A strength training session consists of work and rest periods in its simplest form. To improve strength and power, an understanding of how to maximize the effects of the work and rest periods to produce the desired neuromuscular adaptation associated with various loading schemes is needed. With the advent of linear position transducer and force plate technology, there is an increased awareness of the kinematics and kinetics associated with a single repetition, set, and workout (13).
Improving our mechanical (kinematic and kinetic) understanding of the training stresses that will be imposed on muscle is important as it is thought that strength and power adaptation is mediated by mechanical stimuli and their interaction with other hormonal and metabolic factors. However, our knowledge in this area is in its infancy, the kinematics and kinetics associated with different resistance strength training programs, and associated adaptations will remain a topic of research for many years to come if researchers are genuinely interested in and committed to understanding the adaptational effects of resistance exercise.
Apart from the research that has investigated the effect of rest durations between sets on kinematics and kinetics (15,38,43,44), there has been a lack of research that has investigated how athletes might optimize the rest period to enhance session kinematics and kinetics. That is, there may be activities that can be engaged in during the rest period that may enhance the ensuing set and total workout kinematics and kinetics. The net result could be a session with increased mechanical, hormonal, and metabolic responses and hence the opportunity for improved strength and power adaptation.
This article will explore the concept of engaging in activities in the rest period in terms of increasing hypertrophic adaptation. That is, activities that can be performed during the rest period that promote recovery and/or maximize the mechanical stimuli associated with a training session to maximize the outcomes of training. Specifically, the role of stretching in the recovery period, as a means of increasing hypertrophic adaptation and subsequent strength and power performance, will be described.
Throughout the article, the terms passive and active stretching will be used. Passive stretching implies holding an extended range of motion with little or no neural activation. Active stretching on the other hand can mean (a) the muscle being active while being extended or lengthened (eccentric contraction) or (b) the muscle passively extended to end range of motion and then activated (isometric contraction) or (c) a combination of both.
HYPERTROPHY LOADING PARAMETERS AND REST
Studies have shown that strength gains from resistance training are not only the result of neural adaptation but also because of increases in the cross-sectional area of muscle (10,23,25,54). Researchers and organization's recommendations (5,6,15,34,40,42,52) for increasing muscle hypertrophy include the use of moderate loading (70-85% of 1 repetition maximum [RM]) for 8-12 repetitions per set for 1-3 sets per exercise, for novice and intermediate individuals. Furthermore, slow to moderate repetition velocities are recommended (31), with slow tempos of 1-5 seconds concentric and 1-5 seconds eccentric (29). In terms of time under tension, these slower tempos and contraction velocities result in significantly greater time under tension (29). For experienced athletes, it has been recommended that a loading range of 70-100% of 1RM be used for 1-12 repetitions per set for 3-6 sets per exercise in a periodized manner (31).
With regard to rest period durations, researchers recommended durations of 1-3 minutes depending on athlete training status (42). There is no doubt that longer recoveries allow more complete recovery of the energy and neuromuscular systems; however, short rest periods (1-2 minutes), coupled with moderate- to high-intensity loading and volume, have elicited the greatest acute anabolic hormone and metabolic responses to resistance exercise in comparison with programs using very heavy loads with long rest periods (32,33). Therefore, it is of interest how to magnify the mechanical, hormonal, and/or metabolic responses during the rest period to enhance hypertrophic adaptation. To achieve this, some understanding of the stimuli that determine hypertrophic adaptation is needed.
STIMULI FOR HYPERTROPHY (RADIAL GROWTH)
There is no doubt that there are many interacting factors responsible for hypertrophic adaptation. To ensure that protein synthesis exceeds protein degradation, appropriate loading needs to optimize the muscles mechanical, metabolic, and hormonal responses; signaling pathways; nutrition and recovery (3,7,9,59,60,66). In terms of mechanical loading, Toigo and Boutellier (61) identified the distinct role of active tension in generating muscle hypertrophy, reporting that time under tension is one of the important stimuli in promoting cross-sectional or radial growth of skeletal muscle. They summarized that elongated muscles placed under tension triggered protein synthesis, which is important for muscle growth and is the reverse process to what can be observed during muscle atrophy associated with immobilization (61). It is also widely accepted that the eccentric or lengthening phase in resistance exercise training is an important contributor to muscle growth (16,20,25,28).
It seems that moderate to high forces and time under tension, particularly during lengthening contractions, and subsequent hormonal and metabolic responses are important stimuli for the radial growth of the muscle. Therefore, if hypertrophy is the goal of training, it would seem important to maximize these stimuli during a training session. There is no doubt that this occurs throughout the work periods during a resistance strength training session; however, it may be that what practitioners do during the rest period may provide an additional hypertrophic response, this contention to provide the focus of subsequent discussion.
Topics such as stretch-induced hypertrophy, restricted blood flow, hormonal and metabolic responses, and signalling pathways are briefly discussed. The discussion on these topics is far from definitive statements as there are substantive bodies of research associated with each of the topics listed. The aim of the discussion is to present a rationale why stretching during the rest period may add to the hypertrophic effect and thereafter stimulate dialogue and research among interested practitioners and scientists.
In terms of animal research, there is a body of literature that has documented stretch-induced hypertrophy. Goldspink (18) compared 2 conditions where rat soleus and extensor digitorum longus muscles were immobilized in shortened and lengthened positions and reported that the lengthened muscles increased in size, whereas shortened position muscles atrophied. This suggests that passive stretch at long muscle length stimulates protein synthesis and induces the growth of muscles.
Holly et al. (27) reported increases in length and cross-sectional area of 4 chicken wing muscles stretched to different extents over a 5-week duration. Essentially, length changes were complete after 1 week of stretching; however, increases in cross-sectional area of 73-206% were recorded over the 5-week duration of the study depending on the type of the muscle. The researchers concluded that muscle grew and adapted enzymatically (oxidative enzymes) to stretch, but these responses are dissimilar in twitch and tonic muscles.
Goldspink et al. (19) investigated the effect of passive stretch, electrical stimulation at 10 Hz, and a combination of both stretch and electrical stimulation, on the expression of insulin-like growth factor I (IGF-I) and the rates of protein turnover and growth of the rabbit extensor digitorum longus muscle. It was found that static stretch caused significant adaptive growth and increases in IGF-I either with or without electrical stimulation, whereas continuous electrical stimulation alone failed to induce muscle growth. Yang et al. (67) studying rabbit's lower limb muscles found that 6 days of passive stretch while immobilized in a plaster cast not only induced an increase in expression of IGF-I messenger RNA (mRNA) but also increased the percentage of fibers expressing slow myosin. This change in muscle phenotype was accompanied by a rapid and marked increase in muscle mass, total RNA content, and IGF-I gene expression.
Unlike the previous studies that used chronic stretching protocols, a study by Coutinho et al. (12), which was conducted on eighteen 16-week-old Wistar rats for 3 weeks, found that stretching the immobilized soleus muscles for 40 minutes every 3 days did prevent the muscle shortening and reduced the magnitude of muscle atrophy as compared with a immobilized-only group (22 ± 40 versus 37 ± 31%, respectively). Furthermore, muscles that were submitted to a stretching-only group significantly increased the length (5 ± 2%), serial sarcomere number (4 ± 4%), and fiber area (16 ± 44%) compared with the contralateral muscles. This study showed that although the stretching was passive, hypertrophy still resulted. Tension is also an important regulator of skeletal muscle hypertrophy in vivo because when increased constant tension is applied to embryonic skeletal muscle fibers differentiated in a tissue culture environment, many of the same biochemical processes associated with muscle hypertrophy in vivo are also stimulated in vitro, for example, protein synthesis, total protein, and myosin heavy-chain accumulation (62).
Although much of the research in this area is from immobilization studies, it can be observed that active and passive stretch can induce changes in cross-sectional area of the muscle (14). Naturally, a muscle is stretched under load during strength training, and the slow tempos recommended for hypertrophic adaptation magnify the time under tension or stretch load. During the rest periods, if the muscles are actively or passively stretched, the additional mechanical stimulus may enhance the hypertrophic effect. This contention obviously needs to be researched in a systematic manner, ensuring that the stretching protocol does not significantly influence the ensuing repetition and set kinematics and kinetics.
STRETCHING AND RESTRICTED BLOOD FLOW
It is fairly well accepted that passive and in particular active stretching is likely to disrupt regional blood flow and muscle oxygen consumption, which has been attributed to the local pinching of blood vessels (2,22,48,65). A number of other researchers have noted that the restricted blood flow differs regionally within a muscle, for example, blood flow reduced to a greater extent in the central zones of a muscle (26,30). These regional differences have been attributed to differences in regional tissue pressure, as well as the heterogeneous pattern of muscle fiber direction (architecture), which may induce shear forces and subsequent partial occlusion of blood vessels during stretch and contraction.
In this case, Poole et al. (41) found that not only did stretching reduce blood flow and therefore oxygen delivery and metabolite removal but also it altered red blood cell flow dynamics, which may further impair blood tissue oxygenation. These reductions were attributed to stretching causing (a) passive reductions in vessel diameter by compression and axial stretch and (b) pinching of blood vessels because of the different architectural arrangements between muscle fiber and fascicles.
Given the information on restricted blood flow above, it is likely that the ischemia associated with stretching if used in the rest period, in particular active stretching, would likely contribute to both fatigue and metabolite accumulation. The relative occlusion would reduce the clearance capacity of the circulatory system, resulting in accumulation of lactate, hydrogen ions, sodium ions, and phosphate in the working muscle, which has been implicated as important in the growth hormone (GH) response to exercise (21,63). In this case, Rodney et al. (45) and Schott et al. (53) found that fatigue and metabolite accumulation were important in increasing the strength and accretion of muscle mass. Furthermore, it has been argued that the enhanced hypertrophic response, noted with exercise that uses blood flow restriction, may be attributed to the recruitment of larger type 2 motor units and the resulting mechanical load on these muscle fibers (36). The exact mechanism by which acute changes in high-energy phosphates or other metabolites may trigger hypertrophic signaling is unknown. However, Meyer (36) suggested that there is ample evidence that metabolic sensors such as adenosine monophosphate-dependent protein kinase can play an important role in regulating skeletal muscle growth. For a comprehensive discussion of the effects of restricted blood flow on skeletal muscle, the reader is directed to a recent review by Manini and Clark (35).
STRETCHING AND HORMONE RELEASE
With regard to the restricted blood flow research cited previously, Takarada et al. (57,58) have reported very large acute increases in plasma GH levels, resulting from low-load occlusion training. It is likely that during ischemic conditions, such as stretching during rest periods, metabolites and ions accumulate rather than dissipate, which in turn lead to GH secretion and increased levels of IGF-1. According to Perrone et al. (39), stretch-induced skeletal muscle growth may involve increased autocrine secretion of IGF-1, because IGF-1 is a potent growth factor for skeletal muscle hypertrophy, and stretch elevates IGF-1 mRNA levels in vivo. They believed that extracellular matrix protein type I collagen and stretch stimulate the autocrine secretion of IGF-1 but with different time kinetics. This endogenously produced growth factor may be important for the growth response of skeletal myofibers to both types of external stimuli (39).
STRETCHING AND SIGNALING PATHWAYS
Several factors intrinsic to the muscle are involved in the hypertrophic response of muscle, such as intracellular signaling (transduction of mechanical tension into intracellular signals) (11). Many potential key molecules (e.g., IGF-I, myogenic growth factor, protein kinase B (PKB)/serine/threonine-specific protein kinase (Akt) mammalian target of rapamycin (mTOR) and P70S6K) have been identified as having a role in the hypertrophy associated with skeletal muscle (4,11,37). It is beyond the scope of this article, however, to extensively review the possible mechanisms by which tension is transduced into intracellular signals. Nonetheless, a brief discussion of 1 enzyme (Akt, also referred to as PKB) will give insight into the regulatory effects of contractile activity on adaptation, in particular, the effect of stretch. Akt is thought important in the activation of the hypertrophic response in skeletal muscle (4,50). Although muscle contraction is known to activate Akt in skeletal muscle composed of various fiber types (49), the extent to which different mechanical stimuli activate Akt for the most part remains unclear.
A study found that passive stretch for 10 minutes significantly increased Akt activity (2-fold) in the fast-twitch extensor digitorum longus muscle, in which the researcher of the study concluded that mechanical tension might be a part of the mechanism by which contraction activates Akt in fast-twitch muscles (49). However, a study by Russ (47) found that stimulation frequency in muscle contraction did not contribute significantly to the signaling pathway that is thought important for hypertrophic adaptation, but passive and particularly active muscle tension were the critical signaling factors. Russ (47) also documented that the degree of Akt phosphorylation in isometric contractions was substantially less than forced lengthening (eccentric) contractions and concluded that if tension was indeed the main stimulus for Akt activation, then it was not surprising that using forced lengthening type contractions induced greater levels of Akt. This is consistent with findings that eccentric contractions for the most part induce greater hypertrophic adaptation than other contraction modes (16).
The implications of these findings although speculative are that holding a passive or active stretch at a long length may increase time under tension and/or the magnitude of the tension, which in turn will increase Akt activation and subsequent hypertrophic signaling. For further information on this topic, the readers are referred to the article of Sandri (51), which explains the signaling pathways in hypertrophy and atrophy of the muscles more clearly.
STRETCHING AND STRETCH-ACTIVATED CHANNELS
Stretch-activated channels (SACs) are calcium- and sodium-permeable channels that increase their permeability in response to mechanical loading such as stretch. There is evidence that these channels may play a vital role in mechanotransduction, linking mechanical deformation and cell signaling (8). There is a great deal of research in this area. A snapshot of the importance of stretch on SACs is provided in a study of Spangenburg and McBride (56). They (56) showed that eccentric contractions increased the degree of Akt or p70S6K phosphorylation, whereas 2 different SAC inhibitors reduced activation of the Akt or p70S6K signaling pathway, the signaling pathway thought to be a major regulator in the initiation of protein synthesis in skeletal muscle. They concluded that in skeletal muscle, SAC activity appears to only occur during lengthening or stretch-induced contractions; therefore, SACs are only contributing to hypertrophic signaling mechanisms after eccentric or lengthening contractions.
STRETCHING AND STRENGTH PERFORMANCE
If stretching is to be used within a single workout and repeated workouts as with hypertrophy training, then some understanding of its influence on muscular performance is fundamental. A more full appraisal of the effects of stretching on muscular performance can be found in 2 recent reviews scrutinizing the effects of acute and regular stretching (46,55). The author of a systematic review of 23 articles reported that an acute bout of stretching did not improve isometric and isokinetic force or jump height, and the results for running speed were contradictory (55). Shrier (55) stated that the contradiction for running speed could be attributed to running economy, which was found to be improved by stretching, whereas force and velocity of contraction were decreased after stretching.
Rubini et al. (46) concluded that although most studies found acute decreases (−4.5 to −28%) in strength (isometric, isotonic, and isokinetic) and jump performance (−3.2 to −7.3%) after stretching and that such decreases seemed to correlate to the length of the stretching protocol, the number of exercises and sets, and the duration of each set, in most studies, exceeded the ranges normally recommended in the literature. For example, 30 minutes of passive stretching of the plantar flexors decreased voluntary strength by 28% (17), 20 minutes of passive stretching resulted in a 10% decrease in the plantar flexors voluntary peak torque (24), 7% decrease of maximal isometric voluntary contraction after 10 minutes of acute passive stretching (64), and nonsignificant decreases in explosive force production (0.3-3.6%) after a 5-minute warm-up of either treadmill run or bicycling and 1-4 minutes of static stretching (1,68).
It seems that as the stretching duration decreases, the negative effect of static stretching on performance reduces to nonsignificance. Given these findings, it may be speculated that a 30- to 60-second stretch between sets may have a limited effect on subsequent set kinematics and kinetics, especially as the duration between the stretch and onset of performance increases. However, such a contention needs to be investigated with regard to both active and passive stretching. Furthermore, the influence of active and passive stretch on agonist-antagonist or upper- to lower-body work to rest protocols would benefit from research exploration.
From the literature reviewed, both passive and active stretching will influence the time under tension and the associated neuromuscular, metabolic, and/or hormonal responses. Active stretching by the nature of the added contractile activity should provide greater time under tension and hence adaptational effect. With regard to hypertrophy, it is unlikely that hypertrophic adaptation is caused by one single mechanism, and more likely, it depends on the integration of multiple local and systemic factors, which are influenced by the mechanical stimuli presented to the muscle and the resultant hormonal and metabolic responses. The tension developed within a session (i.e., the magnitude and time under tension) appears to be the critical mechanical stimuli in this process.
Our understanding of how to develop tension throughout the work period during resisted strength training has been well researched, that is, using slow contraction velocities (slow tempos), maximizing both the eccentric and the concentric contraction duration. However, it has been argued that there seems compelling reasons to stretch (active and/or passive) during the interset rest periods while hypertrophic strength training, as it is likely to increase the total time under tension of the muscle, which may have a number of mechanical, neural, metabolic, and hormonal advantages compared with not stretching.
At this stage, it is yet to be determined if the stretching protocol will adversely affect the kinematics and kinetics of the ensuing sets (i.e., magnitude of the tension) given variables such as force are also thought critical to adaptation. The status of the stretching literature does not assist our understanding in any great depth as to the negative influence of stretching on a traditional strength session because the literature for the most part has focused on the influence of stretch on expressions of force and power over excessively long stretch durations. The proposed negative influence of stretch on set and session kinematics and kinetics may be minimized by stretching the antagonist while training the agonist or stretching the lower body while training the upper body and vice versa. The net effect of such work to rest paradigms warrants investigation.
If stretch does influence the set and session kinetics negatively, we need to quantify the magnitude of this decrement and determine whether the increase in time under tension and associated neuromuscular adaptations compensates for the decrement in mechanical stimuli such as force and work. Furthermore, the differential influences of active and passive tension/stretching also need investigation, and how one can maximize tension during the work period also is worthy of research (using weights to stretch muscles at extended positions, pause training at long muscle lengths). Once a greater understanding of these questions is gained, the application of the findings into long-term training protocols assessing hypertrophic adaptation is needed.
1. Alpkaya U and Koceja D. The effects of acute static stretching on reaction time and force. J Sports Med Phys Fitness
47: 147-150, 2007.
2. Astrom M and Westlin N. Blood flow in the human achilles tendon assessed by laser doppler flowmetry. J Orthop Res
12: 246-254, 1994.
3. Biolo G, Tipton KD, Klein S, and Wolfe RR. An abundant supply of amino acids enhances the metabolic effect of exercise on muscle protein. Am J Physiol Endocrinol Metab
273: E122-E129, 1997.
4. 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.
5. Bompa TO. Periodization of Strength
. Toronto, Ontario: Veritas Publishing Inc, 1993. pp. 132-137.
6. Brown LE. Are multiple reps required for hypertrophy? Strength Cond J
24: 23-24, 2002.
7. Burd NA, Tang JE, Moore DR, and Phillips SM. Exercise training and protein metabolism: Influences of contraction, protein intake, and sex-based differences. J Appl Physiol
106: 1692-1701, 2009.
8. Butterfield TA and Best TM. Stretch-activated ion channel blockade attenuates adaptations to eccentric exercise. Med Sci Sports Exerc
41: 351-356, 2009. doi: 10.1249/MSS.0b013e318187cffa.
9. Carraro F, Stuart CA, Hartl WH, Rosenblatt J, and Wolfe RR. Effect of exercise and recovery on muscle protein synthesis in human subjects. Am J Physiol Endocrinol Metab
259: E470-E476, 1990.
10. Charette SL, McEvoy L, Pyka G, Snow-Harter C, Guido D, Wiswell RA, and Marcus R. Muscle hypertrophy response to resistance training in older women. J Appl Physiol
70: 1912-1916, 1991.
11. Coffey VG, Zhong Z, Shield A, Canny BJ, Chibalin AV, Zierath JR, and Hawley JA. Early signaling responses to divergent exercise stimuli in skeletal muscle from well-trained humans. FASEB J
20: 190-192, 2005.
12. Coutinho EL, Gomes ARS, França CN, Oishi J, and Salvini TF. Effect of passive stretching on the immobilized soleus muscle fiber morphology. Braz J Med Biol Res
37: 1853-1861, 2004.
13. Crewther B, Cronin J, and Keogh J. Possible stimuli for strength and power adaptation: Acute mechanical responses. Sports Med
35: 967-989, 2005.
14. Czerwinski SM, Martin JM, and Bechtel PJ. Modulation of IGF mRNA abundance during stretch-induced skeletal muscle hypertrophy and regression. J Appl Physiol
76: 2026-2030, 1994.
15. Denton J and Cronin JB. Kinematic, kinetic and blood lactate profiles of continuous and intraset rest loading schemes. J Strength Cond Res
20: 528-534, 2006.
16. 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.
17. Fowles JR, Sale DG, and MacDougall JD. Reduced strength after passive stretch of the human plantarflexors. J Appl Physiol
89: 1179-1188, 2000.
18. Goldspink DF. The influence of immobilization and stretch on protein turnover of rat skeletal muscle. J Physiol
264: 267-282, 1977.
19. Goldspink DF, Cox VM, Smith SK, Eaves LA, Osbaldcston NJ, Lee DM, and Mantle D. Muscle growth in response to mechanical stimuli. Am J Physiol Endocrinol Metab
268: E288-E297, 1995.
20. Goldspink G. Changes in muscle mass and phenotype and the expression of autocrine and systemic growth factors by muscle in response to stretch and overload. J Anat
194: 323-334, 1999.
21. 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.
22. Gray SD and Staub NC. Resistance to blood flow in leg muscles of dog during tetanic isometric contraction. A J Physiol
213: 677-682, 1967.
23. Hakkinen K, Newton RU, Gordon SE, McCormick M, Volek JS, Nindl BC, Gotshalk LA, Campbell W, Evans W, Hakkinen A, Humphries BJ, and Kraemer WJ. Changes in muscle morphology, electromyographic activity, and force production characteristics during progressive strength training in young and older men. J Gerontol A Biol Sci Med Sci
53: B415-B423, 1998.
24. Herda TJ, Ryan ED, Smith AE, Walter AA, Bemben MG, Stout JR, and Cramer JT. Acute effects of passive stretching vs vibration on the neuromuscular function of the plantar flexors. Scand J Med Sci Sports
19: 703-713, 2009.
25. 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.
26. Hirche H, Raff WK, and Grün D. The resistance to blood flow in the gastrocnemius of the dog during sustained and rhythmical isometric and isotonic contractions. Eur J Physiol
314: 97-112, 1970.
27. Holly RG, Barnett JG, Ashmore CR, Taylor RG, and Mole PA. Stretch-induced growth in chicken wing muscles: A new model of stretch hypertrophy. Am J Physiol Cell Physiol
238: 62-71, 1980.
28. Hortobagyi T, Hill JP, Houmard JA, Fraser DD, Lambert NJ, and Israel RG. Adaptive responses to muscle lengthening and shortening in humans. J Appl Physiol
80: 765-772, 1996.
29. Keogh JWL, Wilson GJ, and Weatherby RE. A cross-sectional comparison of different resistance training techniques in the bench press. J Strength Cond Res
13: 247-258, 1999.
30. Kirkebo A and Wisnes A. Regional tissue fluid pressure in rat calf muscle during sustained contraction or stretch. Acta Physiol Scand
114: 551-556, 1982.
31. Kraemer WJ, Adams K, Enzo C, Dudley GA, Dooly C, Feigenbaum MS, Fleck SJ, Franklin B, Fry AC, Hoffman JR, Newton RU, Potteiger J, Michael HS, Ratamess NA, and Triplett-McBride T. Progression models in resistance training for healthy adults. Med Sci Sports Exerc
34: 364-380, 2002.
32. Kraemer WJ, Gordon SE, Fleck SJ, Marchitelli L, Mello R, Dziados J, Friedl K, Harman E, Maresh CM, and Fry AC. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females Int J Sports Med
12: 228-235, 1991.
33. Kraemer WJ, Marchitelli L, Gordon SE, Harman E, Dziados JE, Mello R, Frykman P, McCurry D, and Fleck SJ. Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol
69: 1442-1450, 1990.
34. Kraemer WJ and Ratames NA. Fundamentals of resistance training: Progression and exercise prescription. Med Sci Sports Exerc
36: 674-688, 2004.
35. Manini TM and Clark BC. Blood flow restricted exercise and skeletal muscle health. Exerc Sport Sci Rev
37: 78-85, 2009.
36. Meyer RA. Does blood flow restriction enhance hypertrophic signaling in skeletal muscle? J Appl Physiol
. 100: 1443-1444, 2006.
37. Nader GA, McLoughlin TJ, and Esser KA. mTOR function in skeletal muscle hypertrophy: Increased ribosomal RNA via cell cycle regulators. Am J Physiol Cell Physiol
289: C1457-C1465, 2005.
38. Parcell AC, Sawyer RD, Tricoli VA, and Chinevere TD. Minimum rest period for strength recovery during a common isokinetic testing protocol. Med Sci Sports Exerc
34: 1018-1022, 2002.
39. Perrone CE, Fenwick-Smith D, and Vandenburgh HH. Collagen and stretch modulate autocrine secretion of insulin-like growth factor-1 and insulin-like growth factor binding proteins from differentiated skeletal muscle cells. J Biol Chem
270: 2099-2106, 1995.
40. Poliquin C. Loading Parameters for Strength Development
. Forcelite Inc, 1990. pp. 1-20.
41. Poole DC, Musch TI, and Kindig CA. In vivo microvascular structural and functional consequences of muscle length changes. Am J Physiol Heart Circ Physiol
272: H2107-H2114, 1997.
42. Ratamess NA, Alvar BA, Evetovich TK, Housh TJ, Kibler WB, Kraemer WJ, and Triplett NT. Progression models in resistance training for healthy adults. Med Sci Sports Exerc
41: 687-708, 2009. doi: 10.1249/MSS.0b013e3181915670.
43. Richmond SR and Godard MP. The effects of varied rest periods between sets to failure using the bench press in recreationally trained men. J Strength Cond Res
18: 846-849, 2004.
44. Robinson JM, Stone MH, Johnson RL, Penland CM, Warren BJ, and Lewis RD. Effects of different weight training exercise/rest intervals on strength, power, and high intensity exercise endurance. J Strength Cond Res
9: 216-221, 1995.
45. Rodney KJ, Herbert RD, and Balnave RJ. Fatigue contributes to the strength training stimulus. Med Sci Sports Exerc
26: 1160-1164, 1994.
46. Rubini EC, Costa ALL, and Gomes PSC. The effects of stretching on strength performance. Sports Med
37: 213-244, 2007.
47. Russ DW. Active and passive tension interact to promote Akt signaling with muscle contraction. Med Sci Sports Exerc
40: 88-95, 2008.
48. Sadamoto T, Bonde-Petersen F, and Suzuki Y. Skeletal muscle tension, flow, pressure, and EMG during sustained isometric contractions in humans. Eur J Appl Physiol Occup Physiol
51: 395-408, 1983.
49. Sakamoto K, Aschenbach WG, Hirshman MF, and Goodyear LJ. Akt signaling in skeletal muscle: Regulation by exercise and passive stretch. Am J Physiol Endocrinol Metab
285: E1081-E1088, 2003.
50. Sakamoto K and Goodyear LJ. Invited review: Intracellular signaling in contracting skeletal muscle. J Appl Physiol
93: 369-383, 2002.
51. Sandri M. Signaling in muscle atrophy and hypertrophy. Physiology
23: 160-170, 2008.
52. Schoenfeld B. Repetitions and muscle hypertrophy. Strength Cond J
22: 67-69, 2000.
53. Schott J, McCully K, and Rutherford OM. The role of metabolites in strength training. Eur J Appl Physiol
71: 337-341, 1995.
54. Seynnes OR, de Boer M, and Narici M. Early skeletal muscle hypertrophy and architectural changes in response to high-intensity resistance training. J Appl Physiol
102: 368-373, 2007.
55. Shrier I. Does stretching improve performance? A systematic and critical review of the literature. Clin J Sport Med
14: 267-273, 2004.
56. Spangenburg EE and McBride TA. Inhibition of stretch-activated channels during eccentric muscle contraction attenuates p70S6K activation. J Appl Physiol
100: 129-135, 2006.
57. 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.
58. Takarada Y, Tsuruta T, and Ishii N. Cooperative effects of exercise and occlusive stimuli on muscular function in low-intensity resistance exercise with moderate vascular occlusion. Jpn J Physiol
54: 585-592, 2004.
59. Tipton KD, Borsheim E, Wolf SE, Sanford AP, and Wolfe RR. Acute response of net muscle protein balance reflects 24-h balance after exercise and amino acid ingestion. Am J Physiol Endocrinol Metab
284: E76-E89, 2003.
60. Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, Petrini BE, and Wolfe RR. Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab
281: E197-E206, 2001.
61. Toigo M and Boutellier U. New fundamental resistance exercise determinants of molecular and cellular muscle adaptations. Eur J Appl Physiol
97: 643-663, 2006.
62. Vandenburgh HH. Motion into mass: How does tension stimulate muscle growth? Med Sci Sports Exerc
19: S150-S156, 1987.
63. Viru M, Jansson E, Viru A, and Sundberg CJ. Effect of restricted blood flow on exercise-induced hormone changes in healthy men. Eur J Appl Physiol
77: 517-522, 1998.
64. Weir DE, Tingley J, and Elder GCB. Acute passive stretching alters the mechanical properties of human plantar flexors and the optimal angle for maximal voluntary contraction. Eur J Appl Physiol
93: 614-623, 2005.
65. Wigmore D, Propert K, and Kent-Braun J. Blood flow does not limit skeletal muscle force production during incremental isometric contractions. Eur J Appl Physiol
96: 370-378, 2006.
66. Wilkinson SB, Phillips SM, Atherton PJ, Patel R, Yarasheski KE, Tarnopolsky MA, and Rennie MJ. Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle. J Physiol
586: 3701-3717, 2008.
67. Yang S, Alnaqeeb M, Simpson H, and Goldspink G. Changes in muscle fibre type, muscle mass and IGF-I gene expression in rabbit skeletal muscle subjected to stretch. J Anat
190: 613-622, 1997.
68. Young W, Elias G, and Power J. Effects of static stretching volume and intensity on plantar flexor explosive force production and range of motion. J Sports Med Phys Fitness 46: 403-411, 2006.