Share this article on:

Brief Review: Maximizing Hypertrophic Adaptation—Possible Contributions of Aerobic Exercise in the Interset Rest Period

Mohamad, Nur Ikhwan PhD1,3; Cronin, John PhD1,2; Nosaka, Kazunori PhD1

Strength & Conditioning Journal: February 2012 - Volume 34 - Issue 1 - pp 8-15
doi: 10.1519/SSC.0b013e3182308969


1School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia; 2Sports Performance Research Institute New Zealand, Auckland University of Technology, North Shore City, Auckland, New Zealand; and 3Faculty of Sports Science and Coaching, Sultan Idris Education University, Tanjong Malim, Perak, Malaysia

Nur Ikhwan Mohamad is a senior lecturer in strength & conditioning and head of the Department of Coaching Science at Sultan Idris Education University.

John Cronin is a professor in Strength and Conditioning at AUT University and holds an adjunct professorial position at Edith Cowan University.

Kazunori Nosaka is a professor in Exercise, Biomedical and Health Sciences at the Edith Cowan University, Perth, Western Australia.

Back to Top | Article Outline


Given that a resistance strength training session consists of work and rest periods in its simplest form, it would seem intuitive that to improve strength and power adaptation, optimizing work and rest for a given purpose is fundamental. A great deal of research has investigated the work period during resistance strength training with the intent of maximizing the mechanical stimuli (kinematics and kinetics). Improving our understanding of the training stresses that we impose on muscle is important because it is thought that strength and power adaptation is mediated by mechanical stimuli and their interaction with hormonal and metabolic factors. In terms of rest, however, apart from research that has investigated rest durations between sets (2,28,61,62,77), a paucity of research has investigated how the rest period may be optimized to enhance session kinematics and kinetics.

The research dealing with an active recovery (20,44) suggests that low-intensity activity during the rest period could enhance the ensuing set and workout kinematics and kinetics. The net result could be a session with increased mechanical, hormonal, neural, and metabolic outputs and hence the opportunity for improved strength and power adaptation. For this to occur, the interset rest periods need to be viewed not as a period of passive rest but as recovery periods. With this in mind, current practice with reference to rest and hypertrophic training, in particular, is discussed. The discussion is not exhaustive but does review the possible benefits of adding an active interset routine (cycling at 50–70 rpm, for example) during the interset rest/recovery period that may optimize the total session training stimulus and hence adaptation.

Back to Top | Article Outline


Studies have shown that strength gains from resistance training are not only the result of improved neural functioning (e.g., increased motor unit activation and firing frequencies) but also because of increases in muscle cross-sectional area (17,40,45,85). Recommendations for increasing muscle hypertrophy include the use of moderate loading (70–85% of 1 repetition maximum [1RM]) for 8–12 repetitions per set for 1 to 3 sets per exercise, for novice and intermediate individuals (12,15,28,56,73,84). 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 (51,54,58,76). With regard to the duration of rest period, 1–3 minutes have been suggested depending on the athlete's training status (76).

Providing longer rest periods 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 (52,53). Toigo and Boutellier (90) highlight recovery time as an important mechanobiological factor for developing strength. Of interest, however, is not only the duration of the rest/recovery period but also the effects of activity, such as aerobic exercise on the metabolic, hormonal, neural, and mechanical profiles of a resistance strength training session. The next sections explore the possible benefits of such interset recovery activity.

Back to Top | Article Outline


The energetic contribution to resistance strength training will, in its most simplest form, depend on the intensity and duration of the work-rest (set) periods, the total number of work-rest periods within a session (i.e., session duration), and repletion kinematics. In terms of the work period, typical hypertrophic loading as described previously consists of 10 repetitions of approximately 3- to 4-second coupled eccentric-concentric contractions per repetition. This equates to an approximate work period of 40 seconds per set, the metabolic cost of which is obviously influenced by variables such as the size of the muscle mass involved and the emphasis on the eccentric phase. Given the recommended loading stated previously and that typical hypertrophic training is suggested to be high in volume and include at least 6–8 exercises per session, the total sets per session could be between 24 and 32 sets per session (23,25,56,68,71,76). This combined with interset rest periods of approximately 60–90 seconds results in total session duration of at least 60 minutes and total session recovery of approximately 20–40 minutes.

Given this information regarding work-rest ratios and session duration, all energy systems would be mobilized during a session aimed at increasing muscle mass. This contention is supported by a previous study that found bodybuilding type of training being associated with a high rate of energy utilization through phosphagen breakdown and activation of glycogenolysis (89). Marked increases in blood lactate and intramuscular lactate, indicative of a high rate of anaerobic glycolysis, have also been reported after intense and prolonged heavy-resistance exercise comprising 5 sets of front squats, back squats, leg presses, and knee extensions (89). Even though anaerobic nonglycolytic and glycolytic energy sources were used, lipolysis (utilization of lipids/fats) has also been found to provide energy during resistance exercise, as shown by the reduced triglyceride content observed in muscle after training (29). However, based on the evidence given, anaerobic metabolism provides the majority of energy for hypertrophic training.

With anaerobic energy systems identified as the main contributor to energy production during hypertrophic training, the rate of energy repletion that occurs in the 60- to 90-second rest periods could influence the amount of work completed in ensuing exercise bouts. The rate of repletion is closely related to the efficiency of the energetic and cardiovascular systems (44,68,76,78,80). However, given the nature of the hypertrophic training stimulus and the short rest period, there is not enough time for complete repletion of energy stores and there is an increase in metabolic by-products, such as lactate, H+ ions, and inorganic phosphate (83). The regeneration of ATP during hypertrophy training using anaerobic pathways (i.e., for the most part without the presence of oxygen) increases lactic acid levels (79,81). The increase in lactic acid will affect session kinematics and kinetics, resulting in decreased force production (70). For example, hypertrophy-type resistance training has been shown to elicit greater lactate accumulation compared with other types of resistance training (50). Accumulation of lactic acid in the skeletal muscle cell can be buffered or resolved by the presence of oxygen; this process would be less likely to occur during the work component of a hypertrophic resistance training session (46,72).

Typically, most interset rest periods are relatively passive in nature. Given that there are increases in lactate in the muscle during hypertrophy-type loading, engaging in interset active recovery may enhance lactate clearance, without adversely affecting session kinematics and kinetics. Light aerobic exercise, such as low-intensity cycling, would increase blood flow, which in turn could assist with: (a) the oxygenation of lactate to pyruvate, which is subsequently used as fuel in the Krebs cycle; and/or (b) conversion to glucose via gluconeogenesis in the liver and then released back into the circulation (Cori circulation). Both outcomes may facilitate an increase in workload. For example, active recovery consisting of low-intensity cycling at 25% onset of blood lactate accumulation between sets of parallel squats was shown to be the most effective means of significantly reducing blood lactate concentration during recovery and increasing performance by an additional 5 parallel squats as compared with a passive recovery (20). Similarly, 2 minutes on a bicycle ergometer at 45% V̇o2max during the interset rest period of 4 sets of maximum repetition bench presses at 65% 1RM was found to be more effective in clearing lactate (10%) and producing greater (10%) isometric force as compared with passive rest (44). Although the effectiveness of active recovery after moderate-duration exercise is well documented (4,27,60,66), few investigations (10,86,93) have determined the impact of short-duration active recovery (<10 minutes) on high-intensity exercise, and most of these studies are not specific to resistance strength training nor have investigated active recovery specific to the 60- to 90-second interset duration common to hypertrophy training. To our knowledge, the studies of Corder et al. (20) and Hannie et al. (44) were the only research that investigated active recovery in relation to resistance strength training, so further research is needed in this area.

Active recovery during hypertrophy resistance training may have a positive influence on rate of energetic repletion and lactate clearance; however, it needs to be established whether metabolic stress is an important mediator of increased muscle mass or not. Scientific studies have suggested that acute metabolite buildup may increase the secretion of various anabolic hormones or lead to greater motor unit activation at a given load (34,57,87,88) and longitudinally may contribute to hypertrophic adaptation (34). Therefore, if metabolite accumulation is an important mediator for hypertrophy by promoting better anabolic hormonal responses, faster lactate clearance may have a negative influence. Conversely, a greater mechanical stimulus (higher forces or greater time under tension) may result from faster lactate clearance and provide a better hypertrophic stimulus. More research is needed to determine the exact interaction of mechanical and metabolic responses.

Back to Top | Article Outline


Hormones, especially the growth-related hormones, have been known to be important in initiating/stimulating the skeletal muscle growth process (34). It is well documented that physical exercise triggers the production of growth hormones, testosterone, and insulin-like growth factor-1, along with epinephrine and norepinephrine, which support the muscle growth adaptational process (1,30,32,33,35,55). Hypertrophy-type loading schemes have been found to cause greater acute endogenous hormone responses as compared with heavy or explosive-type loading schemes (63). The hormonal responses differ in magnitude, depending on the type and/or volume of the stress of the exercise protocol used (22,36,41). These hormone responses can remain elevated for up to 30 minutes posttraining (42,55), along with elevated metabolic by-products, such as lactic acid (55).

Although the magnitude of the mechanical stimulus imposed (volume load, time under tension, etc.) seems to be responsible for greater hormonal secretion during hypertrophic loading schemes (23-25), the length of the interset rest period seems to be less important. Interset rest periods less than 5 minutes have been shown to have no influence on the magnitude of acute hormonal and neuromuscular responses or long-term training adaptations in muscle strength and mass in previously strength-trained men (2).

It is well documented that aerobic/anaerobic exercise can cause an increase in acute hormonal responses, with repeated bouts of exercise elevating human growth hormone (HGH) (21) and that exercise intensity has been shown to influence HGH output (49). A study involving 6 well-trained cyclists and 6 untrained subjects found that after 4 successive 7 minutes of cycling exercise at 30, 45, 60, and 75% of maximal work capacity, plasma HGH rose to a greater extent during exercise and remained elevated after the end of exercise in the untrained group but not in the trained group (9). It has also been reported that concentrations of anabolic hormones, such as growth hormones, are augmented with repeated bouts of exercise, such as cycling (19,48). Intermittent cycling for 1 minute at 285 W followed by 2 minutes of rest repeated 7 times (total session of approximately 21 minutes) was found to elicit greater growth hormone levels than continuous cycling at 100 W for 20 minutes (92). These findings support the contention that aerobic exercise can have an influential effect on the hormonal milieu of the muscle.

From this brief treatise of some of the literature around the elevation of growth hormones with aerobic/anaerobic cycling, evidence for use of such activity in the interset rest period to magnify the total hormonal responses for the entire session do exist. Engaging in activity in the work period (resistance strength training) and rest period (cycling) may result in greater total anabolic hormone production within a session and subsequent hypertrophy. Much research is needed to determine the thresholds of aerobic intensity needed to increase the hormonal response to a practically significant level during the rest/recovery periods. However, it should be remembered that the net available time for aerobic (cycling) activity within a session is quite substantial (i.e., approximately 18–34 minutes) and may be somewhere between 30 and 40 interset rest periods of approximately 60- to 90-second duration within a training session. Research is also needed to determine the thresholds of aerobic activity needed to stimulate greater hormonal responses but at the same time do not negatively affect the kinematics and kinetics of ensuing sets. In other words, interset rest/recovery with aerobic exercise could also potentially lead to greater hormonal responses by reducing available hormone levels in the blood because of increased uptake into the tissue or it might also increase clearance (as with lactate) which might negatively affect the ensuing kinematics and kinetics.

Back to Top | Article Outline


Scientific evidence indicates that strenuous heavy resistance loading results in considerable acute fatigue in the neuromuscular system leading not only to decreased force production capacity of the muscles but also to a decrease in the voluntary neural activation of the exercised muscles (38,39). Integrated electromyography (EMG) recordings have been found to decrease by 10 and 32% after 3 sets of either 100% 10RM to failure or 10 repetitions for the first 2 sets using a 90% 10RM load using 3-minute rest periods (7). Another study found that mean neuromuscular efficiency (measured by EMG) decreased linearly with repetitions and sets (−41.1, −33.9, and −24.4% for sets 1, 2, and 3, respectively) during knee extensions using a loading of 3 sets of 8 repetitions with 2 minutes interset rest period, at 80% of maximum voluntary contraction (78).

Regarding the interset rest period, the working muscle typically is rested so neural drive to the muscle recovers. Thus, the inclusion of aerobic exercise, such as, cycling in the interset rest periods may have positive benefits to neural functioning and subsequent hypertrophic adaptation. Given that dynamic movement processes dependent on contractile rates are temperature dependent (6,80), increasing muscle temperature to normal physiological levels (37°C) can increase the speed of neural transmission and nerve receptor sensitivity, which may positively affect the kinematics and kinetics during the work period (37) and therefore might affect longitudinal adaptation. It should be noted, however, that temperatures above and below certain thresholds have inhibitory effects on muscle function. For example, maximal dynamic strength, power output, jumping, and sprinting performance were positively related to Tm (Tm ranged from 30.0 to 39°C). The changes were in the same order of magnitude for all the parameters (4–6%× C−1) Maximal isometric strength decreased by 2% × C−1 with decreasing Tm, and the force-velocity relationship was shifted to the left at subnormal Tm (8).

An example of the benefits of active recovery is found in a study by Mika et al. (65), who reported that active recovery of low-intensity cycling for 30 seconds increased motor unit activation during 3 sets of leg extensions performed at 50% of maximal voluntary contraction (MVC), with no increase observed with passive recovery and stretching-type recovery. However, whether resistance exercise alone or resistance exercise coupled with interset aerobic exercise optimizes muscle temperature and neural functioning and thereafter hypertrophic adaptation needs investigation.

Back to Top | Article Outline


Studies have shown that manipulating certain loading parameters will have a direct impact on the mechanical stimulus associated with various resistance strength training loading schemes (e.g., hypertrophic loading schemes) (26,31,47,91). As mentioned previously, the mechanical stimuli associated with typical hypertrophic loading schemes influence both the metabolic and/or the hormonal responses. Therefore, finding methods to maintain or maximize the kinematics and kinetics of a session is important if hypertrophic adaptation is to be optimized. The methods available to achieve these ends are many, ranging from nutrition and supplementation to electrical stimulation and technology that allows accentuated eccentric loading.

Similar to the theme of previous sections, it may be that performing light aerobic exercise during the interset rest periods may provide a mean to optimize session kinematics and kinetics, especially because of the temperature-regulating properties of such exercise. For example, different muscle temperatures have been shown to influence the force-velocity relationship and muscle tension of fast and slow rat muscles (74,75). Mechanical isometric force for both slow and fast rat muscle decreased by 35–42%, velocity (muscle fiber length per second) decreased by 83–89%, and maximal power decreased by 63–64% when muscle temperature decreased from 35 to 30, 25, 20, 15, and 10°C (75).

The mechanical behavior of muscle depends on the stiffness-compliance of the musculotendinous unit, which determines the elasticity and extensibility of muscle (18). Increasing muscle temperature can affect both active stiffness (e.g., neural mechanisms discussed previously) and passive stiffness by increasing the elasticity of the muscle-tendon unit (82), which may have positive benefits to the work (force × distance) performed by a muscle and/or muscle tensile behavior (69). For example, 10 minutes of aerobic exercise (jogging) at 60% of the subject's maximum age–predicted heart rate has been found to effectively decrease (7%; p < 0.05) series elastic muscle stiffness (64) and thus increase muscle compliance. Furthermore, a more compliant muscle might be able to resist mechanical fatigue better because the passive components (i.e., connective tissues like tendons) may compensate for fatigue of the active component (i.e., contractile elements) in generating the prerequisite force output (11,59).

Elevating muscle temperature toward optimum working level has also been shown to increase mechanical efficiency (ratio of energy turnover and mechanical power out) from 32 to 34% (5). However, it is unknown how muscle temperature is affected across a resisted strength training session and if aerobic exercise would influence this in any manner.

Back to Top | Article Outline


Currently, most typical resistance loading schemes use passive recovery in between sets with shorter rest periods for hypertrophic loading and longer rest periods for neuronal loading schemes. It is important to note that active recovery using low-intensity aerobic exercises may have beneficial effects to hypertrophic adaptation. Some of the proposed benefits of including light aerobic activity in the interset rest period are summarized in Table 1. However, whether such adaptations occur is likely dependent on the intensity and duration of the aerobic activity used in the interset rest period, some basic examples of which are detailed in Table 2.

Back to Top | Article Outline


1. Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, and Hakkinen K. Muscle hypertrophy, hormonal adaptations and strength development during strength training in strength-trained and untrained men. Eur J Appl Physiol 89: 555–563, 2003.
2. Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, and Hakkinen K. Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men. J Strength Cond Res 19: 572–582, 2005.
3. Bandy WD, Lovelace-Chandler V, and McKitrick-Bandy B. Adaptation of skeletal muscle to resistance training. J Orthop Sports Phys Ther 12: 248–255, 1990.
4. Belcastro AN and Bonen A. Lactic acid removal rates during controlled and uncontrolled recovery exercise. J Appl Physiol 39: 932–936, 1975.
5. Bell MP and Ferguson RA. Interaction between muscle temperature and contraction velocity affects mechanical efficiency during moderate-intensity cycling exercise in young and older women. J Appl Physiol 107: 763–769, 2009.
6. Bennett AF. Thermal dependence of muscle function. Am J Physiol 247: R217–R229, 1984.
7. Benson C, Docherty D, and Brandenburg J. Acute neuromuscular responses to resistance training performed at different loads. J Sci Med Sport 9: 135–142, 2006.
8. Bergh U and Ekblom B. Influence of muscle temperature on maximal muscle strength and power output in human skeletal muscles. Acta Physiol Scand 107: 33–37, 1979.
9. Bloom SR, Johnson RH, Park DM, Rennie MJ, and Sulaiman WR. Differences in the metabolic and hormonal response to exercise between racing cyclists and untrained individuals. J Physiol 258: 1–18, 1976.
10. Bogdanis GC, Nevill ME, Lakomy HKA, Graham CM, and Louis G. Effects of active recovery on power output during repeated maximal sprint cycling. Eur J Appl Physiol 74: 461–469, 1996.
11. Bojsen-Moller J, Magnusson SP, Rasmussen LR, Kjaer M, and Aagaard P. Muscle performance during maximal isometric and dynamic contractions is influenced by the stiffness of the tendinous structures. J Appl Physiol 99: 986–994, 2005.
12. Bompa TO. Periodization of Strength. Toronto, ON: Veritas Publishing Inc, 1993. pp. 132–137.
13. Borg G. Perceived exertion as an indicator of somatic stress. Scand J Rehabil Med 2: 92–98, 1970.
14. Bradenburg JP and Docherty D. The effects of accentuated eccentric loading on strength, muscle hypertrophy, and neural adaptations in trained individuals. J Strength Cond Res 16: 25–32, 2002.
15. Brown LE. Are multiple reps required for hypertrophy? Strength Cond J 24: 23–24, 2002.
16. Carroll TJ, Riek S, and Carson RG. Neural adaptations to resistance training: Implications for movement control. Sports Med 31: 829–840, 2001.
17. 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.
18. Cook C and McDonagh M. Measurement of muscle and tendon stiffness in man. Eur J Appl Physiol Occup Physiol 72: 380–382, 1996.
19. Copeland JL, Consitt LA, and Tremblay MS. Hormonal responses to endurance and resistance exercise in females aged 19-69 years. J Gerontol A Biol Sci Med Sci 57: B158–B165, 2002.
20. Corder KP, Potteiger JA, Nau KL, Figoni SF, and Hershberger SL. Effects of active and passive recovery conditions on blood lactate, rating of perceived exertion, and performance during resistance exercise. J Strength Cond Res 14: 151–156, 2000.
21. Craig BW and Kang H-Y. Growth hormone release following single versus multiple sets of back squats: Total work versus power. J Strength Cond Res 8: 270–275, 1994.
22. Crewther B, Cronin J, and Keogh J. Possible stimuli for strength and power adaptation: Acute metabolic responses. Sports Med 36: 215–238, 2006.
23. Crewther B, Cronin JB, Keogh J, and Cook C. The salivary testosterone and cortisol response to three loading schemes. J Strength Cond Res 22: 250–255, 2008.
24. Crewther B, Keogh J, Cronin J, and Cook C. Possible stimuli for strength and power adaptation: Acute hormonal responses. Sports Med 36: 215–238, 2006.
25. Crewther BT, Cronin J, and Keogh JWL. The contribution of volume, technique, and load to single-repetition and total-repetition kinematics and kinetics in response to three loading schemes. J Strength Cond Res 22: 1908–1915, 2008.
26. Cronin JB and Crewther B. Training volume and strength and power development. J Sci Med Sport 7: 144–155, 2004.
27. Davies C, Knibbs A, and Musgrove J. The rate of lactic acid removal in relation to different baselines of recovery exercise. Eur J Appl Physiol Occup Physiol 28: 155–161, 1970.
28. Denton J and Cronin JB. Kinematic, kinetic and blood lactate profiles of continuous and intra-set rest loading schemes J Strength Cond Res 20: 528–534, 2006.
29. Essén-Gustavsson B and Tesch P. Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise. Eur J Appl Physiol Occup Physiol 61: 5–10, 1990.
30. Felsing NE, Brasel JA, and Cooper DM. Effect of low and high intensity exercise on circulating growth hormone in men. J Clin Endocrinol Metab 75: 157–162, 1992.
31. Frost DM, Cronin JB, and Newton RU. A comparison of the kinematics, kinetics and muscle activity between pneumatic and free weight resistance. Eur J Appl Physiol 104: 937–956, 2008.
32. Frystyk J. Exercise and the growth hormone-insulin-like growth factor axis. Med Sci Sports Exerc 42: 58–66, 2010.
33. Goto K, Ishii N, Kizuka T, Kraemer R, Honda Y, and Takamatsu K. Hormonal and metabolic responses to slow movement resistance exercise with different durations of concentric and eccentric actions. Eur J Appl Physiol 106: 731–739, 2009.
34. 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.
35. Goto K, Ishii N, Kurokawa K, and Takamatsu K. Attenuated growth hormone response to resistance exercise with prior sprint exercise. Med Sci Sports Exerc 39: 108–115, 2007.
36. Goto K, Nagasawa M, Yanagisawa O, Kizuka T, Ishii N, and Takamatsu K. Muscular adaptations to combinations of high- and low-intensity resistance exercise. J Strength Cond Res 18: 730–737, 2004.
37. Gray SR, De Vito G, Nimmo MA, Farina D, and Ferguson RA. Skeletal muscle ATP turnover and muscle fiber conduction velocity are elevated at higher muscle temperatures during maximal power output development in humans. Am J Physiol Regul Integr Comp Physiol 290: R376–R382, 2006.
38. Hakkinen K. Neuromuscular fatigue and recovery in male and female athletes during heavy resistance exercise. Int J Sports Med 14: 53–59, 1993.
39. Hakkinen K. Neuromuscular fatigue in males and females during strenuous heavy resistance loading. Electromyogr Clin Neurophysiol 34: 205–214, 1994.
40. 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.
41. Hakkinen K and Pakarinen A. Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes. J Appl Physiol 74: 882–887, 1993.
42. Hakkinen K, Pakarinen A, Hannonen P, Hakkinen A, Airaksinen O, Valkeinen H, and Alen M. Effects of strength training on muscle strength, cross-sectional area, maximal electromyographic activity, and serum hormones in premenopausal women in fibromyalgia. J Rheumatol 29: 1287–1295, 2002.
43. Hakkinen K, Pakarinen A, and Kallinen M. Neuromuscular adaptations and serum hormones in women during short-term intensive strength training. Eur J Appl Physiol 64: 106–111, 1992.
44. Hannie PQ, Hunter GR, Kekes-Szabo T, Nicholson C, and Harrison PC. The effects of recovery on force production, blood lactate, and work performed during bench press exercise. J Strength Cond Res 9: 8–12, 1995.
45. 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.
46. Hunter GR, Seelhorst D, and Snyder S. Comparison of metabolic and heart rate responses to super slow vs. traditional resistance training. J Strength Cond Res 17: 76–81, 2003.
47. Jones K, Bishop P, Hunter G, and Fleisig G. The effects of varying resistance-training loads on intermediate- and high-velocity-specific adaptations. J Strength Cond Res 15: 349–356, 2001.
48. Kanaley JA, Weltman JY, Veldhuis JD, Rogol AD, Hartman ML, and Weltman A. Human growth hormone response to repeated bouts of aerobic exercise. J Appl Physiol 83: 1756–1761, 1997.
49. Kang H-Y, Martino PF, Russo V, Ryder JW, and Craig BW. The influence of repetitions maximum on GH release following the back squat and leg press in trained men: Preliminary results. J Strength Cond Res 10: 148–152, 1996.
50. 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.
51. Kraemer WJ, Adams K, Enzo C, Dudley GA, Dooly C, Feigenbaum MS, Fleck SJ, Franklin B, Fry AC, Hoffman JR, Newton RU, Potteiger J, Stone HM, Ratamess NA, and Triplett-McBride T. Progression models in resistance training for healthy adults. Med Sci Sports Exerc 34: 364–380, 2002.
52. 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.
53. 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.
54. Kraemer WJ, Nindl BC, Ratamess NA, Gotshalk LA, Volek JS, Fleck SJ, Newton RU, and Hakkinen K. Changes in muscle hypertrophy in women with periodized resistance training. Med Sci Sports Exerc 36: 697–708, 2004.
55. Kraemer WJ, Noble BJ, Clark MJ, and Culver BW. Physiologic responses to heavy-resistance exercise with very short rest periods. Int J Sports Med 8: 247–52, 1987.
56. Kraemer WJ and Ratames NA. Fundamentals of resistance training: Progression and exercise prescription. Med Sci Sports Exerc 36: 674–688, 2004.
57. Kraemer WJ, Staron RS, Hagerman FC, Hikida RS, Fry AC, Gordon SE, Nindl BC, Gothshalk LA, Volek JS, Marx JO, Newton RU, and Häkkinen K. The effects of short-term resistance training on endocrine function in men and women. Eur J Appl Physiol 78: 69–76, 1998.
58. Kramer JB, Stone MH, O'Bryant HS, Conley MS, Johnson RL, Nieman DC, Honeycutt DR, and Hoke TP. Effects of single vs. multiple sets of weight training: Impact of volume, intensity, and variation. J Strength Cond Res 11: 143–147, 1997.
59. Kubo K, Kawakami Y, and Fukunaga T. Influence of elastic properties of tendon structures on jump performance in humans. J Appl Physiol 87: 2090–2096,1999.
60. Lars H and Inger S. Production and removal of lactate during exercise in man. Acta Physiol Scand 86: 191–201, 1972.
61. Lawton TW, Cronin JB, Drinkwater E, Lindsell R, and Pyne D. The effect of continuous repetition training and intra-set rest training on bench press strength and power. J Sports Med Phys Fitness 44: 361–367, 2004.
62. Lawton TW, Cronin JB, and Lindsell RP. Effect of interrepetition rest intervals on weight training repetition power output. J Strength Cond Res 20: 172–176, 2006.
63. McCaulley G, McBride J, Cormie P, Hudson M, Nuzzo J, Quindry J, and Travis Triplett N. Acute hormonal and neuromuscular responses to hypertrophy, strength and power type resistance exercise. Eur J Appl Physiol 105: 695–704, 2009.
64. McNair PJ and Stanley SN. Effect of passive stretching and jogging on the series elastic muscle stiffness and range of motion of the ankle joint. Br J Sports Med 30: 313–317, 1996.
65. Mika A, Mika P, Fernhall B, and Unnithan VB. Comparison of recovery strategies on muscle performance after fatiguing exercise. Am J Phys Med Rehabil 86: 474–481, 2007.
66. Monedero J and Donne B. Effect of recovery interventions on lactate removal and subsequent performance. Int J Sports Med 21: 593–597, 2000.
67. Moritani T and DeVries HA. Neural factors versus hypertrophy in the time course of muscle strength gain. Am J Phys Med 58: 115–130, 1979.
68. Mulligan SE, Fleck SJ, Gordon SE, Koziris LP, Triplett-McBride NT, and Kraemer WJ. Influence of resistance exercise volume on serum growth hormone and cortisol concentrations in women. J Strength Cond Res 10: 256–262, 1996.
69. Noonan TJ, Best TM, Seaber AV, and Garrett WE. Thermal effects on skeletal muscle tensile behavior. Am J Sports Med 21: 517–522, 1993.
70. Nummela A, Vuorimaa T, and Rusko H. Changes in force production, blood lactate and EMG activity in the 400-m sprint. J Sports Sci 10: 217–228, 1992.
71. Peterson MD, Kampert M, Haff GG, and Gordon PM. The contribution of volume load variation on strength and hypertrophy during unilateral resistance training in the elbow flexors. J Strength Cond Res 24(Suppl): 1, 2010.
72. Poehlman ET and Melby C. Resistance training and energy balance. Int J Sport Nutr 8: 143–159, 1998.
73. Poliquin C. Loading parameters for strength development. Forcelite Inc 1–20, 1990.
74. Ranatunga KW. Temperature-dependence of shortening velocity and rate of isometric tension development in rat skeletal muscle. J Physiol 329: 465–483, 1982.
75. Ranatunga KW. Temperature dependence of mechanical power output in mammalian (rat) skeletal muscle. Exp Biol 83: 371–376, 1998.
76. 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.
77. Ratamess NA, Falvo MJ, Mangine GT, Hoffman JR, Faigenbaum AD, and Jie K. The effect of rest interval length on metabolic responses to the bench press exercise. Eur J Appl Physiol 100: 1–17, 2007.
78. Remaud A, Cornu C, and Guevel A. A methodologic approach for the comparison between dynamic contractions: Influences on the neuromuscular system. J Athl Train 40: 281–287, 2005.
79. Reynolds TH, Frye PA, and Sforzo GA. Resistance training and the blood lactate response to resistance exercise in women. J Strength Cond Res 11: 77–81, 1997.
80. Rossi R, Maffei M, Bottinelli R, and Canepari M. Temperature dependence of speed of actin filaments propelled by slow and fast skeletal myosin isoforms. J Appl Physiol 99: 2239–2245, 2005.
81. Rozenek R, Rosenau L, Rosenau P, and Stone MH. The effect of intensity on heart rate and blood lactate response to resistance exercise. J Strength Cond Res 7: 51–54, 1993.
82. Safran MR, Garrett WE, Seaber AV, Glisson RR, and Ribbeck BM. The role of warmup in muscular injury prevention. Am J Sports Med 16: 123–129, 1988.
83. Sahlin K. Muscle fatigue and lactic acid accumulation. Acta Physiol Scand 556: 83–91, 1986.
84. Schoenfeld B. Repetitions and muscle hypertrophy. Strength Cond J 22: 67–69, 2000.
85. 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.
86. Signorile JF, Ingalls C, and Tremblay LM. The effects of active and passive recovery on short-term, high intensity power output. Can J Appl Physiol 18: 31–42, 1993.
87. 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.
88. Taylor JM, Thompson HS, Clarkson PM, Miles MP, De Souza MJ, and Taylor JM. Growth hormone response to an acute bout of resistance exercise in weight-trained and non-weight-trained women. J Strength Cond Res 14: 220–227, 2000.
89. Tesch P, Colliander E, and Kaiser P. Muscle metabolism during intense, heavy-resistance exercise. Eur J Appl Physiol Occup Physiol 55: 362–366, 1986.
90. Toigo M and Boutellier U. New fundamental resistance exercise determinants of molecular and cellular muscle adaptations. Eur J Appl Physiol 97: 643–663, 2006.
91. Tran QT, Docherty D, and Behm D. The effects of varying time under tension and volume load on acute neuromuscular responses. Eur J Appl Physiol 98: 402–410, 2006.
92. Vanhelder W, Goode R, and Radomski M. Effect of anaerobic and aerobic exercise of equal duration and work expenditure on plasma growth hormone levels. Eur J Appl Physiol Occup Physiol 52: 255–257, 1984.
93. Weltman A, Stamford B, Moffat RJ, and Katch VL. Exercise recovery, lactate removal, and subsequent high intensity exercise performance. Res Q 48: 786–796, 1977.

active recovery; hypertrophy; mechanical; metabolic; hormonal; neural; strength training

© 2012 National Strength and Conditioning Association