6
The Use of Specialized Training Techniques to Maximize Muscle Hypertrophy Brad Schoenfeld, MSc, CSCS Global Fitness Services, Scarsdale, New York SUMMARY A VARIETY OF SPECIALIZED TRAINING TECHNIQUES HAVE BEEN ADVOCATED AS A MEANS TO HEIGHTEN MUSCLE GROWTH. FORCED REPETITIONS/DROP SETS, SUPERSETS, AND HEAVY NEGATIVES, IN PARTICULAR, HAVE BEEN PURPORTED TO ENHANCE THE HYPERTROPHIC RESPONSE TO RESISTANCE EXERCISE. THIS ARTICLE WILL EXPLORE THE POTENTIAL ROLE OF THESE TECHNIQUES IN PROMOTING MUSCLE HYPERTROPHY AND PROVIDE AN INSIGHT INTO POS- SIBLE APPLICATIONS TO RESIS- TANCE TRAINING PROGRAMS. I t is a well-accepted fact that pro- gressive resistance training can promote significant increases in muscle size. Enlargements in muscle cross-sectional area (CSA) of approxi- mately 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 individ- uals attributed to neural and architec- tural 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 espe- cially 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 muscu- larity. 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 appli- cations to resistance training programs. MECHANISMS OF MUSCLE HYPERTROPHY Although the mechanisms of exercise- induced muscle hypertrophy have not been fully elucidated, current theory suggests that it is mediated by mecha- nochemically stimulated intracellular signaling and involves a complex int- eraction 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 syn- thetic rate and/or decreases the rate of proteolysis, leading to a greater accu- mulation of myofibrillar proteins (61). Three basic factors have been impli- cated in promoting exercise-induced muscle hypertrophy: mechanical ten- sion, 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 molec- ular and cellular responses in myofibers and satellite cells (72). With respect KEY WORDS: forced repetitions; drop sets; supersets; paired sets; heavy negatives; muscle hypertrophy; muscle development VOLUME 33 | NUMBER 4 | AUGUST 2011 60

Use of Specialized Training Techniques

Embed Size (px)

DESCRIPTION

Use of Specialized Training Techniques

Citation preview

Page 1: Use of Specialized Training Techniques

The Use of SpecializedTraining Techniques toMaximize MuscleHypertrophyBrad Schoenfeld, MSc, CSCSGlobal Fitness Services, Scarsdale, New York

S U M M A R Y

A VARIETY OF SPECIALIZED

TRAINING TECHNIQUES HAVE

BEEN ADVOCATED AS A MEANS

TO HEIGHTEN MUSCLE GROWTH.

FORCED REPETITIONS/DROP

SETS, SUPERSETS, AND HEAVY

NEGATIVES, IN PARTICULAR, HAVE

BEEN PURPORTED TO ENHANCE

THE HYPERTROPHIC RESPONSE

TO RESISTANCE EXERCISE. THIS

ARTICLE WILL EXPLORE THE

POTENTIAL ROLE OF THESE

TECHNIQUES IN PROMOTING

MUSCLE HYPERTROPHY AND

PROVIDE AN INSIGHT INTO POS-

SIBLE APPLICATIONS TO RESIS-

TANCE TRAINING PROGRAMS.

It is a well-accepted fact that pro-gressive resistance training canpromote significant increases in

muscle size. Enlargements in musclecross-sectional area (CSA) of approxi-mately 10–15% have been reported afterjust 10–14 weeks of dynamic heavy-resistance training (48,58,32). Musclehypertrophy is limited during the initialweeks of training, with the majority ofstrength increases in untrained individ-uals attributed to neural and architec-tural adaptations (63). Thereafter,hypertrophy becomes increasinglyevident, with the upper extremitiestending to display growth before thelower extremities (52,70). Although

muscle hypertrophy is apparent in bothtype I and type II fibers, significantlygreater gains are seen in type II fibers(42,70). Factors that mitigate the rateand absolute limits of muscular gainsinclude genetics, age, and gender (43).

A significant number of those who liftweights do so to maximize musculardevelopment. Hypertrophy is espe-cially important to strength athletes(e.g., football linemen, shot putters, etc)given that a direct correlation existsbetween strength and muscle CSA(29,37,46) and bodybuilders, who arejudged on the extent of their muscu-larity. A variety of specialized trainingtechniques have been advocated asa means to heighten muscle growth.Forced repetitions (reps), drop sets,supersets, and heavy negatives, inparticular, have been purported toenhance the hypertrophic response toresistance exercise. Thus, the purposeof this article will be to explore thepotential role of these techniques inpromoting muscle hypertrophy and toprovide an insight into possible appli-cations to resistance training programs.

MECHANISMS OF MUSCLEHYPERTROPHY

Although the mechanisms of exercise-induced muscle hypertrophy have notbeen fully elucidated, current theorysuggests that it is mediated by mecha-nochemically stimulated intracellularsignaling and involves a complex int-eraction of hormones, growth factors,

myokines, and other signaling agents.These upstream regulators act onvarious myogenic pathways, such asPI3K/Akt/mTOR (6,39,71), MAPK(44,60), and calcium signaling pathways(11,12). Initiation of 1 or more of thesepathways sets off an enzymatic cascadethat ultimately increases protein syn-thetic rate and/or decreases the rate ofproteolysis, leading to a greater accu-mulation of myofibrillar proteins (61).

Three basic factors have been impli-cated in promoting exercise-inducedmuscle hypertrophy: mechanical ten-sion, muscle damage, and metabolicstress. Depending on the stimulus,these factors may work in tandem toproduce a synergistic effect on muscledevelopment (61). The following isa brief overview of these factors. Foran in depth exploration of the topic,refer to the review article bySchoenfeld (61).

Mechanical tension is perhaps themost dominant mediator of musclehypertrophy (18,33,34,73). It is believedthat mechanical tension disturbs theintegrity of skeletal muscle, causingmechanochemically transduced molec-ular and cellular responses in myofibersand satellite cells (72). With respect

KEY WORDS :

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

VOLUME 33 | NUMBER 4 | AUGUST 201160

Page 2: Use of Specialized Training Techniques

to resistance training, the degree ofmechanical tension is primarily a func-tion of intensity (amount of load) andtime under tension (duration of appliedload). An optimal combination of thesevariables will maximize the motor unit(MU) recruitment and rate coding,thereby bringing about the fatigue ofa wide spectrum of MUs and thusa greater hypertrophic response (59).

Localized muscle damage caused byresistance training has also been impli-cated in mediating muscle growth(14,31). The onset of myodamageinitiates an inflammatory response in-volving neutrophils, macrophages, andlymphocytes. This leads to the pro-duction of myokines, which are believedto potentiate the release of variousgrowth factors that regulate satellite cellproliferation and differentiation (72,74).Mechano growth factor (MGF), a splicevariant of insulin-like growth factor(IGF-1) that is locally expressed inmuscle fibers, appears to be particularlysensitive to muscle damage (5,18) andthus may be directly responsible for theincreased satellite cell activity seen withmyotrauma.

Finally, an emerging body of researchindicates that exercise-induced meta-bolic stress can act as a potenthypertrophic stimulus (59,62,65,66).Metabolic stress arises from the perfor-mance of resistance exercise that reliespredominantly on anaerobic glycolysisfor the production of adenosine tri-phosphate, which in turn results in theintramuscular accumulation of metabo-lites, such as lactate, hydrogen ion, andinorganic phosphate (67,70). Metabolicbuildup is believed to promote positivealterations in an anabolic milieu, con-ceivably modulated by a combination ofhormonal factors (including IGF-1,testosterone, and growth hormone[GH]), cellular hydration, free radicalproduction, and/or activity of growth-oriented transcription factors (19,20,68). Some researchers have speculatedthat the lower pH associated with fastglycolysis may further augment hyper-trophic adaptation by stimulating sym-pathetic nerve activity and increasingfiber degradation (8).

SPECIALIZED TRAININGTECHNIQUES FOR MUSCLEHYPERTROPHY

Forced reps, drop sets, supersets, andheavy negatives are popular trainingtechniques for increasing muscle de-velopment. Although research is lack-ing as to their direct impact on musclehypertrophy, a large body of implieddata provide a sound theoretical ratio-nale for beneficial effect. The followingsections explore the applicability ofthese techniques with respect to ahypertrophy-oriented routine.

FORCED REPETITIONS

Forced reps (i.e., assisted reps) involvethe use of a spotter who assists the lifterin the performance of additional repsafter the concentric failure is reached,often to help move the weight pasta ‘‘sticking point.’’ It is theorized thatforced reps may enhance the hyper-trophic stimulus by augmenting MUfatigue and/or metabolic stress.

Ahtiainen et al. (1) investigated theeffects of forced reps on acute GHsecretion after a performance of 4 setsof 12 reps of the leg press and 2 sets of12 reps for the squat and leg extension.The maximum rep (MR) group per-formed all sets at their 12 repetitionmaximum (RM), whereas the forcedrepetition (FR) group used a loadhigher than MR so that the subjectsrequired assistance to complete 12reps. Thirty minutes after workout,GH levels were significantly greater inthe FR group compared with thosewho did not perform forced reps.Volume (as measured by total repsperformed) was equated betweengroups, implying that elevated hor-monal concentrations were attribut-able to the use of forced reps.

There is some disagreement amongresearchers as to whether GH actuallyis involved in the anabolic response toexercise. However, studies indicatethat an exercise-induced increase inGH is in fact highly correlated with themagnitude of both type I and type IImuscle fiber hypertrophies andstrength-related muscular adaptations(26,49). Evidence suggests that this

may be related to GH’s ability topotentiate the upregulation of theIGF-1 gene in muscle so that moreIGF-1Ea is spliced toward the MGFisoform (27,36). Additional research isneeded to elucidate what, if any, roledoes exercise-induced elevations inGH play in the hypertrophic processand, if so, whether this is a benefit toemploying forced reps in a musclebuilding program.

DROP SETS

Similar to forced reps, drop sets (alsoknown as descending sets) involveperforming a set to muscular failurewith a given load and then immedi-ately reducing the load and continuingto train until subsequent failure. It isbelieved that this technique can stim-ulate greater muscular growth by in-ducing greater MU fatigue (75). Theincreased time under tension associ-ated with drop sets would likely alsoheighten metabolic stress and ische-mia, enhancing anabolic milieu. Multi-ple drops can be performed in the sameset to elicit even greater levels of fatigueand metabolic stress.

There is some evidence that drop setscan indeed enhance the body’s ana-bolic environment after resistance ex-ercise. Goto et al. (22) assessed theinclusion of a low-intensity set (50% of1RM) immediately after the perfor-mance of a high-intensity set. Resultsshowed a significant spike in GH levelsassociated with the additional low-intensity drop set. Follow-up work byGoto et al. (21) showed that theaddition of a drop set to a standardstrength training protocol resulted ina significant increase in the muscleCSA as opposed to the strengthtraining protocol alone. Neither ofthese studies controlled for total train-ing volume, leaving open the possibilitythat the elevated hormonal responseand associated muscle protein accre-tion were caused by an increasedvolume.

As opposed to forced reps, drop setsdo not necessarily require the presenceof a spotter. This allows for greaterindependence when training and

Strength and Conditioning Journal | www.nsca-lift.org 61

Page 3: Use of Specialized Training Techniques

affording lifters with a greater controlover the intensities used.

Given that both forced reps and dropsets involve training to muscular fail-ure, caution must be used whenintegrating these techniques into a hy-pertrophy-oriented program. Repeat-edly training to muscle failure overtime has been shown to increase thepotential for overtraining and psycho-logical burnout (17) and may lead toreductions in resting IGF-1 concen-trations and a blunting of restingtestosterone levels (38). Hence, a gen-eral recommendation is to use forcedreps and drop sets sparingly in thecontext of a periodized routine. It isusually prudent to limit their use toa select few sets in a given microcycle,making sure to intersperse periods ofunloading to allow for necessary re-cuperation. That said, recuperativeabilities are highly dependent on theindividual and are impacted by nutri-tional supplementation, the use ofanabolic steroids, and other factorsthat may allow for more frequent useof these techniques.

SUPERSETS

Supersets (also known as paired sets)can be defined as 2 exercises performedin succession without rest (56).Although supersets have long beenused in bodybuilding routines, a searchof the literature failed to reveal anystudies directly investigating whethertheir use facilitates increases in musculargrowth. However, it is conceivable thatthe reduced rest between sets increasesmuscular fatigue and metabolic stress(41), which may enhance hypertrophy.

Hypothetically, any 2 exercises can becombined to form a superset. Perhaps,the most common superset techniqueinvolves the performance of exercisesthat share an agonist/antagonist re-lationship, which is sometimes calledagonist-antagonist paired set (APS)training. Multiple studies have shownthat contracting an antagonist muscleincreases force output during subse-quent contractions of the agonist(9,23,24,40). This has been attributedto reduced antagonist inhibition

and/or an increase in stored elasticenergy in the muscle-tendon complex(4,40). The greater mechanical tensiongenerated by the agonist could poten-tially lead to increases in musculargrowth. There is some evidencethat the benefits associated with pre-contractions may be limited to fastermovements (47), suggesting that hy-pertrophy would be optimizedby performing concentric reps explo-sively during the second exercise ina superset.

Robbins et al. (57) demonstrated thatAPS training allows for a greaternumber of reps to be performed pergiven unit of time without significantlyreducing the intensity or total trainingvolume. This increased ‘‘training den-sity’’ is achieved through acute im-provements in training efficiency,which necessarily heightens the extentof fatigue. The elevated levels offatigue, in turn, may contribute to thehypertrophic stimulus (59). Althoughmarkers of metabolic stress were notstudied, an increased training densitywould conceivably require a greaterreliance on anaerobic glycolysis, en-hancing anabolic milieu.

HEAVY NEGATIVES

Heavy negatives (supramaximal loadedeccentric actions) involve the perfor-mance of eccentric contractions ata weight greater than concentric1RM. This usually requires a spotterto help raise the weight concentricallyafter the lifter performs the eccentricrep. The lifter may perform multiplereps depending on training intensity.Given that a muscle is not fully fatiguedduring concentric training (75), the useof heavy negatives may elicit greaterMU fatigue and thus provide anadditional hypertrophic stimulus.

A significant body of research showsthat eccentric exercise elicits greatergains in lean muscle compared withconcentric and isometric contractions(15,16,30,54). Hather et al. (28) foundthat maximal muscle hypertrophy inresponse to resistance exercise is notattained unless eccentric muscle ac-tions are performed. To this end,

eccentric actions are associated witha more rapid rise in protein synthesis(51), greater increases in IGF-1 mes-senger RNA (mRNA) expression (64),and more pronounced elevations inp70S6k (13), when compared with othertypes of contractions.

Several explanations have been pro-posed to account for the hypertrophicsuperiority of eccentric exercise. Forone, it is associated with greater muscledamage, which has been shown tomediate a hypertrophic response, aspreviously noted (14,31). Damage tomuscle manifests as Z-line streaming,which the current research suggests isan indicative of myofibrillar remodel-ing (10,76). Z-bands are critical sites formechanotransduction, and localizedtrauma is believed to facilitate hyper-trophic signaling (34). c-Jun NH2–terminal kinase (JNK), a signalingmodule of MAPK, appears to beparticularly sensitive to eccentricallyinduced muscle damage (7). The acti-vation of JNK by eccentric contractionsis coupled with significant elevations inmRNA of transcription factors involvedin cell proliferation and DNA-mediatedtissue repair (2,3,7).

Eccentric exercise has also been shownto provoke a preferential recruitment offast twitch muscle fibers (53,64,69) andpossibly elicit recruitment of previouslyinactive MUs (50,53). Increased high-threshold MU recruitment occurs inconjunction with a reduced activationof slow twitch fibers, resulting ina greater amount of stress per MU(25,45). The net result is an increasedmechanical tension in type II fibers,which have the greatest potential formuscle growth because of their anaer-obic phenotype (42,70). This wasdemonstrated by Hortobagyi et al.(35), who investigated the effects ofeccentric contractions versus concen-tric contractions on muscle CSA in thequadriceps. After 12 weeks, type 1 fiberdiameter was not significantly differentbetween the groups, but eccentricexercise resulted in a 10-fold increasein the diameter compared with con-centric exercise.

62

Specialized Hypertrophy Techniques

VOLUME 33 | NUMBER 4 | AUGUST 2011 Copyright � National Strength and Conditioning Association

Page 4: Use of Specialized Training Techniques

Finally, eccentric training is associatedwith an increased metabolic stress.Ojasto and Hakkinen (55) reportedan elevated lactate buildup and a cor-responding spike in anabolic hormonallevels after accentuated eccentric train-ing, with the greatest increases notedwhen training at higher eccentricintensities.

Given that the eccentric strength isapproximately 20–50% greater thanthe concentric strength (5), a generalrecommendation is to perform heavynegatives with a load between 105 and125% of concentric 1RM. This willallow the lifter to complete multiplereps at a supramaximal intensity. A2- to 3-second eccentric tempo ishypothesized to be ideal for maximizinga hypertrophic response (61).

As with forced reps, a downside ofheavy negatives is that a spotter isrequired for performance, and in in-stances where free weights are used,2 spotters may be required if theloads are sufficiently heavy. Moreover,forced reps also overtax the neuromus-cular system and therefore can hastenthe onset of overtraining. Moderationis therefore required when integratingthis technique into hypertrophy-oriented programs.

CONCLUSION

Evidence suggests a beneficial effect forselectively including forced reps, dropsets, supersets, and heavy negatives ina hypertrophy-oriented resistancetraining routine. The lack of directresearch examining the hypertrophiceffect of these techniques makes itdifficult to provide specific guidelinesfor volume and frequency. However,their fatiguing nature increases the riskfor overreaching and overtraining, andit is generally prudent to limit their useto no more than a few microcyclesover the course of a periodized pro-gram. That said, people have differingrecuperative abilities, and experimen-tation is therefore necessary to de-termine an appropriate volume andfrequency for the individual. Potentialsigns of overtraining should be contin-ually monitored to optimize results.

Moreover, these techniques should beconsidered advanced training strate-gies. Their use has a taxing effect on theneuromuscular system that is likely toexceed a beginner’s capacity for adap-tation. Based on the author’s experi-ence, a minimum of several months ofregimented training is warranted be-fore integrating the techniques intoa routine.

Brad

Schoenfeld isthe owner/directorof Global FitnessServices.

REFERENCES1. Ahtiainen JP, Pakarinen A, Kraemer WJ,

and Hakkinen 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,

Muller, H, Kucera K, Borisch S, Richter G,

Bartsch 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.

Strength and Conditioning Journal | www.nsca-lift.org 63

Page 5: Use of Specialized Training Techniques

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. Hakkinen 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. Hortobagyi, 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. HumMov 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, Hakkinen, 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, Romano, 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.

VOLUME 33 | NUMBER 4 | AUGUST 201164

Specialized Hypertrophy Techniques

Page 6: Use of Specialized Training Techniques

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 Hakkinen 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 StrengthCondAssoc 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.

Strength and Conditioning Journal | www.nsca-lift.org 65