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maximal muscle force

By Iris Saar, Masters of Applied Exercise Science candidate,Concordia univeristy of Chicago, ACSM PT.

Please make sure you are well versed in the instruction of performing a 1-RM test before reading this more advanced article.

Execution of 1-RM, or maximal force per 1 repetition, requires a structured understanding of muscle force production and factors limiting them. This is vital for initial assessments of clients in gyms, at-home setting for personal trainers and for applied clinical interventions.

Factors that limit force production during a maximal effort

Maximal effort required a significant amount of energy utilization by the muscle cells. Exercise induced fatigue inhibits a constant rate of ATP breakdown and together with other factors, will limit force production during maximal effort. Fatigue is a decrease in the muscle’s ability to produce power and can be measured from the point of time in which contraction time is decreased or slowed down. Fatigue will affect both the central and the peripheral nervous systems. Fatigue itself is related to the following causes:

  • Fitness level of an athlete: an untrained individual will likely experience exercise induced fatigue at an earlier point of the exercise onset due to less efficient mechanism of force production.

  • Diet and nutrition: a diet rich in CHO can promote the economical use of readily-available glucose resources in the blood and liver. Consumption of CHO during recovery periods can add to the utilization of glycogen. Hence, CHO-deprived diets protocols may bring the athlete to a faster state of fatigue (Williams, 1985).

  • Fiber type composition: since the higher amount of energy comes from fast-twitch muscle fibers (types ɪɪx and ɪɪa ), muscle cells which contain them will enhance force production. Conversely, slow-twitch muscle fibers (type ɪɪa ) produce less force and if the athlete is genetically prone to a higher composition of those fibers, likely they will eventually produce less force.

  • Velocity: maximal at initial application of force or onset of exercise. Velocity is greater when force is low. The more force that is required by the muscle as the exercise continues (in our case, resistance is the athletes’ own body-weight, the slower the velocity of the shortening of the muscle tissue.

  • Intensity and duration of an exercise: it is reasonable to assume that higher intensities in which an exercise if performed will result in a lesser amount of force produced, over the timeline of the entire exercise cycle. This is explained by the onset of fatigue, which tends to show after the initial effort and is caused by an impaired force production at the cross bridges of the filaments. Similarly, the duration of the exercise can also contribute to force production; the longer the duration, the higher the impairment in the myosin-actin cross bridges and their power output.

  • Type of exercise performed: isometric or dynamic- an isometric contraction is the strengthening of a muscle with no change in length, while dynamic contraction involves shortening or lengthening of muscles. Eccentric contraction will cause more stress to sarcolema than concentric contraction, for instance. Most maximal efforts do not require eccentric contractions; however this aspect should still be noted.

Factors other than muscle fatigue muscle fatigue can also influence force production. Among them is the initial length of the muscle. In an “optimal” length, the muscle will produce power in its maximal capabilities (figure 1). If the length is not optimal, force production will be less than maximal.

Figure 1: the length-tension relation in the sarcomere

Image source: The (sarcomere) length-tension relation. Retrieved from: http://www.bristol.ac.uk/phys-pharm-neuro/media/plangton/ugteach/ugindex/m1_index/nm_tension/page2.htm

Additional factors that limit force production include the number and type of motor units recruited, the persistent or incremental neural stimulation to the muscle, the contractile history of the muscle and the postactivation potentation if offered.

Muscle structure and its effect on force production

The muscle’s structure affects its force production is the following way: in contrast to other cells in the human body, muscle cells are multinucleated. They can therefore enhance cell polarization, eventually receiving numerous action potentials use ATP to generate muscle actions. It follows that the location of the nuclei are located in proximity to the neuromuscular junctions (Cadot, Gache and Gomes, 2015).

The muscle fibers are called myofibers and consist of striated thick and thin filaments, named Myosin and Action respectably. They generate force by sliding upon each other in that is known as the “Sliding filament theory” (Powers and Howley, 2019). The force production amount is dependent on the speed in which they either slide upon, or detach from each other. In general, more force is generated when the velocity of the contraction (sliding filaments) is at its lowest and vice versa. This is due to the rapid movement required from the filaments and their somewhat compromised ability to adhere and produce a larger amount of force in a short period of time.

Rest periods and physiological processes between max attempts

Rest periods between maximal repetition attempts are intended for the cessation of muscle contraction. The ability of the skeletal muscles to contact is not indefinite; an effort has a maximal “ceiling” and reaches an exercise-induced fatigue which halts a further biomechanical power output.

Exercise-induced fatigue is caused by several factors; among them are higher levels of lactate and lower sensitivity of the myofibrils to calcium, which by itself is reduced to a lower and slower rate of release into the muscle cells (Fitts, 2008).

A rest period taken in between exercise assists in the restoration of the metabolic systems involved into a replenished state, albeit not identical to the pre-exercise condition. During the rest break the motor neurons no longer “fire” action potentials. The myofibril goes through repolarization, which bring the cell into is resting state potential of negative charge. Ions can no longer enter the membrane due to the temporary closure of the protein-made pathways and the average charge of the cell might bounce back to around 60mV. Afferent nerves reduce their activity and promote the inhibition of further action potentials. A regulatory protein called Tropomyosin is bounded to the Actin molecule and blocks the connection sites where active cross bridges would try to connect to in an active state. Calcium is also being drawn back, outside of the cytosol and causes the positive change in Tropomyosin. As mentioned earlier, less Ca2+ (Calcium) will correlate to a lesser degree of Mysoin and Action binding, hence muscle relation or a rest period occurs.

Desired changes to increase force production

The ability to theoretically increase muscle production is dependent on the following factors. Changes in each will increase muscle force production in the following manner.

  • Maximal force production: since larger muscles produce more force than smaller muscles, a competitive exercise program could include a majority of larger muscles as agonists. For example, a shot put competition versus an arm wrestling match. From a cellular point of view, increasing the myosin filaments in the myofibril can increase binding sites, hence creating more muscle force potential. Larger muscles might be more responsive to this theoretical increase in thick filaments.

  • Speed of contraction: Individual fibers contract at a certain Vmax. Perhaps a concentrated cluster of fast-twitch muscle fibers, mainly type ɪɪx, could increase muscle force by the unequal allocation of fast twitch fibers and a relative lack of type ɪ fibers. This can also be viewed by increasing ATPase activity (faster breakdown of ATP). Adequate quantities of both blood and liver glucose are needed for this hypothetical implementation.

  • Maximal power output: more myosin filaments multiplied by increased Vmax can “push” the maximal effort into a new, higher level. In numerical terms, higher values in the following equation can work: maximal power = force * Vmax. So the overall force as a product of this (practical) equation will increase. This will require, as mentioned, more myosin as well as a higher rate of shortening velocity.

  • Efficiency of contraction: type ɪ fibers are more efficient in creating muscle contraction since they are allowed the time frame needed for the sliding of the filaments in the myofibril. A hypothetical allocation of this ability into fast twitch muscle fibers (both types ɪɪx and ɪɪa ) may increase the economy of the force production, I.e. reduce the energy amount required for it to contract. This will desirably not take away from the max power output of the muscle but will operate hand in hand.

  • Muscle fiber types (fast twitch produce more power than slow twitch fibers): a simple (imaginary) reduction of slow twitch muscle fibers and a simultaneous increase in fast twitch fibers can increase muscle force. This is due to the characteristics of types ɪɪx and ɪɪa . since the later produce more power through higher ATPase activity and more mitochondria units in the cell. A higher Vmax is another contributing factor and so preferencing fast (or faster) twitch muscle fibers in the cell may increase force production in the muscles.

Additional exogenous factors such as CHO-rich diet and environmental factors such as living in training camp conditions could increase force production as well due to psychological reasons. This was historically implemented in the days of the Soviet Union.

Factors limiting performance in max repetition assessment

Assessments of max repetitions require a highly attentive observer and a pre-planned protocol. Performance during those assessments can be impacted due to the following factors:

  • Muscle fatigue: as explained above, the onset of fatigue will negatively affect performance. Especially in a max repetition setting, one can except to exhibit exercise-induced fatigue at an earlier time (compared, for example, to endurance training such as low velocity running).

  • Sudden and previous injuries: as opposed to fatigue, since an injury is not reversible in the term that rest period can rehab the affected muscle and restore its force production abilities. An injury can limit range of motion, coordination and power output in affected muscles. Proper screening of athlete prior to max repetition testing will reflect a more accurate 1RM load.

  • Generalization of assumed 1RM: inaccurate assumption of the maximal load an athlete can exercise upon. This may be biased both as a too-light or too-heavy 1RM resistance given during assessments.

  • Incorrect instruction regarding body position: accurate anatomical cueing is important, as it can prevent injury, promote force production and enhance observation of intolerance to resistance and the result determination of 1RM. If the anatomical cueing is incorrect, force production will be affected due to lower recruitment of motor units in the prime movers and a potential reciprocal inhibition.

  • Age: Sarcopenia, or muscle mass loss over time, can affect force production. Depends on the age of the assessed athlete and starting from 25 years of age, certain limitations in force production can be related to the relative loss of muscle mass.

Causes for fatigue during a maximal repetition assessment

Fatigue is a decreased muscular ability to produce force and is primarily caused by slower shortening velocity and lower force generation. As mentioned earlier, the more force that is required by the muscle as the exercise continues (in our case, resistance is the athletes’ own body-weight), the slower the velocity of the shortening of the muscle tissue. This demonstrated the Vmax mechanism leading to fatigue.

Lower force generation is another major cause for fatigue. This occurs at the cross-bridge level. The rate of ATP breakdown is slower, creating less of a trigger for the myosin to operate cross bridges which then bind to actin and pull the thin filament inwards, creating muscle shortening or muscle contraction. Muscle contractions are regulated by the presence of Calcium. When calcium ion levels are high enough, it binds to Troponin however when there’s an insufficient amount of Calcium, the protein Tropomysoin is released and blocks the cross bridges, hence preventing contraction. In a state of prolonged or heavy exercise, Calcium levels drop.

The muscle cells contain two important effort-sensing organelles which regulate the above mentioned physiological changes. Those are the muscle spindle and the Golgi tendon organ or GTO. Muscle spindle observe changes in length of muscles. They signal the CNS to recruit more motor units or alternatively to enable stretch / relaxation of the muscle.

The GTO monitors the tension levels generated by the muscles. It created action potential to elicit muscular response. In terms of fatigue, our ability to resist the inhibition created by the GTO may be a threshold to the onset of exercise induced fatigue.

An adaptable factor to consider in exercise induced fatigue is the neuromuscular junction (NMJ). In contrast to the earlier causes for fatigue, the NMJ may change its size (enlarge) as a response to training. This enables more synaptic responses through a rise in the number of vesicles and acetylcholine receptors (the latter will break down ATP and create energy for the muscle to contract).

Sensation of “burn” during max repetition assessment and its cause

An accumulation of lactate products in the blood, during high-intensity exercise, can create a sensation that is perceived as “burning” in the muscles. This type of exercise relies on the anaerobic energy systems (mainly ATP-PC) to produce energy. While doing so, lactate products are released into the bloodstream. An inability to sync the removal of the lactate products, or to create a harmonized resynthesis, can cause a “burning” sensation and is one of the factors to limit force production and participate in the exercise-induced fatigue. This is not to imply that lactate is a factor in DOMS. The point in which the body is able to remove the by-products from the bloodstream is known as the “Lactate threshold or also as the “Anaerobic” threshold. This may be affected by the individual’s level of fitness, mainly their cardiovascular capacity.

Physical, tactical, and exogenous suggestions to maximize performance

Performance can be improved through physiological adaptations in various organs and organelles, and vast literature on this topic is available. From a physical point of view, simply increasing an individual’s level of fitness (sports-specific, to enable appropriate abilities) can enhance performance. A study compared trained versus untrained runners and cyclists and found significant differences in time to exhaustion and VO2 Max for endurance exercise (Caputo, Mello and Denadai, 2003).

Tactical factors that may improve performance can be the design of the exercise program. In marathon running, for example, an elite or competitive athlete usually follows a yearly plan of periodization called macrocycle. Goals are set in tactical way, considering the athletes’’ current and potential fitness level. Mesocycles are then designed with rest periods separating them, a microcycles detail specific workouts based on heart rate and / or pace goals. This way of planning demonstrated a tactical thinking into maximal and educated implementation of an athlete’s capabilities.

Exogenous can include environmental and behavioral factors. In one of my blog posts (https://www.siyofitness.com/post/it-takes-a-village-elite-runners-unite)

I reviewed a study which concluded that factors such as place of birth, spoken language, distance and methods of arrival to school had a significant event on Kenya’s elite runners (Onywera, Scott, Boit and Pitsiladis, 2006; Saar, 2019) . Also, training camps might maximize performance as earlier suggested. This environmental factor is used in various sports such as rhythmic gymnastics, swimming, ice skating and more. A study in ice hockey players (Eler, 2016) showed lowered heart rate on sprint-run testing following a 15-days training camp.


Cadot, B., Gache, V., & Gomes, E. R. (2015). Moving and positioning the nucleus in skeletal muscle - one step at a time. Nucleus (Austin, Tex.), 6(5), 373–381.

Caputo, F., Mello, M. T., & Denadai, B. S. (2003). Oxygen uptake kinetics and time to exhaustion in cycling and running: a comparison between trained and untrained subjects. Archives of Physiology and Biochemistry, 111(5), 461-466.

Eler, S. (2016). Effects of short term camp periods on aerobic and anaerobic performance parameters in ice hockey national team athletes. International Journal of Environmental and Science Education, 11(5), 973-977.

Fitts, R. H. (2008). The cross-bridge cycle and skeletal muscle fatigue. Journal of applied physiology, 104(2), 551-558.

Onywera, V. O., Scott, R. A., Boit, M. K., & Pitsiladis, Y. P. (2006). Demographic characteristics of elite Kenyan endurance runners. Journal of sports sciences, 24(4), 415-422.

Powers, S.K. & Howley, E.T. (2019). Exercise physiology: Theory and application to fitness and performance. (10th ed.). New York, NY: McGraw-Hill.

Saar, I. (2019) It takes a Village, retrieved from https://www.siyofitness.com/post/it-takes-a-village-elite-runners-unite

The (sarcomere) length-tension relation. Retrieved from: http://www.bristol.ac.uk/phys-pharm-neuro/media/plangton/ugteach/ugindex/m1_index/nm_tension/page2.htm

Williams, C. (1985). Nutritional aspects of exercise-induced fatigue. Proceedings of the Nutrition Society, 44(2), 245-256.

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