Muscle hypertrophy involves an increase in size of skeletal muscle through a growth in size of its component cells. Two factors contribute to hypertrophy: sarcoplasmic hypertrophy, which focuses more on increased muscle glycogen storage; and myofibrillar hypertrophy, which focuses more on increased myofibril size.
- 1 Hypertrophy stimulation
- 2 Factors affecting hypertrophy
- 3 Changes in protein synthesis and muscle cell biology associated with stimuli
- 4 Myofibrillar vs. sarcoplasmic hypertrophy
- 5 In sports
- 6 See also
- 7 References
- 8 Further reading
A range of stimuli can increase the volume of muscle cells. These changes occur as an adaptive response that serves to increase the ability to generate force or resist fatigue in anaerobic conditions.
Strength training typically produces a combination of the two different types of hypertrophy: contraction against 80 to 90% of the one-repetition maximum for 2–6 repetitions (reps) causes myofibrillated hypertrophy to dominate (as in powerlifters, Olympic lifters and strength athletes), whereas several repetitions (generally 8–12 for bodybuilding or 12 or more for muscular endurance) against a submaximal load facilitates mainly sarcoplasmic hypertrophy (professional bodybuilders and endurance athletes).
Progressive overload is considered[by whom?] the most important principle behind hypertrophy, so increasing the weight, repetitions (reps), and sets will all have a positive impact on growth. Some experts create complex plans that manipulate weight, reps, and sets, increasing one while decreasing the others to keep the schedule varied and less repetitive.
The best approach to specifically achieve muscle growth remains controversial (as opposed to focusing on gaining strength, power, or endurance); it was generally considered that consistent anaerobic strength training will produce hypertrophy over the long term, in addition to its effects on muscular strength and endurance. Muscular hypertrophy can be increased through strength training and other short-duration, high-intensity anaerobic exercises. Lower-intensity, longer-duration aerobic exercise generally does not result in very effective tissue hypertrophy; instead, endurance athletes enhance storage of fats and carbohydrates within the muscles, as well as neovascularization.
Factors affecting hypertrophy
Several biological factors such as age and nutrition can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at an increased rate. Natural hypertrophy normally stops at full growth in the late teens. An adequate supply of amino acids is essential to produce muscle hypertrophy. As testosterone is one of the body's major growth hormones, on average, males find hypertrophy much easier to achieve than females. Taking additional testosterone, as in anabolic steroids, will increase results. It is also considered a performance-enhancing drug, the use of which can cause competitors to be suspended or banned from competitions. Testosterone is also a medically regulated substance in most countries, making it illegal to possess without a medical prescription. Anabolic steroid use can cause testicular atrophy, cardiac arrest, and gynecomastia.
Changes in protein synthesis and muscle cell biology associated with stimuli
The message filters down to alter the pattern of gene expression. The additional contractile proteins appear to be incorporated into existing myofibrils (the chains of sarcomeres within a muscle cell). There appears to be some limit to how large a myofibril can become: at some point, they split. These events appear to occur within each muscle fiber. That is, hypertrophy results primarily from the growth of each muscle cell, rather than an increase in the number of cells. Skeletal muscle cells are however unique in the body in that they can contain multiple nuclei, and the number of nuclei can increase.
Cortisol decreases amino acid uptake by muscle tissue, and inhibits protein synthesis. The short-term increase in protein synthesis that occurs subsequent to resistance training returns to normal after approximately 28 hours in adequately fed male youths. Another study determined that muscle protein synthesis was elevated even 72 hours following training.
A small study performed on young and elderly found that ingestion of 340 grams of lean beef (90 g protein) did not increase muscle protein synthesis any more than ingestion of 113 grams of lean beef (30 g protein). In both groups, muscle protein synthesis increased by 50%. The study concluded that more than 30 g protein in a single meal did not further enhance the stimulation of muscle protein synthesis in young and elderly. However, this study didn't check protein synthesis in relation to training; therefore conclusions from this research are controversial.
It is not uncommon for bodybuilders to advise a protein intake as high as 2–4 g per kilogram of bodyweight per day. However, scientific literature has suggested this is higher than necessary, as protein intakes greater than 1.8 g per kilogram of body weight showed to have no greater effect on muscle hypertrophy. A study carried out by American College of Sports Medicine (2002) put the recommended daily protein intake for athletes at 1.2–1.8 g per kilogram of body weight. Conversely, Di Pasquale (2008), citing recent studies, recommends a minimum protein intake of 2.2 g/kg "for anyone involved in competitive or intense recreational sports who wants to maximize lean body mass but does not wish to gain weight. However athletes involved in strength events (..) may need even more to maximize body composition and athletic performance. In those attempting to minimize body fat and thus maximize body composition, for example in sports with weight classes and in bodybuilding, it's possible that protein may well make up over 50% of their daily caloric intake."
Microtrauma, which is tiny damage to the fibers, may play a significant role in muscle growth. When microtrauma occurs (from weight training or other strenuous activities), the body responds by overcompensating, replacing the damaged tissue and adding more, so that the risk of repeat damage is reduced. Damage to these fibers has been theorized as the possible cause for the symptoms of delayed onset muscle soreness (DOMS), and is why progressive overload is essential to continued improvement, as the body adapts and becomes more resistant to stress. However, work examining the time course of changes in muscle protein synthesis and their relationship to hypertrophy showed that damage was unrelated to hypertrophy. In fact, in that study the authors showed that it was not until the damage subsided that protein synthesis was directed to muscle growth.
Myofibrillar vs. sarcoplasmic hypertrophy
In the bodybuilding and fitness community and even in some academic books skeletal muscle hypertrophy is described as being in one of two types: Sarcoplasmic or myofibrillar. According to this hypothesis, during sarcoplasmic hypertrophy, the volume of sarcoplasmic fluid in the muscle cell increases with no accompanying increase in muscular strength, whereas during myofibrillar hypertrophy, actin and myosin contractile proteins increase in number and add to muscular strength as well as a small increase in the size of the muscle. Sarcoplasmic hypertrophy is greater in the muscles of bodybuilders while myofibrillar hypertrophy is more dominant in Olympic weightlifters. These two forms of adaptations rarely occur completely independently of one another; one can experience a large increase in fluid with a slight increase in proteins, a large increase in proteins with a small increase in fluid, or a relatively balanced combination of the two.
|This section does not cite any sources. (November 2011) (Learn how and when to remove this template message)|
Examples of increased muscle hypertrophy are seen in various professional sports, mainly strength related sports such as boxing, olympic weightlifting, mixed martial arts, rugby, professional wrestling and various forms of gymnastics. These athletes train extensively in strength as well as cardiovascular and muscular endurance training.
- Baechle, Thomas R.; Earle, Roger W., eds. (2008). Essentials of strength training and conditioning (3rd ed.). Champaign, IL: Human Kinetics. ISBN 978-0-7360-5803-2.[page needed]
- "Ben Pakulski Mi40X". Archived from the original on 24 March 2016. Retrieved 24 March 2016.
- van Loon LJ, Goodpaster BH (2005). "Increased intramuscular lipid storage in the insulin-resistant and endurance-trained state". Pflügers Archiv - European Journal of Physiology. 451 (5): 606–16. doi:10.1007/s00424-005-1509-0. PMID 16155759.
- Soares JM (1992). "Effects of training on muscle capillary pattern: intermittent vs continuous exercise". The Journal of sports medicine and physical fitness. 32 (2): 123–7. PMID 1279273.
- Prior BM, Yang HT, Terjung RL (2004). "What makes vessels grow with exercise training?". Journal of Applied Physiology. 97 (3): 1119–28. doi:10.1152/japplphysiol.00035.2004. PMID 15333630.
- "Search National Drug Schedule - NAPRA".
- "Controlled Substances Act".
- Fineschi V, Riezzo I, Centini F, Silingardi E, Licata M, Beduschi G, Karch SB (2007). "Sudden cardiac death during anabolic steroid abuse: morphologic and toxicologic findings in two fatal cases of bodybuilders". Int. J. Legal Med. 121 (1): 48–53. doi:10.1007/s00414-005-0055-9. PMID 16292586.
- Basaria S (2010). "Androgen abuse in athletes: detection and consequences". J. Clin. Endocrinol. Metab. 95 (4): 1533–43. doi:10.1210/jc.2009-1579. PMID 20139230.
- Bruusgaard JC, Johansen IB, Egner IM, Rana ZA, Gundersen K (2010). "Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining". Proceedings of the National Academy of Sciences. 107 (34): 15111–6. doi:10.1073/pnas.0913935107. PMID 20713720.
- Manchester KL (1970). "33 – Sites of Hormonal Regulation of Protein Metabolism". Mammalian Protein Metabolism. Academic Press, New York. p. 229. doi:10.1016/B978-0-12-510604-7.50011-6. ISBN 978-0-12-510604-7.
- Tang JE, Perco JG, Moore DR, Wilkinson SB, Phillips SM (2007). "Resistance training alters the response of fed state mixed muscle protein synthesis in young men". AJP: Regulatory, Integrative and Comparative Physiology. 294: R172. doi:10.1152/ajpregu.00636.2007. PMID 18032468.
- Miller BF, Olesen JL, Hansen M, Døssing S, Crameri RM, Welling RJ, Langberg H, Flyvbjerg A, Kjaer M, Babraj JA, Smith K, Rennie MJ (2005). "Coordinated collagen and muscle protein synthesis in human patella tendon and quadriceps muscle after exercise". The Journal of Physiology. 567 (3): 1021–33. doi:10.1113/jphysiol.2005.093690. PMID 16002437.
- Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D (2009). "A Moderate Serving of High-Quality Protein Maximally Stimulates Skeletal Muscle Protein Synthesis in Young and Elderly Subjects". Journal of the American Dietetic Association. 109 (9): 1582–1586. doi:10.1016/j.jada.2009.06.369. PMC . PMID 19699838.
- "Bodybuilders and Protein – Part 2". Leehayward.com. Retrieved 2011-06-19.
- Tarnopolsky MA, Atkinson SA, MacDougall JD, Chesley A, Phillips S, Schwarcz HP (1992). "Evaluation of protein requirements for trained strength athletes". Journal of applied physiology (Bethesda, Md. : 1985). 73 (5): 1986–95. PMID 1474076.
- Rankin JW (2002). "Weight Loss and Gain in Athletes". Current Sports Medicine Reports. 1 (4): 208–13. doi:10.1249/00149619-200208000-00004. PMID 12831697.
- Lemon PW (1991). "Effect of exercise on protein requirements". Journal of Sports Sciences. 9: 53–70. doi:10.1080/02640419108729866. PMID 1895363.
- Di Pasquale, Mauro G. (2008). "Utilization of Proteins in Energy Metabolism". In Ira Wolinsky, Judy A. Driskell. Sports Nutrition: Energy metabolism and exercise. CRC Press. p. 79. ISBN 978-0-8493-7950-5.
- Chargé SB, Rudnicki MA (2004). "Cellular and molecular regulation of muscle regeneration". Physiol. Rev. 84 (1): 209–38. doi:10.1152/physrev.00019.2003. PMID 14715915. Lay summary – Len Kravitz.
- Damas, Felipe; Phillips, Stuart M.; Libardi, Cleiton A.; Vechin, Felipe C.; Lixandrão, Manoel E.; Jannig, Paulo R.; Costa, Luiz A. R.; Bacurau, Aline V.; Snijders, Tim; Parise, Gianni; Tricoli, Valmor; Roschel, Hamilton; Ugrinowitsch, Carlos (2016). "Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage". The Journal of Physiology. 594: 5209–22. doi:10.1113/JP272472. PMC . PMID 27219125.
- Kraemer, William J.; Zatsiorsky, Vladimir M. (2006). Science and practice of strength training. Champaign, IL: Human Kinetics. p. 50. ISBN 0-7360-5628-9.
- Bodine, Sue C.; Stitt, Trevor N.; Gonzalez, Michael; Kline, William O.; Stover, Gretchen L.; Bauerlein, Roy; Zlotchenko, Elizabeth; Scrimgeour, Angus; Lawrence, John C.; Glass, David J.; Yancopoulos, George D. (2001). "Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo". Nature Cell Biology. 3 (11): 1014–9. doi:10.1038/ncb1101-1014. PMID 11715023.
- Frontera, WR; Meredith, CN; O'Reilly, KP; Knuttgen, HG; Evans, WJ (1988). "Strength conditioning in older men: skeletal muscle hypertrophy and improved function". Journal of Applied Physiology. 64 (3): 1038–44. PMID 3366726.
- Glass, David J. (2005). "Skeletal muscle hypertrophy and atrophy signaling pathways". The International Journal of Biochemistry & Cell Biology. 37 (10): 1974–84. doi:10.1016/j.biocel.2005.04.018. PMID 16087388.
- Schuelke, Markus; Wagner, Kathryn R.; Stolz, Leslie E.; Hübner, Christoph; Riebel, Thomas; Kömen, Wolfgang; Braun, Thomas; Tobin, James F.; Lee, Se-Jin (2004). "Myostatin Mutation Associated with Gross Muscle Hypertrophy in a Child". New England Journal of Medicine. 350 (26): 2682–8. doi:10.1056/NEJMoa040933. PMID 15215484.
- Charette, SL; McEvoy, L; Pyka, G; Snow-Harter, C; Guido, D; Wiswell, RA; Marcus, R (1991). "Muscle hypertrophy response to resistance training in older women". Journal of Applied Physiology. 70 (5): 1912–6. PMID 1864770.
- Cureton, Kirk J.; Collins, Mitchell A.; Hill, David W.; McElhannon, Fayette M. (1988). "Muscle hypertrophy in men and women". Medicine and Science in Sports and Exercise. 20 (4): 338–44. doi:10.1249/00005768-198808000-00003. PMID 3173042.
- Glass, David J. (2003). "Signalling pathways that mediate skeletal muscle hypertrophy and atrophy". Nature Cell Biology. 5 (2): 87–90. doi:10.1038/ncb0203-87. PMID 12563267.