Power is one of the most important features of muscular performance and is measured in watts. It has become evident to everyone in sports today that muscular “power” is as important if not more so than strength alone. Although there is an intimate relationship between force and velocity that make up the power equation, the ability to produce force at a rapid velocity of movement is what seems to characterize the elite athlete in many sports today. Power produced during exercise is highly dependent on the type of exercise performed. A long-distance runner may produce only 50 W with each stride cycle during a long-distance race. In contrast, a weightlifter may produce more than 7,000 W during the second phase of the pull during the clean and jerk (10). The underlying physiology of power plays a crucial role in helping the strength and conditioning specialist better understand how to train the power equation. The purpose of this review will be to give some basic insights into the underlying physiology of muscular power.
The classic force-velocity curve demonstrates that as the velocity of movement increases concentrically from zero velocity (4), the force produced is decreased. Conversely, as the velocity of movement increases eccentrically from zero velocity, the force increases (Figure 1a). The pattern of a force-velocity curve can also vary from joint to joint but a similar relationship for force and velocity for the 2 different muscle actions is maintained.
Typically, power is evaluated during the concentric muscle action of the force-velocity curve. Power can be defined as force × distance/time or force × velocity (10). Force (i.e., strength) plays a key role in power production and if not maintained with training can result in a decrease or no change in power production. Force refers to the mass of the resistance that is being displaced times its acceleration whereas velocity is the distance that the resistance is being displaced over the time of the movement (19). Peak power is achieved with moderate to minimal force at an intermediate velocity (14) (Figure 1b).
Compared with eccentric actions, concentric actions of muscles are capable of producing substantially less force (14). However, power output can be further increased when eccentric and concentric movements are used together to take advantage of the elastic properties of muscle within the stretch-shortening cycle (SSC) (17,23). This cycle begins with a rapid countermovement resulting in the stretching of the target muscle through eccentric action. A muscle is capable of being stretched because of its elastic component, which consists of the connective tissue that surrounds each organizational layer of muscle tissue. When a muscle is stretched, specific mechanoreceptors located within the muscle itself known as muscle spindle fibers are also stretched and send feedback to the central nervous system. This feedback causes an immediate signaling of the muscle fibers to contract to prevent potential tissue damage from overstretching. When synchronized with a concentric muscle action, this stretch reflex results in the increased acceleration of the body or limb involved in the movement. Inclusion of that SSC in an exercise results in greater power output as can be seen when a squat jump that has no SSC is compared with a countermovement vertical jump that has a rapid descent before an explosive ascent off the ground producing much greater power output. Plyometric training takes advantage of the SSC by using it in various exercises to help in the development of power with training.
MOTOR UNIT RECRUITMENT
The recruitment of motor units provides the physiological basis for force production at any velocity of movement. Although athletic movements occur as a direct result of skeletal muscle action, they occur in response to a variety of signals sent and received from the nervous system. The conscious controlled movements that generate power during physical activity are initiated in the motor cortex located in the frontal lobes of the cerebrum. Electrical signals making up the information quanta are then passed from the higher brain centers down the brain stem to the spinal cord where it can be used to stimulate specific motor units to ultimately dictate muscle actions (11) (Figure 2).
A motor unit consists of an alpha motor neuron and all the muscle fibers innervated by it. Motor units contain variations of either Type I or Type II muscle fibers and therefore are homogenous for one fiber type. An alpha motor neuron is an electrically excitable cell that initiates, receives, and transmits information concerning skeletal muscle activity. In classic neurons, dendrites are structures extending out at the top of the motor neuron that receive information and send it to the cell body located within the spinal cord, known as the soma, which processes the information received. Signals in the form of electrical charges known as action potentials can then be sent from the axon hillock, the junction between the soma and an axon, down a chain of axons to the neuromuscular junction, which connects the motor neuron with one of its muscle fibers, to stimulate the fiber to contract (7). The generation of an action potential in a motor neuron requires the summation of incoming electrical signals from the dendrites in the axon hillock to exceed a specific amount of stimuli termed the recruitment threshold (30).
The recruitment threshold of a motor neuron is directly related to the size of its axon; the larger the axon, the greater the amount of stimulation required (12). This principle is fundamental to the understanding of power because the size of the soma is in direct proportion to the size of the motor unit or the number of the muscle fibers innervated by the alpha motor neuron (8). Because smaller motor units have lower recruitment thresholds, they are recruited first. Larger motor units have higher recruitment thresholds but produce greater amounts of force. This order of motor unit recruitment progresses in the same manner regardless of the type of muscle action performed. As each muscle possesses a wide variety of motor units ranging in size, motor units are recruited in ascending order of size in what is referred to as “Henneman’s size principle” (12,13). In resistance training, the resistance load and the rate of acceleration will play a major role in dictating how many fibers are stimulated as a part of motor units that produce force. Some have proposed that there are motor units used primarily for power production although evidence to support this remains speculative.
In Figure 3, one can see this translated into terms of resistance loading because it relates to the number of motor units recruited. Those motor units not activated or stimulated by the external load or resistance used in the exercise essentially remain untrained except for the external profusion of metabolites and ions that are exposed to the fibers in a passive state. Thus, anabolism within the neuromuscular system occurs only with activation of motor units; yet, catabolism can occur with exposure of nonactivated motor unit’s fibers to catabolic substances such as oxygen reactive species, inflammatory cytokines, free radicals, cortisol, and so on. Thus, optimizing training session sequences is a vital concern not only for power development but for optimal conditioning in general.
Again, once a facilitatory signal reaches the neuromuscular junction, if enough quanta of neurotransmitter (i.e., acetylcholine, [ACh]) binds with the postjunctional receptors, the energy transformation (i.e., electrical to chemical to electrical) is completed and the muscle fibers are activated. With motor unit recruitment, if enough facilitatory neurotransmitters bind, then an “all-or-none” firing of the neuron occurs in that there is no partial firing or selective contraction of muscle fibers within a motor unit: either the fibers contract or they do not. Although facilitatory neurons interface with the postjunctional gap, one also finds inhibitory neurons that produce inhibitory neurotransmitters (gamma-aminobutyric acid) capable of neutralizing the facilitatory ACh signal. Such a mechanism can be used to modify movement direction, force, and power production necessary in many sport skills (e.g., making final alterations in a bat swing). Thus, skeletal muscles are capable of producing a wide spectrum of power production, ranging from slow precise movements to rapid forceful ones. The fluctuations in power development can be attributed to a number of different factors.
Rate coding or the frequency of signaling from the central nervous system to the motor unit is also an essential element of power production. Increasing signal frequency can result in greater power production because of an increase in the firing rate of motor units and a continual increase in a stepwise fashion of force (18). When the signal frequency reaches a high enough speed that the muscle fibers cannot completely relax in between, the muscle fiber can be restimulated while previous contractile activity is still occurring. The contractions combine on top of the previous contraction, resulting in a stronger more forceful contraction thereby contributing to the power via the force component of the power equation. This mechanism does have its so-called zone of contribution as the signal frequency increases. At some point there are diminishing contributions to power. When signal frequency is fast enough that the muscle fibers cannot relax to any degree, tetanus or a maximal force level is produced and this typically occurs at the higher end of the force-time curve. By that time, power is not the dominant outcome of the rate coding mechanism.
NUMBER OF MOTOR UNITS RECRUITED
The number of motor units recruited for a movement is one of the most important determinants of the amplitude of power produced because it dictates the amount of muscle cross-sectional area and the corresponding number of actin-myosin cross bridges to be used in the movement. Henneman’s size principle is probably the most important principle in understanding neuromuscular function as to the orderly recruitment of motor units (12,13). At the lowest levels of activation, only the smallest motor units are recruited and minimal power is generated. As this level of activation increases, the recruitment thresholds of larger motor units are surpassed, resulting in a greater number of motor units recruited and successively greater force and power production. At a certain level of stimulation, all the available motor units within the muscle are recruited, resulting in the highest force production. Again, based on the force-velocity curve for concentric actions, as force increases velocity gets slower and therefore again at some point the recruitment of more high-force motor units does not enhance the power equation as the velocity is slowed. This magnitude of force capable by a specific muscle is in part determined by the muscle fiber type and the amount of coverage (i.e., cross-sectional area of the fibers) of that type in a muscle along with the number of fibers.
NUMBER OF MOTOR UNITS IN A MUSCLE
Each skeletal muscle possesses a differing number of motor units varying in size corresponding to the functional role of the muscle itself. Finer control of power output can be achieved with a smaller ratio of muscle fibers to motor units. This is observed in extraocular muscles, which control the movement of the eye, which only contain between 5 and 10 muscle fibers per motor unit and are important in sports that depend upon hand-eye coordination (e.g., baseball). In contrast, the gastrocnemius, which has the capability of generating substantial amounts of power, may contain approximately 1,000 muscle fibers per motor unit. Thus, each skeletal muscle contains a ratio of muscle fibers to motor units according to the physiological functions it performs. Highly skilled movements will use motor units in combination that have fewer muscle fibers associated with it. For example, in a jump shot, maximal power is needed to get off the ground to reach a height in the air that is optimal for a shot but as one goes up the kinetic chain of movement and reaches the musculature in the hand that makes the final adjustments in the release of the ball, smaller motor units needed for fine control of that skill are used.
SLIDING FILAMENT THEORY
The process of muscular contraction is best explained by the sliding filament theory in which the sliding of the actin filaments over the myosin filaments causes the shortening of the muscle (15). After the motor unit has been recruited and the action potential travels down to the presynaptic terminal, the neurotransmitter ACh is released from vesicles inside the presynaptic terminal, a quanta is released into the neuromuscular junction where it binds to receptors on postjunctional region that is integrated into the sarcolemma of the muscle fiber. Channels on the sarcolemma open for the influx of Na+ ions, generating an action potential that descends through the transverse tubules (T-tubules) toward the core of the muscle fiber. The electrical charge disrupts an adenosine triphosphate (ATP)–mediated pump mechanism in the sarcoplasmic reticulum that allows Ca++ to be released into the sarcoplasm of the muscle fiber (cell). In other words, the action potential triggers voltage sensors within the T-tubules known as dihydropyridine receptors, which in turn stimulate Ca++ channels in the membrane of the sarcoplasmic reticulum called ryanodine receptors to release Ca++ions into the cytosol.
Once the Ca++ ions enter the cytosol (sarcoplasm of the cell), they can bind to a troponin C subunit of the troponin complex, causing a conformational change in the tropomyosin to move away from the active sites on the actin filament. Myosin crossbridges can now weakly bind to the exposed active sites on actin starting the formation of actomyosin complexes leading to stronger binding interaction with the active site on the actin filament that was not previously allowed because of the coverage of the tropomyosin protein. At rest, the myosin heads are normally bound to adenosine diphosphate (ADP) and phosphate (27) molecules. After the reaction and formation of the actomyosin complex, the Pi molecule is released from the myosin head, which causes the power stroke step in which myosin heads swivel at their hinged pivot point, pulling the actin filament over the myosin filament in a ratcheting-like movement toward the center of the sarcomere. Subsequently, the ADP molecule is released from the myosin head that now strongly binds to the active site on the actin filament.
As a single power stroke results in the shortening of a muscle by only approximately 1% of its resting length, this process must continue a number of times to fully contract the muscle (29). To detach from active sites on the actin filament, a myosin head must bind to an ATP molecule. Myosin ATPase, an enzyme that makes up the majority of the myosin head, hydrolyzes the ATP molecule into ADP and Pi, returning the myosin head back into its original resting position. The initial source for all muscular contractions is the free ATP within the muscle fiber (5). However, intramuscular ATP stores are limited and must be replenished by using one or more of the body’s energy systems. Maximal power is dependent upon immediate availability of ATP and thus the predominant energy source arises from the ATP- PCr system that consists of the ATP and phosphocreatine (PCr) stored in the muscle and its immediate chemical reactions to produce ATP.
When powerful muscle actions are required within a minimal time frame, high quantities of ATP must be produced and replenished immediately. Although ATP can be derived from both the anaerobic breakdown of glucose (anaerobic glycolysis) and the utilization of the aerobic pathway (Krebs cycle), it cannot meet the high instantaneous demands of the typical power actions in sport movements. As a result, ATP is provided by means of the PCr stores within the muscle fiber itself through the ATP-PCr system.
In the ATP-PCr system, the ADP produced during muscular contraction can be converted back to ATP by the enzyme creatine kinase because it promotes the reaction with intramuscular PCr. This process is responsible for producing the majority of ATP used during exercises lasting between 2 and 10 seconds. Although effective in limited time periods, PCr stores are rapidly depleted during the first 10 seconds of maximal exercise. In certain muscles, PCr stores can be fully depleted in approximately 4 seconds. Generally, muscle PCr stores are 50% replenished from full depletion after 1 minute of rest and fully restored upon 5–6 minutes of rest. Here is where creatine supplementation influences power and power endurance by increasing the intramuscular creatine pool (20).
Thus, strength and conditioning professionals should take the bioenergetic elements of the PCr system into account when prescribing training sessions involving maximal power output. The key here is that the rest period length between sets should be longer to optimize power output, and sets should not consist of more than 5 reps to optimize the quality of each repetition. One cannot get more powerful by training at lower-power outputs as in this case, it is quality of the repetition that counts. When to train power is also a concern as lower-power outputs will be observed when performing power training after practice or when chronically fatigued from previous workouts (Figure 4). Optimizing the power output is a function of using a small number of repetitions, allowing adequate rest periods, and having well-rested athletes to allow optimal training.
MUSCLE FIBER TYPES
Although the availability of ATP does play a role in preventing fatigue, it is the rate at which the myosin ATPases breaks down ATP that is the limiting component of contractile velocity (18). This means that although inadequate ATP may hinder performance, excessive amounts of ATP do not provide any physiological benefit for power output. Myosin ATPase exists in a number of different variations or isoforms, each possessing unique functional characteristics. Different isoforms of myosin ATPase break down ATP at different rates and thus impact contraction velocity and therefore power.
MYOSIN ATPASE HISTOCHEMICAL ANALYSIS
The specific isoforms of myosin ATPase present can be used to classify the specific muscle fiber type (20,26,27). In a myosin ATPase histochemical analysis, cross-sections from a muscle biopsy are stained and exposed to 3 different conditions of pH 4.3, 4.6, and 10.0, respectively. The intensity of the stain of each muscle type under the 3 conditions indicates which classification the muscle fiber type belongs to as a result of the myosin ATPase’s lability under different pH conditions (32,33). Muscle fiber types ranked from the most oxidative to the least are Type I—Type IC—Type IIC—Type IIA—Type IIAX—Type IIX. Additionally, one can identify small hybrid transition changes across the Type II profile by pH modulation of the assay (e.g., Type IIaX would be between the Type IIAX and Type IIX isoforms). An example of muscle fiber stains can be seen in Figure 5.
CHARACTERISTICS OF MUSCLE FIBER CLASSIFICATIONS
The rate at which the myosin ATPases of a muscle fiber type can breakdown ATP is inversely proportional to its oxidative capacity (20). This means that although the Type II muscle fiber subclasses have greater power output potential, they are more susceptible to fatigue and are less capable of buffering increasingly acidic intracellular environments. However, Type II muscle fibers do possess greater intramuscular ATP and PCr stores and increased activity of glycolytic enzymes, making them better suited for intermittent high-intensity exercise of short duration.
MUSCLE FIBER TYPE COMPOSITION
Fiber type percentages that make up the functional units of a motor unit vary by the role of a muscle in human motion and by individual. For example, a muscle in the abdominal area that is involved primarily with postural support is made up of primarily Type I muscle fibers, whereas in major prime mover muscles or in locomotive muscles such as the vastus lateralis one typically sees fiber types ranging from approximately 40 to 60% Type I to Type II (32). When ranges are higher or favor Type I or Type II fibers and their coverage, a more elite status exists in the performance potential. An elite marathon runner may have upward of 80 to 90% Type I muscle fibers. This allows for the physiological capability to run a sub-2:10.00 marathon. With the need to recruit over 80% of their motor unit pool, high percentages of Type II muscle fibers would be metabolically and mechanically inefficient leading to more rapid fatigue in such long distance races. Conversely, high levels of power cannot be produced unless the athlete has higher percentages and coverage of Type II motor units in the prime movers; yet, such extreme percentages of Type II muscle fibers (e.g., >70%) do not typically exist (9). Additionally, it is very important to remember that the coverage of the fiber type in the muscle is the vital concept as one can have 50% Type I fibers; yet, for example, 4 Type I muscle fibers may fit into 1 Type II fiber because coverage is a function of the cross-sectional area of the fibers themselves. Type II muscle fibers can be as large as 10,000 μm2, whereas Type I fibers are seen to be approximately 3,000–5,000 μm2.
Although fiber type percentages are similar in men and women, the cross-sectional areas of muscle fibers in men are typically larger than women. Type IIA fibers are the largest in men and are the predominant Type II fiber after a progressive resistance training program has occurred. In untrained women, interestingly, the Type I muscle fiber is larger than their Type II fibers but after training this relationship changes to what is seen in men; yet, even women body builders tend to have smaller fibers compared with the average man (2,3). To date, size differences between men and women provide one of the true sex-linked differences in human physiology. Still, one must be clear that equity of the comparisons made is paramount in this generalization and more research is needed comparing elite women power lifters with the average man.
Thus, the muscle fiber type composition and area coverage can play a vital role in determining an athlete’s success in a particular type of competition. More specifically, although anyone can improve power output, the absolute magnitude of power capabilities is influenced by muscle fiber type, size, and number of fibers. In fact, even more simplistically, body mass in men is a large determinant of maximal power output (25).
MUSCLE FIBER TRANSITION WITH TRAINING
The conversion of muscle fiber types from Type I to Type II or vice versa seems improbable except for minor changes because of neural sprouting during a damage and repair phenomenon as one’s muscle fiber composition seems to be set by genetics (21). An exception to this concept might be aging that can result in a loss of Type II motor units. However, changes in Type I and Type II fiber subtypes do occur with training exposure (1). In untrained individuals, many Type II fibers are classified the IIX subtype (approximately 30%) (32). However, a shift toward the Type IIA subtype occurs after undergoing a resistance training program that activates the higher threshold motor units that these fibers are associated with. Once activated, the transition toward the Type II A subtype starts. By the end of effective resistance training, almost all Type II muscle fibers are classified as Type IIA (1,21). If after training a high percentage of Type IIX fibers exist, the resistance used in the training program was not high enough to activate the motor units that these IIX fibers were a part of.
INHIBITION OF POWER
Animal studies monitoring electrically stimulated muscle actions have observed larger power output values than those with voluntary contractions (31). This indicates the maximal power output potential of a muscle is inhibited by certain physiological processes. Achieving maximal power output may be a result of disinhibition or the loss of inhibition by certain processes within the body (20). However, many types of inhibition are necessary processes to prevent tissue damage. As such, the strategy for improving athletic performance may be both the enhancement of certain physiological processes and disinhibition of others.
A great deal of research has focused upon the phenomenon of coactivation, or the activation of antagonist muscles along with the agonist muscles of a movement (6). Because antagonist muscles are used in movements in opposing directions by definition, increased activity results in a decrease in power output in the direction of the movement. Although they may be detrimental toward maximal power output, current research indicates that the antagonist muscles contract to stabilize the joint, allow for finer control of the movement, and prevent potential tissue damage from overextension (4).
GOLGI TENDON ORGAN
The Golgi tendon organ (GTO) is a proprioceptor organ located within the tendon that attaches the muscle to bone and monitors the amount of force being applied to the tendon (28). When a muscle contracts, it pulls on the tendon to move the bone. If the amount of force is too great on the tendon, the GTO is activated and inhibits the muscle to prevent any damage to the muscle, tendon, or bone. Although the GTO acts as a safety measure against injury, it limits the amount of force that can be developed by the muscle. Disinhibition of the GTO has been theoretically thought to help improve power output, however, at the possible expense of potential injury (16). Thus, reducing GTO activity without putting the joint at risk may be a potential mechanism mediating improved power output; whether this would work safely requires more research.
Power is part of any movement whether minimal or high intensity. The underlying mechanisms that mediate power involve a host of physiological characteristics within an individual’s neuromuscular system. The composition of the motor units as to muscle fiber size, type, and number play important roles as to the inherent strategies that an athlete brings to a sport or event. Optimal training based on understanding the bioenergetics of recovery and timing of the training session is a vital design concern for program development (22,24). Training concepts for optimizing central or peripheral facilitation versus inhibition within the nervous system remains an area that needs more research. Henneman’s size principle is a major concept that needs to be understood and governs much of what we understand of how loading affects motor unit recruitment (8). The underlying mechanisms of power development give important insights into conditioning program designs for improving all athletes’ power capabilities and performance.
1. Adams GR, Hather BM, Baldwin KM, Dudley GA. Skeletal muscle myosin heavy chain composition and resistance training. J Appl Physiol 74: 911–915, 1993.
2. Alway SE, Grumbt WH, Stray-Gundersen J, Gonyea WJ. Effects of resistance training on elbow flexors of highly competitive bodybuilders. J Appl Physiol 72: 1512–1521, 1992.
3. Alway SE, Stray-Gundersen J, Grumbt WH, Gonyea WJ. Muscle cross-sectional area and torque in resistance-trained subjects. Eur J Appl Physiol Occup Physiol 60: 86–90, 1990.
4. Behm DG, Anderson K, Curnew RS. Muscle force and activation under stable and unstable conditions. J Strength Cond Res 16: 416–422, 2002.
5. Brooks GA, Fahey TD, White TP. Exercise Physiology: Human Bioenergetics and Its Applications. Mountain View, CA: Mayfield Publishing, 1996.
6. De Luca CJ, Mambrito B. Voluntary control of motor units in human antagonist muscles: Coactivation and reciprocal activation. J Neurophysiol 58: 525–542, 1987.
7. Deschenes MR, Covault J, Kraemer WJ, Maresh CM. The neuromuscular junction. Muscle fibre type differences, plasticity and adaptability to increased and decreased activity. Sports Med 17: 358–372, 1994.
8. Duchateau J, Enoka RM. Human motor unit recordings: Origins and insight into the integrated motor system. Brain Res 1409: 42–61, 2011.
9. Fry AC, Schilling BK, Staron RS, Hagerman FC, Hikida RS, Thrush JT. Muscle fiber characteristics and performance correlates of male Olympic-style 1lifters. J Strength Cond Res 17: 746–754, 2003.
10. Garhammer J. A review of power output studies of Olympic and powerlifting: Methodology, performance prediction, and evaluation tests. J Strength Cond Res 7: 76–89, 1993.
11. Gordon T, Thomas CK, Munson JB, Stein RB. The resilience of the size principle in the organization of motor unit properties in normal and reinnervated adult skeletal muscles. Can J Physiol Pharmacol 82: 645–661, 2004.
12. Henneman E. Relation between size of neurons and their susceptibility to discharge. Science 126: 1345–1347, 1957.
13. Henneman E. The size-principle: A deterministic output emerges from a set of probabilistic connections. J Exp Biol 115: 105–112, 1985.
14. Hoffman JR. NSCA's Guide to Program Design. Champaign, IL: Human Kinetics, 2012.
15. Huxley AF. Cross-bridge action: Present views, prospects, and unknowns. J Biomech 33: 1189–1195, 2000.
16. Issurin VB. Vibrations and their applications in sport. A review. J Sports Med Phys Fitness 45: 324–336, 2005.
17. Jones NL, McCartney N, McComas AJ. Human Muscle Power. Champaign, IL: Human Kinetics, 1986.
18. Kamen G, Roy A. Motor unit synchronization in young and elderly adults. Eur J Appl Physiol 81: 403–410, 2000.
19. Knuttgen HG, Kraemer WJ. Terminology and measurement in exercise performance. J Appl Sport Sci Res 1: 1–10, 1987.
20. Kraemer WJ, Fleck SJ, Deschenes MR. Exercise Physiology: Integrating Theory and Application. Baltimore, MD: Lippincott Williams & Wilkins, 2012.
21. Kraemer WJ, Patton JF, Gordon SE, Harman EA, Deschenes MR, Reynolds K, Newton RU, Triplett NT, Dziados JE. Compatibility of high-intensity strength and endurance training on hormonal and skeletal muscle adaptations. J Appl Physiol 78: 976–989, 1995.
22. Newton RU, Kraemer WJ, Hakkinen K. Effects of ballistic training on preseason preparation of elite volleyball players. Med Sci Sports Exerc 31: 323–330, 1999.
23. Newton RU, Murphy AJ, Humphries BJ, Wilson GJ, Kraemer WJ, Hakkinen K. Influence of load and stretch shortening cycle on the kinematics, kinetics and muscle activation that occurs during explosive upper-body movements. Eur J Appl Physiol Occup Physiol 75: 333–342, 1997.
24. Newton RU, Rogers RA, Volek JS, Hakkinen K, Kraemer WJ. Four weeks of optimal load ballistic resistance training at the end of season attenuates declining jump performance of women volleyball players. J Strength Cond Res 20: 955–961, 2006.
25. Patton JF, Kraemer WJ, Knuttgen HG, Harman EA. Factors in maximal power production and in exercise endurance relative to maximal power. Eur J Appl Physiol Occup Physiol 60: 222–227, 1990.
26. Pette D, Staron RS. Myosin isoforms, muscle fiber types, and transitions. Microsc Res Tech 50: 500–509, 2000.
27. Pirani A, Vinogradova MV, Curmi PM, King WA, Fletterick RJ, Craig R, Tobacman LS, Xu C, Hatch V, Lehman W. An atomic model of the thin filament in the relaxed and Ca2+-activated states. J Mol Biol 357: 707–717, 2006.
28. Potts JT. Inhibitory neurotransmission in the nucleus tractus solitarii: Implications for baroreflex resetting during exercise. Exp Physiol 91: 59–72, 2006.
29. Ruegg J. Calcium in Muscle Activation. Berlin, Germany: Springer-Verlag, 1992.
30. Scalettar BA. How neurosecretory vesicles release their cargo. Neuroscientist 12: 164–176, 2006.
31. Schwindt PC. Membrane-potential trajectories underlying motoneuron rhythmic firing at high rates. J Neurophysiol 36: 434–439, 1973.
32. Staron RS, Hagerman FC, Hikida RS, Murray TF, Hostler DP, Crill MT, Ragg KE, Toma K. Fiber type composition of the vastus lateralis muscle of young men and women. J Histochem Cytochem 48: 623–629, 2000.
33. Staron RS, Hikida RS, Hagerman FC. Myofibrillar ATPase activity in human muscle fast-twitch subtypes. Histochemistry 78: 405–408, 1983.