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.

 

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.

 

 

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