The Use of Specialized Training Techniques to Maximize Muscle Hypertrophy : Strength & Conditioning Journal

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The Use of Specialized Training Techniques to Maximize Muscle Hypertrophy

Schoenfeld, Brad MSc, CSCS

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Strength and Conditioning Journal 33(4):p 60-65, August 2011. | DOI: 10.1519/SSC.0b013e3182221ec2
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It is a well-accepted fact that progressive resistance training can promote significant increases in muscle size. Enlargements in muscle cross-sectional area (CSA) of approximately 10-15% have been reported after just 10-14 weeks of dynamic heavy-resistance training (48,58,32). Muscle hypertrophy is limited during the initial weeks of training, with the majority of strength increases in untrained individuals attributed to neural and architectural adaptations (63). Thereafter, hypertrophy becomes increasingly evident, with the upper extremities tending to display growth before the lower extremities (52,70). Although muscle hypertrophy is apparent in both type I and type II fibers, significantly greater gains are seen in type II fibers (42,70). Factors that mitigate the rate and absolute limits of muscular gains include genetics, age, and gender (43).

A significant number of those who lift weights do so to maximize muscular development. Hypertrophy is especially important to strength athletes (e.g., football linemen, shot putters, etc) given that a direct correlation exists between strength and muscle CSA (29,37,46) and bodybuilders, who are judged on the extent of their muscularity. A variety of specialized training techniques have been advocated as a means to heighten muscle growth. Forced repetitions (reps), drop sets, supersets, and heavy negatives, in particular, have been purported to enhance the hypertrophic response to resistance exercise. Thus, the purpose of this article will be to explore the potential role of these techniques in promoting muscle hypertrophy and to provide an insight into possible applications to resistance training programs.


Although the mechanisms of exercise-induced muscle hypertrophy have not been fully elucidated, current theory suggests that it is mediated by mechanochemically stimulated intracellular signaling and involves a complex interaction of hormones, growth factors, myokines, and other signaling agents. These upstream regulators act on various myogenic pathways, such as PI3K/Akt/mTOR (6,39,71), MAPK (44,60), and calcium signaling pathways (11,12). Initiation of 1 or more of these pathways sets off an enzymatic cascade that ultimately increases protein synthetic rate and/or decreases the rate of proteolysis, leading to a greater accumulation of myofibrillar proteins (61).

Three basic factors have been implicated in promoting exercise-induced muscle hypertrophy: mechanical tension, muscle damage, and metabolic stress. Depending on the stimulus, these factors may work in tandem to produce a synergistic effect on muscle development (61). The following is a brief overview of these factors. For an in depth exploration of the topic, refer to the review article by Schoenfeld (61).

Mechanical tension is perhaps the most dominant mediator of muscle hypertrophy (18,33,34,73). It is believed that mechanical tension disturbs the integrity of skeletal muscle, causing mechanochemically transduced molecular and cellular responses in myofibers and satellite cells (72). With respect to resistance training, the degree of mechanical tension is primarily a function of intensity (amount of load) and time under tension (duration of applied load). An optimal combination of these variables will maximize the motor unit (MU) recruitment and rate coding, thereby bringing about the fatigue of a wide spectrum of MUs and thus a greater hypertrophic response (59).

Localized muscle damage caused by resistance training has also been implicated in mediating muscle growth (14,31). The onset of myodamage initiates an inflammatory response involving neutrophils, macrophages, and lymphocytes. This leads to the production of myokines, which are believed to potentiate the release of various growth factors that regulate satellite cell proliferation and differentiation (72,74). Mechano growth factor (MGF), a splice variant of insulin-like growth factor (IGF-1) that is locally expressed in muscle fibers, appears to be particularly sensitive to muscle damage (5,18) and thus may be directly responsible for the increased satellite cell activity seen with myotrauma.

Finally, an emerging body of research indicates that exercise-induced metabolic stress can act as a potent hypertrophic stimulus (59,62,65,66). Metabolic stress arises from the performance of resistance exercise that relies predominantly on anaerobic glycolysis for the production of adenosine triphosphate, which in turn results in the intramuscular accumulation of metabolites, such as lactate, hydrogen ion, and inorganic phosphate (67,70). Metabolic buildup is believed to promote positive alterations in an anabolic milieu, conceivably modulated by a combination of hormonal factors (including IGF-1, testosterone, and growth hormone [GH]), cellular hydration, free radical production, and/or activity of growth-oriented transcription factors (19,20,68). Some researchers have speculated that the lower pH associated with fast glycolysis may further augment hypertrophic adaptation by stimulating sympathetic nerve activity and increasing fiber degradation (8).


Forced reps, drop sets, supersets, and heavy negatives are popular training techniques for increasing muscle development. Although research is lacking as to their direct impact on muscle hypertrophy, a large body of implied data provide a sound theoretical rationale for beneficial effect. The following sections explore the applicability of these techniques with respect to a hypertrophy-oriented routine.


Forced reps (i.e., assisted reps) involve the use of a spotter who assists the lifter in the performance of additional reps after the concentric failure is reached, often to help move the weight past a “sticking point.” It is theorized that forced reps may enhance the hypertrophic stimulus by augmenting MU fatigue and/or metabolic stress.

Ahtiainen et al. (1) investigated the effects of forced reps on acute GH secretion after a performance of 4 sets of 12 reps of the leg press and 2 sets of 12 reps for the squat and leg extension. The maximum rep (MR) group performed all sets at their 12 repetition maximum (RM), whereas the forced repetition (FR) group used a load higher than MR so that the subjects required assistance to complete 12 reps. Thirty minutes after workout, GH levels were significantly greater in the FR group compared with those who did not perform forced reps. Volume (as measured by total reps performed) was equated between groups, implying that elevated hormonal concentrations were attributable to the use of forced reps.

There is some disagreement among researchers as to whether GH actually is involved in the anabolic response to exercise. However, studies indicate that an exercise-induced increase in GH is in fact highly correlated with the magnitude of both type I and type II muscle fiber hypertrophies and strength-related muscular adaptations (26,49). Evidence suggests that this may be related to GH's ability to potentiate the upregulation of the IGF-1 gene in muscle so that more IGF-1Ea is spliced toward the MGF isoform (27,36). Additional research is needed to elucidate what, if any, role does exercise-induced elevations in GH play in the hypertrophic process and, if so, whether this is a benefit to employing forced reps in a muscle building program.


Similar to forced reps, drop sets (also known as descending sets) involve performing a set to muscular failure with a given load and then immediately reducing the load and continuing to train until subsequent failure. It is believed that this technique can stimulate greater muscular growth by inducing greater MU fatigue (75). The increased time under tension associated with drop sets would likely also heighten metabolic stress and ischemia, enhancing anabolic milieu. Multiple drops can be performed in the same set to elicit even greater levels of fatigue and metabolic stress.

There is some evidence that drop sets can indeed enhance the body's anabolic environment after resistance exercise. Goto et al. (22) assessed the inclusion of a low-intensity set (50% of 1RM) immediately after the performance of a high-intensity set. Results showed a significant spike in GH levels associated with the additional low-intensity drop set. Follow-up work by Goto et al. (21) showed that the addition of a drop set to a standard strength training protocol resulted in a significant increase in the muscle CSA as opposed to the strength training protocol alone. Neither of these studies controlled for total training volume, leaving open the possibility that the elevated hormonal response and associated muscle protein accretion were caused by an increased volume.

As opposed to forced reps, drop sets do not necessarily require the presence of a spotter. This allows for greater independence when training and affording lifters with a greater control over the intensities used.

Given that both forced reps and drop sets involve training to muscular failure, caution must be used when integrating these techniques into a hypertrophy-oriented program. Repeatedly training to muscle failure over time has been shown to increase the potential for overtraining and psychological burnout (17) and may lead to reductions in resting IGF-1 concentrations and a blunting of resting testosterone levels (38). Hence, a general recommendation is to use forced reps and drop sets sparingly in the context of a periodized routine. It is usually prudent to limit their use to a select few sets in a given microcycle, making sure to intersperse periods of unloading to allow for necessary recuperation. That said, recuperative abilities are highly dependent on the individual and are impacted by nutritional supplementation, the use of anabolic steroids, and other factors that may allow for more frequent use of these techniques.


Supersets (also known as paired sets) can be defined as 2 exercises performed in succession without rest (56). Although supersets have long been used in bodybuilding routines, a search of the literature failed to reveal any studies directly investigating whether their use facilitates increases in muscular growth. However, it is conceivable that the reduced rest between sets increases muscular fatigue and metabolic stress (41), which may enhance hypertrophy.

Hypothetically, any 2 exercises can be combined to form a superset. Perhaps, the most common superset technique involves the performance of exercises that share an agonist/antagonist relationship, which is sometimes called agonist-antagonist paired set (APS) training. Multiple studies have shown that contracting an antagonist muscle increases force output during subsequent contractions of the agonist (9,23,24,40). This has been attributed to reduced antagonist inhibition and/or an increase in stored elastic energy in the muscle-tendon complex (4,40). The greater mechanical tension generated by the agonist could potentially lead to increases in muscular growth. There is some evidence that the benefits associated with precontractions may be limited to faster movements (47), suggesting that hypertrophy would be optimized by performing concentric reps explosively during the second exercise in a superset.

Robbins et al. (57) demonstrated that APS training allows for a greater number of reps to be performed per given unit of time without significantly reducing the intensity or total training volume. This increased “training density” is achieved through acute improvements in training efficiency, which necessarily heightens the extent of fatigue. The elevated levels of fatigue, in turn, may contribute to the hypertrophic stimulus (59). Although markers of metabolic stress were not studied, an increased training density would conceivably require a greater reliance on anaerobic glycolysis, enhancing anabolic milieu.


Heavy negatives (supramaximal loaded eccentric actions) involve the performance of eccentric contractions at a weight greater than concentric 1RM. This usually requires a spotter to help raise the weight concentrically after the lifter performs the eccentric rep. The lifter may perform multiple reps depending on training intensity. Given that a muscle is not fully fatigued during concentric training (75), the use of heavy negatives may elicit greater MU fatigue and thus provide an additional hypertrophic stimulus.

A significant body of research shows that eccentric exercise elicits greater gains in lean muscle compared with concentric and isometric contractions (15,16,30,54). Hather et al. (28) found that maximal muscle hypertrophy in response to resistance exercise is not attained unless eccentric muscle actions are performed. To this end, eccentric actions are associated with a more rapid rise in protein synthesis (51), greater increases in IGF-1 messenger RNA (mRNA) expression (64), and more pronounced elevations in p70S6k (13), when compared with other types of contractions.

Several explanations have been proposed to account for the hypertrophic superiority of eccentric exercise. For one, it is associated with greater muscle damage, which has been shown to mediate a hypertrophic response, as previously noted (14,31). Damage to muscle manifests as Z-line streaming, which the current research suggests is an indicative of myofibrillar remodeling (10,76). Z-bands are critical sites for mechanotransduction, and localized trauma is believed to facilitate hypertrophic signaling (34). c-Jun NH2-terminal kinase (JNK), a signaling module of MAPK, appears to be particularly sensitive to eccentrically induced muscle damage (7). The activation of JNK by eccentric contractions is coupled with significant elevations in mRNA of transcription factors involved in cell proliferation and DNA-mediated tissue repair (2,3,7).

Eccentric exercise has also been shown to provoke a preferential recruitment of fast twitch muscle fibers (53,64,69) and possibly elicit recruitment of previously inactive MUs (50,53). Increased high-threshold MU recruitment occurs in conjunction with a reduced activation of slow twitch fibers, resulting in a greater amount of stress per MU (25,45). The net result is an increased mechanical tension in type II fibers, which have the greatest potential for muscle growth because of their anaerobic phenotype (42,70). This was demonstrated by Hortobagyi et al. (35), who investigated the effects of eccentric contractions versus concentric contractions on muscle CSA in the quadriceps. After 12 weeks, type 1 fiber diameter was not significantly different between the groups, but eccentric exercise resulted in a 10-fold increase in the diameter compared with concentric exercise.

Finally, eccentric training is associated with an increased metabolic stress. Ojasto and Häkkinen (55) reported an elevated lactate buildup and a corresponding spike in anabolic hormonal levels after accentuated eccentric training, with the greatest increases noted when training at higher eccentric intensities.

Given that the eccentric strength is approximately 20-50% greater than the concentric strength (5), a general recommendation is to perform heavy negatives with a load between 105 and 125% of concentric 1RM. This will allow the lifter to complete multiple reps at a supramaximal intensity. A 2- to 3-second eccentric tempo is hypothesized to be ideal for maximizing a hypertrophic response (61).

As with forced reps, a downside of heavy negatives is that a spotter is required for performance, and in instances where free weights are used, 2 spotters may be required if the loads are sufficiently heavy. Moreover, forced reps also overtax the neuromuscular system and therefore can hasten the onset of overtraining. Moderation is therefore required when integrating this technique into hypertrophy-oriented programs.


Evidence suggests a beneficial effect for selectively including forced reps, drop sets, supersets, and heavy negatives in a hypertrophy-oriented resistance training routine. The lack of direct research examining the hypertrophic effect of these techniques makes it difficult to provide specific guidelines for volume and frequency. However, their fatiguing nature increases the risk for overreaching and overtraining, and it is generally prudent to limit their use to no more than a few microcycles over the course of a periodized program. That said, people have differing recuperative abilities, and experimentation is therefore necessary to determine an appropriate volume and frequency for the individual. Potential signs of overtraining should be continually monitored to optimize results.

Moreover, these techniques should be considered advanced training strategies. Their use has a taxing effect on the neuromuscular system that is likely to exceed a beginner's capacity for adaptation. Based on the author's experience, a minimum of several months of regimented training is warranted before integrating the techniques into a routine.


1. Ahtiainen JP, Pakarinen A, Kraemer WJ, and Häkkinen K. Acute hormonal and neuromuscular responses and recovery to forced vs maximum repetitions multiple resistance exercises. Int J Sports Med 24: 410-418, 2003.
2. Aronson D, Boppart MD, Dufresne SD, Fielding RA, and Goodyear LJ. Exercise stimulates c-Jun NH2 kinase activity and c-Jun transcriptional activity in human skeletal muscle. Biochem Biophys Res Commun 251: 106-110, 1998.
3. Aronson D, Dufresne SD, and Goodyear LJ. Contractile activity stimulates the c-Jun NH2-terminal kinase pathway in rat skeletal muscle. J Biol Chem 272: 25636-25640, 1997.
4. Baker D and Newton RU. Acute effect on power output of alternating an agonist and antagonist muscle exercise during complex training. J Strength Cond Res 19: 202-205, 2005.
5. Bamman MM, Shipp JR, Jiang J, Gower BA, Hunter GR, Goodman A, McLafferty CL, and Urban RJ. Mechanical load increases muscle IGF-1 and androgen receptor mRNA concentrations in humans. Am J Physiol Endocrinol Metab 280: E383-E390, 2001.
6. Bodine SC, Stitt TN, Gonzalez M, Kline WO, Stover GL, Bauerlein R, Zlotchenko E, Scrimgeour A, Lawrence JC, Glass DJ, and Yancopoulos GD. Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nat Cell Biol 3: 1014-1019, 2001.
7. Boppart MD, Aronson D, Gibson L, Roubenoff R, Abad LW, Bean J, Goodyear LJ, and Fielding RA. Eccentric exercise markedly increases c-Jun NH 2 terminal kinase activity in human skeletal muscle. J Appl Physiol 87: 1668-1673, 1999.
8. Buresh R, Berg K, and French J. The effect of resistive exercise rest interval on hormonal response, strength, and hypertrophy with training. J Strength Cond Res 23: 62-71, 2009.
9. Caiozzo VJ, Laird T, Chow K, Prietto CA, and McMaster WC. The use of precontractions to enhance the in vivo force-velocity relationship. Med Sci Sports Exerc 14: 162, 1982.
10. Crameri RM, Langberg H, Magnusson P, Jensen CH, Schroder HD, Olesen JL, and Kjaer M. Changes in satellite cells in human skeletal muscle after a single bout of high intensity exercise. J Physiol 558: 333-340, 2004.
11. Dunn SE, Burns JL, and Michel RN. Calcineurin is required for skeletal muscle hypertrophy. J Biol Chem 274: 21908-21912, 1999.
12. Dunn SE, Chin ER, and Michel RN. Matching of calcineurin activity to upstream effectors is critical for skeletal muscle fiber growth. J Cell Biol 151: 663-672, 2000.
13. Eliasson J, Elfegoun T, Nilsson J, Kohnke R, Ekblom B, and Blomstrand E. Maximal lengthening contractions increase p70 S6 kinase phosphorylation in human skeletal muscle in the absence of nutritional supply. Am J Physiol Endocrinol Metabol 291: E1197-E1205, 2006.
14. Evans WJ. Effects of exercise on senescent muscle. Clin Orthop Relat Res 403(Suppl): S211-S220, 2002.
15. Farthing JP and Chilibeck PD. The effects of eccentric and concentric training at different velocities on muscle hypertrophy. Eur J Appl Physiol 89: 578-586, 2003.
16. Friedmann B, Kinscherf R, Vorwald S, Müller, H, Kucera K, Borisch S, Richter G, Bärtsch P, and Billeter R. Muscular adaptations to computer-guided strength training with eccentric overload. Acta Physiol Scand 182: 77-88, 2004.
17. Fry AC and Kraemer WJ. Resistance exercise overtraining and overreaching: Neuroendocrine responses. Sports Med 23: 106-129, 1997.
18. Goldspink G. Gene expression in skeletal muscle. Biochem Soc Trans 30: 285-290, 2002.
19. Gordon SE, Kraemer WJ, Vos NH, Lynch JM, and Knuttgen HG. Effect of acid-base balance on the growth hormone response to acute high-intensity cycle exercise. J Appl Physiol 76: 821-829, 1994.
20. Goto K, Ishii N, Kizuka T, and Takamatsu K. The impact of metabolic stress on hormonal responses and muscular adaptations. Med Sci Sports Exerc 37: 955-963, 2005.
21. Goto K, Nagasawa M, Yanagisawa O, Kizuka T, Ishii N, and Takamatsu K. Muscular adaptations to combinations of high- and low-intensity resistance exercises. J Strength Cond Res 18: 730-737, 2004.
22. Goto K, Sato K, and Takamatsu K. A single set of low intensity resistance exercise immediately following high intensity resistance exercise stimulates growth hormone secretion in men. J Sports Med Phys Fitness 43: 243-249, 2003.
23. Grabiner MD. Maximum rate of force development is increased by antagonist conditioning contraction. J Appl Physiol 77: 807-811, 1994.
24. Grabiner MD and Hawthorne DL. Conditions of isokinetic knee flexion that enhance knee extension. Med Sci Sports Exerc 22: 235-240, 1990.
25. Grabiner MD and Owings TM. EMG differences between concentric and eccentric maximum voluntary contractions are evident prior to movement onset. Exp Brain Res 145: 505-511, 2002.
26. Häkkinen K, Pakarinen A, Kraemer WJ, Hakkinen A, Valkeinen H, and Alen M. Selective muscle hypertrophy, changes in EMG and force, and serum hormones during strength training in older women. J Appl Physiol 91: 569-580, 2001.
27. Hameed M, Lange KH, Andersen JL, Schjerling P, Kjaer M, Harridge SD, and Goldspink G. The effect of recombinant human growth hormone and resistance training on IGF-I mRNA expression in the muscles of elderly men. J Physiol 555: 231-240, 2004.
28. Hather BM, Tesch PA, Buchanan P, and Dudley GA. Influence of eccentric actions on skeletal-muscle adaptations to resistance training. Acta Physiol Scand 143: 177-185, 1991.
29. Haxton HA. Absolute muscle force in the ankle flexors of man. J Physiol 103: 267-273, 1944.
30. Higbie EJ, Cureton KJ, Warren GL III, and Prior BM. Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation. J Appl Physiol 81: 2173-2181, 1996.
31. Hill M and Goldspink G. Expression and splicing of the insulin-like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage. J Physiol 549: 409-418, 2003.
32. Holm L, Reitelseder S, Pedersen TG, Doessing S, Petersen SG, Flyvbjerg A, Andersen JL, Aagaard P, and Kjaer M. Changes in muscle size and MHC composition in response to resistance exercise with heavy and light loading intensity. J Appl Physiol 105: 1454-1461, 2008.
33. Hornberger TA and Chien S. Mechanical stimuli and nutrients regulate rapamycin-sensitive signaling through distinct mechanisms in skeletal muscle. J Cell Biochem 97: 1207-1216, 2006.
34. Hornberger TA, Chu WK, Mak YW, Hsiung JW, Huang SA, and Chien S. The role of phospholipase D and phosphatidic acid in the mechanical activation of mTOR signaling in skeletal muscle. Proc Natl Acad Sci U S A 103: 4741-4746, 2006.
35. Hortobágyi, T, Barrier J, Beard D, Braspennincx J, and Koens J. Greater initial adaptations to submaximal muscle lengthening than maximal shortening. J Appl Physiol 81: 1677-1682, 1996.
36. Iida K, Itoh E, Kim DS, del Rincon JP, Coschigano KT, Kopchick JJ, and Thorner MO. Muscle mechano growth factor is preferentially induced by growth hormone in growth hormone-deficient lit/lit mice. J Physiol 560: 341-349, 2004.
37. Ikai M and Fukunaga T. Calculation of muscle strength per unit cross-sectional area of human muscle by means of ultrasonic measurement. Int Z Angew Physiol 26: 26-32, 1968.
38. Izquierdo M, Ibanez J, Gonzalez-Badillo JJ, Hakkinen K, Ratamess NA, Kraemer WJ, French DN, Eslava J, Altadill A, Asianin X, and Gorostiaga EM. Differential effects of strength training leading to failure versus not to failure on hormonal responses, strength and muscle power increases. J Appl Physiol 100, 1647-1656, 2006.
39. Jacinto E and Hall MN. Tor signalling in bugs, brain and brawn. Nat Rev Mol Cell Biol 4: 117-126, 2003.
40. Kamimura T, Yoshioka K, Ito S, and Kusakabe T. Increased rate of force development of elbow flexors by antagonist conditioning contraction. Hum Mov Sci 28: 407-414, 2009.
41. Kelleher AR, Hackney KJ, Fairchild TJ, Keslacy S, and Ploutz-Snyder LL. The metabolic costs of reciprocal supersets vs. traditional resistance exercise in young recreationally active adults. J Strength Cond Res 24: 1043-1051, 2010.
42. Kosek DJ, Kim JS, Petrella JK, Cross JM, and Bamman MM. Efficacy of 3 days/wk resistance training on myofiber hypertrophy and myogenic mechanisms in young vs. older adults. J Appl Physiol 101: 531-544, 2006.
43. Kraemer WJ, Häkkinen, K, Newton RU, Nindl BC, Volek JS, McCormick M, Gotshalk LA, Gordon SE, Fleck SJ, Campbell WW, Putukian M, and Evans WJ. Effects of heavy-resistance training on hormonal response patterns in younger vs. older men. J Appl Physiol 87: 982-992, 1999.
44. Kramer HF and Goodyear LJ. Exercise MAPK, and NF-kappaB signaling in skeletal muscle. J Appl Physiol 103: 388-395, 2007.
45. Linnamo V, Strojnik V, and Komi PV. EMG power spectrum and features of the superimposed M-wave during voluntary eccentric and concentric actions at different activation levels. Eur J Appl Physiol 86:534-540, 2002.
46. Maughan RJ, Watson JS, and Weir J. Strength and cross-sectional area of human skeletal muscle. J Physiol 338: 37-49, 1983.
47. Maynard J and Ebben WP. The effects of antagonist prefatigue on agonist torque and electromyography. J Strength Cond Res 17: 469-474, 2003.
48. McCall GE, Byrnes WC, Dickinson A, Pattany PM, and Fleck SJ. Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training. J Appl Physiol 81: 2004-2012,1996.
49. McCall GE, Byrnes WC, Fleck SJ, Dickinson A, and Kraemer WJ. Acute and chronic hormonal responses to resistance training designed to promote muscle hypertrophy. Can J Appl Physiol 24: 96-107, 1999.
50. McHugh MP, Connolly DA, Eston RG, and Gleim GW. Electromyographic analysis of exercise resulting in symptoms of muscle damage. J Sport Sci 18: 163-172, 2000.
51. Moore DR, Phillips SM, Babraj JA, Smith K, and Rennie MJ. Myofibrillar and collagen protein synthesis in human skeletal muscle in young men after maximal shortening and lengthening contractions. Am J Physiol Endocrinol Metabol 288: E1153-E1159, 2005.
52. Mulligan SE, Fleck SJ, Gordon SE, and Koziris LP. Influence of resistance exercise volume on serum growth hormone and cortisol concentrations in women. J Strength Cond Res 10, 256-262, 1996.
53. Nardone A, Romanò, C, and Schieppati M. Selective recruitment of high-threshold human motor units during voluntary isotonic lengthening of active muscles. J Physiol 409: 451-471, 1989.
54. Norrbrand L, Fluckey JD, Pozzo M, and Tesch PA. Resistance training using eccentric overload induces early adaptations in skeletal muscle size. Eur J Appl Physiol 102: 271-281, 1989.
55. Ojasto T and Häkkinen K. Effects of different accentuated eccentric loads on acute neuromuscular, growth hormone, and blood lactate responses during a hypertrophic protocol. J Strength Cond Res 23: 946-953, 2009.
56. Pauletto B. Choice and order of exercises. Natl Strength Cond Assoc J 8: 71-73, 1986.
57. Robbins DW, Young WB, and Behm DG. The effect of an upper body agonist-antagonist resistance training protocol on volume load and efficiency. J Strength Cond Res 24: 2632-2640, 2010.
58. Ronnestad BR, Egeland W, Kvamme NH, Refsnes PE, Kadi F, and Raastad T. Dissimilar effects of one- and three-set strength training on strength and muscle mass gains in upper and lower body in untrained subjects. J Strength Cond Res 21: 157-163, 2007.
59. Rooney KJ, Herbert RD, and Balnave RJF. Fatigue contributes to the strength training stimulus. Med Sci Sports Exerc 26: 1160-1164, 1994.
60. Roux PP and Blenis J. ERK and p38 MAPK-activated protein kinases: A family of protein kinases with diverse biological functions. Microbiol Mol Biol Rev 68: 320-344, 2004.
61. Schoenfeld BJ. The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res 24: 2857-2875, 2010.
62. Schott J, McCully K, and Rutherford OM. The role of metabolites in strength training. II. Short versus long isometric contractions. Eur J Appl Physiol 71: 337-341, 1995.
63. Seynnes OR, de Boer M, and Narici MV. Early skeletal muscle hypertrophy and architectural changes in response to high-intensity resistance training. J Appl Physiol 102: 368-373, 2007
64. Shepstone TN, Tang JE, Dallaire S, Schuenke MD, Staron RS, and Phillips SM. Short-term high- vs. low-velocity isokinetic lengthening training results in greater hypertrophy of the elbow flexors in young men. J Appl Physiol 98: 1768-1776, 2005.
65. Shinohara M, Kouzaki M, Yoshihisa T, and Fukunaga T. Efficacy of tourniquet ischemia for strength training with low resistance. Eur J Appl Physiol 77: 189-191, 1998.
66. Smith RC and Rutherford OM. The role of metabolites in strength training. I. A comparison of eccentric and concentric contractions. Eur J Appl Physiol Occup Physiol 71: 332-336, 1995.
67. Suga T, Okita K, Morita N, Yokota T, Hirabayashi K, Horiuchi M, Takada S, Takahashi T, Omokawa M, Kinugawa S, and Tsutsui H. Intramuscular metabolism during low-intensity resistance exercise with blood flow restriction. J Appl Physiol 106: 1119-1124, 2009.
68. Takarada Y, Nakamura Y, Aruga S, Onda T, Miyazaki S, and Ishii N. Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion. J Appl Physiol 88: 61-65, 2000.
69. Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, and Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol 88: 2097-2106, 2000.
70. Tesch PA. Skeletal muscle adaptations consequent to long-term heavy resistance exercise. Med Sci Sports Exerc 20(5 Suppl): S132-S134, 1988.
71. Thomas G and Hall MN. TOR signalling and control of cell growth. Curr Opin Cell Biol 9: 782-787, 1997.
72. Toigo M and Boutellier U. New fundamental resistance exercise determinants of molecular and cellular muscle adaptations. Eur J Appl Physiol 97: 643-663, 2006.
73. Vandenburgh HH. Motion into mass: How does tension stimulate muscle growth? Med Sci Sports Exerc 19(5 Suppl): S142-S149, 1987.
74. Vierck J, O'Reilly B, Hossner K, Antonio J, Byrne K, Bucci L, and Dodson M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 24: 263-272, 2000.
75. Willardson JM. The application of training to failure in periodized multiple-set resistance exercise programs. J Strength Cond Res 21: 628-631, 2007.
76. Yu JG and Thornell LE. Desmin and actin alterations in human muscles affected by delayed onset muscle soreness: A high resolution immunocytochemical study. Histochem Cell Biol 118: 171-179, 2002.

forced repetitions; drop sets; supersets; paired sets; heavy negatives; muscle hypertrophy; muscle development

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