Lesson 1: Movement Physiology and Strength Training Adaptations

Table of Contents


Introduction

There are many different body systems that contribute to movement and regular exercise leads to adaptations in these systems. In the first two lessons of this course I will discuss this in detail. First I will discuss the nervous and musculoskeletal systems and the adaptations that occur with strength training. In the next lesson I will discuss energy production as well as the respiratory and cardiovascular systems and the adaptations that occur with aerobic training.


Overview of movement

The above listed systems all play a role in movement. The central and peripheral nervous systems connect your brain to your muscles. Your musculoskeletal system translates thoughts into actual movement. The cardiovascular and respiratory systems provide the nutrients your muscles need to undergo contractions.

Note: Much of this lesson provides theoretical knowledge that some may not find very interesting. You do not need to read through all of this in detail to move through this course. You can feel free to skim through to the “Summary of Movement” section below and refer to the rest of the material for clarification if desired.


Central and peripheral nervous systems

In order to move, chemical and electrical signals generated in your brain travel through your central nervous system in the spinal cord. These signals transfer to the peripheral nervous system that then carries the signals to skeletal muscle.

In the image below the central nervous system is in yellow and the peripheral nervous system is in blue. The peripheral nervous system branches out to all places in the body where muscles are located.

Note: Unless otherwise stated I took all of the following images from Wikipedia.

an image showing the central and peripheral nervous systems

Skeletal muscle structure

Skeletal muscle generally has an outer layer of connective tissue called epimysium. A middle layer of connective tissue called perimysium surrounds distinct muscle fascicles within this epimysium. Lastly, an inner layer of endomysium surrounds individual muscle fibers within the fascicles. To be clear, this is somewhat of a simplification and the connective tissue structures are intricately connected to various components of the muscle to allow force transmission.(Purslow, 2020) The image below shows all of the basic structures of skeletal muscle. I will discuss the bottom part of the image further below.

a cartoon depicting skeletal muscle structure
This image was reproduced from: Jorgenson KW, Phillips SM, Hornberger TA. Identifying the Structural Adaptations that Drive the Mechanical Load-Induced Growth of Skeletal Muscle: A Scoping Review. Cells. 2020 Jul 9;9(7):1658. doi: 10.3390/cells9071658. PMID: 32660165; PMCID: PMC7408414.

Neuromuscular junction

Peripheral nerves penetrate muscle to abut skeletal muscle fibers. When activated they release neurotransmitters; these are small chemical molecules that interact with muscle fibers. Additionally, in the image below a blue myelin sheath surrounds the yellow peripheral nerve. The myelin sheath allows signals to propagate more quickly. The nerve releases many chemical neurotransmitters (acetylcholine is the primary one for skeletal muscle) that bind to receptors on the skeletal muscle fiber. Of note, one “motor unit” consists of one motor neuron (generally a lower motor neuron that is part of the peripheral nervous system) and all of the muscle fibers it innervates; these activate in an “all or none” fashion where the motor neuron will either activate all of its muscle fibers or none of them.

an image showing a neuromuscular junction

The schematic below shows a zoomed in cartoon of this. When the released acetylcholine binds to the receptors, this causes sodium ions to enter the cell.

Part 1 of 3 of a schematic of a neuromuscular junction
Part 2 of 3 of a schematic of a neuromuscular junction
Part 3 of 3 of a schematic of a neuromuscular junction

Action potential propagation

When the sodium ions enter the skeletal muscle fiber this generates an action potential; this is a rapid rise and then fall in voltage across the sarcolemma (muscle fiber membrane) due to the positive charge of the sodium. This action potential transcends through transverse tubules (“t tubules”), ultimately leading to calcium entering the core of the muscle fiber. The following cartoon shows a muscle fiber, its component myofibrils, the location of the sarcoplasmic reticulum (a storage network for calcium) and t-tubules. It also shows the presence of many mitochondria (organelles that generate the adenosine triphosphate (“ATP”) needed to fuel muscle contractions). MItochondria are discussed further in Lesson 2.

a cartoon image of a muscle fiber

Skeletal muscle contraction

Once calcium enters from the sarcoplasmic reticulum it acts on the core components of the myofibrils. Subsequently this triggers the actin (thin) and myosin (thick) filaments to interact. The following cartoon shows the location of the sarcoplasmic reticulum in relation to the core components of myofibrils.

The image below shows that calcium binds to the troponin complex. This shifts tropomyosin to expose active sites on the actin filaments. The thicker myosin filaments then bind to these active sites, forming cross bridges. When this occurs, inorganic phosphate (“Pi”) releases from the myosin heads and the myosin heads hinge. This “power stroke” moves the actin filament slightly. After this hinge movement adenosine diphosphate (“ADP”) releases from the myosin head as well.

A single power stroke shortens the skeletal muscle a small amount; you need recurrent power strokes to generate a full contraction. After the power stroke the hinged myosin head binds to ATP and releases from the active site. Myosin ATPase, a protein within the myosin head, hydrolyzes this ATP molecule to generate ADP & Pi again. The myosin head can then bind to a subsequent active site, allowing another power stroke to occur.


Sliding filament theory

As seen in the below cartoon of a sarcomere (the basic contractile unit within myofibrils), recurrent power strokes when a muscle contracts lead to the myosin and actin filaments overlapping more readily; this is the “sliding filament theory” of skeletal muscle contraction. As greater overlapping correlates with greater contraction, skeletal muscle shortens during a contraction.

a cartoon image of actin & myosin sliding over each other

Movement generation

So how does this generate movement? The epimysium, perimysium, and endomysium of skeletal muscle fuse together into a tendon that attaches to a bone. When the muscle contracts and shortens, it pulls on the attached tendon(s) which pull on the bones, causing movement.

a cartoon image of a bicep contraction causing arm movement

Note: A key aspect of movement is that when skeletal muscles contract they always shorten. Keeping this in mind helps to make it much easier to visualize and understand which muscles perform different actions in the body. I’ll discuss movements and exercises of the major muscle groups in Lessons 9-12.


Length-tension relationship

Looking at the last two figures:

  • sarcomeres are in a more relaxed state when muscles are in a lengthened position
  • sarcomeres are in a more contracted state when muscles contract into a shortened position

When sarcomeres are “too relaxed” or “too contracted” only a subset of possible cross bridges can form; this leads to submaximal force production. This phenomenon is termed the “length-tension relationship” and it is depicted in the figure I created below.

an image depicting the length-tension relationship
Active force is force generated with muscular contraction. Passive force is force generated when a muscle is stretched as the elastic structures attempt to return to their baseline length. Combined force is a summation of active and passive force. Along the active force line there are depictions of sarcomeres with different degrees of cross bridge formation and overall contraction.

Motor unit recruitment, rate coding, and the force-velocity relationship

When you want to initiate movement you generally do not use every motor unit available. Rather, according to “Henneman’s size principle”, the smaller motor units activate first and the larger motor units only activate if needed.(Kraemer, 2012) Additionally, motor units can alter the frequency of action potentials (called “rate coding”). When you need to generate more force, two primary events occur:

  • motor unit recruitment increases (allowing more muscle fibers to take part in force generation)
  • rate coding increases (allowing each individual muscle fiber to contribute a greater amount of force by increasing the number of contractions per unit time)

As a result of these two factors, plus the fact that cross bridge formation is not instantaneous as well as other potential considerations like fluid viscosity within the muscle itself, it takes some amount of time to generate maximum force. Therefore, maximum force cannot be generated at a maximum velocity of contraction; at maximum velocity there is not enough time for all possible cross bridges to form. This is depicted in the figure I created below.

an image depicting the force-velocity relationship and its association with power production.
The blue line represents force. The red line represents power (of note, power = force * velocity, though you can see a caveat to this in the note below). As velocity of movement increases total possible force production decreases; this is due to less time and less need for motor unit recruitment, rate coding, and cross bridge formation at faster contraction velocities. Regarding power output, this is low when velocity is very low or when force is very low. Power output is maximized when force and velocity are both proportionally significant relative to their maximum possible values.

Note: Technically speaking, “power = force * velocity” is not completely accurate/applicable in the context of exercise science, and an argument can be made that the term “impulse” should be used instead.(Winter, 2016) However, as the vast majority of the exercise science literature uses “power” in this manner, I will as well for consistency. A similar argument can be made for other terms such as “explosiveness” (ie, nothing in humans explode) and “workload” (“work” is technically measured in joules while “load” is technically measured in newtons). On the other hand, the authors of (Winter, 2016) favor the term intensity for describing various aspects of sporting performance, yet as I will discuss in Lesson 4 the term “intensity” has variable definitions in the exercise literature.

In general I will use terminology that is consistent with the majority of the literature as well as colloquial use and I will attempt to clarify at any point when this is confusing.


Muscle fiber types

The smaller motor units are more typically comprised of type I muscle fibers while the larger motor units are more typically comprised of type II muscle fibers. Muscle fiber type refers to the predominant type of myosin ATPase present (if you recall this was mentioned above). There are three types:

  • Type IA is slow oxidative.
  • Type IIA is fast oxidative.
  • Type IIX is glycolytic (some refer to this as type IIB but technically type IIX is more appropriate(Jorgenson, 2020)).

The terms “oxidative” and “glycolytic” are discussed in the next lesson, as are the involved energy production pathways. Being more oxidative, type I muscle fibers are better able to use aerobic pathways for energy production. Therefore, this is helpful for sustaining muscular activity over longer time periods (ie, aerobic activity). As type IIx fibers more prominently use anaerobic & glycolytic pathways, they are better for shorter bursts of activity (ie, sprinting or lifting weights explosively). Type IIA is in between these but are functionally more like type IIX.

In general(Kraemer, 2022):

  • Type I fibers (compared to type II) have greater muscle contractile efficiency, endurance capabilities, triglyceride stores, aerobic enzymes, capillary density, mitochondrial density, and density of noncontractile proteins.
  • Type II fibers (compared to type I) have greater cross-sectional area fiber size, contraction speed, force generating capabilities, glycolytic enzymes, and glycogen stores.

Note: Some fibers can have properties of multiple types as well as shift along a spectrum to some degree between them.(Kraemer, 2012) Over time as you continue to exercise the fibers will shift properties to a limited degree to better meet the demands of the training stimulus you provide them.

Example: Conceptually, the motor unit recruitment order makes sense when considering walking vs jogging vs sprinting. When walking you are going to predominantly use the smaller motor units with primarily type I muscle fibers; this is because you do not need to generate large amounts of force to walk but you do need to be able to sustain walking for extended periods of time. As you move on the spectrum towards jogging and then sprinting, you will need to impart more force into the ground to propel yourself forward at faster speeds; this will utilize more of your larger motor units with predominantly type II muscle fibers. This allows you to generate more force and move faster but only for a short period of time prior to fatiguing and needing to slow down.


Pennation angle

For some muscles the fascicles actually join the tendon at an angle relative to the primary direction of pull of the muscle. This angle, called the “pennation angle”, allows a greater number of fibers to be packed in parallel, and with more fibers a greater amount of force can be generated.

The cartoon below illustrates how the pennation angle allows more fibers to be present. The black lines represent tendons, the red lines represent fascicles, the blue line represents the anatomic cross sectional area (“aCSA”), and the green line represents the physiologic cross sectional area (“pCSA”). Image A is a fusiform arrangement, B is unipennate, C is bipennate, and D is multipennate. In A the pennation angle (the angle between the blue and the green line) is 0.

The aCSA is essentially equivalent to the width of the muscle, but when fascicles run through the muscle at an angle the aCSA does not fully approximate the amount of fibers that are present. The pCSA essentially represents the area perpendicular to the fascicles themselves and not just the area of the muscle as a whole; this is a better approximation of the total number of fibers and force production capability. As the pennation angle increases, the pCSA increases, and the amount of force that can be generated increases.

This image was reproduced from Jorgenson KW, Phillips SM, Hornberger TA. Identifying the Structural Adaptations that Drive the Mechanical Load-Induced Growth of Skeletal Muscle: A Scoping Review. Cells. 2020 Jul 9;9(7):1658. doi: 10.3390/cells9071658. PMID: 32660165; PMCID: PMC7408414.

Note: Technically when calculating the amount of force that can be produced you must multiply the pCSA by the cosine of the pennation angle (this yields an “effective pCSA” by determining the component of the muscle fascicles that pull along the longitudinal axis); this still overall favors greater force production with a larger pennation angle given the increase in pCSA that is observed. For further discussion of the relationship between muscle size, structure, and strength, see (Vigotsky, 2018).

Having said that, a recent study found that muscle volume correlates just as well as effective pCSA with force production (in fact the volume measurement was non-statistically significantly superior), either due to inaccuracies in measuring the latter or the fact that effective pCSA does not account for lateral force transmission between fibers, fascicles, or muscles while muscle volume may also account for these factors.(Balshaw, 2021)

While this is all complicated and much research remains to be done, thankfully none of this is very relevant for practical considerations of exercise program design or execution for the purpose of health or performance benefits. These various factors do however help explain why two people with similarly sized muscles may have different levels of strength.


Summary of movement

In order to move several steps must occur. First you generate signals in your brain that travel through your central nervous system to your peripheral nervous system. Then motor neurons of the peripheral nervous system transfer these signals to several muscle fibers by releasing small neurotransmitters. One motor unit consists of one motor neuron and all of the muscle fibers it innervates. Subsequently, these neurotransmitters lead to sodium ions entering the muscle fiber; this generates an electrical signal that results in calcium binding to the core components of muscle fibers. This triggers the core components to interact using ATP to generate a muscle contraction. Ultimately this process leads to muscles shortening and pulling on their tendons. Since these tendons pull on bones, this generates movement.

Your muscles are more effective at generating large amounts of force at certain lengths; when they are stretched too long or placed in a shortened position they may be unable to generate maximum force. Additionally, if you need to generate more force to carry out a specific movement your body increases motor unit recruitment (initially smaller motor units are utilized and larger ones are recruited as needed) and rate coding (the frequency at which each motor unit generates a contraction). Another contributing factor to greater force production is a slower velocity of contraction, though if the contraction is too slow this will hinder power output as power = force * velocity. Lastly, several intrinsic properties of muscle fibers can impact for production, such as their pennation angle (their orientation relative to the line of force) and their composition (ie, type IA vs. type IIA vs. type IIX).

This has not been an exhaustive discussion of factors contributing to movement. However, the above should be plenty for an introduction to how muscles work and sets the stage to see what physiologic changes occur with exercise as described below.


Strength Training Adaptations

Strength training induces several different physiologic adaptations that lead to greater strength levels.(Reggiani, 2020) Strength training leads to several neural adaptations (including increased motor unit recruitment/synchronization, decreased corticospinal & intracortical inhibition, and a decrease in the motor unit recruitment threshold)(Siddique, 2020; Lysenko, 2021) as well as connective tissue adaptations that allow more efficient transfer of energy, and this allows a rapid increase in strength when people begin training.(Hughes, 2018) Beneficial mitochondrial changes also occur with resistance training.(Parry, 2020; Mang, 2022)

Over longer periods of time strength training contributes to increased cross-sectional area of skeletal muscle via skeletal muscle hypertrophy due to an increase in muscle protein synthesis, presumably as a result of an increase in ribosome content.(Lysenko, 2021) This is currently thought to occur primarily via the addition of sarcomeres (the individual contractile units within myofibrils) as well as the addition of myofibrils to muscle fibers.(Haun, 2019) However, there are many gaps in our current understanding.(Jorgenson, 2020) Furthermore, the exact triggers for this are unclear(Schiaffino, 2021), but various considerations include tension placed on the muscle while training, metabolic stress generated by the buildup of metabolites, and exercise-induced muscle damage.(Wackerhage, 2019) In addition to this, the muscle fiber types will transition to a degree to better suit the training stimulus.(Reggiani, 2020) Additional muscle properties can change, such as the pennation angle of the muscle fascicles as well as the length of the fascicles when sarcomeres are added in series.(Maestroni, 2020)

Note: When skeletal muscle hypertrophy occurs with strength training this is not necessarily a uniform process throughout the entire muscle.(Vigotsky, 2018) Different portions of a muscle can grow at different rates. Additionally when new sarcomeres or myofibrils are added this may occur in parallel or in series. I drew a simple diagram to illustrate this below.

With sarcomeres added in parallel the overall cross sectional area of the muscle increases and thus the ability to generate force increases. However, with sarcomeres added in series the muscle fibers lengthen. Of interest, when fibers lengthen their contraction speed may increase and this alters the length-tension & force-velocity relationships of the muscle. While theoretical, it is possible that different training styles may induce hypertrophy in different ways that could prove beneficial for specific athletic tasks or other goals.(Travis, 2020)

We actually do not have a great understanding of how skeletal muscle hypertrophy occurs.(Roberts, 2020) For a greater discussion of this topic, please read (Jorgenson, 2020 and Lim, 2022). This lack of understanding extends to a degree to the various contributing factors for strength gains.(Duchateau, 2021) If curious, several of the theoretical key factors are demonstrated in the figure below(Lim, 2022):

Reproduced from: Lim C, Nunes EA, Currier BS, McLeod JC, Thomas ACQ, Phillips SM. An Evidence-Based Narrative Review of Mechanisms of Resistance Exercise-Induced Human Skeletal Muscle Hypertrophy. Med Sci Sports Exerc. 2022 Sep 1;54(9):1546-1559. doi: 10.1249/MSS.0000000000002929. Epub 2022 Apr 6. PMID: 35389932.

Conclusion

Overall, the nervous and musculoskeletal systems are intricately connected to allow you to generate movement, and when you exercise regularly several physiologic adaptations occur. Many of these adaptations are associated with significant health benefits. Additionally, you can design an exercise program with specific goals in mind and you can tailor your training style to induce the adaptations necessary to help you achieve your goals. I will discuss how to design exercise programs for improved health and fitness in upcoming lessons.

In this lesson I briefly mentioned that mitochondria help supply ATP to fuel skeletal muscle contractions. In the next lesson I’ll discuss energy production in more detail to help explain how this occurs and I will discuss the physiologic adaptations that occur with aerobic training.

Click here to proceed to Lesson 2


References

  1. Balshaw TG, Maden-Wilkinson TM, Massey GJ, Folland JP. The Human Muscle Size and Strength Relationship: Effects of Architecture, Muscle Force, and Measurement Location. Med Sci Sports Exerc. 2021 Oct 1;53(10):2140-2151. doi: 10.1249/MSS.0000000000002691. PMID: 33935234.
  2. Duchateau J, Stragier S, Baudry S, Carpentier A. Strength Training: In Search of Optimal Strategies to Maximize Neuromuscular Performance. Exerc Sport Sci Rev. 2021 Jan;49(1):2-14. doi: 10.1249/JES.0000000000000234. PMID: 33044332.
  3. Haun CT, Vann CG, Roberts BM, Vigotsky AD, Schoenfeld BJ, Roberts MD. A Critical Evaluation of the Biological Construct Skeletal Muscle Hypertrophy: Size Matters but So Does the Measurement. Front Physiol. 2019 Mar 12;10:247. doi: 10.3389/fphys.2019.00247. PMID: 30930796; PMCID: PMC6423469.
  4. Hughes DC, Ellefsen S, Baar K. Adaptations to Endurance and Strength Training. Cold Spring Harb Perspect Med. 2018 Jun 1;8(6):a029769. doi: 10.1101/cshperspect.a029769. PMID: 28490537; PMCID: PMC5983157.
  5. Jorgenson KW, Phillips SM, Hornberger TA. Identifying the Structural Adaptations that Drive the Mechanical Load-Induced Growth of Skeletal Muscle: A Scoping Review. Cells. 2020 Jul 9;9(7):1658. doi: 10.3390/cells9071658. PMID: 32660165; PMCID: PMC7408414.
  6. Kraemer WJ, Looney DP. Underlying Mechanisms and Physiology of Muscular Power. Strength and Conditioning Journal. 2012 December;34(6):13-19 doi: 10.1519/SSC.0b013e318270616d
  7. Kraemer WJ, Nitka M. Choice of Resistance Used in an Exercise: Simple to Complex Interactions. Strength and Conditioning Journal. 2022. doi: 10.1519/SSC.0000000000000696.
  8. Lim C, Nunes EA, Currier BS, McLeod JC, Thomas ACQ, Phillips SM. An Evidence-Based Narrative Review of Mechanisms of Resistance Exercise-Induced Human Skeletal Muscle Hypertrophy. Med Sci Sports Exerc. 2022 Sep 1;54(9):1546-1559. doi: 10.1249/MSS.0000000000002929. Epub 2022 Apr 6. PMID: 35389932.
  9. Lysenko EA., Vinogradova OL, Popov DV. The Mechanisms of Muscle Mass and Strength Increase during Strength Training. J Evol Biochem Phys.  2021;57: 862–875. doi: 10.1134/S0022093021040104
  10. Maestroni L, Read P, Bishop C, Papadopoulos K, Suchomel TJ, Comfort P, Turner A. The Benefits of Strength Training on Musculoskeletal System Health: Practical Applications for Interdisciplinary Care. Sports Med. 2020 Aug;50(8):1431-1450. doi: 10.1007/s40279-020-01309-5. PMID: 32564299.
  11. Mang ZA, Ducharme JB, Mermier C, Kravitz L, de Castro Magalhaes F, Amorim F. Aerobic Adaptations to Resistance Training: The Role of Time under Tension. Int J Sports Med. 2022 Sep;43(10):829-839. doi: 10.1055/a-1664-8701. Epub 2022 Jan 27. PMID: 35088396.
  12. Parry HA, Roberts MD, Kavazis AN. Human Skeletal Muscle Mitochondrial Adaptations Following Resistance Exercise Training. Int J Sports Med. 2020 Jun;41(6):349-359. doi: 10.1055/a-1121-7851. Epub 2020 Mar 11. PMID: 32162291.
  13. Purslow PP. The Structure and Role of Intramuscular Connective Tissue in Muscle Function. Front Physiol. 2020 May 19;11:495. doi: 10.3389/fphys.2020.00495. PMID: 32508678; PMCID: PMC7248366.
  14. Reggiani C, Schiaffino S. Muscle hypertrophy and muscle strength: dependent or independent variables? A provocative review. Eur J Transl Myol. 2020 Sep 9;30(3):9311. doi: 10.4081/ejtm.2020.9311. PMID: 33117512; PMCID: PMC7582410.
  15. Roberts MD, Haun CT, Vann CG, Osburn SC, Young KC. Sarcoplasmic Hypertrophy in Skeletal Muscle: A Scientific “Unicorn” or Resistance Training Adaptation? Front Physiol. 2020 Jul 14;11:816. doi: 10.3389/fphys.2020.00816. PMID: 32760293; PMCID: PMC7372125.
  16. Schiaffino S, Reggiani C, Akimoto T, Blaauw B. Molecular Mechanisms of Skeletal Muscle Hypertrophy. J Neuromuscul Dis. 2021;8(2):169-183. doi: 10.3233/JND-200568. PMID: 33216041; PMCID: PMC8075408.
  17. Siddique U, Rahman S, Frazer AK, Pearce AJ, Howatson G, Kidgell DJ. Determining the Sites of Neural Adaptations to Resistance Training: A Systematic Review and Meta-analysis. Sports Med. 2020 Jun;50(6):1107-1128. doi: 10.1007/s40279-020-01258-z. PMID: 31993949.
  18. Travis SK, Ishida A, Taber CB, Fry AC, Stone MH. Emphasizing Task-Specific Hypertrophy to Enhance Sequential Strength and Power Performance. J Funct Morphol Kinesiol. 2020 Oct 27;5(4):76. doi: 10.3390/jfmk5040076. PMID: 33467291; PMCID: PMC7739346.
  19. Vigotsky AD, Schoenfeld BJ, Than C, Brown JM. Methods matter: the relationship between strength and hypertrophy depends on methods of measurement and analysis. PeerJ. 2018 Jun 27;6:e5071. doi: 10.7717/peerj.5071. PMID: 29967737; PMCID: PMC6026459.
  20. Wackerhage H, Schoenfeld BJ, Hamilton DL, Lehti M, Hulmi JJ. Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise. J Appl Physiol (1985). 2019 Jan 1;126(1):30-43. doi: 10.1152/japplphysiol.00685.2018. Epub 2018 Oct 18. PMID: 30335577.
  21. Winter EM, Abt G, Brookes FB, Challis JH, Fowler NE, Knudson DV, Knuttgen HG, Kraemer WJ, Lane AM, van Mechelen W, Morton RH, Newton RU, Williams C, Yeadon MR. Misuse of “Power” and Other Mechanical Terms in Sport and Exercise Science Research. J Strength Cond Res. 2016 Jan;30(1):292-300. doi: 10.1519/JSC.0000000000001101. PMID: 26529527.
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