Neuromuscular Adaptations to Exercise

Original Editor - Wanda van Niekerk


Top Contributors - Wanda van Niekerk, Kim Jackson, Lucinda hampton, Naomi O'Reilly, Tarina van der Stockt and Ewa Jaraczewska  

Introduction[edit | edit source]

Exercise group.jpg

Regular exercise is an effective way to maintain health. It also results in various physiological adaptations in the neuromuscular, cardiovascular and respiratory systems of the human body. These adaptations can improve physical performance.[1]

Adaptation to Exercise: The Overload Principle[edit | edit source]

The overload principle is responsible for the improvement in exercise as well as the adaptation to exercise. The muscular system can be mechanically or metabolically overloaded. These mechanisms result in specific and different adaptations that enhance performance.[1]

The magnitude of these adaptations are dependent on:[1]

  • The type of exercise
  • The intensity of exercise
  • The frequency of exercise
  • The duration of exercise

There is also emerging evidence for other factors also playing a role such as:[2]

  • The initial level of fitness
  • Genetic influences that determine the body's responsiveness (responders and non-responders) to given training interventions

The mode of exercise (e.g. strength training or endurance training) influences the type and magnitude of adaptation in the neuromuscular system. For example, if endurance training (high repetition, low load contractions) is undertaken the muscular system will undergo specific changes that target aerobic metabolism and improved fatigue resistance. Strength training (low repetitions with high load contractions), in contrast, will cause muscle adaptations such as increased myofibrillar protein synthesis. As a result muscle size, strength and power may increase and improve.[1]

Another principle to consider is specificity. The type of exercise performed is important to consider within the context of training. The principle of specificity states that only the system or body part repeatedly stressed will adapt to chronic overload. Thus, "specific exercise elicits specific adaptations creating specific training effects."[3]

[4]

Adaptations to High-Resistance Strength Training[edit | edit source]

Progressive resistance training refers to any type of training that aims to increase muscle strength, power and size through muscular contraction. This mode of exercise relies on the overload principle where strength is improved and muscle growth stimulated by exercising/working a muscle close to its maximal force-generating capacity. A typical programme might involve 6-8 repetitions of lifting and lowering a weight, with these sets being repeated 3-4 times and using loads that are equal to approximately 70-80% of the maximum weight that can be lifted once (1-RM).[1]

[5]

Neural Adaptations[edit | edit source]

  • Increased central drive (from the higher centres of the brain) after resistance training is partly responsible for the increase in strength[6]
  • Increased Motor Unit (MU) synchronization (several MU's firing at similar times)[7]
  • Decrease in the force threshold at which Motor Units are recruited[8]
  • Increased Motor Unit firing rate[9]
  • Decrease in the level of co-activation of antagonist's muscles after training[10]

[11]

Muscular Adaptations[edit | edit source]

Skeletal muscle will adapt to mechanical overload by increasing muscle size. With resistance training various signalling mechanisms are activated and these initiate the creation of new proteins and the enlargement of muscle fibre and muscle cell size leading to hypertrophy with little evidence showing an increase in the number of muscle fibres (hyperplasia) taking place.[1][12]Various adaptations include:

  • Increase in the cross-sectional area of the muscle[13][14]
  • Changes in muscle architecture[13][14]
    • Ultrasound studies have shown changes in the angle of fibre pennation (the angle at which fibres are aligned in regards to their insertion to the aponeuroses of the muscle). This will affect force output by determining the physiological cross-sectional area (where the cross-section area is determined perpendicular to the line of pull of the muscle fibres).[13]
  • Hypertrophy of fibre types at cellular level, especially in Type II fibres:[13]
    • Research shows a decrease in the number of Type IIb (also known as type IIx) fibres, together with an increase in Type IIa fibres[13]
    • Fast-twitch muscle fibres are inherently stronger (greater force per unit area) and have a high speed of shortening, therefore "a given enlargement of a fast-twitch fibre should have a proportionately greater effect on strength and power than the same growth of a slow-twitch fibre."[13]

Muscle Protein Synthesis[edit | edit source]

It is well-known that muscle is sensitive to training loads. The muscular system is a dynamic system with proteins being synthesised and degraded. For muscle growth, the balance between protein synthesis and degrading needs to be changed. This can occur by either increasing the synthesis rate or decreasing the rate of degrading or a combination of both.[1]

Important findings to know about human muscle protein turnover:

  • Muscle protein synthesis is ~ 0.04% per hour in the fasted state[15]
  • Exercise and feeding stimulate muscle myofibrillar protein synthesis[15]
  • Following resistance training muscle protein synthesis increases 2x - 5x post exercise[15]
  • Increases in protein synthesis occur 1 - 2 hours post-exercise, but in the fed state it can remain increased for 48 - 72 hours[16]
  • An elevated protein breakdown accompanies this increase in protein synthesis post exercise[17]
  • In a fed state, protein synthesis is greater than protein breakdown, resulting in a net gain of protein[17]
  • The accumulated effect of this process over multiple exercise bouts leads to a net gain in protein and therefore muscle growth.[1]

The above-mentioned findings clearly show that adaptations to muscle are dependent on nutrition availability. The protein synthesis and breakdown response post-exercise can be adjusted by altering the availability of certain nutrients. Both, resistance training and amino acid ingestion increases protein synthesis[1][18]. When these two factors are combined it has an even bigger effect.[19] The consumption of protein post-exercise does the following:

  • Promotes protein synthesis[19]
  • Suppresses protein breakdown[19]

With the suppression of protein breakdown post-exercise in the fed state, there is also an increase in insulin levels which further aids this suppression of protein breakdown. It is therefore important to maintain adequate nutrition to maximise the benefits of resistance training.[20]

Satellite Cells[edit | edit source]

Satellite cells are specialised muscle stem cells located in a niche between the basal lamina and the sarcolemma of a muscle fibre. They aid in the growth and repair of all skeletal muscle. These cells are activated by muscle damage and/or sufficient exercise. Once these cells are activated they proliferate differentiate and fuse to an existing myofibre, and in this way forming new contractile proteins and repairing the damage.[1] Resistance training results in an increase in the number of satellite cells within four days of training[21]. With continued resistance training over an extended period of time satellite cell numbers can increase by ~30% and can furthermore remain elevated even if training is stopped.[22]

Another important role of satellite cells is the donation of their nuclei to act as post-mitotic nuclei in the growing muscle fibre.[1]

Adaptations to Endurance Training[edit | edit source]

Endurance training is focused on increasing muscle fatigue resistance for the exercise of a longer duration.[1] Fatigue is defined as: "a loss in the capacity for developing force and/or velocity of a muscle, resulting from muscular activity under load and which is reversible by rest."[23] Performance in endurance activities is dependent on the body's ability to produce sufficient ATP through aerobic respiration. This process requires the neuromuscular, cardiovascular and respiratory systems to interact. The focus will be more on the local adaptations that happen in skeletal muscle for the purpose of this page.

Essentially, endurance training and activity enhances the oxidative capacity and metabolic efficiency of skeletal muscle. The adaptations that it achieves this through are: oxygen utilisation (mitochondrial adaptations), oxygen delivery (angiogenesis) and local substrate availability.[1]

[24]

Mitochondrial Adaptations (Oxygen Utilisation)[edit | edit source]

Mitochondria are the "powerhouse" of the cell. These organelles generate the majority of the cell's supply of ATP through aerobic respiration.[1] Endurance training can:

  • increase the volume and number of mitochondria and the magnitude of these changes is dependent on the frequency and intensity of training[25]
  • increase oxygen utilisation by skeletal muscle[26]

With the increased number and size of mitochondria, the proportion of pyruvate formed during glycolysis passing into the mitochondria for oxidative phosphorylation is increased with less use for the production of lactate and its by-products. As a result the exercise intensity, which can be sustained through relying on aerobic metabolism, is higher.[1]

Angiogenesis (Oxygen Delivery)[edit | edit source]

The network of capillaries adjacent to the muscle fibres is responsible for the diffusive exchange of gasses, substrates and metabolites between the circulation and the working muscle fibres. Endurance training results in:

  • the growth of new capillaries (a process of angiogenesis), with an increase of ~20% being present after 8 weeks of training in both Type I and Type II fibres[27]

Substrate Utilisation[edit | edit source]

During submaximal exercise the main fuel sources are carbohydrates (mainly muscle glycogen) and fats (local and circulating fatty acids).[1] Endurance training leads to a key adaptation in substrate utilisation:

  • for a given level of submaximal exercise the contribution of fatty acid oxidation to the total energy requirement increases with a marked increase in the muscle's ability to utilise intramuscular triglycerides as the primary fuel source.[28]
  • Training results in more glycogen being stored in muscle fibres, in form of granules, this leads to a greater number of intramuscular lipid droplets being in contact with the mitochondria[29]
  • Endurance athletes rely on improved fatty acid oxidation as it conserves muscle glycogen stores (these are more needed during the exercise of high intensity)[1]

Neural Adaptations[edit | edit source]

With endurance training the following adaptations occur in the neural system:

  • Motor unit discharge rate decreases[9]
  • Slower rate of decline in Motor unit conduction velocity during sustained contractions is found after endurance training[30]
  • Decrease in Motor unit recruitment thresholds[1]

Comparison of Neuromuscular Adaptations to Strength and Endurance Training[edit | edit source]

Variable Strength Training Endurance Training
Muscle fibre size increase no change
Number of muscle fibres no change no change
Movement speed increase no change
Strength increase no change
Aerobic capacity no change increase
Anaerobic capacity increase no change
Capillary density no change or decrease increase
Mitochondrial density decrease increase
Type II muscle fibre

subtype conversion

almost all to Type IIa with sprint interval

majority to Type IIa

References[edit | edit source]

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 Pollock R, Harridge S. Neuromuscular Adaptations to Exercise. In Jull GA. Grieve's Modern Musculoskeletal Physiotherapy. Edinburgh: Churchill Livingstone, 2015. p68-77.
  2. Bouchard C, Rankinen T. Individual differences in response to regular physical activity. Med Sci Sports Exerc. 2001; 33: S446-51.
  3. McArdle W, Katch F, Katch V. Exercise Physiology: Energy, Nutrition and Human Performance.8th ed. Philidelphia: Lippincott, Williams & Wilkens; 2014.
  4. Osiris Salazar.Published on Feb 7, 2018 The Energetics of Exercise. Available from https://www.youtube.com/watch?v=q-NWIDlUCuY&t=341s (last accessed 28 March 2019)
  5. Osirus Salazar. Adaptations to Strength Training. Published on 7 February 2018. Available from https://www.youtube.com/watch?v=aM9N_gcoh_Q
  6. Aagaard P, Simonsen E, Andersen J et al. Neural adaptation to resistance training: changes in evoked V-wave and H-reflex responses. J Appl Physiol. 2002;92: 2309-18.
  7. Pucci AR, Griffin L, Cafarelli E. Maximal motor unit firing rates during isometric resistance training in men. Exp Physiol. 2006; 91: 171-8.
  8. Van Cutsem M, Duchateau J, Hainaut K. Changes in single motor unit behaviour contribute to the increase in contraction speed after dynamic training in humans. J Physiol. 1998; 513: 295-305.
  9. 9.0 9.1 Vila-Cha C, Falla D, Farina D. Motor unit behaviour during submaximal contractions following six weeks of either endurance or strength training. J Appl Physiol. 2010; 109: 1455-66.
  10. Hakkinen K, Alen M, Kraemer WJ et al. Neuromuscular adaptations during concurrent strength and endurance training versus strength training. Eur J Appl Physio. 2003;89:42-52.
  11. Sandoo A. Human Physiology video tutorials. The Neural adaptions to resistance training. Published 16 February 2017. Available from: https://www.youtube.com/watch?v=5TAN-o_7Miw( last accessed 16 March 2019
  12. McCall GE, Byrnes WC, Dickinson A et al. Muscle fibre hypertrophy, hyperplasia, and capillary density in college men after resistance training. J Appl Physiol. 2004;81:2004-12.
  13. 13.0 13.1 13.2 13.3 13.4 13.5 Aagaard P, Andersen J, Dyhre-Poulsen P et al. A mechanism for increased contractile strength of the human pennate muscle in response to strength training: changes in muscle architecture. J Physiol. 2001; 534:613-23.
  14. 14.0 14.1 Tumkur Anil Kumar N, Oliver JL, Lloyd RS, Pedley JS, Radnor JM. The influence of growth, maturation and resistance training on muscle-tendon and neuromuscular adaptations: A narrative review. Sports. 2021 May;9(5):59.
  15. 15.0 15.1 15.2 Burd N, West DWD, Staples AW, et al. Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men. PLoS ONE 2010;5:e12033.
  16. Kumar V, Selby A, Rankin D, et al. Age-related differences in the dose-response relationship of muscle protein synthesis to resistance exercise in young and old men. J Physiol. 2009;587:211-217.
  17. 17.0 17.1 Phillips SM, Tipton KD, Aarsland A, et al. Mixed muscle protein synthesis and breakdown after resistance exercise in humans. Am J Physiol. 1997;273:E99-107.
  18. Joanisse S, McKendry J, Lim C, Nunes EA, Stokes T, Mcleod JC, Phillips SM. Understanding the effects of nutrition and post-exercise nutrition on skeletal muscle protein turnover: insights from stable isotope studies. Clinical Nutrition Open Science. 2021 Mar 2.
  19. 19.0 19.1 19.2 Tipton KD, Ferrando AA, Phillips SM, et al. Postexercise net protein synthesis in human muscle from orally administered amino acids. Am J Physiol. 1999;276:E628-34.
  20. Hawley JA, Burke LM, Phillips SM, et al. Nutritional modulation of training-induced skeletal muscle adaptations. J Appl Physiol. 2011;110:834-45.
  21. Crameri RM, Langberg H, Magnusson P, et al. Changes in satellite cells in human skeletal muscle after a single bout of high-intensity exercise. J Physiol. 2004;558:333-40.
  22. Kadi F, Schjerling P, Andersen LL, et al. The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol. 2004;558:1005-12.
  23. NHLBI Workshop Summary. Respiratory muscle fatigue. Report of the respiratory muscle fatigue workshop group. Am Rev Respir Dis. 1990;142:474-80.
  24. Reynolds B. Muscular adaptations to endurance training. Published 9 April 2015. Available from https://www.youtube.com/watch?v=k0nziaiGxSU (last accessed 17 April 2019)
  25. Hickson RC. Skeletal muscle cytochrome c and myoglobin, endurance, and frequency of training. J Appl. Physiol. 1981;51:746-9.
  26. Lin YN, Tseng TT, Knuiman P, Chan WP, Wu SH, Tsai CL, Hsu CY. Protein supplementation increases adaptations to endurance training: A systematic review and meta-analysis. Clinical Nutrition. 2020 Dec 15.
  27. Ingjer F. Effects of endurance training on muscle fibre ATP-ase activity, capillary supply and mitochondrial content in a man. J Physiol. 1979;294:419032.
  28. Martin W. Effect of endurance training on fatty acid metabolism during whole-body exercise. Med Sci Sport Exerc. 1997;29:635-9.
  29. Tarnapolsky MA, Rennie CD, Robertshaw HA, et al. Influence of endurance exercise training and sex on intramyocellular lipid and mitochondrial ultrastructure, substrate use and mitochondrial enzyme activity. Am J Physiol Regul Integr Comp Physiol. 2007;292:R1271-8.
  30. Vila-Cha C, Falla D, Correia MV, et al. Adjustments in motor unit properties during fatiguing contractions after training. Med Sci Sports Exerc. 2012;112:54-63.