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Lab 8 Muscle Physiology Measures of Strength Development & Fatigue - Biology

Lab 8 Muscle Physiology  Measures of Strength Development & Fatigue - Biology


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Learning Objectives:
At the end of the lab each student will be asked to:

1) Determine the differences in strength development between subjects based on gender and between the concepts of “dominance” of use.
2) Observe, record, and correlate relative amount of total motor unit recruitment that occurs within a muscle group with increased strength production.
3) Distinguish between mechanical (peripheral) fatigue and cognitive (central) fatigue.

Pre-Lab:

1) What is the importance of a recovery period of 5-minutes for each participant?
2) What principle explains why strength increases when recruiting larger fibers in the muscle?
3) Complete your hypothesis to test in the lab.

Introduction:

Skeletal muscle is an excitable tissue made of several tubular cells (muscle fibers) that form a cylindrical collection of tissues (fascicles). These fascicles run the length of the muscle from the tendon of origin to the tendon of insertion see figure 1. Additionally, skeletal muscles possess unique characteristics. Skeletal muscles are voluntarily controlled tissue (needs nervous system control, whether the control is conscious or not) and exhibit electrical characteristics that make the tissues irritable (can change its membrane potential when stimulated). These two features enable us to explain the basis for the function of skeletal muscle through what is generally referred to as the excitation-contraction coupling of strength production. Additionally, skeletal muscle tissue is contractile (able to shorten when electrically stimulated), extensible (able to stretch beyond its resting length), elastic (able to return to its original shape), and plastic (able to change to meet new demands for strength, power, or work production). The principle of contractility, elasticity and extensibility explains how active (actin and myosin) and passive (connective proteins) forces form the tension within the fascicles and motor units of the skeletal muscle that results in the visible morphological changes of a muscle during active force production. The sequence events in force production, that leads to ever greater response from the muscle fiber, is based on a continuum of responses within the fascicles and motor units beginning with a twitch (due to a single contraction episode), and with continuous excitation progresses through Treppe effect (as the summation events occur within the fascicles and between motor units due to repeated excitations), eventually leading to the full muscle Tetany (whole muscle contraction) based on the pattern of recruitment, figure 2.

Figure 1. Anatomy of the skeletal muscle displaying the pattern of tissue interaction and divisions of the functional units of the muscle.

Figure 2. The relationship between timing stimulation and the contraction strength (mechanical force) development within a muscle fiber based on the Treppe effect leading to tetany of contraction that we normally associate as a muscle contraction.

Since the process of formation of a muscular contraction is under voluntary control and can be modified by cognitive desire or focus. As such, a person modulates the recruitment, and strength produced, from a muscle thereby leading to greater, or reduced, strength production based on desire for strength. All activity along the path of voluntary control is due to the excitation-contraction coupling between the skeletal muscle and the motor neuron that innervates that skeletal muscle’s motor end plate, all of which begins with the release of neurotransmitter acetylcholine (ACh) onto the skeletal muscle which leads to whole muscle fiber depolarization to threshold of stimulus and initiates the contraction of the muscle gaster. The way this interaction occurs is through the motor unit, single motor neuron and all fibers it innervations. Within each of muscle there will be a varying number of motor units (m.u.); the total number of m.u. within the muscle is dependent upon the type of muscle and the type of movement that is being controlled. Generally, the finer (more dexterous) the motor movement, the greater number of m.u. are involved (fewer muscle fibers per motor neuron) in the recruitment, while less motor control fewer units (fewer motor neurons per muscle fiber) in the recruitment.
When developing contractile strength, units are selectively recruited based on a continuum of threshold for excitation (the Size Principle) from the lowest, easy to recruit, to the highest, hardest to recruit, threshold based on the amount of strength development necessary, figure 3. This pattern of recruitment is developed in relation to the diameter of the muscle fiber, with the larger cross-sectional area providing a greater strength capacity but also needing a higher level of stimulation to cause excitation of the membrane. This concept is referred to as Henneman’s size principle. Each muscle fiber is being recruited along a gradient of a threshold potential reached by the individual muscle fibers within the muscle gaster, see figure 4. The selection of recruitment for different m.u. will proceed to meet the demand for strength production in such a way that a continuous contraction can be maintained throughout the length of the muscle for the duration of contraction time, referred to as the time under tension. This pattern of contraction within the muscle is based on the recruitment of individual muscle fibers beginning from the central region of the muscle gaster and traversing laterally until the entire recruited muscle is contracting to meet the demand. Because of the plasticity that muscles show, as you learn to recruit the muscle to produce a desired level of strength, you alter the way that you recruit the muscle. Where instead of recruiting throughout the continuum, you only recruit what is needed at any point in time within the contraction for that amount of strength.

Figure 3. Graphical representation of the generalized pattern of recruitment of motor units of skeletal muscles based on fiber type, activation threshold, and force production capacity of the fiber type and motor units based on Henneman’s size principle.

Figure 4. Overview of the relative activation/non-activation of skeletal muscle tissue) based excitation to match the demand for strength along with the relative threshold of activation of the motor unit within the skeletal muscle being recruited based on Henneman’s size principle.

The pattern of recruitment throughout the muscle can be measured not only by the elicited motion, but also through the electrical activity at the muscle during activation, known as electromyography (EMG). This analysis of electrical activity gives insight into the amount of muscle recruitment that occurs during periods of rest versus periods of maximal and near maximal force production. For most clinical situations, such EMG analysis is performed via surface electrodes placed near the origin and insertion tendons of single muscles or groups of muscles. These electrodes do two things: 1) record the change in electrical activity across the muscle and 2) indicate the relative amount of muscle being recruited in relation to either the external load being applied, or the stimulation of a motor neuron linked with a nerve conduction velocity test. When coupled with a recording of force production (via dynamometry), this gives a clinician an integrated level of data to determine the amount of muscle being recruited and thus the maximal volitional contraction (MVC). This understanding of MVC provides both clinician and patient with an understanding of differential recruitment during biofeedback within a course of neurological treatment, and, in addition, provides insight into the course of degeneration and atrophy that accompanies many degenerative neurological diseases.
A combination of muscle contraction patterns is involved in most EMG studies. Typically, they involve the use of a prolonged isometric (no movement) contraction. The use of the isometric contraction allows for the recruitment of various m.u. to provide the constant state of tension throughout the length of contraction time. This graph of force production is generally noted by a gradual “ramping up” to “plateau” to rapid “ramping down” graph of strength, see figure 5. In creating this graph, the individual and clinician obtain an understanding of recruitment, as well understanding the general order of fiber recruitment based on the fundamentals of the size principle. This pattern of recruitment and graph will mirror the continuum of increasing force production and the inverse relationship with respect to time needed to fatigue the fibers.

Figure 5. Graphical representation of the isometric contraction based on the time of contraction and the maximal force.

Additionally, discussion of any unit must also find the rate of twitch formation, i.e. slow-twitch and fast-twitch. Twitch formation describes the rate that the excitation-contraction coupling occurs, or how quickly the binding sites on the actin become exposed once exposed to calcium (Ca++) ions and the movement of the myosin heads. The rate of twitch formation within the muscle fiber will be influenced by the metabolic process utilized to regenerate ATP necessary for the contraction. When combined, the relative thresholds, the twitch speed and the metabolic process for regenerating ATP gives rationale to how the continuum of motor units seen within the size principle and the progressive loss of strength that is demonstrated in sustained isometric contractions. As those small fibers and units have a low force capacity but is long to fatigue whereas the larger fibers and units that have high force capacity but are quick to fatigue. The skeletal muscle is thus recruited to provide the force for movement with the smaller fibers and unit continually recruited and the progressively larger ones being selectively and intermittently recruited to meet the requirement for the activity and relative to the level of fatigue, see figure 6.

Figure 6. Description of the relationship between muscle fiber recruitment relative to the maximal force production (%1RM) and time to fatigue.

There are key aspects to responses noted in relation to EMG studies. First, there is often a relationship that shows that men are able to produce greater force than women. This gender difference is based on a) the larger muscle mass that men tend to have compared to women, and b) the basal level of testosterone and integrated testosterone response to periods of exertion leading to greater muscle excitation. Second, the cognitive involvement controlling the recruitment of the skeletal muscle means that changing cognitive involvement (or encouragement) to develop the skeletal muscle force will modulate. As such, EMG activity, force development and time to fatigue can all be adjusted; where fatigue is any reduction of force capacity across the muscle from the level of force produced at the beginning of the sustained contraction. This fatigue in contraction is based on several aspects of muscle anatomy and physiology. There is only a limited concentration of ATP within the skeletal muscle of the body (enough to perform less than a few seconds of cellular activities) and as ATP is required to sustain the energetics of the muscle contraction it must be regenerated, regardless of the type of motor unit being recruited. It begins with the use of the ATP-cP pathway and then progresses into catabolism of molecules to provide the free energy required to regenerate ATP for the cell. The very moment that the skeletal muscle changes to the use of catabolism for ATP regeneration, the muscle has entered fatigue (as there is a delay in the cycle of ATP to allow for muscle contraction to continue). This reduction of force capacity continues as the catabolic pathways of energetics proceeds into what are called the aerobic pathways. This is not due to the “accumulation of metabolic wastes” but instead due to the smaller fibers that are being recruited for force production, see figure 6. Since the aerobic pathways require a high concentration of oxygen within the cell, these aerobic muscle fibers must remain relatively close to the capillaries within the skeletal muscle and thus have a limited CSA. As there is less CSA, these fiber types have a lower force capacity than the large fibers that were being recruited at the maximal level of force production; resulting in the progressive decrease in force from the maximum that is seen in sustained “isometric” contractions. Along with this issue of ATP regeneration comes the idea of cognitive recruitment (i.e. central drive) and cognitive withdrawal from exercise (i.e. central fatigue). When performing sustained contractions, these central issues focus on the sensation of wanting to do the activity. Central fatigue is due to several factors: changes in the muscle morphology (microdamage from the contraction), accumulation of heat within the muscle (byproduct of metabolic processes not being 100% efficient), or even boredom. It is not due to what some text ascribes to accumulation of metabolites (most discuss lactate, which is shuttled out of the fiber and transported to other tissues) or restriction of blood flow (which does occur but only after extremely prolonged, whole gaster isometric contraction), figure 7. More importantly, when there is high self-efficacy, or external motivation for the exertion, central drive will override many peripheral signals that would normally lead to central fatigue and allow for prolonged sustained contraction at moderately elevated levels from the point where fatigue first is noticed.

Figure 7. Feedback initiating muscle inhibition leading to the onset of fatigue through reduced activation and recruitment of the muscle due to the accumulation of metabolic wastes, intracellular damage and alteration of temperature following sustained muscle contraction.

Strength Comparison
Along with examining the changes in strength that occurs during sustained contractions, we can also use isometric contractions for comparison of strength between individuals. In this case, we will examine how strength of contractions can vary based on the use of the limb (i.e. dominant versus non-dominant hand) as well as between genders (i.e. males versus females). In these comparisons there are several concepts of muscle physiology that are important to recall. First of which is related to the concept of the S.A.I.D. (Specific Adaptations to Imposed Demands) principle and muscle adaptations that will occur with greater use. Based on this principle, the more often we use a muscle or pattern of recruitment within the muscle, more efficient we are at recruiting the muscle and the larger the muscle will become (hypertrophy). As such, the more used a muscle is the greater the work and strength capacity the muscle will exhibit. Therefore, one might expect that the dominant hand would be more efficiently recruited than the non-dominant hand in the analysis of the handgrip strength leading to lower EMG recordings at relatively the same level of strength seen in the non-dominant hand. Secondly, there are gender differences in muscle cross-sectional areas stemming from residual effects of higher levels of testosterone. As such, males tend to have higher latent strength capacity than females. These gender differences are noted in the standardized grip-strengths used to establish aspects of fitness for individuals. Additionally, using these normative we can also gradate how individual compare to the whole population, table 1. In which, lower (i.e. “weaker”) handgrip is associated with poor musculoskeletal fitness and linked with impaired health status issues associated with overfatness. From which one can evaluate and determine one aspect of their overall relative fitness. Within these normative values, secondary demographic aspects of muscle physiology can be seen, as grip strength reduces (along with overall musculoskeletal fitness) with age. Studies show that among men, peak values of 49–52 kg/cm2 are reached in the fourth decade of life, whereas females exhibit peak values of 31 kg/cm2 in third to fourth decade. In which these demographic differences can be attributed to sarcomere and muscle fascicle CSA, use and disuse of digital flexors and overall robustness of anabolic and growth signals across the life span. Moreover, based on differences in growth signals and responses to use and disuse it would not be surprising to see those that regularly stress the muscles (i.e. physical activity and recruitment of the muscle) to exhibit higher levels of strength, S.A.I.D. principle adaptations, relative to those muscles less regularly recruited.

Table 1. Grip strength (kg/cm2) norms and classifications for musculoskeletal fitness by age and gender.

Age (year)

Gender

Grip Strength

“Weak”

“Normal”

“Strong”

18-19

Female

< 19.2 kg/cm2

19.2-31.0 kg/cm2

> 31.0 kg/cm2

Male

< 35.7 kg/cm2

35.7-55.5 kg/cm2

> 55.5 kg/cm2

20-24

Female

< 21.5 kg/cm2

21.5-35.3 kg/cm2

> 35.3 kg/cm2

Male

< 36.8 kg/cm2

36.8-56.6 kg/cm2

> 56.6 kg/cm2

25-29

Female

< 25.6 kg/cm2

25.6-41.4 kg/cm2

> 41.4 kg/cm2

Male

< 37.7 kg/cm2

37.7-57.5 kg/cm2

> 57.5 kg/cm2

30-34

Female

< 21.5 kg/cm2

21.5-35.3 kg/cm2

> 35.3 kg/cm2

Male

< 36.0 kg/cm2

36.0-55.8 kg/cm2

> 55.8 kg/cm2

35-39

Female

< 20.3 kg/cm2

20.3-34.1 kg/cm2

> 34.1 kg/cm2

Male

< 35.8 kg/cm2

35.8-55.6 kg/cm2

> 55.6 kg/cm2

40-44

Female

< 18.9 kg/cm2

18.9-32.7 kg/cm2

> 32.7 kg/cm2

Male

< 35.5 kg/cm2

35.5-55.3 kg/cm2

> 55.3 kg/cm2

45-49

Female

< 18.6 kg/cm2

18.6-32.4 kg/cm2

> 32.4 kg/cm2

Male

< 34.7 kg/cm2

34.7-54.5 kg/cm2

> 54.5 kg/cm2

50-54

Female

< 18.1 kg/cm2

18.1-31.9 kg/cm2

> 31.9 kg/cm2

Male

< 32.9 kg/cm2

32.9-50.7 kg/cm2

> 50.7 kg/cm2

Thus, the purpose of the experiment is to examine the aspects of strength development and fatigue of forearm flexors. In which we will examine the relationship between strength and fatigue based on the gender of the participants (male/female), regularity of having to lift a heavy object each day, days of weight training (resistance training) per week, and age. In this we will have a secondary purpose of examining the role that central drive has on the development and then maintaining of maximal contraction.

References:

Aagaard P. 2004. Making muscles “stronger”: exercise, nutrition, drugs. J Musculoskelet Neuronal Interact. 4(2). 165-174.
Clark JE, Rompolski K, Comstock BA. 2018. Rethinking how we talk about and teach muscle fatigue. HAPS Educator 22(3).229-241.
Henneman E, Olson CB. 1965. Relations between structure and functions in design of skeletal muscles. J Neurophysiol. 28; 581-598.
Henneman E. 1985. The size-principle: a deterministic output emerges from a set of probabilistic connections. J. Exp. Biol. 115; 105-112
Keener J, Sneyd J. ED. 2009. Ch. 15: Muscle, from Mathematical Physiology I: Cellular Physiology. Springer. 717-772
Massy-Westropp NM, Gill TK, Taylor AW, Bohannon RW, Hill CL. 2011. Hand grip strength age and gender stratified normative data in a population-based study.BMC Research Notes 4:127
Narici M, Maganaris C. 2006. 9: Muscle architecture and adaptations to functional requirements, from: Skeletal Muscle Plasticity in Health and Disease, From Genes to Whole Muscle, ED: Bottinelli R and Reggiani. Springer, 265-288
Pette D. Ch.1: Skeletal muscle plasticity- history, facts and concepts, from: Skeletal Muscle Plasticity in Health and Disease, From Genes to Whole Muscle, ED: Bottinelli R and Reggiani. Springer, 1-27Sandri M. 2008. Signaling in muscle atrophy and hypertrophy. Physiology (Bethesda) 23; 160-170
Roberts HC, Denison HJ, Martin HJ, Patel HP, Syddall H, Cooper C, Sayer AA. A review of the measurement of grip strength in clinical and epidemiological studies: towards a standardized approach. Age Ageing 40 (4): 423-429
Schiaffino S, Sandri M, Murgia. 4: Signalling pathways controlling muscle fiber size and type in response to nerve activity, from: Skeletal Muscle Plasticity in Health and Disease, From Genes to Whole Muscle, ED: Bottinelli R and Reggiani. Springer, 91-119

Hypothesis:

Procedures:

Materials:

Handgrip dynameter

Stopwatch

Methods:

PART 1: Maximal Volitional Contraction:

1. Explain to the test subject that they will now be performing the strength-testing portion of the experiment. In the test, they will begin to squeeze the dynamometer without allowing for any movement or deviation from the testing position. The clench should build up over a 5-second period with a hold for 10-seconds and then a ramp down over 5-seconds

Figure 8 Positioning for testing of strength via handgrip dynamometer, note that you may have subject either standing or seated (but seated in unsupported position)

2. After explaining the process, have the test subject assume the position shown in figure 8

a. Give the subject a countdown, “3… 2… 1… GO!” where on “GO” then begin to squeeze, at 5-seconds give encouragement to “squeeze as hard as possible” and then continued encouragement to “Keep holding” for the 5-second isometric hold
b. Record the grip force (strength) during 5-second hold
c. As they get toward 5-sconds of holding, give the cue to “slowly start relaxing” and give count down of “4…3…2…1…Relax”

3. Have subject 1 rest for 2-minutes. During the rest, have subject 2 perform their isometric grip test
4. After 2-minute rest, repeat step 2 for the non-dominant side
5. Repeat for subject 2.
6. Repeat for 3 total trials, for each hand and each subject. Average the three trials
7. Determine the 100%, 50% and 25% grip strength

a. 100% is the maximal strength that was obtained during the maximal isometric hold
b. 50% is ½ of that number and 25% is ¼ of that number

SUBJECT 1:

Dominant:100 % =kg/cm2; 50%= kg/cm2; 25%= kg/cm2

Non-Dominant:100 % =kg/cm2; 50%= kg/cm2; 25%= kg/cm2

SUBJECT 2:

Dominant:100 % =kg/cm2; 50%= kg/cm2; 25%= kg/cm2

Non-Dominant:100 % =kg/cm2; 50%= kg/cm2; 25%= kg/cm2

PART 2: Time to Fatigue
1. Following 5-minutes of rest, have the test subject grasp the handgrip dynameter with their dominant-hand and assume the testing position that has been used throughout the experiment
2. Make sure that the instructor has started the “Workout Music” so that the testing environment provides an external motivation to allow for maximal performance
3. Explain to the test subject that they’re now going to be performing a prolonged maximal clench where they need to “squeeze as hard as possible” for the entirety of the test either until they are no longer able to continue to hold the clench or you have instructed them to relax as they are no longer able to maintain a clench strength of at least 25% of their MVC
4. Giving a countdown “3…2…1… GO!” Have your test subject now clench (keeping upper extremity in the neutral testing position) to maximal force as measured previously obtained in part 2. As they clench their fist, click “Start” on the stopwatch and give them constant encouragement “Keep Squeezing” as they ramp up to maximal strength.

a. Once maximal force had been reached start the stopwatch and continue to have test subject clench at what they perceive to be maximal force until they are unable to maintain 25% of MVC. (Note that force will waiver as contraction continues, note the number of times that the subject is able to get force above 50% MVC until force production is at 25% MVC and unable to return to 25% MVC)

i. Once the test subject is unable to maintain 50% MVC record the time from the stopwatch, do not stop the timer on the stopwatch and the grip strength

b. As contraction continues past the first few seconds, the test subject will need continuous encouragement that cannot be solely provided by the “Workout Music” in the lab room

i. (Using positive and negative reinforcements) provide constant positive encouragement to the test subject “You got this… don’t stop”; “Don’t let (fill-in name) beat you”

c. Remind them to breathe throughout the hold
d. As contraction continues allow the subject to get feedback from the computer screen as you both see a reduction in contraction strength, verbally cue them to get the strength curve back towards maximal force.
e. Once test subject is consistently below 25% MVC, tell them to “Stop” note that some test subjects may have stopped before this time. Click “stop” on the stopwatch and record the time and grip strength and the moment that the subject stopped holding the squeeze.

5. Give your test subject 5-minutes of rest. While resting, have the second test subject complete their dominant hand grip test
6. Repeat steps 4-6 for the non-dominant hand.
7. Input data into large group data tables (Google Doc), based on where subject falls for gender and determine averages for contraction strength, EMG activity, and times to fatigue.

Results:

Demographic Information:

Gender:

Age:

Days of Weightlifting/week:

Regularly Required to Carry Objects Heavier than 20-lbs.:(Yes/No)

Table 2. Grip strength (kg/cm2) produced via handgrip dynamometer during the test for maximal volitional contraction.

SUBJECT 1

SUBJECT 2

Measurement Segment

Dominant Hand Strength (kg/cm2)

Non-dominant Hand Strength (kg/cm2)

Dominant Hand Strength (kg/cm2)

Non-dominant Hand Strength (kg/cm2)

Grip 1

Grip 2

Grip 3

Average Isometric

Maximal Volitional

Contraction

Table 3. Results for the measures of maximal strength (MVC) production via handgrip dynamometer (kg/cm2) and time (seconds) for subject to degrade in force production from 100% MVC to 50 % MVC and then 25% MVC.

SUBJECT 1

100% MVC (kg/cm2)

50% MVC (kg/cm2)

25% MVC (kg/cm2)

Time of contraction 100%-to-50% MVC

(sec)

Time of contraction

50%-to-25% MVC

(sec)

Total time of contraction 100-to-25% MVC

(sec)

Dominant

Non-Dominant

SUBJECT 2

100% MVC (kg/cm2)

50% MVC (kg/cm2)

25% MVC (kg/cm2)

Time of contraction 100%-to-50% MVC

(sec)

Time of contraction

50%-to-25% MVC

(sec)

Total time of contraction 100-to-25% MVC

(sec)

Dominant

Non-Dominant

Note time is in seconds, convert each minute to 60 seconds: Time of Contraction= (# minutes*60) + seconds of the minute

Example: 3:30 contraction time has a Time= (3x60) + 30=180+30 = 210 seconds

**Upload your data to the data table in Google Documents for Analysis and Lab Report**

Discussion: Using the Google Doc Data Tables for group data and analysis.

In at least 2 well-formulated and coherent paragraphs, discuss the findings of the experiment based on the concepts of muscle physiology related to strength, recruitment, and fatigue. (In the analysis of results and presentation of findings think about do not answer as individual questions: What differences can be seen between dominant and non-dominant sides for the test subjects? To what can you ascribe these differences in observations? What gender differences are observed? What can be a possible explanation for the differences observed between genders? What are other factors that can influence the results observed in your experiment? Why would there be variability in someone’s ability to produce additional force after “fatigue” has begun? What factors are involved in that variability of force production? Why?)


RATE OF FORCE DEVELOPMENT (RFD)

This article explains everything you need to know about the RFD, including how to measure it and improve it.

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By Owen Walker
9 Mar 2016 | 7 min read

Contents of Article

  1. Summary
  2. What is the Rate of Force Development (RFD)?
  3. What causes an increase in Rate of Force Development?
  4. Why is the Rate of Force Development important for Sports?
  5. How to Calculate the Rate of Force Development
  6. Validity and Reliability
  7. Practical Application: How to improve the Rate of Force Development
  8. Conclusion
  9. References
  10. About the Author
  11. Comments

Summary

The rate of force development (RFD) is a measure of explosive strength, or simply how fast an athlete can develop force. Athletes with higher rates of force development have been shown to perform better during numerous physical performance tests. This, therefore, highlights the potential importance this value has in the role of athletic development. Whilst many forms of training have been shown to improve the rate of force development in untrained individuals, only resistance and ballistic training have shown to enhance this quality in trained athletes. Lastly, though there are multiple ways to measure the rate of force development, the time-interval sampling windows appear to be the most reliable.

What is the Rate of Force Development (RFD)?

The rate of force development (RFD) is a measure of explosive strength, or simply how fast an athlete can develop force – hence the ‘rate’ of ‘force development’. This is defined as the speed at which the contractile elements of the muscle can develop force (1). Therefore, improving an athlete’s RFD may make them more explosive as they can develop larger forces in a shorter period of time. Developing a more explosive athlete may improve their sporting performance. In fact, higher RFDs have been directly linked with better jump (2-8), sprint (9), cycling (10), weightlifting (5, 6), and even golf swing performances (11).

The RFD is commonly believed to be manifested during the stretch-shortening cycle (SSC) . Depending upon the duration of the stretch-shortening cycle (SSC), exercises are classified as either slow- (≥250 milliseconds) or fast-SSC (≤250 milliseconds) movements (12). For example, a countermovement jump (CMJ) is classified as a slow-SSC movement as the duration of the SSC lasts approximately 500 milliseconds (3). On the other hand, sprinting is classified as a fast-SSC movement as the duration of the SSC lasts between 80-90 milliseconds (13). Table 1 displays the SSC durations of some common exercises.

Because the movement is slower, exercises with slow-SSC have a longer timeframe to develop force than those with a fast-SSC, this means slow-SSC exercises can typically create higher peak forces (7, 19). However, as there is typically less urgency to develop force during the slow-SSC movements, they often do not develop force as quickly as fast-SSC movements. This means that exercises with a slow-SSC produce lower RFDs than fast-SSC movements (7, 19). Therefore, slow-SSC exercises produce higher peak forces, but lower RFD than fast-SSC movements.

On the other hand, as it takes 140-710 milliseconds to develop peak force during various jump exercises (7, 5, 20), fast-SSC exercises may struggle to produce peak forces because the SSC simply does not last long enough. Whilst they may not be capable of producing peak forces, they can produce large a RFD due to the speed of the movement (Table 2).

It is suggested that exercises characterised by larger joint displacements (i.e. work through a larger range of movement) are typically categorised as slow-SSC movements. Whereas exercises with smaller joint displacements are commonly referred to as fast-SSC movements (21). For example, a CMJ (slow-SSC movement) experiences larger joint displacements than sprinting (fast-SSC) (Figure 1). This helps to dissociate between what are slow-SSC movements and what are fast-SSC movements when no research has determined what classification they belong too.

What causes an increase in Rate of Force Development?

Improvements in RFD are likely to be the result of increases in muscle-tendon stiffness (22, 23), enhanced muscle force production via changes in muscle fibre type or type area (from type I to type IIA) (24, 25), and increases in neural drive during the early phase of the SSC (

Why is the Rate of Force Development important for Sports?

As power is a key determinant in the performances of many sports, optimising an athlete’s explosiveness may be of great importance (30-35). Research has identified that the RFD has been directly linked to performances during jumping (2-8), weightlifting (5, 6), cycling (10), sprinting (9), and even during the golf swing (11) – suggesting a better RFD can lead to a better athletic performance. Moreover, elite sprinters have been shown to possess greater RFD than well-trained sprinters (9). Collectively, this information suggests that RFD may be an important contributor to athletic performance.

  • RFD linked to better jump, sprint, cycling, weightlifting . and golf swing performances
  • Elite-level sprinters have better RFD than well-trained sprinters
  • Power trained athletes have greater RFD than non-power trained athletes (36).
  • Power trained athletes have greater RFD than endurance athletes (36).

How to Calculate the Rate of Force Development

As RFD is an expression of explosive strength, it is measured in Newtons per second squared (N·s -1 ). The RFD can be calculated for isometric, concentric and eccentric muscle contractions, with the latter two otherwise referred to in the research as the ‘positive’ and ‘negative’ acceleration phases of the SSC (2, 3). In fact, one study suggests that eccentric RFD is a better predictor of jump performance than concentric RFD because it summarises several intrinsic properties of muscle and tendons during a key moment (2). However, this is yet to be validated by other research.

Multiple measures of RFD have been developed in order to measure various components of performance during both isometric and dynamic movements:

  1. Average RFD or IES (Index of Explosiveness) (2, 3, 5, 6, 8, 9, 11, 37, 38)
  2. Time-interval RFD (11, 39)
  3. Instantaneous RFD (40, 41)
  4. Peak or maximal RFD (42, 4, 5, 7, 10, 11, 36)
  5. Time to peak RFD (11, 7)

Average RFD: This value is identical to the IES discussed by Zatsiorsky (37), and is calculated by dividing the peak force by the time to achieve peak force (39). However, this form of measuring average RFD has been shown to have lower levels of reliability in comparison to time-interval RFD and peak RFD (39). These lower levels of reliability may be associated with each athlete’s time to achieve peak force, as not all athletes can achieve peak force in the same time frame. Therefore, measuring RFD using predetermined time-intervals can accommodate for these variances.

How to calculate Average RFD

Example – Calculating Average RFD

Average RFD [N·s -1 ] = Peak Force [N] / Time to achieve peak force [s][/toggle]

Time-Interval RFD: Though this measure of RFD is effectively the same as average RFD, it is calculated at various time-intervals (e.g. 0-30, 0-50, 0-90, 0-100, 0-150, 0-200, and 0-250 milliseconds [39]). This value simply represents a change in force divided by a change in time. It is calculated by dividing the force at the end of the time interval by the duration of the time interval (39) (Table 3). Just note that when calculating RFD, the time should be calculated in seconds, not milliseconds.

How to calculate Time-Interval RFD

Example – Calculating RFD with a 0-30 millisecond time-interval:

RFD [N·s -1 ] = Change in Force [N] / Change in Time [s]

RFD [N·s -1 ] = Force [N] at 30 milliseconds / 0.03 second time-interval [s]

The strength and conditioning coach should select the time-intervals they wish to use based upon the nature of the exercise. For example, if the exercise has a fast-SSC movement (e.g. Sprinting – 80-90 milliseconds), then it may be suggested that time-intervals of ≤100 milliseconds may be most appropriate (e.g. 0-50, 0-90, and 0-100 milliseconds). Furthermore, the early time-intervals ( 100s time-intervals are referred to as ‘late phase’ RFD.

Instantaneous RFD: This value is measured by using the maximal tangential slope between two adjacent data points. In other words, the data is recorded using 1-milliseconds time-intervals, and from this, the change in force is divided by the change in time at every 1-millisecond time interval. As this value of RFD is calculated every 1-millisecond, it provides a very precise measure of RFD.

Peak or Maximal RFD: This value of RFD is really as simple as it sounds, it is the largest amount of RFD produced during the movement. Most commonly, the value is identified by measuring the peak RFD during numerous sampling windows of 1, 2, 5, 10, 20, 30, and 50 (40, 39). For example, if the strength and conditioning coach selected a sampling window of 5 milliseconds, they would measure peak RFD every 5-milliseconds (e.g. 0-5, 5-10, and 10-15 milliseconds and so forth). They would then simply identify the largest RFD value out of those recorded – this value is then the peak RFD. Whilst all of these sampling windows have been reported as reliable measures of peak RFD, the 20-millisecond sampling window has been shown to be the most reliable (39). Table 4 demonstrates how to identify peak RFD during an isometric performance.

From this data, the coach is able to calculate the athlete’s peak RFD, time to peak RFD, and average RFD. These variables are useful tools for comparing a group of athletes to identify who the best and worst individuals are at developing force quickly.

Time to Peak RFD: As displayed in Table 4, this value of RFD is extremely straight-forward. It is a useful tool for measuring performance as it provides the coach with information on how quickly the athlete is able to achieve their maximal explosive strength (i.e. peak RFD). Decreasing an athlete’s time to achieve peak RFD will allow them to produce higher forces in shorter periods of time, and therefore may increase their explosiveness and overall athletic performance.

Validity and Reliability

The RFD and its various measures (Average RFD, Time-Interval RFD, Peak RFD, and Time to Peak RFD) have all been shown to be a valid and reliable tool for assessing explosive strength (11, 39). However, the most reliable measures for assessing RFD appears to be any of the time-interval sampling windows (i.e. 0-30, 0-50, 0-90, 0-100, 0-150, 0-200, and 0-250 milliseconds), and peak RFD using 20-millisecond windows (39). It is therefore recommended that these two variables should be preferable when measuring RFD.

Practical Application: How to improve the Rate of Force Development

Increasing the RFD whilst simultaneously reducing the time in which peak RFD occurs, will result in a left and upward shift in the force-time curve (Figure 2). This left and upward shift enables the athlete to produce greater forces in a shorted period of time, ultimately improving their explosiveness.

Figure 2 – Shift in the Force-Time curve after a successful training programme.

It is often suggested that athletes must train at various sections along the force-time curve if improvements in RFD are to occur. By only training on one part of the force-time curve (e.g. maximum strength), it is likely that the athlete will only improve their performance at that section on the paradigm. For example, only training maximal strength may lead to improvements in force production, but it may also result in a reduction in the time to achieve that force (Figure 3).

As training programmes which combine strength and power training have been repeatedly shown to improve athletic performance more than strength or speed training alone (43), there is no surprise that most exercise professionals commonly use an all-rounded approach within their programming.

Figure 3 – Force-time curve after training specific elements

The following types of training have all shown to improve RFD:

  • Resistance training (44, 45, 46, 47, 48)
  • Ballistic training (49, 50, 51, 52)
  • Olympic Weightlifting (53)
  • Plyometric training (54, 55, 50, 56)
  • Balance training (57, 58)

However, only those listed below have shown RFD improvements in trained or athletic subjects:

So whilst numerous training methods have been shown to improve RFD in untrained and elderly males and females, little research has shown RFD improvements in trained or athletic subjects.

Conclusion

RFD is a reliable measure of explosive strength, with higher RFDs have been linked with better athletic performance. Improvements in RFD are likely to be the result of increases in muscle-tendon stiffness, enhanced muscle force production via changes in muscle fibre type (from type I to type IIA), and increases in neural drive. The most reliable values for measuring this component of performance appear to be calculating RFD at various time-intervals and peak RFD using 20-millisecond sampling windows. Though various methods of training have been shown to improve performance (resistance, ballistic, Olympic Weightlifting , plyometrics , and balance training), only resistance and ballistic training have been proven to increase RFD in trained and athletic populations.

What now?

Some coaches believe that reading one article will make them an expert on strength and conditioning. Here’s why they’re wrong…

Strength and conditioning entails many, many topics. By choosing to simply read up on The Rate of Force Development and ignore the sea of other crucial S&C topics, you run the risk of being detrimental to your athlete’s success and not realising your full potential.

To make you an expert coach and make your life as easy as possible, we highly suggest you now check out this article on Basic Movement Patterns.

References

Reference List (click here to open)

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About the Author

Owen Walker MSc CSCS
Founder and Director of Science for Sport

Owen is the founder and director of Science for Sport. He was formerly the Head of Academy Sports Science and Strength & Conditioning at Cardiff City Football Club, and an interim Sports Scientist for the Welsh FA. He also has a master’s degree in strength and conditioning and is a NSCA certified strength and conditioning coach.


Run Muscle Fatigue Test

The question here is: "How can we explain the decline in maximal force during a sustained contraction?"

This phenomenon is called "muscle fatigue".

Before you begin

Ensure the volunteer can see the computer screen where their signal will appear.

Procedure

  1. Begin recording. Ask the volunteer to apply and maintain 25% of their maximal grip strength while watching the recorded trace. Enter "25%" in as a comment or label on the recording.
  2. After 25 s, tell the volunteer to relax and stop recording.
  3. Wait for 30 s to allow recovery of muscle function.
  4. Repeat steps 1–3 for contractions of 50%, 75%, and 100% of maximal grip strength. Add a comment for each trial.

Analysis

In this analysis students will determine how fatigue affects grip force at different intensities.

  1. Create a table like this:
  2. Ask students to scroll to their 25% grip force data.
  3. Place a marker on the baseline just before the increase in force. Place the point selector at 1 s into the contraction. Note the change in grip force from the baseline.
  4. Note this value in the appropriate cell in the table (above).
  5. Repeat steps 2–3 for 5 s, 10 s, and 20 s into the contraction.
  6. Repeat steps 2–4 for 50%, 75%, and 100% grip force.

Check students’ understanding

Question: Did this experiment help you decide which of the factors proposed to explain fatigue are important?

Answer: You may have noticed that there is a greater decline in your volunteer's grip force during the more strenuous contractions (75%, 100%) compared with the less strenuous contractions (25%, 50%). This is with "visual feedback" present, where the volunteer can see the decline, and can attempt to correct for it. There is clearly more fatigue occurring during the more strenuous contractions. A decline in "central drive" will also have affected some of the results.


What Happens during Exercise [ edit | edit source ]

Musculoskeletal System [ edit | edit source ]

Exercise is about movement, and the muscular system is primarily responsible for creating movement. Therefore, the responses and adaptations of the muscular system to exercise are important parts of exercise physiology. During exercise, many changes take place in skeletal muscle, such as changes in temperature, acidity, and ion concentrations. These changes affect muscle performance and may lead to fatigue. Indeed, the mechanisms of muscle fatigue is an important area of inquiry in exercise physiology. [11] [12] In addition, the adaptations of the muscular system to exercise lead to long-term changes in exercise capability.

Depending on the type of exercise, changes in enzyme concentrations, contractile protein content, and vascularisation affect the ability of the muscle to perform work. For example, endurance exercise increases concentrations of enzymes in skeletal muscle that are involved in the aerobic production of energy. [13] [14] In contrast, strength training is associated with increases in the size of the muscle due to increased synthesis of contractile proteins, with little change in anaerobic enzyme content. [15] These types of adaptations are appropriate for a certain type of activity in that these adaptations will improve muscle performance in the types of activities that stimulated these adaptations.

If muscles are under loaded, it does not matter how much they are exercised, they will increase little in strength. On the other side, if they are trained with at least 50 percent of maximal force of contraction, they will develop strength rapidly even if the contractions are performed only a few times each day. Using this principle, experiments on muscle building have shown that six nearly maximal muscle contractions performed in three sets 3 days a week give approximately optimal increase in muscle strength, without producing chronic muscle fatigue.

The musculoskeletal system is fundamental in exercise physiology. The strength of a muscle is mostly determined by its cross sectional area. [16] Therefore size is key.

  • Mechanical Work performed by a muscle is the amount of force applied by the muscle multiplied by the distance over which the force is applied. [17]
  • Muscle Strength is the maximal amount of tension or force that a muscle or a muscle group can voluntarily exert on a maximal effort[18] when the type of muscle contraction, segment velocity and joint angle is specified. [19] .
  • The power of muscle contraction is different from muscle strength because power is a measure of the total amount of work that the muscle performs in a unit period of time and is generally measured in kilogram meters (kg-m) per minute. [17]
  • Another important concept is endurance, defined as the ability to perform repeated contractions against a resistance or maintain a contraction for a period of time. [18]

Muscle Structure and Contraction [ edit | edit source ]

Types of Skeletal Muscle Actions [ edit | edit source ]

There are several types of skeletal muscle actions: [22] [23]

  • Static (Isometric): it occurs when tension is developed in the muscle without movement, therefore the muscle origin and insertion does not move and there is no changes in muscle length. During a static muscle contraction, the myosin and actin myofilaments form cross-bridges and generate force, but the external force is greater than the muscle-produced force. No mechanical work (force x distance) is done, as there is no displacement, even though there is energy expenditure. [22]
  • Dynamic (Isotonic) Muscle Actions:
    • Concentric: The muscle produces enough force to overcome the external resistance. The muscle shortens and there is movement at the joint. The myosin and actin myofilaments form cross-bridges, and the filaments slide past each other causing muscle shortening. Energy expenditure results in positive mechanical work as force production and displacement occurs. [22]
    • Eccentric: The muscle lengthens while producing force. This happens because the external resistance moves in the direction opposite to the standard concentric (shortening) action. [22] A high force is produced by the contractile elements and this makes these type of muscle actions an important training stimulus. Eccentric muscle actions are also associated with muscle damage and soreness and it is advised that the eccentric component of exercise training should initially be limited. [22] Furthermore, eccentric contractions have clinical value during the rehabilitation of tendinopathies. [24][25]

    Skeletal Muscle Fibre Types [ edit | edit source ]

    Human skeletal muscle fibres vary in terms of their mechanical, physiological and biochemical characteristics. Generally, human skeletal muscles have three types of fibres: Type I, Type IIa and Type IIx.

    Fast Twitch (FT) or Type II fibers have two primary subdivisions, Type IIa and Type IIx. Type IIa fibres have intermediate properties - they are fast contracting fibres but also have a oxidative metabolic profile. Both Type IIa and Type IIx show rapid contraction speed, high capacity for anaerobic ATP production through glycolysis and a larger diameter. Type IIx fibres are fatigable fibres. [22]

    Slow Twitch (ST) or type I fibers generate energy primarily through aerobic system. This type of fibre shows a relatively slow contraction speed, a higher number of larger mitochondria and larger amounts of myoglobin. These fibres are the slow, oxidative, fatigue-resistant fibres. [22]

    Muscle Hypertrophy [ edit | edit source ]

    Muscle sizes are determined mainly by genetic and anabolic hormone secretion. Training can add another 30 to 60 percent of muscle hypertrophy, mostly from increased muscle fibers diameter, but in a small part also from increased number of fibers (hyperplasia).

    Hypertrophied muscle is characterized by:

    • an increased number of myofibrils
    • increased number of mitochondrial enzymes
    • increase in ATP and phosphocreatine amounts available
    • increased stored glycogen and triglyceride

    thus enhancing both aerobic and anaerobic systems.

    Muscle Strength Determinants [ edit | edit source ]

    The amount of force that a muscle can generate varies individually. Genetics play a big role in this force generation, but there are other determinants as well: [26]

    • Nerve supply: The number of motor units recruited determine the amount of force. Slow twitch (Type I fibre) motor units are easily recruited, whereas Fast twitch (Type IIx) motor units hold more muscle fibres and can therefore generate more force. [26]
    • Muscle length: Most force is produced when muscles are working in mid-range. Mid-range is the position where there is optimal overlap of the thin and thick filaments at sarcomere level. [26]
    • Speed of shortening: More force is generated with slower movement. A dynamic (isotonic) muscle action produces more force than a static (isometric) contraction. [26]
    • Mechanical advantage: Most muscles work at a mechanical disadvantage due to the position of the muscle insertion point in relation to the portion of the limb being moved. [26] (Think of knee extension, where the quadriceps acts across the bone levers of the femur and tibia, the knee joint is the fulcrum and the quadriceps inserting onto the upper end of the tibia).
    • Muscle fibre pennation: The fascicles in muscle are arranged according to the shape of the muscle. More force will be produced by muscles where the fascicles are parallel with the longitudinal axis of the muscle. [26]
    • Connective tissue: Connective tissue in and around the muscle provides support and also increases the muscle's ability to produce force. [26]

    Energy Systems [ edit | edit source ]

    In order to meet the increased demands for ATP when exercising, there is an increase in the chemical reactions in the body providing ATP. In aerobic metabolism, the chemical reactions use oxygen to completely break down carbohydrates e.g. glycogen, glucose and fats for energy. [27] With moderate levels of exercise, the muscles can use aerobic metabolism to meet the increased energy requirements. [22] Aerobic metabolism does not allow for maximum power output of the muscles but aerobic activity can be sustained for long periods of time. [27] The body first uses the stored oxygen available in the body and then the exercise level is limited by the capacities of the respiratory and cardiovascular systems to provide more oxygen to the active cells.

    These systems do not work on an on-off base but rather in a conveniently mixed mode with considerable overlap between them.

    Phosphocreatine-Creatine System [ edit | edit source ]

    Phosphocreatine is another chemical compound that has a high-energy phosphate bond that can be hydrolysed to provide energy and resynthesize ATP. This occurs within a small fraction of a second. Therefore, all the energy stored in the muscle phosphocreatine is almost instantaneously available for muscle contraction, just as is the energy stored in ATP.

    At the start of exercise ATP is broken down into ADP + Pi, resulting in ATP being reformed by the creatine phosphate (CP) reaction. A phosphate is donated to ADP from CP to reform ATP. This method is the fastest and simplest way to produce energy for a muscle contraction. This energy source lasts for about 5 seconds as muscle cells only store a small amount of ATP and CP. This reaction provides energy for the start of the exercise and short-term high intensity exercise. This energy production is done without oxygen, thus an anaerobic method of energy production. [26]

    Thus, the energy from the phosphagen system (ATP and Phosphocreatine stored in the muscle) is used for maximal short bursts of muscle power.

    Anaerobic Glycolysis (Lactic Acid System) [ edit | edit source ]

    The stored glycogen in muscle can be split into glucose and the glucose then used for energy. Glycolysis is the first part of this process, which occurs without use of oxygen and, therefore, is said to be anaerobic metabolism. During glycolysis, each glucose molecule is split into two pyruvic acid molecules, and energy is released to form four ATP molecules for each original glucose molecule. [22] [26]

    These pyruvic acid molecules can then be used by mitochondria in muscle cells, reacting with oxygen and providing more ATP molecules (oxidative stage), but if the exercise is too intense then it is likely the oxygen is insufficient for this second stage to occur, therefore pyruvic acid is converted into lactic acid. By doing so considerable amount of ATP are formed without oxygen, but also of lactic acid which will diffuse into interstitial fluid and bloodstream.

    Another characteristic of the glycogen-lactic acid system is that it can form ATP molecules about 2.5 times as rapidly as can the oxidative mechanism of the mitochondria. Therefore, when large amounts of ATP are required for short to moderate periods of muscle contraction, this anaerobic glycolysis mechanism can be used as a rapid source of energy. It is, however, only about one half as rapid as the phosphagen system. Under optimal conditions, the glycogen-lactic acid system can provide 1.3 to 1.6 minutes of maximal muscle activity in addition to the 8 to 10 seconds provided by the phosphagen system, although at somewhat reduced muscle power. [22]

    Oxidative Phosphorylation (Aerobic System) [ edit | edit source ]

    The aerobic system is the oxidation of glucose, fatty acids and amino acids. Combined with oxygen these compounds are able to release great amounts of energy used to provide ATP. This occurs in the mitochondria of the cell. Two metabolic pathways, the Krebs cycle and the electron transport chain, work together. These pathways remove hydrogen from from carbohydrates, fats and proteins so that the potential energy in the hydrogen can be implemented to produce ATP. [26]

    This system provides less ATP per minute than the phosphagen system and the lactic acid system, but can last as long as there are nutrients to provide substrates.

    The aerobic system is thus useful for less powerful but longer-term aerobic exercise activities. [27]

    Cardiovascular System [ edit | edit source ]

    The cardiovascular system is responsible for the transport of blood, and therefore oxygen and nutrients, to the tissues of the body. Similarly, the cardiovascular system facilitates removal of waste products such as carbon dioxide from the body. In addition, the cardiovascular system is centrally involved in the dissipation of heat, which is critical during prolonged exercise.

    The primary components of the cardiovascular system are the heart, which pumps the blood, and the arteries and veins, which carry the blood to and from the tissues. Although all systems (i.e. pulmonary, respiratory, skeletal muscle and cardiovascular system) are involved in constructing an appropriate response to exercise training, the cardiovascular system can be seen as the central hub. [29] Therefore, a large proportion of study and research in exercise physiology focuses on the responses and adaptations of the cardiovascular system to exercise.

    Important beneficial effects of exercise on the cardiovascular system include a decrease in resting blood pressure (an important risk factor in cardiovascular disease) and a decrease in blood cholesterol levels (reducing the risk for developing atherosclerosis). Furthermore, exercise is an important component of the cardiac rehabilitation process following a cardiac event such as a heart attack. [30]

    Individuals with training in exercise physiology are playing important roles in the research and implementation of exercise programs for the prevention of cardiovascular disease and the rehabilitation of individuals with cardiovascular disease. [31]

    Exercises increase some components of the cardiovascular system, such as:

    • stroke volume (SV) [29]
    • cardiac output [29]
    • systolic blood pressure (BP) [29]
    • mean arterial pressure [29]

    To meet the metabolic demands of skeletal muscle during exercise, 2 major adjustments to blood flow must occur. First, cardiac output from the heart must increase. Second, blood flow from inactive organs and tissues must be redistributed to active skeletal muscle. At rest, muscles receive approximately 20% of the total blood flow, but during exercise, the blood flow to muscles increases to 80-85%.

    Generally, the longer the duration of exercise, the greater the role the cardiovascular system plays in metabolism and performance during the exercise bout. An example would be the 100-meter sprint (little or no cardiovascular involvement) versus a marathon (maximal cardiovascular involvement).

    Heart Rate [ edit | edit source ]

    During exercise heart rate (HR) increases. This happens alongside oxygen uptake during exercise in order to reach steady-state heart rate during constant workload, sub-maximal exercise. In incremental maximal exercise heart rate increases up to maximal heart rate (HRmax). Initially cardiac output during exercise increases as a result of an increase in stroke volume. With a further increase in exercise workload, further increases in cardiac output becomes dependent on heart rate. In healthy people maximal exercise is limited by maximal heart rate (HRmax). Maximal heart rate can be estimated using the equation of 220 - age. In trained athletes an increase in stroke volume is noticed. This therefore allows for a greater cardiac output in trained individuals for a given heart rate. [26]

    Blood Flow and Pressure [ edit | edit source ]

    During exercise various factors in the exercising muscle cause vasodilation and opening of dormant capillaries. These factors are:

    • increase in temperature
    • decrease in oxygenation
    • decrease in metabolic products

    As a result an significant increase in blood flow to the muscle is observed. [26]

    To maintain a sufficient blood pressure, systemically vasoconstriction causes blood to move from the periphery to the central circulation. This kept balance between vasoconstriction vasodilation, ensures that there is little change in blood pressure during steady-state exercise. [26] During incremental exercise, the large increase in cardiac output required during high levels of exercise, can cause an increase in the systolic pressure up to around 200mmHg, but the diastolic pressure remains stable. [26]

    Pulmonary System [ edit | edit source ]

    The pulmonary system is important for the exchange of oxygen and carbon dioxide between the air and blood. The primary component of the pulmonary system is the lungs, which vary in volume from 4-6L and if laid out flat would cover a huge surface area from 60 - 80m 2. [31] Exercise places a great deal of stress on the pulmonary system as oxygen consumption and carbon dioxide production are increased during exercise, thus increasing the pulmonary ventilation rate. The control and regulation of the pulmonary system during exercise are areas of much research. As with the cardiovascular system, the interplay of exercise and the neurological control of breathing is not completely understood. Surprisingly, most evidence indicates that there are few, if any, adaptations to exercise in the pulmonary system itself in healthy individuals. [35] However, adaptations in the musculature structures that controls breathing are apparent. [36]

    Oxygen Uptake [ edit | edit source ]

    Oxygen uptake (VO2) is the amount of oxygen that the body takes up and utilises. [26] Oxygen consumption rises exponentially during the first minutes of exercise, reaching a steady rate around the third minute and then remaining relatively stable. In such conditions, the energy required by the working muscles and ATP production in aerobic metabolism are balanced, without lactate accumulation in the blood.

    VO2Max or Maximal Oxygen Uptake [ edit | edit source ]

    Maximal oxygen consumption (VO2max) is the region where oxygen consumption reaches a steady-state or increases only slightly with additional increases in exercise intensity. [26] It provides a quantitative measures of a person's capacity for aerobic ATP resynthesis. Maximal oxygen uptake is dependent on a person's:

    • gender
    • height
    • weight
    • lung function
    • fitness level
    • type of activity being performed

    VO2max is exercise specific and is greater in activities involving large muscle groups. [26] Trained athletes can have a higher Maximal Oxygen Uptake than sedentary individuals because of their enhanced stroke volume, improved myocardial function and a higher capacity for oxidative metabolism in active muscles. [22] VO2max in short-term studies is found to increase only 10% with the effect of training. However, that of a person who runs in marathons is 45% greater than that of an untrained person. This is believed to be partly genetically determined (e.g, stronger respiratory muscles, larger chest size in relation to body size) and partly due to long-term training.

    Oxygen Diffusing Capacity [ edit | edit source ]

    Oxygen diffusing capacity is a measure of the rate at which oxygen can diffuse from the alveoli into the blood. An increase in diffusing capacity is observed in a state of maximal exercise.

    During exercise, increased blood flow through the lungs causes all of the pulmonary capillaries to be perfused at their maximal level, providing a greater surface area through which oxygen can diffuse into the pulmonary capillary blood. Athletes who require greater amounts of oxygen per minute have been found to have higher diffusing capacities.

    Both arterial blood oxygen pressure and carbon dioxide pressure remains almost at normal level even during strenuous exercise, as they are well compensated.

    Ventilation [ edit | edit source ]

    During light to moderate intensity exercise/sports activities, ventilation increases linearly with oxygen uptake and carbon dioxide production. This is necessary to meet the body's oxygen requirement and to expel the additional produced carbon dioxide. Initially the increase in ventilation is achieved by an increase in the tidal volume, and with increasing demand by increasing the respiratory rate. [26] During heavy to maximal exercise a rise in ventilation is observed in response to the lactate threshold. This is known as the ventilatory threshold. Should a person continue exercising a further rise in ventilation is observed at the onset of blood lactate accumulation (OBLA). This happens in order to expel more carbon dioxide in an effort to reduce the acidity in the blood. This rise in ventilation at the OBLA is known as respiratory compensation. [26]

    Arteriovenous Oxygen Difference [ edit | edit source ]

    The arteriovenous oxygen difference is a measure of the amount of oxygen taken up from the blood by the tissues. Cardiac output and arteriovenous oxygen difference are the determinants of overall oxygen uptake. During exercise blood flow increases to the tissues haemoglobin dissociates quicker and easier. This results in a greater arteriovenous oxygen difference during exercise. In trained athletes, the arteriovenous oxygen difference is greater as a result of the tissues becoming more efficient in oxygen uptake with aerobic training. [26]

    Thermoregulation during Exercise [ edit | edit source ]

    The heat produced by the increase in metabolism during exercise must be dissipated in order to prevent a dangerous increase in core temperature. [26] This is best accomplished by vasodilation of the blood vessels in the skin. This allows for the heated blood to pass close to the body surface and losing heat through radiation and conduction. The sweat glands is stimulated by the heated blood resulting in an increase in sweat production and thus losing more heat through evaporation. This evaporation of sweat leads to fluid and electrolyte loss, which can result in dehydration. [26]

    Dehydration may lead to impaired cognitive and exercise performance and heat stroke. Vasoconstriction happens at the viscera to maintain blood pressure in response to the fluid loss and redirection of blood to the skin. [26]

    Nervous System [ edit | edit source ]

    Among the many functions of the nervous system is the control of movement by way of the skeletal muscles, which are under voluntary (and reflex) control. Most of the study of the neural control of movement is considered the domain of motor control and learning. However, certain areas of inquiry are also of interest to exercise physiologists. Two notable areas are neuromuscular fatigue and neurological adaptations to strength training. With respect to neuromuscular fatigue, research suggests that under certain conditions the Central Nervous System may play an important role in the development of fatigue. [12] For example, changes in brain levels of serotonin and dopamine may influence fatigue. [37] [38] In addition, the firing rate of motor units can change during fatigue [39] , which may be due to an elegant interplay between peripheral receptors and the CNS.

    Similarly, strength training may influence the CNS control of muscle activation by changing the number of motor units that the CNS will activate during a contraction and the firing rate of the active muscle [40] . Much of the data regarding neurological adaptations to strength training are contradictory, but this remains an important area of study. These areas of study are important to basic researchers in exercise physiology, and new information in these areas may also have implications in the rehabilitation of individuals with neuromuscular disorders.

    The Autonomic Nervous System (ANS) is involved in the involuntary control of body functions. The ANS has two divisions. The Sympathetic Nervous System becomes active during situations of increased stress, such as during exercise. The Parasympathetic Nervous System is more active during resting conditions. Most notable in exercise physiology is the autonomic control of the cardiovascular system. For example, during exercise an increase in Sympathetic Activity and a decrease in Parasympathetic Activity result in an increase in activity of the heart and an increase in blood pressure. In addition, the ANS is involved in the redistribution of blood flow away from inactive tissues, such as the gastrointestinal tract, and toward the active tissues during exercise.

    Endocrine System [ edit | edit source ]

    The endocrine system is the system of hormones, which are chemicals released into the blood by certain types of glands called endocrine glands. Many hormones are important during exercise and may affect performance. For example, during exercise the hormone called growth hormone increases in concentration in the blood. This hormone is important in regulating blood glucose concentrations. Similarly, other hormones, such as cortisol, epinephrine, and testosterone, increase during exercise. Their effects may be short term in that they affect the body during the exercise bout. Other effects are prolonged and may be important in the long-term adaptation to regular exercise.


    Ca 2+ SENSITIZATION MECHANISM AND CONTRACTION OF SMOOTH MUSCLE

    In addition to the Ca 2+ -dependent activation of MLC kinase, the state of myosin light chain phosphorylation is further regulated by MLC phosphatase [aka myosin phosphatase (1, 4, 9, 11–16)], which removes the high-energy phosphate from the light chain of myosin to promote smooth muscle relaxation (Fig. 1). There are three subunits of MLC phosphatase: a 37-kDa catalytic subunit, a 20-kDa variable subunit, and a 110- to 130-kDa myosin-binding subunit. The myosin-binding subunit, when phosphorylated, inhibits the enzymatic activity of MLC phosphatase, allowing the light chain of myosin to remain phosphorylated, thereby promoting contraction. The small G protein RhoA and its downstream target Rho kinase play an important role in the regulation of MLC phosphatase activity. Rho kinase, a serine/threonine kinase, phosphorylates the myosin-binding subunit of MLC phosphatase, inhibiting its activity and thus promoting the phosphorylated state of the myosin light chain (Fig. 1). Pharmacological inhibitors of Rho kinase, such as fasudil and Y-27632, block its activity by competing with the ATP-binding site on the enzyme. Rho kinase inhibition induces relaxation of isolated segments of smooth muscle contracted to many different agonists. In the intact animal, the pharmacological inhibitors of Rho kinase have been shown to cause relaxation of smooth muscle in arteries, resulting in a blood pressure-lowering effect (2, 17).

    An important question facing the smooth-muscle physiologist is: what is the link between receptor occupation and activation of the Ca 2+ -sensitizing activity of the RhoA/Rho kinase-signaling cascade? Currently, it is thought that receptors activate a heterotrimeric G protein that is coupled to RhoA/Rho kinase signaling via guanine nucleotide exchange factors (RhoGEFs Fig. 1). Because RhoGEFs facilitate activation of RhoA, they regulate the duration and intensity of signaling via heterotrimeric G protein receptor coupling. There are ∼70 RhoGEFs in the human genome, and three RhoGEFs have been identified in smooth muscle: PDZ-RhoGEF, LARG (leukemia-associated RhoGEF), and p115-RhoGEF. Increased expression and/or activity of RhoGEF proteins could augment contractile activation of smooth muscle and therefore play a role in diseases where an augmented response contributes to the pathophysiology (hypertension, asthma, etc.).

    Several recent studies suggest a role for additional regulators of MLC kinase and MLC phosphatase (13–16). Calmodulin-dependent protein kinase II promotes smooth muscle relaxation by decreasing the sensitivity of MLC kinase for Ca 2+ . Additionally, MLC phosphatase activity is stimulated by the 16-kDa protein telokin in phasic smooth muscle and is inhibited by a downstream mediator of DG/protein kinase C, CPI-17.


    Treppe

    When a skeletal muscle has been dormant for an extended period and then stimulated to contract, with all other things being equal, the initial contractions generate about one-half the force of later contractions. The muscle tension increases in a graded manner that to some looks like a set of stairs. This tension increase is called treppe, a condition where muscle contractions become more efficient. It’s also known as the “staircase effect” (Figure 10.4.5).

    Figure 10.4.5 – Treppe: When muscle tension increases in a graded manner that looks like a set of stairs, it is called treppe. The bottom of each wave represents the point of stimulus.

    It is believed that treppe results from a higher concentration of Ca ++ in the sarcoplasm resulting from the steady stream of signals from the motor neuron. It can only be maintained with adequate ATP.


    Richard L. Lieber, PhD

    Richard L. Lieber, PhD, oversees all research endeavors throughout the Shirley Ryan AbilityLab system of care. He joined the organization (then the Rehabilitation Institute of Chicago or RIC) in March 2014, bringing an extensive research focus on the science and physiology of skeletal muscle. Dr. Lieber is the established expert in the field, both nationally and internationally, and is a pioneer in conducting translational research.

    Dr. Lieber, along with Chief Medical Officer James Sliwa, DO, is jointly responsible for implementing the novel translational approach embedded in the Shirley Ryan AbilityLab medical and research enterprise, and for demonstrating its tangible and cultural progress.

    Dr. Lieber also led the design of Shirley Ryan AbilityLab’s Biologics Lab, in which studies of living human cells are used to solve human problems, particularly in the context of rehabilitation and recovery. The lab’s state-0f-the-art equipment allows scientists to monitor living cells as they perform testing of various types. Shirley Ryan AbilityLab’s Biologics Lab is the only one in the world placed in a rehabilitation setting and brings together biologists, physiologists, stem-cell biologists and molecular biologists — all sharing ideas and expertise, and speeding discoveries.

    As Chief Scientific Officer, Dr. Lieber oversees the work of more than 200 researchers. Under his leadership, Shirley Ryan AbilityLab has more than 300 research studies and clinical trials under way, all of which will benefit its patient population.

    Specifically, Dr. Lieber’s research is studying the design and plasticity of skeletal muscle. Currently, he is developing state-of-the-art technical and biological approaches to understanding and solving painful and debilitating muscle contractures that result from cerebral palsy, stroke and spinal cord injury.

    He has published more than 300 articles in scientific journals, from the fundamental journals such as Biophysical Journal and the Journal of Cell Biology to the more applied-science publications such as the Journal of Hand Surgery and Clinical Orthopaedics and Related Research.

    Over the span of his career, Dr. Lieber has won numerous prestigious awards, among them Kappa Delta Young Investigator Award, American Academy of Orthopaedic Surgeons, February 1994 Fulbright Scholarship (Sweden), 2007 The Göteborg University Medal, Sahlgrenska University Hospital, June 2007 Giovanni Borelli Award, American Society of Biomechanics, August, 2007 Kappa Delta Award, American Academy of Orthopaedic Surgeons, February 2013, Chicago, IL and most recently, Fellow, American Institute of Medical and Biological Engineering (AIMBE), March 2019, Washington DC.

    Dr. Lieber’s laboratory has been supported by the National Institutes of Health in both investigator-initiated grants, as well as center grants for more than 35 years. He is also Senior Research Career Scientist in the U.S. Department of Veteran’s Affairs, where he receives support from the Rehabilitation Engineering Research and Development service.

    Prior to joining Shirley Ryan AbilityLab, Dr. Lieber was Professor and Vice Chairman of the Department of Orthopaedic Surgery at the University of California, San Diego (UCSD), and principal investigator of the San Diego Skeletal Muscle Research Center — an NIH-funded center designed to leverage muscle expertise on behalf of patients in the San Diego community. He earned his doctorate in Biophysics, with a minor in Electrical Engineering, from the University of California, Davis, where he also earned a BS in Physiology. He earned his MBA from the Rady School of Management at UCSD.


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    Results

    Across our Nile crocodiles (N = 9), experiments were successfully executed on the following muscle bundles (and N = numbers of samples): Rhm (N = 6), BB (N = 5), and FTI4 (N = 4). In one case, two preparations of Rhm muscle were obtained from the same muscle of the same animal.

    F-L and force-hold examples

    The crocodile muscles displayed classic “Hill-type” active F–L relationships ( Fig. 2). The resulting partial F–L relationships were a typical shape, with broad plateau regions. Average (±SEM) L0 across all of the preparations was 34.9 ± 3.35 mm and a near-plateau region of maximal force encompassed approximately L0 ± 10%. Passive force increased gradually in most preparations when resting lengths exceeded ∼1.1 L0. One BB muscle displayed a sharp rise in passive force at lengths >1.2 L0. The margins of the active F–L plateau for this one preparation were, however, in line with the general ±10% shown as an approximation, and it was the shortening length-changes in this region that were most relevant to the subsequent determinations of muscle force and speed during shortening and, in turn, to the calculations of muscle power.

    In the examples in Fig. 3, force-control began in each case at 500 ms into the stimulus time-course. The three time courses depicted overlay each other during the periods of force rise and isometric plateau, indicating that the muscles responded consistently to the maximal stimulation. For a full series with any one muscle bundle, 10–13 stimulations were required. Across the 15 muscle bundles tested, only in one case, force at the end of the simulation series was <90% of peak value measured at the beginning of the series on average, isometric force during the final measurement in a series was 97.6 ± 0.04% of the first measurement. The low, medium, and high levels of force-clamp depicted in the example in Fig. 3 are 3 of the total of 13 different levels of force-clamp measured for this bundle of BB. The full series of force clamps were used to generate the power–force relationship shown in Fig. 4 (see also Curtin et al. 2015). As a reminder, the chief aim of fitting a power–force relationship was to extract the peak value of normalized power (Qmax). Figure 4 shows values for Q ( Equation 1), calculated for each of the 13 force clamps, plotted against values of relative force (i.e., mN during force-clamp normalized to mN of isometric force). The least-squares curve fit for Q as a function of relative force, as detailed in the Materials and Methods section and in Curtin et al. (2015), found values for peak normalized power (Qmax), and also values for the relative (optimal) force at peak power (FQmax) and the x-intercept of the curve-fit, called F O * . For the example of BB in Fig. 4, the normalized maximum power (Qmax) was 0.284 s −1 and the relative force at peak power (FQmax) was 0.342. The product of Qmax and maximum isometric stress (σ for this preparation, 218.8 kPa) gave power in units W L −1 (62.1). The values shown in the example F–V plot ( Fig. 4B) were derived from the outcomes of the power–force curve fitting, as described in detail in Curtin et al. (2015). The velocity at maximum power for this muscle fiber bundle was 0.83 s −1 and the maximum shortening velocity was 2.42 s −1 .

    Example force-hold contractions of a BB muscle bundle in Nile crocodile. (A) After 200 ms, the stimulus was initiated, and the maximum isometric force was reached after 650 ms. In this example, three separate force time-courses are overlaid force-rise was the same in each record. In the middle (dark grey) record, the targeted submaximal force was pre-set at 200 mN. A step-change of muscle length allowed the system to rapidly achieve the 200 mN target, and thereafter the stable length-change needed to hold the force stable was recorded. (B) Stable rates of muscle shortening (dotted lines) were determined with force clamped at different levels. Length-change was stable for 10 to 30 ms the shortest linear periods were associated with the fastest shortening speeds attained (light grey). For clarity, the time-courses after the stimulus was stopped (at 800 ms) are not shown because the system was still holding force stable for a short period while the muscle relaxed.

    Example force-hold contractions of a BB muscle bundle in Nile crocodile. (A) After 200 ms, the stimulus was initiated, and the maximum isometric force was reached after 650 ms. In this example, three separate force time-courses are overlaid force-rise was the same in each record. In the middle (dark grey) record, the targeted submaximal force was pre-set at 200 mN. A step-change of muscle length allowed the system to rapidly achieve the 200 mN target, and thereafter the stable length-change needed to hold the force stable was recorded. (B) Stable rates of muscle shortening (dotted lines) were determined with force clamped at different levels. Length-change was stable for 10 to 30 ms the shortest linear periods were associated with the fastest shortening speeds attained (light grey). For clarity, the time-courses after the stimulus was stopped (at 800 ms) are not shown because the system was still holding force stable for a short period while the muscle relaxed.

    Experimentally acquired force and velocity and calculated power data from a representative Nile crocodile BB muscle bundle (same sample as in Fig. 3). (A) Power normalized by isometric force and L0 as function of force during shortening normalized by isometric force. The normalized maximum power (Qmax) and the normalized force at maximum power (FQmax) were measured from fitting these data, normalized by FIM. (B) Velocity of shortening normalized by L0, as a function of force during shortening normalized by isometric force.

    Experimentally acquired force and velocity and calculated power data from a representative Nile crocodile BB muscle bundle (same sample as in Fig. 3). (A) Power normalized by isometric force and L0 as function of force during shortening normalized by isometric force. The normalized maximum power (Qmax) and the normalized force at maximum power (FQmax) were measured from fitting these data, normalized by FIM. (B) Velocity of shortening normalized by L0, as a function of force during shortening normalized by isometric force.

    Our results show some differences in performance between the different muscles in power output and contraction velocity. Table 2 summarizes the values and the means for muscle fiber bundles we measured from our Nile crocodiles. Bar graphs of the isometric stress, maximum power (in W L −1 ), maximum velocity of shortening (Vmax), normalized maximum power, optimal velocity of shortening at maximum power, and stress at maximum power compared between muscles are presented in Fig. 5. Several LME models were compared (see Materials and Methods section) to ensure that variance in the data was characterized using the simplest possible model. The resulting LME models that best characterize the variance with the lowest AIC (e.g., best goodness of fit, with penalizing the number of parameters) are presented in Supplementary data, Table S1 . See the Discussion section for more explanation.

    The maximum isometric stress σ (A), maximum power (B), maximum velocity (C) normalized power (D), normalized velocity at maximum power (E) and stress at maximum power (FQmax expressed as stress), and (F) differences between muscles of the Nile crocodile. The error bars indicate the SD results with asterisks show statistical differences between the muscles in our LME models.

    The maximum isometric stress σ (A), maximum power (B), maximum velocity (C) normalized power (D), normalized velocity at maximum power (E) and stress at maximum power (FQmax expressed as stress), and (F) differences between muscles of the Nile crocodile. The error bars indicate the SD results with asterisks show statistical differences between the muscles in our LME models.

    Summation of the measurements and results for muscle physiology and mechanical performance in Nile crocodiles

    . Body mass . Muscle length . Muscle mass . CSA . σ . FQmax . Max power . Vmax . Qmax . V@Qmax . Stress at Qmax . .
    Muscle . (kg) . (mm) . (mg) . (mm 2 ) . (kPa) . . (W L −1 ) . (s −1 ) . (s −1 ) . (s −1 ) . (kPa) . Fatigue .
    Rhm
    Average 3.58 32.6 45.8 1.62 218.0 0.28 66.3 4.27 0.320 1.17 61.4 78
    SD 1.36 17.0 12.6 0.42 82.8 0.06 28.0 1.67 0.102 0.42 25.1 12
    BB
    Average 3.98 29.4 64.6 2.12 183.0 0.34 73.6 3.88 0.420 1.27 61.2 85
    SD 2.01 6.1 13.7 0.54 45.0 0.03 26.7 1.89 0.194 0.59 14.8 12
    FTI4
    Average 3.37 45.3 62.2 1.29 227.9 0.32 145.5 6.44 0.626 1.98 72.1 56
    SD 1.39 7.0 28.6 0.52 50.8 0.04 53.3 1.87 0.082 0.39 12.0 22
    . Body mass . Muscle length . Muscle mass . CSA . σ . FQmax . Max power . Vmax . Qmax . V@Qmax . Stress at Qmax . .
    Muscle . (kg) . (mm) . (mg) . (mm 2 ) . (kPa) . . (W L −1 ) . (s −1 ) . (s −1 ) . (s −1 ) . (kPa) . Fatigue .
    Rhm
    Average 3.58 32.6 45.8 1.62 218.0 0.28 66.3 4.27 0.320 1.17 61.4 78
    SD 1.36 17.0 12.6 0.42 82.8 0.06 28.0 1.67 0.102 0.42 25.1 12
    BB
    Average 3.98 29.4 64.6 2.12 183.0 0.34 73.6 3.88 0.420 1.27 61.2 85
    SD 2.01 6.1 13.7 0.54 45.0 0.03 26.7 1.89 0.194 0.59 14.8 12
    FTI4
    Average 3.37 45.3 62.2 1.29 227.9 0.32 145.5 6.44 0.626 1.98 72.1 56
    SD 1.39 7.0 28.6 0.52 50.8 0.04 53.3 1.87 0.082 0.39 12.0 22

    Averages and SDs presented. Shown: individual body masses, the length of the muscle, muscle mass, CSA, maximal isometric stress (σ), force normalized by FIM at the maximum normalized power (FQmax), volume-normalized maximum power, normalized Vmax, normalized maximum power (Qmax), velocity at maximum power ([email protected]Qmax), stress at maximum normalized power (stress at Qmax), and rate of fatigue (“Fatigue” or fatigability number of activations for a muscle to reach 50% of its initial isometric force).

    Summation of the measurements and results for muscle physiology and mechanical performance in Nile crocodiles

    . Body mass . Muscle length . Muscle mass . CSA . σ . FQmax . Max power . Vmax . Qmax . V@Qmax . Stress at Qmax . .
    Muscle . (kg) . (mm) . (mg) . (mm 2 ) . (kPa) . . (W L −1 ) . (s −1 ) . (s −1 ) . (s −1 ) . (kPa) . Fatigue .
    Rhm
    Average 3.58 32.6 45.8 1.62 218.0 0.28 66.3 4.27 0.320 1.17 61.4 78
    SD 1.36 17.0 12.6 0.42 82.8 0.06 28.0 1.67 0.102 0.42 25.1 12
    BB
    Average 3.98 29.4 64.6 2.12 183.0 0.34 73.6 3.88 0.420 1.27 61.2 85
    SD 2.01 6.1 13.7 0.54 45.0 0.03 26.7 1.89 0.194 0.59 14.8 12
    FTI4
    Average 3.37 45.3 62.2 1.29 227.9 0.32 145.5 6.44 0.626 1.98 72.1 56
    SD 1.39 7.0 28.6 0.52 50.8 0.04 53.3 1.87 0.082 0.39 12.0 22
    . Body mass . Muscle length . Muscle mass . CSA . σ . FQmax . Max power . Vmax . Qmax . V@Qmax . Stress at Qmax . .
    Muscle . (kg) . (mm) . (mg) . (mm 2 ) . (kPa) . . (W L −1 ) . (s −1 ) . (s −1 ) . (s −1 ) . (kPa) . Fatigue .
    Rhm
    Average 3.58 32.6 45.8 1.62 218.0 0.28 66.3 4.27 0.320 1.17 61.4 78
    SD 1.36 17.0 12.6 0.42 82.8 0.06 28.0 1.67 0.102 0.42 25.1 12
    BB
    Average 3.98 29.4 64.6 2.12 183.0 0.34 73.6 3.88 0.420 1.27 61.2 85
    SD 2.01 6.1 13.7 0.54 45.0 0.03 26.7 1.89 0.194 0.59 14.8 12
    FTI4
    Average 3.37 45.3 62.2 1.29 227.9 0.32 145.5 6.44 0.626 1.98 72.1 56
    SD 1.39 7.0 28.6 0.52 50.8 0.04 53.3 1.87 0.082 0.39 12.0 22

    Averages and SDs presented. Shown: individual body masses, the length of the muscle, muscle mass, CSA, maximal isometric stress (σ), force normalized by FIM at the maximum normalized power (FQmax), volume-normalized maximum power, normalized Vmax, normalized maximum power (Qmax), velocity at maximum power ([email protected]Qmax), stress at maximum normalized power (stress at Qmax), and rate of fatigue (“Fatigue” or fatigability number of activations for a muscle to reach 50% of its initial isometric force).

    Muscle performance

    We found wide variation in the isometric stress generated by the muscles. Both the Rhm and the FTI4 had similar average isometric stress measurements (218.0 and 227.9 kPa, respectively), but the measurements within the Rhm muscles ranged from as low as 108 kPa, up to 328.0 kPa ( Supplementary data, Table S2 ). Variation across the three muscles led us to find no statistical differences in stress generation between muscle IDs ( Fig. 5A, Supplementary data, Table S1 : Isometric stress MuscleID Fstat < 1).

    The variation in isometric stress generation also showed in the poor relationship between force and CSA. Figure 6 summarizes the FIMs (mN) and CSA’s (mm 2 ) across all preparations tested most of the values lie within the narrow CSA range of 1–2 mm 2 . No more than a general trend of increased force with increased CSA was found. Figure 6 also shows the range of force variation for each muscle. The Rhm, in particular, showed a relatively wide range of force generation between muscle samples all of the Rhm results appear within the 1–2 mm 2 CSA zone, but they cluster poorly around the force–CSA relationship that the BB and FTI4 bundles seem to form.

    Maximal isometric force capacity (FIM) and muscle fiber cross-sectional area (CSA) relationship in Nile crocodiles. Force (mN) as a function of muscle fiber bundle CSA (mm 2 ). The trendline “linear” is set to intercept the axes at 0, enforcing a proportional relation between CSA and FIM at (CSA [mm 2 ] · 191 [kPa] = FIM [mN] 95% confidence intervals = 164–217 kPa N = 15 P < 0.0001).

    Maximal isometric force capacity (FIM) and muscle fiber cross-sectional area (CSA) relationship in Nile crocodiles. Force (mN) as a function of muscle fiber bundle CSA (mm 2 ). The trendline “linear” is set to intercept the axes at 0, enforcing a proportional relation between CSA and FIM at (CSA [mm 2 ] · 191 [kPa] = FIM [mN] 95% confidence intervals = 164–217 kPa N = 15 P < 0.0001).

    The maximum power output (W L −1 ) did show a clear difference between muscles ( Table 2). We find that the Rhm averaged around 66.3 W L −1 , with some variation in two muscle samples of around 100 W L −1 and the rest closer to 50 W L −1 . The BB had slightly less variation, but similar maximum power output average across the measurements (73.6 W L −1 ). Our statistical analysis showed that the primary variance was attributed to the muscles ( Supplementary data, Table S1 Power [W L −1 ] MuscleID Fstat = 5.3), and secondarily by body mass (Fstat = 3.7). There was no statistically relevant difference between the Rhm and BB ( Fig. 5B and Supplementary data, Table S1 ). The FTI4 stood out from the other two muscles, measuring double the average maximum power output vs. any of the others (145.5 W L −1 ). The maximum power output for the FTI4 tested higher than the Rhm in our statistical analysis, but not relative to the BB ( Fig. 5B and Supplementary data, Table S1 ).

    Peak normalized power (Qmax) is independent of differences in muscle isometric stress and muscle size within a group of preparations and so is a measure of the intrinsic muscle power that allows for comparison of power output between the three muscles. The average normalized powers varied in a pattern similar to that depicted for power in W L −1 , but there were clearly significant differences between the FTI4 and both Rhm and BB. The Qmax of the FTI4 was close to double the average value of the Rhm ( Fig. 5D and Supplementary data, Table S1 ).

    Measurement of the stress that generates maximum power can be calculated from the values of relative force at peak power (FQmax) and the maximum isometric stress. The stress at peak power ( Table 2 and Fig. 5F) was slightly higher in the FTI4 than in the BB and Rhm, but was not statistically different relative to either.

    The average values for Vmax optimal velocity of muscle shortening at maximum power ([email protected]Qmax) showed similar general muscle ID dependency to the that shown among the average Qmax values, with those for the FTI4 being higher than the BB and Rhm muscles, and the BB and Rhm average Vmax and [email protected]Qmax being quite similar to each other ( Table 2, Fig. 5C and E). The FTI4 average Vmax and average [email protected]Qmax were significantly higher than the values for BB and Rhm in our LME analyses. Differences in muscle bundle shortening speed, and not stress at peak power, appear to explain the greater average power in the FTI4 compared to the BB and Rhm muscles.

    The rate of fatigue within Nile crocodile muscles showed a higher fatigability for the FTI4. Both the Rhm and BB were more resistant to fatigue, reaching 50% of their initial isometric force after 78 and 85 consecutive activations, respectively. The FTI4 was more easily fatigued on average, half of the isometric force was reached after 56 activations. As part of the LME model analysis, we tested whether the rate of fatigue had an effect on the performance of the muscle bundles. No statistical influence of fatigue was found on any of our performance measures.

    Muscle immunostaining

    Immunostaining was done to provide a qualitative picture of MHC-I and -II distribution in muscle bundles dissected directly adjacent to the bundles used for mechanics testing. We did not count fiber types partly because reliable identification of MHC-II subtypes and hybrids was not possible, and partly because the bundles that were stained varied in size (cross-section) and total fiber number. Also, the triton-X 100 skinned bundles will have been swollen and lacking both intracellular compartmentation and consistent collagen demarcation of fiber margins. Nevertheless, the actin–myosin lattice remains intact in relaxed skinned fibers and indeed remains functional in the presence of calcium and adenosine–triphosphate. The myosin heads are available for antibody binding in thin sections. We assumed that the MHC content of these small skinned muscle strips is representative of the larger intact bundles used for mechanics testing.

    A total of eight muscle fragments (three each of FTI4 and Rhm and two of BB) from three different crocodiles were cut and stained successfully. An example set of images ( Fig. 7), where the muscles stained all came from the same crocodile, shows that bundles from all three muscle groups contained both MHC-I (slow-twitch) and MHC-II (fast-twitch) fibers. The FTI4 and BB cross-sections showed similar densities of MHC-I fibers, while the Rhm fragment tended to show greater MHC-I content. The BB and FTI4 comparisons were visually consistent across the subset of muscles sampled for immunostaining (see Supplementary Material S1 for images not shown in Fig. 7). The two Rhm samples that were sectioned had quite different densities of MHC-I (compare Fig. 7, Panels C and D), perhaps consistent with the variable degree of surface “pinkness” that we noted in particular the Rhm coloration during dissection.

    Representative images of immunohistochemical staining of Nile crocodile muscle fiber bundles (from “Croc 5”). Muscle ID (BB/Rhm/FTI4) is given followed by “Fast”/“Slow” for Types I or II staining. Blue highlights the Type I (slow-twitch) and red highlights the Type II (fast-twitch) fibers in the images, which all were viewed with ×20 magnification. For all other samples see Supplementary Material S1. Note 50-micron scale bar in bottom right panel.

    Representative images of immunohistochemical staining of Nile crocodile muscle fiber bundles (from “Croc 5”). Muscle ID (BB/Rhm/FTI4) is given followed by “Fast”/“Slow” for Types I or II staining. Blue highlights the Type I (slow-twitch) and red highlights the Type II (fast-twitch) fibers in the images, which all were viewed with ×20 magnification. For all other samples see Supplementary Material S1. Note 50-micron scale bar in bottom right panel.


    Muscular Strength, Power, and Endurance Training

    Muscular strength is the ability to exert maximal force in one single contraction, such as lifting a weight that you could lift only once before needing a short break. Muscular power refers to a great force production over a short period of time, such as in fast leg kicks and explosive jumping. Muscular endurance is when less force is sustained over a longer period of time such as in gallops, skips, pli&eacutes, and swings. Dancers often confuse endurance with strength, so it is sometimes useful to think of endurance as continuous and strength as maximal.

    This dancer displays muscular strength as well as flexibility in this difficult balance.
    CPRowe Photography 2012, University of Utah, Modern Dance.

    In dance you are required to jump, catch partners, move down onto the floor and up out of the floor at fast speeds, and perform other explosive movements. These movements require a level of muscular strength and power. While technique classes can improve muscular strength and power, it is not necessarily the main goal. Some current dance technique classes are increasingly asymmetrical (practicing coordination on one side only) and are more focused on stylistic and artistic aspects of dancing rather than adequate repetitions to develop strength, power, and endurance. Therefore, you should do supplementary exercises for muscular strength, power, and endurance outside of your dance technique classes. Without a certain baseline of these important abilities, you are more likely to incur musculoskeletal imbalances and injuries. Injuries developed from muscular imbalances or from lack of core strength in large, explosive movements are common.

    You need a good level of muscular strength, power, and endurance in order to effectively perform a variety of dance movements such as lifts, jumps, and explosive movements. An adequate level of muscular strength, power, and endurance not only assists the technical and aesthetic aspects of performance, it can also minimize the risk of injury by increasing joint stabilization and improving bone health.

    A common method of strength training is with resistance machines or free weights, such as dumbbells. Even more common for dancers is using exercise bands or stretchy surgical tubing as resistance. You can also do strength training using your own body weight, such as in push-ups and leg lunges. You should exercise larger muscle groups before smaller ones, because smaller ones fatigue more quickly. It is important to alternate muscle groups to allow for recovery before performing another exercise on the same muscle group. For muscular strength gains, you should exercise a muscle through its full range of motion for 8 to 12 repetitions. The amount of weight or resistance should be challenging after the set, you should feel muscular fatigue. Young teens or dancers rehabilitating from an injury should use lower weight or resistance and higher numbers of repetitions. For exercises targeting muscular power, remember to perform fast repetitions. You can repeat exercises two or three times in a given conditioning sequence.

    When exercising for muscle strength, you should isolate the muscles to be strengthened carry out the correct motion fully in a smooth and controlled manner without other muscles compensating. People tend to compensate when they are tired, which is when other muscles take over for the fatigued muscles. When you are exercising, be mindful of this tendency and make adjustments in resistance in order to isolate the appropriate muscles. Whenever possible, exercise a joint through its full range of motion so as to work the entire muscle and not to use too much weight or resistance during the end of a motion.

    Apply the principle of specificity by replicating movement patterns of dance as closely as possible and stressing muscle groups that are most needed in current dance activities. For example, when you are returning to technique class or rehearsals after an ankle sprain, you will need to condition the ankle to be able to jump. It is best for you to incorporate foot exercises that best match the jumping speed and range of motion similar to what occurs in dance jumps. While slow and sustained strengthening exercises, such as work with an exercise band, are recommended, you will benefit from restrengthening the feet with an increase in tempo, coming as close as possible to actual jumping speed and with a similar range of motion.

    To realize gains in strength and power, apply the principle of progressive overload. Overload should happen in a gradual and progressive manner whereby intensity, duration, and frequency of the exercises are steadily increased. It is a good idea to begin with an initial 2-week period of high-repetition (15-25 reps) training with low resistance. Following this period, increase load with fewer (8-12) repetitions, allowing the focus of the exercise to shift from endurance to strength. A rest period of 60 to 90 seconds between each set is important, and exercises for the same body area should not be done on successive days. You may not notice results for 5 to 10 weeks, but do not become discouraged results will occur.

    You can train muscular power by incorporating explosive exercises after seeing initial strength gains. Plyometrics training is a form of jump training in which you exert maximal force in short intervals, which has been shown to effectively increase leg power. Usually exercises are quite short but fairly explosive. An example of a plyometrics exercise is 6 to 8 high tuck jumps followed by a rest and then repeated twice more. If progressive overload is applied here, the frequency of the jumps may increase from 3 to 4 bouts and the number of repetitions may increase from 6 to 8 jumps, to 8 to 10 jumps, and so on.

    Dance technique classes cannot be solely relied on to provide the conditioning exercises needed to target various components of physical fitness such as muscular strength, power, and endurance. These aspects of conditioning allow you to perform dance movements such as jumping, catching a partner, moving down onto the floor and up from the floor at fast speeds, and other explosive movements. It is therefore recommended that you do supplementary exercises for these aspects of conditioning outside of dance technique classes.


    Watch the video: LAB 8 ANATOMY PHYSIOLOGY 1 (September 2022).


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