covers several specific potential benefits.

[ANDROGEL PICTURE] Growing evidence suggests that testosterone administration may actually reduce the risk of heart disease in older men.

Serum Lipids

One of the first potential benefits of testosterone replacement therapy (TRT) reviewed in this paper is the management of triglyceride and cholesterol levels. As detailed in a growing number of studies, testosterone replacement therapy consistently improves the lipid profile in men with hormone deficiency. The most consistent endpoints of improvement appear to be a reduction in total cholesterol, a reduction in LDL (‘bad’) cholesterol, and a lowering of serum triglycerides. The improvements in lipid profile appear to be more pronounced in older men, although both young and old populations tend to show improvements in serum lipids when testosterone is given to correct a deficient state.

The effect of TRT on HDL (‘good’) cholesterol levels is less consistent. Studies giving testosterone gels, patches, or the longest-acting ester (testosterone undecanoate) tend to show improvement or no consistent effect on HDL. Studies with the more common esters such as cypionate and enanthate tend to show minor decreases in HDL during therapy, likely owing to the brief supraphysiological peaks for several days after administration. Note that HDL is often improved when TRT is combined with exercise and other lifestyle modifications.

Inflammatory Markers

Androgen deficiency is associated with an increase in certain inflammatory markers that can support the progression of atherosclerosis. Testosterone replacement therapy has been shown to reduce some of the same inflammatory mediators, specifically TNF-alpha (tumor necrosis factor-alpha) and IL-1B (interleukin-1beta).

Inflammation in the vascular system is an especially important concern with heart disease. For one, vascular inflammation is associated with the deposition of arterial plaque, a key component of this disease. Inflammation of the blood vessels may also damage the arteries, making them both thicker and weaker. Scarring may be noticed, and blood flow may be reduced. All of this can restrict blood flow and reduce the heart’s blood pumping capacity.

By helping to reduce the production of TNF-alpha and IL-1B, hormone replacement therapy may reduce inflammation, vascular damage, and the chance for atherosclerosis. Again, instead of seeing a neutral or ‘negative’ effect, we find a specific improvement in the cardiovascular disease risk profile with the administration of this drug.

Abdominal Obesity, Insulin Resistance

A growing number of studies have linked androgen deficiency to insulin resistance, as well as increased abdominal obesity. These two factors are also common with men suffering from cardiovascular disease, and may directly contribute to (among other things) endothelial cell dysfunction and vascular damage. Androgen substitution has been shown in several studies to reduce midsection fat deposits, increase glucose tolerance, and improve the overall metabolic state. It has additionally been postulated that due to the important role of testosterone in managing insulin sensitivity, androgen deficiency may be a contributing factor to adult-onset (type 2) diabetes. Likewise, the substitution of testosterone in aging men with hypogonadism might reduce the likelihood of developing diabetes.

Endothelial Function

The endothelium is a layer of cells that lines the blood vessels throughout the entire circulatory system. These cells are responsible for managing the passage of some materials in and out of the blood vessels, and supporting the flow of blood through the system. Endothelial cells play a role in vasoconstriction and vasodilation, they regulate certain inflammatory processes, and they’re involved in blood clotting and in supporting the formation of new blood vessels. Endothelial dysfunction is linked to androgen deficiency in men, and may result in elevated blood pressure (hypertension), vascular ‘stiffness,’ and significantly increased risk of cardiovascular disease. Likewise, replacement of testosterone in men with a deficiency has been shown to improve endothelial function, blood vessel dilation, arterial vasoreactivity, and blood flow.

One additional important ‘endpoint’ of improvement to this therapy appears to be an increase in endothelial progenitor cell activity, which helps repair damage to the vascular system.

Conclusion

Traditionally, most physicians are extremely cautious with testosterone drugs. Many family doctors are very willing to prescribe estrogens to their female menopausal patients complaining of symptoms such as sexual dysfunction, but when it comes to their male patients with similar complaints, the response is often different. Many of these same physicians are much more willing to prescribe a drug like Viagra than the basic male androgen testosterone. Some mistakenly consider testosterone to be ‘too dangerous’ to give most of their patients, and reserve its use for extreme cases. And when testosterone is considered, it is given only for a very narrow and specific set of psychological or physical symptoms.

Of course in the era of AndroGel, some physicians are much more enlightened. Still, the troubling common fear of this hormone remains. Perhaps this is changing, and perhaps the accepted set of symptoms and therapies for prescribing this hormone is changing.

It seems clear that we can no longer paint testosterone as simply a ‘bad’ hormone for the cardiovascular system. While excessive high-level elevations of this hormone may indeed damage an individual’s cardiovascular health, we have strong evidence that within a certain physiological range, it may also protect the cardiovascular system from some of the same health issues. As such, its replacement may indeed turn out to be very important medical intervention for millions of men across the country, helping us to not only live better— but also live longer.

After all this time, it appears that this very controversial hormone, the same steroid demonized in the media, might actually help reduce the risk of cardiovascular disease in aging male patients. The study we reviewed this month is, likewise, something all men should take to heart— literally.

Reference:

1.The Dark Side of Testosterone Deficiency: III. Cardiovascular Disease. Traish AM, Saad F et al. Journal of Andrology, April 2, 2009. ePub, Ahead of Print.

Know Your Gear! William Llewellyn’sANABOLICS 9th Edition (2009) is available NOW. Order your copy of this 800-page anabolic steroid reference guide today by calling 888-918-7888 or visiting www.AnabolicsBook.com.

Understanding the Oxidative Energy System and How to Properly Feed It

http://breakingmuscle.com/nutrition/understanding-the-oxidative-energy-system-and-how-to-properly-feed-it

Kevin Cann

In previous articles I discussed the fueling of two of our energy systems - our ATP-PC systemas well as glycolysis. In the final installment of this series, we are going to dive into fueling the oxidative system. This is our primary source of ATP at rest and during longer duration physical activity. Understanding this energy system and how to fuel it can help increase performance in endurance events.

Enough Calories for the Oxidative System

The oxidative system is also known as the Krebs cycle and the citric acid cycle. In this system, carbohydrates and fats are the primary energy sources converted into ATP and this process takes place in the mitochondria of the cell. Protein is typically not utilized during this energy system except during bouts of exercise greater than ninety minutes and during starvation.¹ This means it is critical to be taking in enough calories of carbohydrates and fats to fuel endurance activity.

Low calorie eating and long, slow distance running are common amongst individuals attempting to lose weight. During these bouts of starvation or prolonged exercise we will use our protein to fuel activity. Our greatest source of protein in the human body is our muscle tissue. If you do not eat enough or work out too much, you run the risk of burning up muscle tissue for energy. This process is known as gluconeogenesis.

Too few calories from under eating or from over exercising can also lead to weight gain. Going too low in calories can decrease our thyroid hormone T3 by as much as 66%.² This puts our body into an energy conservation mode and can make weight loss extremely difficult. Having adequate fats and carbohydrates in the diet can help avoid these negative situations.

Carbohydrates and Fats

At rest, fats contribute 70% to energy needs and carbohydrates about 30%. As we learned from previous articles, as intensity increases we shift to using more carbohydrates for energy. As the activity becomes longer in duration (more than three minutes), we shift to using fats as the primary source of energy. The key to this transition is the amount of oxygen present in the blood.

If we have enough oxygen present in the blood, then pyruvate, the end product of glycolysis, is shuttled to the mitochondria and we enter the oxidative energy system. In this process we get six molecules of NAHD and two molecules of FADH2. These substrates are then brought through the electron transport chain where they are used to convert ADP into ATP. This process is known as oxidative phosphorylation. This yields us approximately 38 ATP from one molecule of glucose. This is a much higher energy yield than the other two energy systems.

Our stored fat can also be utilized in the oxidative system. Free fatty acids can be broken down into acetyl-CoA and hydrogen. The acetyl-CoA enters the Krebs cycle and the hydrogen atoms are brought through the electron transport chain and ATP is produced. A limiting factor of all this is oxygen uptake.

The Importance of Oxygen

Oxygen uptake is literally a person’s ability to take in and use oxygen. The beginning of all activity is anaerobic, or without oxygen. This is roughly the first three minutes of activity. After this three minute period we are left with what is known as an oxygen deficit. This is why we continue to breathe heavily once we stop our activity. We need to replenish the oxygen debt. Remember that enough oxygen being present is what allows us to utilize our long duration energy system. Once the oxygen deficit becomes too high, we will continue to utilize anaerobic mechanisms to fuel activity and blood lactate concentrations will raise and cause fatigue.

This is why it is important to train in all energy systems. Training long, slow distance can help us build an aerobic base and help strengthen this oxidative system by increasing your VO2 max, which is our ability to utilize the oxygen we take in. Interval training can help us recover by increasing our body’s ability to decrease blood lactate levels as well as making us more proficient at replenishing our oxygen debt.

Ketone Bodies

Another form of usable fats for energy are ketone bodies. Ketone bodies can be found in medium chain triglyceride fats. These are unique because they do not require bile salts for digestion. Instead they are shuttled to the liver, converted to ketones, and immediately used by cells. Research has been done on the use of ketone bodies in endurance training.

Depletion of muscle glycogen, our stored sugar reserves, leads to fatigue. Some research suggests supplementation with medium chain triglycerides can stave off fatigue by sparing our stored glycogen.³ This is most likely due to the easy nature in which medium chain triglycerides are converted to usable energy. Medium chain triglycerides can be supplemented in the diet by using MCT oil or by cooking more with coconut oil. Half of the fats in coconut oil are medium chain triglycerides. The evidence in the literature is contradictory on the use of medium chain triglycerides, but I have seen it work for a number of clients.

In conclusion, if we are working out for short term, high intensity bouts we need to make sure we ingest enough carbohydrates to fuel activity and to replenish our stored glycogen for recovery. As we exercise longer there is a shift to utilizing fats as a primary source of energy. Making sure we are getting enough fats in our diet to fuel longer duration activity can help improve performance. Also, adding medium chain triglycerides to the diet may help spare stored glycogen due to the easy conversion to usable energy in the form of ketones. It is important to keep in mind that not everyone is the same. Some people do well higher carb and others do well higher fat. Planning the best diet for you and your performance will take some tinkering around, but at least now with an understanding of how our energy systems work you can have a good starting point.

References:

1. Thomas Baechle and Roger Earle. Essentials of Strength Training and Conditioning. Human Kinetics (2008).

2. Wadden, TA et al., Effects of very low calorie diet on weight, thyroid hormones, and mood. International Journal of Obesity (1990). Accessed on October 11, 2013. 

3. Van Zyl, CG et al., Effects of medium-chain triglyceride ingestion on fuel metabolism and cycling performance. Journal of Applied Physiology (1996). Accessed on October 11, 2013. 

Krebs cycle graphic by RegisFrey (Own work) [CC-BY-SA-3.0 or GFDL], via Wikimedia Commons.

Energy pathways chart property of Breaking Muscle.

Other photos courtesy of Shutterstock.

Understanding Energy Systems: ATP-PC, Glycolytic, and Oxidative, Oh My!

http://breakingmuscle.com/health-medicine/understanding-energy-systems-atp-pc-glycolytic-and-oxidative-oh-my

Tom Kelso

Human bioenergetics is an interesting topic. However, energy systems function is understood by few and/or can be confusing to many. Open a quality exercise physiology text and it can leave you saying “huh?” when reading about aerobic, anaerobic, and immediate energy metabolism. It can get even worse when sifting through all the biochemical processes.

Is it important to be able to explain the chemical breakdown of the oxidative Krebs cycle or anaerobic glycolysis if you’re a coach or an athlete in training? Not really.However, knowing the basics of how we generate energy can be helpful in understanding how we fatigue and what training measures can be used to minimize it. Let’s get going as simply as possible. I will do my best, but some “high-tech” discussion is necessary.

The first thing to remember is that ANY muscle contraction/force exertion is due to a molecule called adenosine triphosphate (ATP). When an ATP molecule is combined with water the last of three phosphate groups splits apart and produces energy. This breakdown of ATP for muscle contraction results in adenosine diphosphate (ADP). The limited stores of ATP must be replenished for work to continue; so chemical reactions add a phosphate group back to ADP to make ATP.

How ATP Is Produced

Take three different activities and put them on a continuum. On one end would be a quick, explosive burst such as throwing a punch. On the other end would be an extended, lower-level event such as walking five miles. Between the two could be anything: an intense twenty-second activity, one minute of constant force exertion, or a five-minute event with varied intensities of effort.

As you can see, there are many expressions of energy output depending on the amount of force required and the length of the activity. What then, is the energy source for activities that fall on the continuum at various points? This is the essence of bioenergetics - so many possibilities and so many factors involved.

The Three Energy Systems

Conventionally, there are three energy systems that produce ATP: ATP-PC (high power, short duration), glycolytic (moderate power/short duration), and oxidative (low power/long duration). All are available and “turn on” at the outset of any activity. What dictates which one (or two) is relied upon the most is the effort required.

Take home point: ATP must be present for muscles to contract. It can be produced via the ATP-PC system, the glycolytic system, or the oxidative system. If depleted, it must be replenished if further muscle contraction is to continue.

Perform an explosive, one-time movement such as a standing long jump or vertical jump and you exert maximal effort, but guess what? You will not become fatigued from this single exertion. However, jump multiple times and eventually you will become fatigued. Going all-out for as long as possible will deplete immediate ATP stores, then glycolytic stores. Continuing effort must be fueled by the oxidative system at a lower intensity, all other factors being equal. The most pure aerobic activity that exists is sleeping or lying comatose.

The ATP-PC Energy System – High Power/Short Duration

ATP and phosphocreatine (PC) compose the ATP-PC system, also sometimes called the Phosphogen system. It is immediate and functions without oxygen. It allows for up to approximately 12 seconds (+ or -) of maximum effort. During the first few seconds of any activity, stored ATP supplies the energy. For a few more seconds beyond that, PC cushions the decline of ATP until there is a shift to another energy system.It is estimated the ATP-PC system can create energy at approximately 36 calories minute.

Examples: a short sprint, lifting a heavy resistance for three repetitions, or pitching a baseball.

The Glycolytic System – Moderate Power/Moderate Duration

Now it becomes more complicated as energy demands shift to this system. The glycolytic system is the “next in line” tool after the ATP-PC system runs its course. Dietary carbohydrates supply glucose that circulates in the blood or is stored as glycogen in the muscles and the liver. Blood glucose and/or or stored glycogen is broken down to create ATP through the process of glycolysis. Like the ATP-PC system, oxygen is not required for the actual process of glycolysis (but it does play a role with the byproduct of glycolysis: pyruvic acid). It is estimated glycolysis can create energy at approximately 16 calories per minute.

Here is where it gets interesting. After maximum power declines around 12 seconds, further intense activity up to approximately 30 seconds results in lactic acid accumulation, a decrease in power, and consequent muscle fatigue. This high, extended effort is labeled “fast” glycolysis. Exerting further effort up to approximately 50 seconds results in another drop in power due to the shift in dependence on the oxidative system. Bottom line: it is getting tougher.

Example: think of an all-out sprint, to a slower jog, to an eventual walk. That is the progression of the three energy systems when going all-out.

Enter “slow” glycolysis into the discussion (warning: more science jargon ahead, but hang in there). Recall the byproduct of glycolysis is pyruvic acid. In fast glycolysis, more power can be generated, but pyruvic acid is converted to lactic acid and fatigue ensues quickly.Slow glycolysis is different. Relatively less power is generated, but pyruvic acid is converted to acetyl coenzyme A (acA), fed through the oxidative Krebs cycle, more ATP is produced, and fatigued is delayed. Thus, extreme fatigue can be avoided (but relatively less-intense effort can continue to be expressed) in slow glycolysis as compared to fast glycolysis.

Examples: any moderately-long runs such as 200-400 yards, a 1:30 effort of all-out MMA maneuvers, or a one-minute full-court press - offense display - and another full-court press effort in basketball.

The Oxidative System – Low Power/Long Duration

Your maximal effort was fueled initially by the ATP-PC, but your performance declines. Continued effort results in further decline, either via fast glycolysis (quick decline) or slow glycolysis (slower decline). You’re now entering the complex world of the low power but longer duration oxidative system, which is estimated to create approximately 10 calories per minute.

Examples: 6-mile run, low-level manual labor on an eight-hour work shift, or a 3-mile walk.

The effort demand is low, but ATP in this system can be produced three ways:

1. Krebs cycle
2. Electron Transport Chain
3. Beta Oxidation.

Let me explain the science, and then I’ll get back to you in plain English. The Krebs cycle is a sequence of chemical reactions that continues to oxidize the glucose that was initiated during glycolysis. Remember the acA? It enters the Krebs cycle, is broken down in to carbon dioxide and hydrogen, and “poof” two more ATP molecules are formed.

Here is the problem: the hydrogen produced in the Kreb’s cycle and during glycolysis causes the muscle to become too acidic if not tended to. To alleviate this, hydrogen combines with the enzymes NAD and FAD and is sent to the electron transport chain. Through more chemical reactions in the electron transport chain, hydrogen combines with oxygen, water is produced, and acidity is prevented.Notice this takes time due to the need of oxygen, which is why the oxidative energy takes a while and intensity of effort declines (i.e., all-out sprinting becomes slow jogging/walking).

The Krebs cycle and the electron transport chain metabolize triglycerides (stored fat) and carbohydrates to produce ATP. The breakdown of triglycerides is called lipolysis. The byproducts of lipolysis are glycerol and free fatty acids. However, before free fatty acids can enter the Krebs cycle they must enter the process of beta oxidation where a series of chemical reactions downgrades them to acA and hydrogen. The acA now enters the Krebs cycle and fat is metabolized just like carbohydrates.

In Plain English:

Due to the time-line, the oxidative system provides energy much more slowly than the other two systems, but has an almost unlimited supply (in your adipose sites - yeah, that stuff you can pinch!). The oxidative system by itself is used primarily during complete rest and low-intensity activity. It can produce ATP through either fat (fatty acids) or carbohydrate (glucose).

Because fatty acids take more time to breakdown than glucose, more oxygen is needed for complete combustion. If efforts are intense and the cardiovascular system cannot supply oxygen quickly enough, carbohydrate must produce ATP. However, in very long duration activities (i.e., marathons), carbohydrates can become depleted and the body looks to fat as the energy producer.

A Few Words on Protein

In extended activities protein can be used as a “last resort” for energy production (in rare cases where carbohydrates are depleted and stored fat is minimal). In such cases, it can supply as much as 18% of total energy requirements. The building blocks of protein - amino acids - can be either converted into glucose (via gluconeogenisis) or other sources used in the Krebs cycle, such as acA. But understand protein cannot supply energy at the same rate as carbohydrates and fats, thus it’s basically a non-issue).

Programming for the Energy Systems

It is estimated that the ATP-PC and glycolytic systems can be improved up to 20% and the oxidative system by a whopping 50% (but in untrained subjects only). Regardless, sport-specific conditioning plans and optimal nutritional intake need to be implemented. But be aware of the reality of genetics: your unalterable muscle fiber composition plays a huge role. If you possess predominately slow type I fibers (endurance) or fast type II fibers (strength), you can only do so much. For me, this explains why I never got a sniff of any national-level competitions back in the early 1980s.

What else can you do to maximize each energy system? I will provide specific recommendations in a forthcoming article. Stay in touch.

Understanding Glycolysis: What It Is and How to Feed It

 http://breakingmuscle.com/health-medicine/understanding-glycolysis-what-it-is-and-how-to-feed-it

Kevin Cann

In a previous article I explained the first of three energy systems, our ATP-PC system. In this article I would like to dive into glycolysis. Glycolysis takes over as the main energy system in activities that are slightly longer in duration and have a smaller energy demand than our ATP-PC system. Many of us train in this pathway and many sports require a high demand of the glycolytic pathway for fuel. Understanding the system and substrates involved can help increase you performance in these areas.

Glycolysis is the breakdown of carbohydrates. It lasts from roughly ten seconds into physical activity up to about two to three minutes. The energy for glycolysis comes from glucose, or our stored form of glucose - glycogen. Glycogen is stored in muscle tissue and the liver, and the average person holds about 1,500-2,000 calories of stored glycogen. Broken down there are about 100g of glycogen in the liver and upwards of 400g of stored glycogen in muscle tissue.

Glycogen in the Liver and Muscles

Storing glycogen in the liver and muscles serves an important function in human metabolism. Our liver is the organ responsible for controlling blood sugar between meals. When insulinlevels fall, the opposing hormone, glucagon, is released. Glucagon stimulates the liver to release some of its stored glycogen into the blood to maintain blood sugar levels.

Glycogen stored in the muscle tissue serves an important role as well. Our muscles main function is to move bones. This allows us to do all the locomotive tasks associated with daily living. What better place to store energy then within the tissues that require this energy to move us around? After the first seven to ten seconds of moving we utilize this glycolytic pathway for energy.

The first ten seconds of activity utilizes the ATP readily available in the cytosol of our cells. After that timeframe our body needs to resynthesize ATP from glucose and our stored glycogen. This process requires quite a few chemical reactions. Due to the increase in reactions, this energy system takes longer to kick in then the ATP-PC system, but it will be able to supply a higher amount of total energy.

Fast Glycolysis and Slow Glycolysis

Glycolysis can be broken up into two different parts - fast glycolysis and slow glycolysis. The determining factor is the direction in which the end product, pyruvate, goes. Within fast glycolysis the pyruvate is converted into lactate. With lactate our body can resynthesize ATP at a much faster rate. This would occur when the activity requires a higher energy demand.

Pyruvate on the left, lactate on the right.

In slow glycolysis the pyruvate is shuttled to our mitochondria and we enter the citric acid cycle, or the oxidative system. In the oxidative system the resynthesis of ATP happens at a much slower rate, but we can maximize the number of ATPs produced, yielding us with the highest amount of energy.

Lactate sometimes gets an undeserving bad wrap. Many people mistakenly associate an increase in lactate with an increase in lactic acid. However, lactic acid cannot exist when the body’s pH is around seven. Instead, exercise decreases the body’s pH and this is known as metabolic acidosis. In fact, lactate may actually be a buffer to this metabolic acidosis.¹Lactate is actually utilized as energy by type 1 muscle fibers and cardiac muscle fibers.

With that said the body’s lactate levels are relatively low at rest and increase with an increase in physical activity. Byproducts of these reactions may be responsible for metabolic acidosis. A clearing of the lactate from the blood is therefore a return to homeostasis. This is one aspect we attempt to train during high intensity interval training.

With enough oxygen present in the mitochondria, the powerhouse of our cell, the pyruvate is converted is shuttled into the mitochondria with NADH, a byproduct of glycolysis, and then converted into acetyl CoA. This is the start of the oxidative metabolism, which we will cover, in my next article.

Glycolysis and Proper Nutrition

Glycolysis is an anaerobic metabolic pathway. The only macronutrient that can be synthesized into usable ATP under anaerobic conditions is carbohydrates. We need to make sure we take in enough carbohydrates to fuel glycolysis during activity. We also need to make sure we take in enough carbohydrates to keep our glycogen stores full. A reduction in muscle glycogen is associated with fatigue.²

This is where the importance of post-workout nutrition comes into play. Studies have shown an increase in glucose uptake by muscle tissue post workout.³ This makes carbohydrates an important piece of our post-workout recovery meal. Simple starch may be the best source of carbohydrates post workout because of their ability to raise blood sugar levels quickly. This can allow for faster uptake by muscle cells to recover. Fruit may even be a better option. Fructose gets immediately shoveled to our liver when ingested. Upon reaching the liver it is converted into glycogen to refill liver stores (it will not refill muscle stores because muscle cells do not contain a receptor for the GLUT5 transporter required to carry fructose). Under conditions of decreased liver glycogen, such as exercise, fruit may have the ability to resupply the liver faster. Sweet potatoes, white potatoes, yams, and even white rice are good additions to the post-workout meal.

Other vitamins such as vitamin A, B2, niacin, and pantothenic acid are important for energy metabolism. This puts a high emphasis on quality foods such as fruits and vegetables for high-level athletes. Foods such as these can be obtained throughout the day. In some cases supplementation may be necessary. Some athletes require such a large amount of nutrients that it becomes difficult to obtain from food alone. In these cases, supplementation would be warranted. Make sure to work with a healthcare practitioner to determine if supplementation is right for you. 

In conclusion, if you participate in sports or gym activities that require high energy outputs for two to three minutes, you need to make sure you are ingesting plenty of carbohydrates. This is to ensure our muscle glycogen stores stay full to keep fatigue away as well as to supply our body with the necessary fuel to perform. The carbohydrates can be ingested from fruit, which may replenish liver glycogen stores more rapidly, or other safe starches such as potatoes.

In my next article we will look at the oxidative system and see how the energy requirements and substrates differ.

References:

1. Robergs, RA, et al., Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology (2004). Accessed on September 30, 2013. 

2. Ortenblad, N et al., Muscle Glycogen Stores and Fatigue. Journal of Physiology (2013). Accessed on September 30, 2013.

3. Poehlman, Eric et al., Effects of resistance training and endurance training on insulin sensitivity in nonobese, young women: A controlled randomized trial. The Journal of Clinical Endocrinology and Metabolism (2000). Accessed on September 30, 2013. 

4. Thomas Baechle and Roger Earle. Essentials of Strength Training and Conditioning. Human Kinetics (2008).

Energy pathways chart property of Breaking Muscle.

Glucose metabolism by Mikael Häggström [Public domain], via Wikimedia Commons.

Pyruvate/Lactate by Yikrazuul (Own work) [Public domain], via Wikimedia Commons.

Photos courtesy of Shutterstock.