Hot or Cold: How Temperature Affects Sports (Technical)

Fig1Crespo

Fig. 1. Organization of vertebrate skeletal muscles (From ref. 1).

Like other tissues, skeletal muscle tissue consists of cells (muscle fibers). The size of these cells ranges from 5 to 100 μm in diameter, and they are up to several centimeters long (Randall et al. 2002). Their parallel arrangement allows for the fibers in a muscle to pull together in a specific direction to exert force. This muscle force is achieved by parallel subunits inside muscle fibers (myofibrils) which in turn consist of sarcomeres, the longitudinally repeated functional units of muscle. The importance of the sarcomere is that its arrangement helps us understand the molecular basis for muscle function. Each sarcomere contains two proteins arranged in a particular geometric pattern, namely actin and myosin, and the interaction between these two proteins explains how a muscle is able to contract (current mechanism known as the sliding-filament theory; see Fig. 1). This contraction requires energy and it is obtained from glucose and lipids that are in turn transformed into adenosine triphosphate (ATP), the energy currency of the cell. Both ATP production (see how chemistry fuels running) and hydrolysis release heat, and it is this heat that contributes to the body’s temperature.

ATP is necessary for muscle work because of two major processes that are energy-dependent. The first process has to do with the cycling of attachment and detachment of myosin cross-bridges to actin, which is mediated by an enzyme called actomyosin ATPase. Without ATP, the myosin heads cannot detach from the actin filament for a new cycle. The second process involves the pumping of Ca2+ (calcium ions) back into the sarcoplasmic reticulum of the muscle fiber by an enzyme called sarcoplamic reticulum ATPase. Free Ca2+ induces muscle contraction by binding to troponin (a muscle protein) which changes the configuration of another protein, tropomyosin, allowing for the myosin heads to access myosin binding sites on the actin filament. During strenuous exercise, muscle energy consumption can surpass that of a resting muscle 100-fold and achieve rates of energy consumption greater than 1.5 kg ATP per minute of activity (McIntosh et al. 2006). If we reflect on the facts that skeletal muscle constitutes about 40% of our total body weight and that muscle contraction is only ~25% efficient, we immediately realize that a lot of expended energy must be released as heat (Sawka and Young 2006). In fact, about 3 joules of energy are released as heat for every joule of chemical energy that is converted into mechanical work4. This extra heat produced during activity is added to the heat generated by our basal metabolism and increases body temperature (2-4°C increase in core temperature is common after strenuous exercise; Randall et al. 2002). Excessively high body temperatures threaten enzymatic activity and thus, avoiding excessive heat storage is of paramount importance when exercising.

Athletes performing different types of exercise rely on the strength of specific muscles. This strength depends on muscle morphology and architecture and myosin isoform composition (see genetic aspects in How Much do Genes Affect Your Athletic Potential?). The phenotypic profiles of muscle fibers cannot only be affected by neuromuscular activity, hormones and aging, but also by the athletic training a person undergoes. Broadly speaking we can define two types of exercise: high-resistance exercise and endurance exercise. The first one results in greater muscle mass and strength by involving some form of high-intensity weightlifting for a short duration (8-12 repetitions) two to three days a week. In contrast, muscular endurance is achieved by low-intensity exercise regimes during 30-60 minutes on an almost daily basis (McCarthy and Esser 2012). Thus, athletes usually bear this in mind when exercising. But, irrespective of the type of exercise, we always feel an increase in body temperature associated with activity. How is it then that our body copes with the excess heat generated during sports or other physically-demanding activities?

Metabolic heat generated by active muscles is transferred to the bloodstream and then to the body core. Whether this heat increases our body temperature or not will depend on different environmental variables, particularly ambient temperature. For example, in cold climates we can suffer from heat loss, which will lower our body temperature and cause our metabolic rate to slow down. If body heat generation cannot keep up with the dissipation of heat to the environment, our body temperature will eventually decrease to dangerous low levels, and may even end in death. The opposite can happen in hot climates. If we cannot dissipate enough heat, we accumulate heat causing our metabolic rate to increase (which generates even more heat) and leads to overheating. This can also end in death. Fortunately, since most of us do not experience extreme weather on a regular basis, our bodies are able to handle this interplay between internal and external temperature in different ways.

Fig2Crespo

Fig. 2. Avenues of heat exchange for an athlete performing exercise in air (From ref. 3).

Humans can be classified as endotherms, which means that our own energy metabolism produces the heat that determines our body temperature. Endothermy allows us to also be homeotherms, because our body temperature is relatively constant and independent of ambient temperature (core body temperature in humans is about 37°C). Thermoregulation in homeotherms occurs through two collaborative processes, namely behavioral and physiological temperature regulation. The first consists of conscious and unconscious behavioral changes influencing heat storage, like modifying activity levels, seeking shade or sunlight, reducing surface area for heat exchange and even changing clothes. Physiological temperature regulation encompasses responses that are unconscious. Our bodies can control the rate of metabolic heat we produce (e.g., by shivering), as well as heat loss by sweating and blood flow distribution (e.g., cutaneous vasodilatation and vasoconstriction). This last mechanism facilitates heat transfer from the skin to the surrounding air or water and is highly dependent on environmental temperature, air humidity, air or water motion, radiation and clothing (Gavin 2003). Biophysically speaking, this heat transfer can be achieved by non-evaporative avenues (conduction, convection, and radiation) called “dry heat exchange” or via evaporative cooling (see Fig. 2). Evaporation is induced by sweating (it can begin after just 2 seconds of engaging in heavy physical work; Randall et al. 2002) when we exercise, and it is the only known mechanism for dissipating heat against a thermal gradient. For example, on a hot day in the desert, our exocrine glands can produce over 12 liters of sweat, effectively cooling our bodies to tolerable temperatures (Jablonski 2006). However, the effectiveness of sweating is low in very humid environments, making it extremely difficult to get rid of excess heat.

Usually our motivation to win or complete a certain task leads us to ignore effective thermoregulatory strategies, and this usually causes lower performance, injuries and/or heat related illnesses. On top of thermoregulatory strategies during activity, there are also several pre- and post-exercise strategies that aid us in performing better and avoiding injuries (Noonan et al. 2012, Ross et al. 2013, Very et al. 2013). For example, warming up and stretching prior to exercising has been shown to deter muscular injuries. In general, warm-up is defined as activities that make us sweat mildly but do not fatigue us, with the purpose of improving muscle dynamics and preparing us for more stringent demands of subsequent exercise. There are two types of warm-up, active and passive. Active warm-up is the most common type of warm-up for both amateur and professional athletes and involves some kind of non-specific body movement (e.g., jogging, cycling or callisthenics). In contrast, passive warm-up results from the increase of muscle temperature or core body temperature by external means, like heating pads, vibrational devices (Cochran 2013), hot showers, saunas, etc. Stretching, as part of warm-up, is recommended within 15 minutes prior to activity to obtain the best results (Woods et al. 2007). Post-exercise strategies are more commonly used by professional athletes after very demanding activities that may lead to muscular fatigue and injuries. These usually involve some kind of muscle cooling technique (DeGroot 2013). Finally, every athlete knows that good nutrition (see Putting Protein in Its Place)  and hydration (see Hydration and Sports Beverages) are essential for safe and effective exercising. In particular, hydration is strongly linked to thermoregulation. Although sweating allows us to get rid of excessive heat efficiently, it also presents the risk of dehydration, if not enough water is consumed.

Regular physical activity enhances and maintains health, but we need to take special considerations (like the ones we saw above) when engaging in sports or other vigorous physical activities. This is particularly true in hot and humid weather, which cannot only lead to poor athletic performance but also to heat stress and even death. Besides inadequate hydration, excessive heat retention can be caused by physical exertion, insufficient recovery time in-between activities, and inappropriate clothing. Heat stress can come in the form of heat cramps (painful cramps in abdominal muscles and muscles of the extremities), heat syncopes (weakness, fatigue and fainting), heat exhaustion due to water and/or salt depletion (causing exhaustion, muscle cramps, nausea, vomiting, dizziness, elevated temperature, weakness headaches, etc.), and heat strokes due to failing thermoregulation (causing nausea, seizures, disorientation, and in severe cases unconsciousness or comatosis). There are also serious risks associated with exercising in cold weather (Castellani and Young 2012). For example, sprains and strains are common, and in very cold-weather, frostbite and hypothermia (core body temperature dropping below that required for normal metabolism) can present a challenge to unprepared athletes.

All of these health related issues can be avoided by learning on the one hand, about the different strategies that our bodies use to control body temperature and, on the other hand, ways of helping our bodies to thermoregulate when external conditions are too harsh. We should always reduce the risks of heat-related illness, by hydrating and eating appropriately, adjusting exercise activity levels according to our current fitness status, having adequate recovery periods between bouts of exercises, and realizing when it is better to cancel athletics and stay home (Heat-Related Illnesses 2014).

By Jose G. Crespo
Jose G. Crespo is a researcher in the field of animal physiology and behavior with an emphasis on insect thermoregulation and neuroscience. He is currently a Postdoctoral researcher at the University of Utah – Department of Biology.

References

Castellani, J. W., & A. J. Young. 2012. Health and performance challenges during sports training and competition in cold weather. British Journal of Sports Medicine. 46: 1-5.

Cochrane, D. 2013. The sports performance application of vibration exercise for warm-up, flexibility and sprint speed. European Journal of Sport Science. 13: 256-271.

DeGroot, D. W., R. P. Gallimore, S. M. Thompson, & R. W. Kenefick. 2013. Extremity cooling for heat stress mitigation in military and occupational settings. Journal of Thermal Biology.   38: 305-310.

Gavin, T, P. 2003. Clothing and thermoregulation during exercise. Sports Medicine. 33: 941-947.

Heat-Related Illnesses (Heat Cramps, Heat Exhaustion, Heat Stroke). University of Utah Health Care, n.d. Web. 1 April 2014. Available at: https://healthcare.utah.edu/healthlibrary/centers/ortho/doc.php?type=90&id=P01611

Jablonski, N.G. 2006. Sweat. In Skin: A Natural History, pp. 39-55. Berkley: University of California Press.

MacIntosh, B. R., P. F. Gardiner, & A. J. McComas. 2006. Muscle Metabolism. In Skeletal Muscle: Form and Function (2nd Ed.), pp. 209-223. Chelsea, MI: Sheridan Books.

McCarthy, J. J., & K. A. Esser. 2012. Skeletal Muscle Adaptation to Exercise. In Muscle: Fundamental Biology and Mechanisms of Disease (ed. J.A. Hill & E.N. Olson), pp. 911-        920. San Diego: Elsevier.

Noonan, B., R. W. Bancroft, J. S. Dines, & A. Bedi. 2012. Heat- and Cold-induced Injuries in Athletes: Evaluation and Management. Journal of the American Academy of Orthopaedic Surgeons. 20: 744-754.

Randall, D., W. Burggren, & K. French. 2002. Energetic Costs of Meeting Environmental Challenges. In Animal physiology: Mechanisms and adaptations (5th Ed.), pp. 699-736. New York: W. H. Freeman.

Randall, D., W. Burggren, & K. French. 2002. Muscles and Animal Movement. In Animal physiology: Mechanisms and adaptations (5th Ed.), pp. 361-424. New York: W. H. Freeman.

Ross, M., C. Abbiss, P. Laursen, D. Martin, & L. Burke. 2013. Precooling methods and their effects on athletic performance: a systematic review and practical applications. Sports Medicine. 43: 207-225.

Sawka, M. N., & A. J. Young. 2006. Physiological Systems and Their Responses to Conditions of Heat and Cold. In ACSM’s Advanced Exercise Physiology (ed. C.M. Tipton),    pp. 535-563. Baltimore: Lippincott Williams & Wilkins.

Versey, N. G., S. L. Halson, & B. T. Dawson. 2013. Water immersion recovery for athletes: effect on exercise performance and practical recommendations. Sports Medicine. 43:       1101-1130.

Woods, K., P. Bishop, & E. Jones. 2007. Warm-up and Stretching in the Prevention of Muscular Injury. Sports Medicine. 37: 1089-1099.

Hot or Cold: How Temperature Affects Sports (Basic)

Fig2CrespoWe wonder whether the day ahead of us is going to be hot or cold in order to decide if we should do certain activities, like practice our favorite outdoor sports. We might think that no matter how hot or cold it gets, we should still go on our running routine because exercise is always good for us. However, we should always remind ourselves that excessive heat or cold can not only make us uncomfortable during exercise, but even put our health at risk.

Based on morphological characteristics, muscles can be classified into two major types, smooth muscle (e.g., the type of muscle found in the walls of hollow organs such as blood vessels) and striated muscle (including heart muscle and skeletal muscle). Skeletal muscles generate most of the heat that causes body temperature to rise during exercise, and thus, it is the main focus of this article.

Muscle contraction requires energy. In muscle cells, like in any other cells, adenosine triphosphate (ATP) is the molecule that stores energy. This energy is transformed into work by the muscles that we use during a specific activity. However, not all the energy is transformed into work. Both the production and hydrolysis (water-mediated cleavage of chemical bonds) of ATP release heat as a by-product, and it is this heat that contributes to the body’s temperature.

Since we are homeotherms (our body temperature is kept relatively constant with respect to ambient temperature), our basal metabolism is higher than that of non-homeotherm animals. When we engage in any type of activity, our body produces extra heat that is added to the heat generated by our basal metabolism and thus, our body temperature increases. If our bodies could not regulate internal temperature, we would store great amounts of heat compromising cell function.

We can regulate body temperature via behavioral and physiological means. For example, we can exercise in the shade to avoid direct sunlight (behavioral) and depending on ambient temperature, we can experience vasodilation (widening of blood vessels) and vasoconstriction (narrowing of blood vessels) to facilitate or restrict heat transfer from the skin to the surrounding air. Thus, thermoregulation can profoundly affect how we perform in different sports and under different ambient conditions.

Furthermore, we need to be extra careful when engaging in sports or other vigorous physical activities in hot and humid weather. Hot weather means that we may accumulate heat more rapidly than what our body can dissipate, and humid conditions imply that sweating (the only known mechanism for dissipating heat against a thermal gradient) may not be possible. Under these circumstances we are prone to suffer from heat stress. Heat stress can lead to cramps, syncopes, exhaustion, and even stroke.

All of these can be avoided by learning about the different strategies to reduce the risks of heat-illness, always hydrating appropriately, adjusting exercise activity levels according to current fitness status, having adequate recovery periods between bouts of exercise, and realizing when it is better to cancel athletics and stay home.

Read the technical details about body temperature and sport.

By Jose G. Crespo
Jose G. Crespo is a researcher in the field of animal physiology and behavior with an emphasis on insect thermoregulation and neuroscience. He is currently a Postdoctoral researcher at the University of Utah – Department of Biology.

Fast and Furious: How Muscle Fiber Type Influences Basketball Performance

Muscle-fibers-631x421Professional athletes use a unique combination of speed, agility, strength, and power to stand apart from the rest. This winning combination of traits is largely due to the slow-twitch (ST) and fast-twitch (FT) fibers found in their muscles. ST fibers are important for endurance, as they allow the muscles to contract at a slow rate for a long time. On the other hand, FT fibers contract fast and hard, but only for a short time, and are important for sprinting. The body first turns to the ST fibers for movement, then focuses on the FT fibers in their legs, calves, and buttocks as the athlete increases speed. A combination of balance, lateral movement, T-drill exercises, and core training are important to increase this muscle response time and maximize gains.

Read about basic muscle fiber and performance or learn the technical physiological explanation.

Articles by Josh Silvernagel

95 miles per hour: Physiology of Pitching

Nationals_Rockies_Baseball-00baa-27438Baseball has been America’s pastime since its early beginnings.  Over time, fans have watched the game evolve. In many cases, the game seems to boil down to a battle between pitchers.  Franchises competing for a spot in the World Series seem to know this, and many (such as the San Francisco Giants) have heavily stacked their pitching rosters with notable talent.  So, physiologically speaking, how do pitchers do what they do, pitch after pitch after pitch?  And what parts of their bodies are most prone to injuries?

These are complex questions. The obvious place to begin is with the arm, shoulder and back muscles.  The most vulnerable joint in pitching is the glenohumeral joint, which is commonly known as the ball and socket of the shoulder.  This joint has the greatest range of motion of any joint in the body.  It is directly supported by four rotator cuff muscles that attach with tough, sinuous tendons.  The pectoral muscle group and the lassitimus dorsi are larger muscles, located in the front and back of the shoulder.  They help stabilize the joint and help keep it from over-rotating and causing injury.

These and other muscle groups work to gather and release energy during a pitch, and others counter the whipping motion of throwing the ball, acting to decelerate and prevent the arm from injury.  In addition to the muscles used in the back and shoulder, leg and core body muscles significantly contribute to the power behind the pitch.  It is this symphony of muscles working in tandem that allows pitchers to throw 100 mph pitches.

Read more about the basics of pitching and physiology or learn the technical physiology behind pitching.

Articles by Josh Silvernagel

Fast and Furious: How Muscle Fiber Type Influences Basketball Performance (Technical)

Introduction 

A unique combination of speed, agility, strength, and power sets professional athletes apart from the rest.  Are these attributes genetic, or do they result from hard work and dedication?  In science, answers are rarely black and white and this question is no different.  It is a complex interplay of genetics and training, which sets off a cascade of physiological and anatomical mechanisms, that produces our professional athletes.  These mechanisms are wide in their scope and intricate in their complexity.  Therefore, this article focuses on explaining muscle fiber properties in the context of basketball related performance.  It also presents some training principles to help the athlete improve his or her performance.

Muscles and Contractions 

When we decide to move a part of our body, the brain sends a signal through the nervous system. The signal, carried by motor neurons, then travels to the muscles required to perform the desired action, causing contraction and movement.  Despite this apparent simplicity, much more actually occurs, making this process quite complex.

The neuromuscular junction is the location where the signal from the nervous system meets the muscular tissue.  Motor neurons branch as they approach muscles to the point where only one individual branch innervates a muscle fiber (Seeley et al. 2006).  There is a small gap between the neuron and the fiber called the synaptic cleft.  The signal carried by the neuron causes a release of particles called neurotransmitters into the synaptic cleft, signaling the muscle fiber to fire (Seeley et al. 2006).

On the molecular scale, muscle contraction is a result of what is known as the sliding filament theory (Huxley and Hanson 1954, Huxley and Niedergerke 1954).  Briefly, each muscle fiber houses a sarcomere.  Inside the sarcomere, a thick filament composed of myosin and a thin filament composed of actin reside.   Upon neurotransmitter signaling, the thick myosin protein uses a ratchet motion to move the actin protein and cause contraction (Seeley et al. 2006, Plowman and Smith 2008).  A more in-depth explanation of the sliding filament theory and muscle contraction is given in another article: 95 miles per hour: Performance Physiology of Pitchers.

Muscle fibers are categorized into two groups: slow-twitch (ST) and fast-twitch (FT).  For the purposes of this article, we will consider the most common forms of these two fibers found in the literature.  Type I fibers are ST fibers and type II fibers are FT.  There are two classifications of type II fibers called type IIa and type IIx (Baechle and Earle 2008).  A surface level difference between fast- and slow-twitch fibers is the amount of blood supplied to the muscle.  Type I fibers have a well established blood supply and stain red during histochemical staining while type II fibers have a less developed blood supply and stain white (Zierath and Hawley 2004).  This can be seen in a chicken or turkey where breast meat is white (fast-twitch) and the legs and thighs are dark (slow-twitch).

Type I fibers have a small diameter with a large population of mitochondria, giving them a high aerobic capacity (Baechle and Earle 2008).  This aerobic capacity directly relates to the slow relaxation and twitch times, but also predisposes the muscle to fatigue slowly (Plowman and Smith 2008).  In physiology, structure always determines function.  The aforementioned structural characteristics give good evidence to say that type I fibers are used primarily in weak or moderately strong contractions that must take place over extended periods of time or that occur in a repetitive manner (MacIntosh et al. 2006).

Type IIx fibers are on the opposite end of the spectrum from ST fibers.  These fibers have a large diameter with a low density of mitochondria, thus, their aerobic capacity is low but their ability to function in the absence of oxygen is extremely high (Baechle and Earle 2008).  In stark contrast to ST fibers, type IIx fibers contract fast and hard but fatigue very easily (Plowman and Smith 2008).

In between type I and type IIx fibers are type IIa fibers.  These fibers are essentially a mix of the properties of the two extremes.  Their diameters could be considered intermediate in size and the density of mitochondria is at moderate levels as well (Baechle and Earle 2008).  They have the ability to work in oxygen rich and oxygen deprived situations, meaning they can function in long duration activities and those of shorter, more intense, effort as well (Plowman and Smith 2008).

So, does this information mean that when you want to go fast your body activates FT muscles and when you want to go slow it uses ST?  The answer to this is no: the body evokes a specific pipeline of recruitment to carry out all skeletal muscle tasks (MacIntosh et al. 2006).  The body starts with type I muscles, and then evokes type IIa in addition to type I as the need for contraction increases.  Finally, type IIx fibers can be recruited if the need for stronger contraction continues to grow (Vollestad et al. 1984, 1992, Vollestad and Blom 1985, Zajac and Faden 1985).  However, in specific fast or sudden corrective movements, the body does allow for type II units to be selectively activated (MacIntosh et al. 2006).  This phenomenon can be clearly seen in many reflexive actions.

The body’s specific protocol for muscle recruitment has implications for athletes.  If there are more ST muscles, it will take longer for the force of contraction to grow large enough to recruit more FT fibers.  Conversely, if there are fewer ST fibers, then type II fibers may be recruited sooner in those individuals.  Therefore, we will next look at the distribution of fibers within individuals and athletes.

The distribution of fiber types can vary from one person to another in the same group (Saltin et al. 1977) and depends on the genetics of individuals (Simoneau and Bouchard 1995).  However, scientists do have a general idea of locations in which each fiber type is in high density.  Muscles that contribute to sustained postural activity tend to have the highest amount of ST fibers (Plowman and Smith 2008), whereas the limbs contain more FT fibers (Seeley et al. 2006).  The percent of ST fibers in sprinters has been shown to be more than half that of endurance cyclists (Fox et al. 1993).  Furthermore, it has been shown that these differences can be attributed, to a degree, to sport specific exercise and training (Saltin et al. 1977).  What these data indicate is part of our distribution of fiber types is due to genetics, and some is due to sport-specific training.

Basketball’s Physiological Requirements 

Understanding the training needs for basketball requires more than just knowing about muscle fiber types.  It requires a thorough knowledge of the systems needed during competition.  Therefore, this section will briefly discuss the muscles, energy systems, and recovery principles that contribute to speed, agility, and power on the basketball court.

The upper body demands of a basketball player are greatly inferior to those of the lower body.  For this reason, the focus will be on the lower body only.  The buttocks, quadriceps, hamstrings, and calves play the most significant role in speed, agility and power.  Core stability has been shown to contribute to running performance (Sato and Mokha 2009), so it must be considered as well.

A study done by McInnes et al. (1995) sought to quantify the physiologic load placed on basketball players, lending insight into training demands for athletes.  They found that players change direction on average every 2.0 seconds.  Additionally, they did about 105 high-intensity sprints per game, one every 21 seconds, lasting an average of 1.7 seconds.  Data indicate glycolysis as the primary energy producer, meaning that anaerobic endurance is required.  Furthermore, players had an average heart rate of about 169 beats per minute throughout the game.  All these data led the authors to conclude that metabolic and cardiovascular demands are high in basketball players (McInnes et al. 1995).

Fitness and Training 

It is important to review the needs and goals of a training program designed around a basketball player.  First and foremost, the program must train for FT fiber development in the legs.  At the same time, the anaerobic energy system must be trained to ensure stamina and recovery during high intensity bursts.  Finally, agility (which is the ability to change direction) needs to be incorporated.

Agility training has been shown to increase muscular response times in the quadriceps and gastrocnemius (calves) (Wojtys et al. 1996).  T-drills, lateral movement drills, and balance drills are all components of agility training.  The type and variety of agility drills is endless, essentially any drill that incorporates quick movements with changes in direction in 5-15 second intervals will improve agility, build anaerobic endurance, and develop FT fibers.

Plyometric (plyos) and ladder drills are two effective means of increasing quickness and explosiveness through FT fiber development.  Plyos are generally very rapid, short distance jumps that occur in 5-20 second sets.  Dot drills and four-square setups are the most common.  In both, there is a pattern of dots or numbers on the ground in which the athlete uses one or two legs to hop about the pattern in a variety of ways.  Speed ladders are similar but all movements move the athlete along the ladder, making these drills less stationary.  These two methods are nearly endless in their variety.

Incorporating core training must be done as well.  Swiss ball, stabilization, lower back, and hip flexor exercises work together to build the entire core.  We have discussed that the stabilizing core muscles are primarily ST fibers, so exercises need to be designed with this in mind.  Rapid repetitions are less important here as the body is genetically predisposed to maintain ST fibers in this region (Plowman and Smith 2008).  Long duration core stabilization exercises like leg raises and planks should be the focus.

Finally, it is important to work the training protocol around the previously mentioned activity data from McInnes et al.  These data tell how to design recovery times between sets and between training sessions.  Recovery should never be taken lightly as it is just as important as the actual activity in improving performance.

Conclusion

The principles presented in this article can be applied to a wide range of sports whose demands are similar to those of basketball.  It is important to remember that there are limits to everyone’s abilities.  Most of us will never get close to the level of Michael Jordan or LeBron James, yet each person does have room to improve in some aspect of their game.  The requirements for improvement are simple: hard work and dedication.  With these two ideas in mind, it is nearly impossible to produce a training program that does not improve performance.

 

By: Josh Silvernagel, Graduate Student, Bioengineering, University of Utah
Josh Silvernagel received undergraduate degrees in Exercise Science and Mathematics from Bemidji State University (BSU) in Bemidji, MN.  During his undergraduate studies, he was a four year starter in baseball for the BSU Beavers, where he both pitched and played infield.  In addition to providing sport specific training for ametuer and professional athletes following school, Josh spent two years coaching the sport at both the collegiate and high school levels.  He is currently working on a Ph. D. in Bioengineering at the University of Utah, where he studies cardiac electrophysiology in the CARMA Center.  Josh and his wife, Danielle, are recently married.

Reference:

Baechle, T. R., and R. W. Earle (Eds.). 2008. Essentials of Strength Training and Conditioning, 3rd edition. Human Kinetics, Champaign, IL.

Fox, E. L., R. W. Bowers, and M. L. Foss. 1993. The Physiological Basis for Exercise and Sport. Pages 94–135. Brown & Benchmark, Dubuque, IA.

Huxley, A. F., and R. Niedergerke. 1954. Structural changes in muscle during contraction: Interference microscopy of living muscle fibres. Nature 173:971–973.

Huxley, H., and J. Hanson. 1954. Changes in the cross-striations of muscle during contraction and stretch and thier structural interpretation. Nature 173:973–976.

MacIntosh, B. R., P. F. Gardiner, and A. J. McComas. 2006. Skeletal Muscle: Form and Function, 2nd edition. Human Kinetics, Champaign, IL.

McInnes, S. E., J. S. Carlson, C. J. Jones, and M. J. McKenna. 1995. The physiological load imposed on basketball players during competition. Journal of Sports Sciences 13:387–397.

Plowman, S., and D. Smith. 2008. Exercise Physiology for Health, Fitness, and Performance, 2nd edition. Kippincott Williams & Wilkins, Philadelphia, PA.

Saltin, B., J. Henriksson, E. Nygaard, P. Andersen, and E. Jansson. 1977. Fiber types and metabolic potentials of skeletal muscles in sedantary man and endurance runners. Annals of the New York Academy of Sciences 301:3–29.

Sato, K., and M. Mokha. 2009. Does Core Strength Training Influence Running Kinetics, Lower-Extremity Stability, and 5000-m Performance in Runners? The Journal of Strength & Conditioning Research 23.

Seeley, R., T. Stephens, and P. Tate. 2006. Anatomy and Physiology, 7th edition. McGraw Hill, New York, NY.

Simoneau, J. A., and C. Bouchard. 1995. Genetic determinism of fiber type proportion in human skeletal muscle. The FASEB Journal 9 :1091–1095.

Vollestad, N. K., and P. C. S. Blom. 1985. Effect of varying exercise intensity on glycogen depletion in human muscle fibres. Acta Physiologica Scandinavica 125:395–405.

Vollestad, N. K., I. Tabata, and J. I. Medbo. 1992. Glycogen breakdown in different human muscle fibre types during exhaustive exercise of short duration. Acta Physiologica Scandinavica 144:135–141.

Vollestad, N. K., O. D. D. Vaage, and L. Hermansen. 1984. Muscle glycogen depletion patterns in type I and subgroups of type II fibres during prolonged severe exercise in man. Acta Physiologica Scandinavica 122:433–441.

Wojtys, E. M., L. J. Huston, P. D. Taylor, and S. D. Bastian. 1996. Neuromuscular Adaptations in Isokinetic, Isotonic, and Agility Training Programs. The American Journal of Sports Medicine 24:187–192.

Zajac, F. E., and J. S. Faden. 1985. Relationship among recruitment order, axonal conduction velocity, and muscle-unit properties of type-identified motor units in cat plantaris muscle. Journal of Neurophysiology 53 :1303–1322.

Zierath, J. R., and J. a Hawley. 2004. Skeletal muscle fiber type: influence on contractile and metabolic properties. PLoS biology 2:e348.

 

Fast and Furious: How Muscle Fiber Type Influences Basketball Performance (Basic)

A unique combination of speed, agility, strength, and power sets professional athletes apart from the rest.  This article focuses on explaining how muscle fiber properties produce this combination in the context of basketball.  It explores muscle fiber type properties and some training implications that can be gleaned from what science knows about these properties.

Muscle fiber types fall into two main categories: slow-twitch (ST) and fast-twitch (FT).  Slow-twitch fibers are also known as type I fibers, and FT fibers have two subcategories: type IIa and type IIx (Baechle and Earle 2008).  Type I fibers have many mitochondria which make them able to contract weakly or mildly for long periods of time at low intensities (MacIntosh et al. 2006).  Type IIx fibers have little mitochondria and function to contract very hard and rapidly for short durations.  Lying between type I and type IIx fibers are type IIa fibers.  These have a moderate amount of mitochondria and contract at intermediate levels for lengths of time that fall between types I and IIx (Plowman and Smith 2008).

It is important for basketball players to have large amounts of FT fibers in their legs, calves, and buttocks.  To sustain these muscles over the course of activity, strongly developed ST core muscles need to be trained as well.  Focusing training on these aspects will allow the athlete to meet the high metabolic and cardiovascular demands required of the sport (McInnes et al. 1995).

Agility training has been shown to increase muscular response times in the quadriceps and gastrocnemius (calves) (Wojtys et al. 1996).  Therefore, a combination of balance training, lateral movement training, and T-drill type exercises are important.  Plyometric exercises (plyos) are important for training in this sport.  Finally, core stabilization and recovery principles must be incorporated to maximize gains.

Learn more about the technical aspects of muscle fibers and their influence on basketball performance.

By: Josh Silvernagel, Graduate Student, Bioengineering, University of Utah
Josh Silvernagel received undergraduate degrees in Exercise Science and Mathematics from Bemidji State University (BSU) in Bemidji, MN.  During his undergraduate studies, he was a four year starter in baseball for the BSU Beavers, where he both pitched and played infield.  In addition to providing sport specific training for ametuer and professional athletes following school, Josh spent two years coaching the sport at both the collegiate and high school levels.  He is currently working on a Ph. D. in Bioengineering at the University of Utah, where he studies cardiac electrophysiology in the CARMA Center.  Josh and his wife, Danielle, are recently married.

References:

Baechle, T. R., and R. W. Earle (Eds.). 2008. Essentials of Strength Training and Conditioning, 3rd edition. Human Kinetics, Champaign, IL.

MacIntosh, B. R., P. F. Gardiner, and A. J. McComas. 2006. Skeletal Muscle: Form and Function, 2nd edition. Human Kinetics, Champaign, IL.

McInnes, S. E., J. S. Carlson, C. J. Jones, and M. J. McKenna. 1995. The physiological load imposed on basketball players during competition. Journal of Sports Sciences 13:387–397.

Plowman, S., and D. Smith. 2008. Exercise Physiology for Health, Fitness, and Performance, 2nd edition. Kippincott Williams & Wilkins, Philadelphia, PA.

Wojtys, E. M., L. J. Huston, P. D. Taylor, and S. D. Bastian. 1996. Neuromuscular Adaptations in Isokinetic, Isotonic, and Agility Training Programs. The American Journal of Sports Medicine 24:187–192.

 

How Chemistry Fuels the Body to Run (Basic)

Usain St. Leo Bolt, World Champion

sports-usain-bolt-in-action-new-hd-wallpaper-usain-bolt-wallpaperUsain St. Leo Bolt, a Jamaican sprinter who competed in the 2012 London Olympics, is widely known as the fastest man ever. Bolt is the first man in history to hold both the world records for the 100 meter and 200 meter sprint. He earned gold medals in both of these events at the 2008 and 2012 Olympics (Usain Bolt 2012). When sprinting, Bolt’s body must produce enough energy to run 100 meters in 9.63 seconds. There are amazing processes going on simultaneously within this runner’s body that are allowing this all to happen.

The Origin of Energy

Metabolic processes begin long before an athlete competes. In fact, the precursors to these processes begin at the dinner table. Energy begins in the form of a healthy meal consisting of carbohydrates, fatty acids, and amino acids. These “fuel” molecules are then metabolized into substances such as glucose, pyruvate, lactate, and the aforementioned acetyl-CoA.

The end product of these metabolic processes is a very important molecule called adenosine triphosphate (ATP). ATP is the molecule that supplies our body with the necessary energy to perform. The cells that make up our body all use ATP to perform many necessary functions such as cell signaling (Bell et al. 2003), transport of molecules in and out of cells (Skou 1965), muscle contraction (Adelstein and Eisenberg 1980), and even for the synthesis of more ATP through our metabolism (Champe and Harvey 1987, Campbell et al. 2005). Through cell signaling, ATP allows our central and peripheral nervous system to function properly (Bell et al. 2003), it allows actin and myosin crossbridges in our muscles to function so that we can flex and contract muscles (Adelstein and Eisenberg 1980), allowing us to move and perform. In our metabolism, ATP is used to allow glycolysis to continue, which in turn produces more ATP (Champe and Harvey 1987, Campbell et al. 2005). When our body has low levels of ATP, it knows when to produce more and will increase the rate of glycolysis and the citric acid cycle accordingly.

Glycolysis

Glycolysis literally translated means to split sugar (Glucose—sugar, lyse—to split). Glycolysis can be aerobic when we have sufficient oxygen, or anaerobic when the oxygen in our system is low. Virtually all sugars can be converted to glucose which is free to diffuse in and out of the cells that make up the different tissues of our body. Glycolysis is a process that ends up in a net formation of two ATP molecules per glucose molecule.

Anaerobic Glycolysis

Anaerobic glycolysis takes place without oxygen and is the way our metabolism supplements the demand for short, intense bursts of energy. Events lasting approximately 10 seconds or somewhat longer (e.g. 100-m run) utilize anaerobic glycolysis for energy in ATP production (Knuttgen and Komi 2003). This can only be sustained for short periods of time (Knuttgen and Komi 2003).  Lactic acid is produced during anaerobic glycolysis and is responsible for the burning sensation sometimes felt in muscle fibers.

Aerobic Glycolysis and The Citric Acid Cycle

When there is adequate oxygen in the body, aerobic glycolysis takes place and is coupled to the citric acid cycle. The citric acid cycle yields much more energy than glycolysis alone. If we add all of the energy yielding products of the breakdown of one glucose molecule, we can obtain 15-17 times more ATP through the breakdown of one glucose molecule.

Learn the technical details about the chemistry of running.

By: Josh Sewell, University of Utah
Joshua Sewell graduated from Brigham Young University-Idaho with a Bachelor’s of Science in chemistry and a minor in biology. He is fascinated by biochemistry and the processes that make the body work. Josh is currently a graduate student working on a Ph.D. in chemical engineering where he is focused on microbially enhanced coalbed methane recovery and applications. Outside of the lab, Josh enjoys spending time with his wife, Sara, and his two daughters, Oakley and Zoe.

References:

Adelstein, R. S., & E. Eisenberg. 1980. Regulation and Kinetics of the Actin-Myosin-ATP Interaction. Annual Review of Biochemistry 49: 921-56.

Bell, P. D., J.Y. Lapointe, R. Sabirov, S. Hayashi, J. Peti-Peterdi, K. Manabe . 2003. Macula densa cell signaling involves ATP release through a maxi anion channel. Proceedings of the National Academy of Sciences of the United States of America 100 (7): 4322-27.

Ericinska, M., & F. Dagani. 1990. Relationships between the neuronal sodium/potassium pump and energy metabolism. Effects of K+, Na+, and adenosine triphosphate in isolated brain synaptosomes. The Journal of General Physiology 95 (4): 591-616.

Knuttgen, H. G., & P.V. Komi. 2003. Basic Considerations for Exercise. In P. V. Komi (Ed.). Strength and Power in Sport (Vol. 3). Blackwell Science, Malden, Massachusetts, USA.

Champe, P., & R.A. Harvey. 1987. Lippincott’s Illustrated Reviews: Biochemistry. J.B. Lippincott Company, Philadelphia, Pennsylvania, USA.

Campbell, P. A. Smith, & T. Peters. 2005. Biochemistry Illustrated, Biochemistry and molecular biology in the post-genomic era (Fifth ed.). Elsevier Churchill Livingstone, Edinburgh, Scotland.

Skou, J. 1965. Enzymatic basis for active transport Na+ and K+ across cell membrane. Physiological Reviews 45 (3): 596-618.

Usain Bolt. (2012, August). Usain Bolt. Retrieved from http://usainbolt.com/bio/.com/bio/

How Chemistry Fuels the Body to Run (Technical)

Usain St. Leo Bolt, World Champion

Usain St. Leo Bolt (See Figure 1), a Jamaican sprinter who competed in the 2012 London Olympics, is widely known as the fastest man ever. Bolt is the first man in history to hold both the world records for the 100 meter and 200 meter sprint. He earned gold medals in both of these events at the 2008 and 2012 Olympics (Usain Bolt 2012). When sprinting, Bolt’s body must produce enough energy to run 100 meters in 9.63 seconds. There are amazing processes going on simultaneously within this runner’s body that are allowing this all to happen.

Figure 1: Usain St. Leo Bolt4

Aerobic and Anaerobic Respiration

To understand what is going on in an athlete’s body, we must first understand the difference between aerobic respiration and anaerobic respiration. When an athlete runs, there is a high demand for oxygen and a limited supply. A Sprinter like Bolt finishes a race before he is able to breathe heavier and accrue more oxygen. For the most part, Bolt’s body is running on a process called anaerobic glycolysis (Kudo et al. 1996). Anaerobic essentially means “without oxygen.” Anaerobic glycolysis allows his body to produce limited energy when he has low levels of oxygen in his system. Every time Bolt takes a breath, his body is supplied with a very limited amount of oxygen that is instantly used to fuel a process that yields much more energy: aerobic glycolysis coupled to the citric acid cycle (also known as Kreb’s cycle or the tricarboxylic acid cycle) by acetyl coenzyme A (Acetyl CoA). Acetyl-CoA is produced when the oxygen supply in our body is abundant. This is one of the reasons we breathe more heavily when we engage in physical activity. Our body has feedback mechanisms that tell us to breathe in more oxygen to allow our body to produce energy at a faster pace (Skou 1965, Lamb and Stephenson 2006b).

The Origin of Energy

Metabolic processes begin long before an athlete competes. In fact, the precursors to these processes begin at the dinner table. Energy begins in the form of a healthy meal consisting of carbohydrates, fatty acids, and amino acids. These “fuel” molecules are metabolized into substances such as glucose, pyruvate, lactate, and the aforementioned acetyl CoA.

The end product of these metabolic processes is a very important molecule called adenosine triphosphate (ATP). ATP is the molecule that supplies our body with the necessary energy to perform. The cells that make up our body all use ATP to perform many necessary functions such as cell signaling (Bell et al. 2003), transport of molecules in and out of cells (Winder and Hardie 1996), muscle contraction (Adelstein and Eisenberg 1980), and metabolism (Skou 1965, Lamb and Stephenson 2006b). Through cell signaling, ATP allows our central and peripheral nervous system to function properly (Bell et al. 2003). It allows actin and myosin crossbridges in our muscles to function so that we can flex and contract muscles (Adelstein and Eisenberg 1980), allowing us to move and perform. In metabolism, ATP allows glycolysis to continue, which in turn produces more ATP (Skou 1965, Lamb and Stephenson 2006b). ATP is one of the most important molecules in our body because essentially, it gives the cells in our body the ability to perform all the functions necessary to sustain life. Studies have shown that a decrease in ATP is the chief factor responsible for increased energy production.5 When our body has low levels of ATP, it knows when to produce more and will increase the rate of glycolysis and the citric acid cycle accordingly.

Glycolysis

Glucose

Glycolysis literally translated means to split sugar (Glucose—sugar, lyse—to split). Virtually all sugars (whether arising from our diet or from catabolic reactions in the body) ultimately can be converted to glucose; glucose is free to diffuse in and out of the cells that make up the different tissues of our body. Diffusion generally occurs from areas of high concentration to areas of low concentration. For this reason, when cells are depleted of glucose, more is able to be supplied through diffusion.

Glycolysis can be aerobic when we have sufficient oxygen, or anaerobic when the oxygen in our system is low. The reactions involved with glycolysis begin in the same pathway, regardless of the amount of oxygen present.

Glycolysis (See Figure 2) begins when a phosphorous molecule is added to the glucose molecule to form glucose 6-phosphate. This process is called phosphorylation and in this case, the phosphorylation is performed by an enzyme called hexokinase. Enzymes are biocatalysts that speed up reactions such as this one. The phosphorylation is irreversible. Once the phosphorylation occurs, the glucose molecule is blocked from leaving the cell without some kind of special carrier molecule. This commits the glucose molecule to the glycolysis process. The phosphorylation of glucose uses the phosphorous from an ATP molecule, which almost seems counterproductive since ATP is what glycolysis is trying to produce, but we can consider this an investment since more ATP will be produced further along in the process. When the ATP gives up a phosphorus molecule, it is converted to adenosine diphosphate (ADP).

Next, the enzyme phosphoglucose isomerase converts glucose 6-phosphate to fructose 6-phosphate. Fructose 6-phosphate is an isomer of glucose 6-phosphate, which means that they have the same chemical formula (i.e. they are made of the same number and type of atoms) but a different structural formula. This means that they are made up of the same atoms, but they are shaped differently. After isomerization, phosphofructokinase (an enzyme) phosphorylates fructose 6-phosphate to form fructose 1,6-bisphophate. An additional investment of ATP is made in the phosphorylation of fructose 6-phosphate. This makes two total ATP molecules invested into glycolysis for each molecule of glucose. Soon we will see why glycolysis is worth the investment of energy in the “payoff” phase.

Once fructose 1,6-bisphophate is made, it is cleaved (or split) into dihydroxyacetone phosphate and glyceraldehyde 3-phosphate by the enzyme Aldolase. This is the ‘lysis or lyse’ step in glycolysis. Dihydroxyacetone phosphate is a precursor molecule only and cannot proceed further down the pathway of glycolysis without modification. Triose phosphate isomerase (an enzyme) catalyzes the reversible conversion of dihydroxyacetone phosphate to another molecule of glyceraldehyde 3-phosphate. This increases the total number of glyeraldehyde 3-phosphate molecules to two per molecule of glucose metabolized.

The glyceraldehyde 3-phosphate molecules are oxidized to 1,3-diphosphoglycerate by glyceraldehyde 3-phosphate dehydrogenase (an enzyme). This is an oxidation-reduction reaction converting nicotinamide adenine dinucleotide (NAD+) to a reduced form (NADH) and phosphorylating each of the glyceraldehyde 3-phosphate molecules to form 1,3-diphosphoglycerate (Skou 1965, Lamb and Stephenson 2006b). Glycolysis is closely regulated by the amount of NAD+ to NADH in our system (Witters et al. 1994). You can imagine that if there is a large buildup of NADH and not much NAD+ available, this step will slow down the rate of glycolysis.

Each 1,3-diphosphoglycerate is used to form an ATP using the enzyme Phosphoglycerate kinase and an ADP molecule (remember that two ADP were created in the investment of ATP in the earlier stages of glycolysis). This forms two ATP molecules so that the net production of ATP is now zero per molecule of glucose. 3-phosphoglycerate is the resulting molecule from each 1,3-diphosphoglycerate.

Next, the phosphate atom is shifted on the #3 carbon of 3-phosphoglycerate to #2 carbon by phosphoglyceromutase to form 2-phosphoglycerate. 2-phopshoglycerate is then dehydrated by the enzyme enolase to form phosphoenolpyruvate (PEP). The next reaction forms the molecule pyruvate. Pyruvate is formed by the enzyme pyruvate kinase producing an additional ATP molecule from each PEP molecule. Two ATP molecules are formed for each glucose molecule. This gives a net of two ATP molecules for each molecule of glucose metabolized. The resulting pyruvate molecule is where anaerobic glycolysis and aerobic glycolysis differ (Skou 1965, Lamb and Stephenson 2006b).

Anaerobic Glycolysis

Sprinting, lifting weights, and short bursts of energy within aerobic exercise are all fueled by anaerobic respiration. When Bolt is sprinting, his oxygen demand exceeds the supply. Anaerobic glycolysis is the way our metabolism supplements the energy demand for these short, intense bursts of activity. Events lasting approximately 10 seconds or somewhat longer (e.g. 100-m run) utilize anaerobic glycolysis for energy in ATP production (Kudo et al. 1996).

Remember, the NADH that was formed in the oxidation-reduction reaction in glycolysis. When oxygen levels are low, this NADH reacts with the pyruvate leftover from glycolysis to form lactate and NAD+. This NAD+ is then recycled and used to allow the glyceraldehyde 3-phosphate molecules to be oxidized to 1,3-diphosphoglycerate in glycolysis allowing the glycolysis cycle to continue to produce more ATP (Skou 1965, Lamb and Stephenson 2006b). This can only be sustained for short periods of time (Kudo et al. 1996). Once our body adjusts to the strenuous activity and the energy demand by breathing in oxygen, aerobic glycolysis kicks in.

It is interesting to know that production of lactate and other metabolites during extreme exertion results in the burning sensation that is felt in active muscles. While lactic acid accumulation inside muscle fibers is responsible for the burning sensation we feel, it is not responsible for decreased muscle performance (“muscle fatigue”). There are several broad types of muscle fatigue, and the contribution of each to the overall decline in performance depends on the muscle fiber type and the intensity and duration of the activity (Tilton et al. 1991). Arguments have been made that lactic acid buildup in active muscles is advantageous and other arguments have countered saying that it is disadvantageous (Witters et al. 1994). Those that advocate that lactate is advantageous make the argument that the lower intracellular pH, due to the acidity of lactate, counters the effects of high potassium levels which inhibit membrane transport channels from functioning at full capacity (Tilton et al. 1991). Those that argue that lactate has an inhibitory effect report that lactate induced an impairment of calcium release channels (Bangsbo and Juel 2006). Calcium plays a crucial role in muscle contraction (Kudo et al. 1995), so this argument makes a valid point as well.

Figure 2: Glycolysis6

Aerobic Glycolysis and Acetyl CoA

For longer distance running, when oxygen supply is able to meet the demand, oxidative decarboxylation of pyruvate occurs to form Acetyl CoA yielding an NADH for each pyruvate. This occurs in cells that contain mitochondria. The mitochondria are considered “the powerhouses of the cell” because they are where the citric acid cycle occurs. Oxidative decarboxylation of pyruvate by the enzyme pyruvate dehydrogenase converts pyruvate (inside the mitochondrial matrix) to acetyl CoA.

Acetyl CoA is the precursor to the citric acid cycle (Skou 1965, Lamb and Stephenson 2006b).

The Citric Acid Cycle

The citric acid cycle is an eight-step process after pyruvate has been converted to acetyl CoA (See Figure 3). It begins by the condensation of acetyl CoA and oxaloacetate to form citrate by the enzyme citrate synthase. Next is the isomerization of citrate to isocitrate, a molecule with the same number of atoms, with a different makeup. After isomerization, oxidation and decarboxylation of the resulting isocitrate occurs. This converts isocitrate to alpha-ketoglutarate and is catalyzed by the enzyme isocitrate dehydrogenase. This is another oxidation-reduction reaction and requires an NAD+ molecule. This forms the first of three NADH molecules.

This reaction is followed by another oxidation-reduction reaction. Oxidative decarboxylation of alpha-ketoglutarate to form succinyl CoA by alpha-ketoglutarate dehydrogenase complex occurs. This forms another NADH from NAD+. Succinate kinase catalyzes the cleavage of succinyl CoA to form succinate. The cleavage of succinyl CoA produces a guanosine triphosphate (GTP), which contains the same energy content as an ATP molecule. After succinate is formed, it is oxidized, in another oxidation-reduction reaction, to form fumarate. Since the reducing power of succinate is not sufficient to reduce NAD+ to NADH, the oxidation-reduction reaction is enabled this time by the molecule flavin adenine dinucleotide (FAD). This forms the reduced form of FAD, FADH2. Fumarate is then hydrated to the molecule malate by the enzyme fumarase.

The final step of the citric acid cycle is the oxidation of malate to oxaloacetate catalyzed by the enzyme malate dehydrogenase. This produces the third and final NADH molecule and leaves an oxaloacetate molecule to react with acetyl CoA to renew the cycle. Keep in mind that for each glucose molecule, two molecules of acetyl CoA are formed. This produces a total of six NADH molecules, two FADH2 molecules, and two GTP molecules for each glucose molecule. If we add all of the energy yielding products of the breakdown of one glucose molecule, we have a total of ten NADH molecules, two FADH2 molecules, two GTP molecules, and a net of four ATP molecules. Each NADH is capable of producing 3 ATP, each FADH2 is capable of producing 2 ATP, and each GTP is equivalent to one ATP. This yields a total of 38 ATP assuming that all of these products go on to produce an ATP. We can now see why we need more oxygen when we work hard over longer distances. The oxygen is essential to allow glycolysis to link to the citric acid cycle and produce more energy to sustain us (Skou 1965, Lamb and Stephenson 2006b).

Figure 3: The Citric Acid Cycle11

Summary – How does this affect running?

As Bolt lines up at the starting line, he listens for the starting gun. His body has already started to produce extra ATP because of his warm-up exercises. As the gun goes off, ATP begins working in conjunction with actin and myosin fibers that make up his muscles, enabling him to contract his muscles and move. His central and peripheral nervous system communicate with his muscles through cell signaling, which is enabled by ATP. His cells start to notice a lack of ATP, which signals the production of pyruvate through glycolysis. With each breath of air, oxygen molecules diffuse from his lungs into his bloodstream and finally into his cells where they allow oxidative decarboxylation of pyruvate forming acetyl CoA. Acetyl CoA allows the metabolism of oxaloacetate in the citric acid cycle to produce more ATP. As his cells are starved of oxygen between breaths, anaerobic glycolysis occurs and pyruvate is fermented into lactate in his muscles, producing a burning sensation in his muscles. Bolt crosses the finish line well ahead of his competitors, all made possible by the adenosine triphosphate produced during metabolism.

 

By: Josh Sewell, University of Utah
Joshua Sewell graduated from Brigham Young University-Idaho with a Bachelor’s of Science in chemistry and a minor in biology. He is fascinated by biochemistry and the processes that make the body work. Josh is currently a graduate student working on a Ph.D. in chemical engineering where he is focused on microbially enhanced coalbed methane recovery and applications. Outside of the lab, Josh enjoys spending time with his wife, Sara, and his two daughters, Oakley and Zoe.

 

 

References:

Adelstein, R. S., and E. Eisenberg. 1980. Regulation and Kinetics of the Actin-Myosin-ATP Interaction. Annual Review of Biochemistry 49: 921-56.

Bangsbo, J., and C. Juel. 2006. Lactic acid accumulation is a disadvantage during muscle activity. Journal of Applied Physiology 100 (4): 1410-12.

Bell, P. D., J.Y. Lapointe, R. Sabirov, S. Hayashi, J. Peti-Peterdi, K. Manabe . 2003. Macula densa cell signaling involves ATP release through a maxi anion channel. Proceedings of the National Academy of Sciences of the United States of America 100 (7): 4322-27.

Ericinska, M., and F. Dagani. 1990. Relationships between the neuronal sodium/potassium pump and energy metabolism. Effects of K+, Na+, and adenosine triphosphate in isolated brain synaptosomes. The Journal of General Physiology 95 (4): 591-616.

Karaki, H., H. Ozaki, M. Hori, M. Mitsui-Saito, K. Amano, K. Harada. 1997. Calcium Movements, Distribution, and Functions in Smooth Muscle. Pharmacological Reviews 49 (2): 157-230.

Knuttgen, H. G., and P.V. Komi. 2003. Basic Considerations for Exercise. In P. V. Komi (Ed.). Strength and Power in Sport (Vol. 3). Blackwell Science, Malden, Massachusetts, USA.

Kudo, N., A. Barr, R. Barr, S. Desai, and G. Lopaschuk. 1995. High rates of fatty acid oxidation during reperfusion of ischemic hearts are associated with a decrease in malonyl-coA levels due to an increase in 5’-AMP-activated protein kinase inhibition of acetyl-coA carboxylase. Journal of Biological Chemistry 270: 17513–17520

Kudo, N., J. Gillespie, K. Kung, L. Witters, R. Schuz, S. Clanachan, and G. Lopaschuk. 1996. Characterication of 5’AMP-activiated kinase activity in the heart and its role in inhibiting acetyl-CoA carboxylases during reperfusion following ischemia. Biochimica et Biophysica Acta 1301: 67–75

Champe, P., and R.A. Harvey. 1987. Lippincott’s Illustrated Reviews: Biochemistry. J.B. Lippincott Company, Philadelphia, Pennsylvania, USA.

Campbell, P. A. Smith, and T. Peters. 2005. Biochemistry llustrated, Biochemistry and molecular biology in the post-genomic era (Fifth ed.). Elsevier Churchill Livingstone, Edinburgh, Scotland.

Lamb, G. D., and D.G. Stephenson. 2006a. Lactic acid accumulation is an advantage during muscle activity. Journal of Applied Physiology 100 (4): 1410-12.

Lamb, G. D., and D.G. Stephenson. 2006b. Point Counterpoint: Lactic acid accumulation is an advantage/disadvantage during muscle activity. Journal of Applied Physiology 100 (4): 1410-12.

Skou, J. 1965. Enzymatic basis for active transport Na+ and K+ across cell membrane. Physiological Reviews 45 (3): 596-618.

Tilton, W., C. Seaman, D. Carriero, and S. Piomelli. 1991. Regulation of glycolysis in the erythrocyte: role of the lactate/pyruvate and NAD/NADH ratios. The Journal of Laboratory and Clinical Medicine 118 (2): 146-52.

Usain Bolt. (2012, August). Usain Bolt. Retrieved from http://usainbolt.com/bio/

Winder, W.W. and D.G. Hardie. 1996. Inactivation of acetyl-CoA carboxylase and activation of AMP-activated protein kinase in muscle during exercise. American Journal of Physiology 270: 299–304.

Witters, L. A., G. Gao, B. Kemp, and B. Quistorff. 1994. Hepatic 5’-AMP-activated protein kinase: zonal distribution and relationship to acetyl-CoA carboxylase activity in varying nutritional states. Arch. Biochem. Biophys. 308: 413–419.

95 miles per hour: Physiology of Pitching (Basic)

Major League pitchers throw the ball extremely hard, some at over 100 miles per hour.  Yet, as much as can be attributed to natural ability, much more can be attributed to strength, technique, and subtle keys revealed by modern science.

A muscle is composed mainly of proteins, with the addition of a few specialized organelles (Plowman and Smith 2008). What most people consider to be one muscle is actually millions of tiny filaments called myofibrils (Plowman and Smith 2008). Within these fibers, proteins and elements work together to create a muscle contraction.  As the requirement for force increases, more and more myofibrils are recruited to carry out the task.

In pitching, there are two important stages to the throw: the acceleration and deceleration phases.  Essentially, the acceleration phase starts when the arm comes forward and ends as the ball is released. The deceleration phases happens right after the ball is released and is where the body is trying to slow down the arm to prevent injury.  Studies have shown that the upper arms contribute to both acceleration and deceleration, as do the shoulders.  The chest and back both play an important role creating velocity (Jobe et al. 1983, Jobe et al. 1984, Escamilla and Andrews 2009). Although the literature is sparse, the core and lower body are thought to contribute a majority of the power during the throw (MacWilliams et al. 1998, Coleman 2009, Lehman 2012).

Since recent studies have alluded to the core and legs being integral parts of the throw, they become the focus of improving velocity.  Not only should the entire core be trained, but also all the muscles in the lower part of the body. In fact, a soon-to-be published study indicates that lateral jumps similar to the movement a pitcher makes are the most effective method to improving throwing velocity among common exercises (Lehman 2012).

The body requires more than just strong muscles to work. A high-performance body results from a combination of good nutrition and hours in the weight room and on the practice field.  Although not everyone can throw as hard as major league pitchers, everyone can improve their ability from where they are today. By applying basic scientific principles and putting in a little hard work, anyone can excel to rise among the ranks in whatever league they find themselves in.

Check out the technical physiology involved in pitching. 

By: Josh Silvernagel, Graduate Student, Bioengineering, University of Utah
Josh Silvernagel received undergraduate degrees in Exercise Science and Mathematics from Bemidji State University (BSU) in Bemidji, MN.  During his undergraduate studies, he was a four year starter in baseball for the BSU Beavers, where he both pitched and played infield.  In addition to providing sport specific training for ametuer and professional athletes following school, Josh spent two years coaching the sport at both the collegiate and high school levels.  He is currently working on a Ph. D. in Bioengineering at the University of Utah, where he studies cardiac electrophysiology in the CARMA Center.  Josh and his wife, Danielle, are recently married.

 

References

Coleman, A.E. 2009. Training the power pitcher. Strength and Conditioning Journal 31: 48–58.

Escamilla, R.F. and J.R. Andrews. 2009. Shoulder muscle recruitment patterns and related biomechanics during upper extremity sports. Sports medicine (Auckland, N.Z.) 39: 569–90.

Jobe, F.W., D.R. Moynes, J.E. Tibone, and J. Perry. 1984. An EMG analysis of the shoulder in a second report * pitching. American Journal of Sports Medicine 12: 218–220.

Jobe, F.W., J.E. Tibone, J. Perry, and D. Moynes. 1983. An EMG analysis of the shoulder in and pitching throwing preliminary report *. American Journal of Sports Medicine 11: 3–5.

Lehman, G., E.J. Drinkwater, and D.G. Behm. 2012. Correlation of throwing velocity to the results of lower body field tests in male college baseball Players. Journal of Strength and Conditioning Research / National Strength and Conditioning Association 3979.

MacWilliams, B., T. Choi, M.K. Perezous, E.Y. Chao, and E.G. McFarland. 1998. Characteristic ground-reaction forces in baseball pitching. The American Journal of Sports Medicine 26: 66–71.

Plowman, S. and D. Smith. 2008. Exercise physiology for health, fitness, and performance. Kippincott Williams and Wilkins, Philadelphia, PA, USA.

95 miles per hour: Physiology of Pitching (Technical)

Introduction

Nationals_Rockies_Baseball-00baa-27438Recent technological advancements through scientific research have had an impact on nearly everything we know, including sports. Research is constantly undertaken in physiology and the basic sciences to develop training protocols that maximize physical gains through optimal training protocols. Additionally, experts using high-speed cameras and sophisticated software programs evaluate technique and movement to find the most efficient way to perform a movement. All this and more is done to improve performance at all levels of athletics.

At the Major League level, pitchers throw at extreme velocities with precise control. No one exemplifies this trend better than the young star in Washington D.C., Stephen Strasburg. In his first 127 innings this season, he leads the league in average fastball velocity at 95.9 mph (FanGraphs Pitching Leaderboard 2012). Not only that, he is also able to effectively change speeds by throwing a curveball at an average speed of 80.5 mph and a change-up at 88.8 mph, leading to a third best 160 strikeouts (FanGraphs Pitching Leaderboard 2012, Major League Baseball Statistics 2012). Furthermore, his control is remarkable as shown by only giving up 34 walks to this point (Major League Baseball Statistics 2012). A common metric for individual pitching performance is the strikeout to walk ratio; Strasburg is third in the league at 4.71 (Major League Baseball Statistics 2012). Clearly, he is one of the most dominant power throwers in professional baseball right now.

Although pitchers do have an advantage in baseball, their job still comes with obstacles.  Strasburg must throw a 9-ounce baseball 60 feet and six inches into what is called the strike zone. The strike zone, as defined by Major League Baseball, is only 17 inches wide and runs upward from just below the kneecap to the midline between the shoulders and the belt (Major League Baseball Commissioner’s Office 2012). Not only is it difficult to throw the ball in this zone consistently, but also the batter at the plate is trying to make contact with the ball whenever it gets close. Experienced pitchers know a combination of throwing hard, changing velocities, and being accurate are the keys to maximizing the chances the ball will miss the sweet spot of the bat. Although Strasburg is an elite athlete who has learned how to do all these things extremely well, the principles behind his ability to throw the ball and be successful are ones that can be applied to any pitcher at any level.

In order to understand the more complex mechanisms at play in the throwing motion, a basic background into the fundamentals of anatomy and physiology is necessary. Many people know that muscles are the functional units that allow the body to move, but most know little else about what a muscle is composed of and how it works to achieve movement. Additionally, few people understand what the body must go through to fuel the movement of muscles.

The human body contains 400 skeletal muscles which work to achieve movement (Fox 1987). At a fundamental level, muscle is made up proteins (Seeley et al 2006). Muscles work by burning energy in order to create contractile force, which shortens the length of the muscle.  Muscle shortening can easily be seen when the arm goes from straight to bent by flexing at the elbow. Contraction occurs in the biceps brachii during this movement, but there is more than just that occurring.

If only one muscle group were associated with that part of the body, once a person flexed their biceps the arm would remain in that position; thankfully, this is not the case.  An antagonist group of muscles, the triceps brachii, which relaxed and extended when the biceps contracted, is now able to contract, straightening the arm. Most muscles within the body have this agonist-antagonist duality that allows us to function in a practical manner (Seeley et al 2006).

In order for triceps, biceps, or other muscles to move the body, they have to be attached to the skeleton in some manner.  This is the function of tendons, which are a type of fibrous connective tissue that have the strength to withstand tensile forces (Medline Plus Dictionary 2012). When a muscle contracts, it exerts a force on the tendon which pulls on the bone, creating movement (Plowman and Smith 2008). The direction of movement is determined by the direction the fibers are orientated and where the tendon is anchored(Plowman and Smith 2008).

What most people consider a single muscle is actually composed of many smaller units called myofibrils or muscle fibers (Plowman and Smith 2008). Each muscle fiber is composed of myofilaments, T tubules, and sarcoplasmic reticulum, among other things (Plowman and Smith 2008). Figure 1 gives a visual of the hierarchy of the muscle fiber.

The smaller myofilament houses the functional unit of the muscle, the sarcomere. The sarcomere consists of two major filaments: a thick filament composed of the protein myosin and a thin one composed of actin and tropomyosin, two proteins (Huxley and Hanson 1954, Seeley et al. 2006, Plowman and Smith 2008, Medline Plus dictionary 2012). A series of steps must take place in order for a signal from the brain to make a muscle contract.  First, calcium is released inside the cell, which changes the alignment of the tropomyosin, exposing sites where the heads of the myosin filaments can attach (Plowman and Smith 2008). After the myosin heads attach to the actin, forming a cross-bridge, they perform a power stoke to shorten the length of the fiber (Plowman and Smith 2008). A simple way to envision this ratchet type movement is to hold the forearm out straight and flex at the wrist. Now, adenosine triphosphate (ATP), the fuel source of cells, attaches to myosin, releasing the cross-bridge bond (Plowman and Smith 2008). The myosin heads return to their initial position so the process can repeat again to continue shortening of the muscle.  This process happens extremely fast and takes place many times over the length of contraction. The number of myofibrils that are recruited to carry out this action depends on the force required by the activity.

The ATP required for muscle contraction is produced in the body through three different systems. Although it is important to note that the three systems are not mutually exclusive, each system is the prime energy producer in different intensities of exercise.  Aerobic cellular respiration takes place when oxygen is present in the system, which generally occurs during long and light exercise like jogging or bicycling (Baechle and Earle 2008). The second system, anaerobic glycolysis, functions at higher intensities and shorter durations, like running a 200-meter sprint or biking up a steep hill (Baechle and Earle 2008). Finally, the ATP-PC system activates during high intensity activities that last only a few seconds (Baechle and Earle 2008). Simply based on this information, it is easy to see that pitching requires the use of the latter two energy systems to supply fuel.

Muscles Involved With the Pitch

When it comes to pitching, the muscles used to throw can be thought of as residing in two main categories: accelerators and decelerators. Of course, the accelerators are the ones that produce the high-speed velocities seen from Strasburg and others. However, decelerators are just as important in the throwing motion. A simple analogy is to think of having a car with a working gas pedal, but lacking any braking system.

During the delivery of the pitch, the muscles in the rotor cuff fire at a moderate intensity (Jobe et al. 1983, Escamilla and Andrews, 2009). Since these muscles function to keep the joint in place, their activity during this stage should be expected (Escamilla and Andrews, 2009). Furthermore, the deltoids show a moderate level of activity, which is attributed to the need for shoulder stabilization during the delivery (Escamilla and Andrews, 2009). Once the ball is released and the deceleration process beings, these muscles increase their activity to aid in injury prevention (Jobe et al. 1983, Escamilla and Andrews, 2009). Since the arm acts as a whip during the acceleration stage; these muscles assist in braking at the shoulder and preventing the ball of the humerus from coming out of the socket.

Moving to the upper arm, the biceps brachii show most activity after release of the ball (Jobe et al. 1984, Escamilla and Andrews, 2009). The biceps work in conjunction with the rotator cuff muscles to keep the shoulder in place.  The opposite is the case with the antagonist group, the triceps brachii.  Since this muscle group functions by extending the arm at the elbow, it should make sense that high muscle activity can be seen during acceleration and low activity during deceleration.

The last two upper body areas of activity that will be examined are the chest (pectoralis major) and the back (latissimus dorsi and the upper part of the subscapularis).  The pectoralis major has a high level of activity during the acceleration phase and a lower moderate level during the deceleration phase (Escamilla and Andrews, 2009). In the back, both aforementioned muscle groups exhibit extremely high levels of activity during acceleration.  Therefore, it can be concluded that these two groups play an important role in force generation. Although their activation levels are still considered high during deceleration, the forces are almost half of what is produced during the acceleration phase (Escamilla and Andrews, 2009).

Although data is somewhat sparse when it comes to force generation in the legs and core, some studies do indicate that these areas are important for force production and injury prevention (MacWilliams et al. 1998, Willardson 2007, Coleman 2009, Lehman et al. 2012). In his 2009 article, Dr. A. Coleman estimates that 50% of the power produced by a pitcher comes from the legs, with 30% initiating in the core and only 20% coming from the shoulder (Coleman 2009) Essentially, both the push off and landing phases have the ability to transfer energy up the trunk and impart force on the baseball.  This means that for as wiry as Strasburg is, he has the ability to generate tremendous amounts of force from his lower body and core.

Implications for Pitchers

Proper care must be taken in any sport to aid in avoiding injury.  For pitchers, the most delicate place is the glenohumeral joint in the shoulder.  Therefore, it is absolutely imperative that the musculature in this region be trained with carefully thought-out protocols (Escamilla and Andrews, 2009). Additionally, shoulder problems can start with inconsistencies in other locations.  For example, some throwers may experience anterior shoulder instability due to weak latissimus dorsi muscles and an overcorrection in the rotator cuff (Escamilla and Andrews, 2009). This indicates the need for strong back muscles to allow for proper muscle recruitment during maximal recruitment.

As stated above, the legs and core can be thought of as contributing approximately 80% to the force production in the throw.  Prepared athletes will use this knowledge to improve flexibility and strength in all aspects of the core.  This means that not only do the abdominal muscles need to be strengthened, but the lower back and hip muscles (flexors, extensors, adductors, abductors) do as well. Since so much power is generated in the legs, total lower body strength should be emphasized during training to create velocity and reduce the reliance on the shoulder (Perelli 1996, Coleman 2009). In a study soon to be published by Lehman et. al., they describe that lateral to medial jumps (side to side) have the highest correlation to an increase in velocity in comparison to other common lower body strengthening techniques (Lehman et al. 2012).

Training the muscles is not enough; the athlete must also train the appropriate fuel systems for optimal performance. It is the author’s opinion that since the duration of the pitching activity falls within the ATP-PC system and anaerobic metabolism, that these are the energy producing systems that should be trained. Although aerobic conditioning is necessary to build endurance, maximal force production likely comes from the other two energy producing systems and should be trained accordingly. This means a training regimen should include many short duration explosive activities done many times to simulate the short explosive nature of a pitch. It is important to remember that any training program should be done under the guidance and direction of trained professionals.  There is no magic formula that will maximize strength while eliminating the risk of injury, as exemplified by Steven Strasburg himself.

By: Josh Silvernagel, Graduate Student, Bioengineering, University of Utah
Josh Silvernagel received undergraduate degrees in Exercise Science and Mathematics from Bemidji State University (BSU) in Bemidji, MN.  During his undergraduate studies, he was a four year starter in baseball for the BSU Beavers, where he both pitched and played infield.  In addition to providing sport specific training for ametuer and professional athletes following school, Josh spent two years coaching the sport at both the collegiate and high school levels.  He is currently working on a Ph. D. in Bioengineering at the University of Utah, where he studies cardiac electrophysiology in the CARMA Center.  Josh and his wife, Danielle, are recently married.

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