Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise

Publication: Applied Physiology, Nutrition, and Metabolism26 April 2012


It is often recommended that heavier training intensities (∼70%–80% of maximal strength) be lifted to maximize muscle growth. However, we have reported that intensities as low as 30% of maximum strength, when lifted to volitional fatigue, are equally effective at stimulating muscle protein synthesis rates during resistance exercise recovery. This paper discusses the idea that high-intensity contractions are not the exclusive driver of resistance exercise-induced changes in muscle protein synthesis rates.


Pour maximiser la croissance musculaire, on recommande souvent de s’entraîner à plus forte intensité (∼70–80 % de la force maximale). Toutefois, nous avons déjà rapporté que soulever jusqu’à épuisement volontaire des charges équivalant à aussi peu que 30 % de la force musculaire stimule la synthèse des protéines dans les muscles durant la phase de récupération consécutive aux exercices contre résistance. Cet article analyse l’idée selon laquelle des contractions de forte intensité ne seraient pas le seul moyen pour modifier le taux de synthèse des protéines musculaires causée par les exercices contre résistance.


Acute studies examining protein phosphorylation or muscle protein synthetic responses after resistance exercise and protein ingestion are often used to predict longer-term training outcomes. Is there concrete evidence suggesting these acute studies provide meaningful information? Indeed, definitive evidence is lacking and it is clear that this is a research gap that needs to be filled. The relevance of using static “snapshots” of protein phosphorylation that represent a single stage of the translational process to represent dynamic measurements of the phenotypic response, such as muscle protein synthesis rates (MPS), is dwindling, at least in humans (Burd et al. 2009). This disconnect between the measurements are likely due to the single point measurement or a minimum threshold where greater protein phosphorylation would have little additive effect on the dynamic rate measurement of MPS. Moreover, the existence of multiple redundant pathways to activate MPS also makes interpretation difficult. Conversely, for a muscle fibre to hypertrophy there must be a period of net muscle protein accretion at some point over the course of a day. Resistance exercise is an effective stimulus to improve muscle protein balance, primarily by the stimulation of MPS (Phillips et al. 1997), and when accompanied by protein ingestion the stimulation of MPS is greater than either stimulus alone (Biolo et al. 1997; Tipton et al. 1999; Moore et al. 2009). The ultimate outcome, therefore, is an acute positive muscle protein balance that will lead to eventual hypertrophy after chronic resistance training (RT). To our knowledge, there is no other physiological mechanism that a muscle fibre can hypertrophy to a substantial extent after RT without some type of muscle proteins being synthesized and incorporated into new muscle proteins. Thus, acute measurements of MPS must have some indication of training-mediated hypertrophy. Furthermore, indirect evidence suggests that acute measurements of MPS after anabolic (Fujita et al. 2007; Wilkinson et al. 2007; West et al. 2009; Holm et al. 2010) or catabolic (Glover et al. 2008) stimuli can translate into muscle growth (Takarada et al. 2000; Hartman et al. 2007; Holm et al. 2008; West et al. 2010) or loss (Yasuda et al. 2005). Given all this, there is scientific evidence to support the idea that acute measurements of MPS are linked to long-term outcomes.
Our laboratory conducted a series of acute experiments that manipulated various resistance exercise variables (e.g., intensity, volume, and muscle time under tension) that has lead to the thesis that maximal fibre activation represents the primary stimulus to maximize MPS during resistance exercise recovery. Our findings uncovered a concept that is commonly not recognized. Specifically, high-intensity contractions (lifting heavy loads) are not the only driver of exercise-induced rates of MPS. The aim of this article, therefore, is to discuss the idea that full muscle fibre recruitment, and not merely high-intensity contractions, is the fundamental variable underpinning resistance exercise-induced MPS rates.

The contraction stimulus driving MPS

There are a myriad of resistance exercise variables, beyond intensity, which can be manipulated to produce diverse training-mediated hypertrophy; these variables can include volume, muscle action, muscle time under tension, lifting cadence, contraction mode, and inter-set rest interval (American College of Sports Medicine 2009). Indeed, for each of these variables to have independent effects on muscle protein turnover, and thus hypertrophic adaptation, the skeletal muscle must be able to “gauge” these variables as distinct mechanical stimuli, such as interacting with the metabolic and hormonal milieu, that can subsequently be transformed into intramuscular signals that leads to the stimulation of MPS. Theoretically, each variable would elicit a specific muscle phenotypic response. However, such evidence is, at least in our view, lacking. From a systems perspective, the input into a skeletal motor unit–muscle fibre to lift a weight would come from the neural signals it received, and these signals would determine whether to fire or not fire and at what frequency. The surrounding nutrient milieu would then dictate (to a variable degree) the response of the fibre in terms of MPS (Biolo et al. 1997), which would ultimately sum to yield hypertrophy over time. When viewed from this perspective, there is an underlying commonality between many RT variables such that application of any variable in such a way to induce muscle activation ultimately serves to activate the same intramuscular signaling pathways necessary to stimulate MPS and potentially training-induced hypertrophy. Indeed, many will argue that the phenotype of ultimate importance with any program of RT is both strength and hypertrophy and we do not disagree with this. However, a common link between these variables is hypertrophy, and thus we focus on gains in muscle protein mass in this review. Strength gains are, however, a product of neuromuscular and muscular adaptations as reviewed elsewhere (Sale 1988).
Resistance exercise intensities of ∼70%–80% of 1 repetition maximum (1RM) for 8–12 repetitions are the classically prescribed protocols to use to maximize training-induced muscle hypertrophy (American College of Sports Medicine 2009). What is so intrinsically unique about high-intensity resistance exercise in terms of promoting exercise-induced MPS? It may be related to the existence of a positive relationship between greater force development and increased muscle electromyographic activity (Alkner et al. 2000). Accordingly, a greater recruitment of muscle fibres at high exercise intensities may occur to stimulate a robust MPS response. Kumar and colleagues (2009) provide support for the concept of a dose–response relationship between external work-equated exercise intensities and MPS. From this work it appears the relationship reaches a plateau between intensities of ∼60–90% of 1RM (Kumar et al. 2009). This outcome, we propose, is likely a product of maximal, or at least near maximal, muscle fibre recruitment at contraction intensities beyond 60% of 1RM. Thus, there would be little reason to expect a large difference in MPS unless the muscle fibre had an intricately sensitive mechanism to detect a difference between 60% and 90% of 1RM, a concept that appears, at least according to all available data, highly unlikely. It is generally accepted that motor units are recruited in accordance with the size principle during voluntary muscle contraction (Henneman et al. 1965). Against this background, it would seem reasonable to assume that lower intensities performed to volitional fatigue (i.e., task failure) could achieve a similar degree of muscle fibre activation to that of high-intensity resistance exercise regimes performed to task failure, and presumably a similar stimulation of MPS during recovery (Fig. 1). Certainly, such a thesis would be dependent on the notion that maximal fibre activation occurs at the moment of fatigue, which is an idea that has support (Wernbom et al. 2009).
Fig. 1.
Fig. 1. An illustration representing the relationship between resistance exercise intensity (x axis) and myofibrillar protein synthesis (left y axis). The bold line represents the reported dose-dependent relationship between resistance exercise intensity and myofibrillar protein synthesis rates that rises to a plateau at 60%–90% of 1 repetition maximum (1RM) after external work-equated exercise (Kumar et al. 2009). During lower intensity work-matched conditions, less muscle fibre activation (right axis) is required to maintain muscle tension and thus results in less stimulation of a myofibrillar protein synthesis. However, based on the orderly recruitment of muscle fibres (Henneman et al. 1965) performance of resistance exercise, even at lower intensities, until volitional fatigue (i.e., failure) will necessitate maximal fibre recruitment and culminate in a similar fibre recruitment resulting in the stimulatory threshold being surpassed. The end result is the maximal stimulation of myofibrillar protein synthesis rates (dashed line).
Our laboratory has recently tested the thesis that eliciting failure during high- or low-intensity resistance exercise leads to maximal muscle fibre activation, and thus a similar stimulation of MPS. It was demonstrated, in resistance-trained young men, that lower intensity (30% of 1RM) and higher volume (24 ± 3 repetitions, means ± SD) resistance exercise performed until failure was equally effective in stimulating myofibrillar protein synthesis rates during 0–4 h recovery as heavy intensity (90% of 1RM) and lower volume (5 ± 1 repetitions) resistance exercise (Burd et al. 2010b). Interestingly, exercise performed at 30% of 1RM induced a longer-lasting effect on MPS at 21–24 h of exercise recovery (Burd et al. 2010b). The observation of a sustained elevation in myofibrillar protein synthesis rates after the low-intensity–higher volume regime corroborates recent data demonstrating that exercise volume is an integral factor for sustaining the myofibrillar protein synthetic response during exercise recovery (Burd et al. 2010a). Thus, an additional benefit of low-intensity resistance exercise is that it allows for higher total number of repetitions to be performed, which is an important variable to sustain the response, and still eventually results in full motor unit recruitment.
For clarity, the performance of dynamic knee extension exercise at 30% of 1RM to failure, as we did previously (Burd et al. 2010b), induces fatigue in the contracting leg within 24 repetitions. This number of repetitions effectively minimizes the time that loaded muscle is under tension and likely prevents a shift toward the synthesis of non-contractile proteins (Burd et al. 2012). Also, leg extension exercise, even at low intensities, is effective at inducing temporary occlusion of blood flow (Wernbom et al. 2009). Thus, other types of resistance exercises (e.g., leg press) would require more repetitions to induce fatigue with an intensity at 30% of 1RM (Hoeger et al. 1990). An argument that is commonly put forward is the sustained elevation in postabsorptive MPS observed after the low-intensity–higher volume condition, such as in our previous study (Burd et al. 2010b), simply represents a state of increased muscle protein turnover as compared with the high-intensity condition. We cannot completely dismiss such an argument as invalid. It is clear the substrates to support MPS, in the fasting state, are the amino acids released from muscle protein breakdown (Phillips et al. 1997). However, examining the 24-h responses after feeding 15 g of high-quality protein, and thus decreasing muscle protein breakdown (Biolo et al. 1997), demonstrates that myofibrillar protein accretion is occurring in similar magnitude to the high-intensity condition (Burd et al. 2011). Thus, we speculate that low-intensity training would result in a similar amount of training-induced muscle mass as high-intensity resistance training.


A central tenet of this review is that achieving maximal muscle fibre activation during acute resistance exercise is fundamental in eliciting robust increase in MPS (Fig. 1). Also, the authors wish to be clear that the prescription of an “optimal” resistance training program will never be possible as substantial variation exists in the ability of individuals to respond to a training stimulus. Moreover, differential training goals among cohorts of individuals will also need to be considered when developing training programs. However, the perspective provided within this review highlights that other resistance exercise protocols, beyond the often discussed high-intensity training (American College of Sports Medicine 2009), can be effective in stimulating an acute anabolic response (Burd et al. 2010b) that may translate into training-mediated increases in hypertrophy (Léger et al. 2006). A larger metabolically active muscle mass, and discussing other avenues beyond high-intensity contractions to achieve this, will have important implications from a public health standpoint. For example, skeletal muscle mass is a large contributor to daily energy expenditure and will assist in weight management. Additionally, skeletal muscle, because of its overall size, is the primary site of blood glucose disposal and thus will likely play a role in reducing the risk for the development of type II diabetes (Wolfe 2006). However, if the goal is to achieve maximal strength development, since neural factors are a significant contributor to this outcome (Sale 1988), then high-intensity training regimes are superior in this regard. Training with high-intensity contractions allows the trainee to get “practice” in activating muscle mass during a single maximal lift. However, greater strength would not require continual training at higher intensity resistance exercise, merely the periodic practice of higher intensity lifts during a low-intensity training program.


This work was funded by the Canadian Natural Science and Engineering Research Council (NSERC). The authors have no conflicts of interests to declare that are directly relevant to the content of this article.


Alkner B.A., Tesch P.A., and Berg H.E. 2000. Quadriceps EMG/force relationship in knee extension and leg press. Med. Sci. Sports Exerc. 32(2): 459–463.
American College of Sports Medicine. 2009. American College of Sports Medicine position stand. Progression models in resistance training for healthy adults. Med. Sci. Sports Exerc. 41(3): 687–708.
Biolo G., Tipton K.D., Klein S., and Wolfe R.R. 1997. An abundant supply of amino acids enhances the metabolic effect of exercise on muscle protein. Am. J. Physiol. 273(1): E122–E129.
Burd N.A., Tang J.E., Moore D.R., and Phillips S.M. 2009. Exercise training and protein metabolism: influences of contraction, protein intake, and sex-based differences. J. Appl. Physiol. 106(5): 1692–1701.
Burd N.A., Holwerda A.M., Selby K.C., West D.W., Staples A.W., Cain N.E., et al. 2010a. Resistance exercise volume affects myofibrillar protein synthesis and anabolic signalling molecule phosphorylation in young men. J. Physiol. 588(16): 3119–3130.
Burd N.A., West D.W., Staples A.W., Atherton P.J., Baker J.M., Moore D.R., et al. 2010b. Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men. PLoS ONE, 5(8): e12033.
Burd N.A., West D.W., Moore D.R., Atherton P.J., Staples A.W., Prior T., et al. 2011. Enhanced amino acid sensitivity of myofibrillar protein synthesis persists for up to 24 h after resistance exercise in young men. J. Nutr. 141(4): 568–573.
Burd N.A., Andrews R.J., West D.W., Little J.P., Cochran A.J., Hector A.J., et al. 2012. Muscle time under tension during resistance exercise stimulates differential muscle protein sub-fractional synthetic responses in men. J. Physiol. 590(2): 351–362.
Fujita S., Abe T., Drummond M.J., Cadenas J.G., Dreyer H.C., Sato Y., et al. 2007. Blood flow restriction during low-intensity resistance exercise increases S6K1 phosphorylation and muscle protein synthesis. J. Appl. Physiol. 103(3): 903–910.
Glover E.I., Phillips S.M., Oates B.R., Tang J.E., Tarnopolsky M.A., Selby A., et al. 2008. Immobilization induces anabolic resistance in human myofibrillar protein synthesis with low and high dose amino acid infusion. J. Physiol. 586(24): 6049–6061.
Hartman J.W., Tang J.E., Wilkinson S.B., Tarnopolsky M.A., Lawrence R.L., Fullerton A.V., and Phillips S.M. 2007. Consumption of fat-free fluid milk after resistance exercise promotes greater lean mass accretion than does consumption of soy or carbohydrate in young, novice, male weightlifters. Am. J. Clin. Nutr. 86(2): 373–381.
Henneman E., Somjen G., and Carpenter D.O. 1965. Functional significance of cell size in spinal motoneurons. J. Neurophysiol. 28: 560–580.
Hoeger W.W.K., Hopkins D.R., Barrette S.L., and Hale D.F. 1990. Relationship between repetitions and selected percentages of one repetition maximum: A comparison between untrained and trained males and females. J. Strength Cond. Res. 4(2): 47–55.
Holm L., Reitelseder S., Pedersen T.G., Doessing S., Petersen S.G., Flyvbjerg A., et al. 2008. Changes in muscle size and MHC composition in response to resistance exercise with heavy and light loading intensity. J. Appl. Physiol. 105(5): 1454–1461.
Holm L., van Hall G., Rose A.J., Miller B.F., Doessing S., Richter E.A., and Kjaer M. 2010. Contraction intensity and feeding affect collagen and myofibrillar protein synthesis rates differently in human skeletal muscle. Am. J. Physiol. Endocrinol. Metab. 298(2): E257–E269.
Kumar V., Selby A., Rankin D., Patel R., Atherton P., Hildebrandt W., et al. 2009. Age-related differences in the dose-response relationship of muscle protein synthesis to resistance exercise in young and old men. J. Physiol. 587(1): 211–217.
Léger B., Cartoni R., Praz M., Lamon S., Dériaz O., Crettenand A., et al. 2006. Akt signalling through GSK-3β, mTOR and Foxo1 is involved in human skeletal muscle hypertrophy and atrophy. J. Physiol. 576(3): 923–933.
Moore D.R., Tang J.E., Burd N.A., Rerecich T., Tarnopolsky M.A., and Phillips S.M. 2009. Differential stimulation of myofibrillar and sarcoplasmic protein synthesis with protein ingestion at rest and after resistance exercise. J. Physiol. 587(4): 897–904.
Phillips S.M., Tipton K.D., Aarsland A., Wolf S.E., and Wolfe R.R. 1997. Mixed muscle protein synthesis and breakdown after resistance exercise in humans. Am. J. Physiol. 273(1): E99–E107.
Sale D.G. 1988. Neural adaptation to resistance training. Med. Sci. Sports Exerc. 20(5 Suppl.): S135–S145.
Takarada Y., Takazawa H., Sato Y., Takebayashi S., Tanaka Y., and Ishii N. 2000. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J. Appl. Physiol. 88(6): 2097–2106.
Tipton K.D., Ferrando A.A., Phillips S.M., Doyle D. Jr, and Wolfe R.R. 1999. Postexercise net protein synthesis in human muscle from orally administered amino acids. Am. J. Physiol. 276(4): E628–E634.
Wernbom M., Jarrebring R., Andreasson M.A., and Augustsson J. 2009. Acute effects of blood flow restriction on muscle activity and endurance during fatiguing dynamic knee extensions at low load. J. Strength Cond. Res. 23(8): 2389–2395.
West D.W., Kujbida G.W., Moore D.R., Atherton P., Burd N.A., Padzik J.P., et al. 2009. Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. J. Physiol. 587(21): 5239–5247.
West D.W., Burd N.A., Tang J.E., Moore D.R., Staples A.W., Holwerda A.M., et al. 2010. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J. Appl. Physiol. 108(1): 60–67.
Wilkinson S.B., Tarnopolsky M.A., Macdonald M.J., Macdonald J.R., Armstrong D., and Phillips S.M. 2007. Consumption of fluid skim milk promotes greater muscle protein accretion after resistance exercise than does consumption of an isonitrogenous and isoenergetic soy-protein beverage. Am. J. Clin. Nutr. 85(4): 1031–1040.
Wolfe R.R. 2006. The underappreciated role of muscle in health and disease. Am. J. Clin. Nutr. 84(3): 475–482.
Yasuda N., Glover E.I., Phillips S.M., Isfort R.J., and Tarnopolsky M.A. 2005. Sex-based differences in skeletal muscle function and morphology with short-term limb immobilization. J. Appl. Physiol. 99(3): 1085–1092.

Information & Authors


Published In

Applied Physiology, Nutrition, and Metabolism cover image
Applied Physiology, Nutrition, and Metabolism
Volume 37Number 3June 2012
Pages: 551 - 554


Received: 10 November 2011
Accepted: 31 January 2012
Published online: 26 April 2012


Request permissions for this article.

Key Words

  1. anabolic signaling
  2. resistance exercise
  3. adaptation
  4. skeletal muscle growth
  5. myofibrillar
  6. mitochondrial
  7. skeletal muscle protein turnover


  1. signalisation anabolique
  2. exercice contre résistance
  3. adaptation
  4. croissance du muscle squelettique
  5. renouvellement des protéines musculaires squelettiques
  6. mitochondriales et myofibrillaires



Nicholas A. Burd
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada.
Cameron J. Mitchell
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada.
Tyler A. Churchward-Venne
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada.
Stuart M. Phillips
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada.


Present address: Department of Human Movement Sciences, Maastricht University Medical Centre, PO Box 616, 6200 MD Maastricht, the Netherlands

Metrics & Citations


Other Metrics


Cite As

Export Citations

If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download.

Cited by

1. May the Force and Mass Be With You—Evidence-Based Contribution of Mechano-Biological Descriptors of Resistance Exercise
2. Acute performance and physiological responses to upper-limb multi-set exercise to failure: Effects of external resistance and systemic hypoxia
3. Effects of Resistance Training Performed with Different Loads in Untrained and Trained Male Adult Individuals on Maximal Strength and Muscle Hypertrophy: A Systematic Review
4. Comparison Between Two Volume-Matched Squat Exercises With and Without Momentary Failure for Changes in Hormones, Maximal Voluntary Isometric Contraction Strength, and Perceived Muscle Soreness
5. Resistance Training Load Effects on Muscle Hypertrophy and Strength Gain
6. Age-related differences in gastrocnemii muscles and Achilles tendon mechanical properties in vivo
7. Intramuscular mechanisms of overtraining
8. Skeletal muscle hypertrophy: molecular and applied aspects of exercise physiology
9. Resistance Exercise–induced Regulation of Muscle Protein Synthesis to Intraset Rest
10. Multiaspective diagnostics of training loads as well as biomechanical parameters and blood indices among leadingelite race walkers preparing for participation in the olympics
11. Moderate vs high-load resistance training on muscular adaptations in rats
12. Moderate Intensity Resistive Training Reduces Oxidative Stress and Improves Muscle Mass and Function in Older Individuals
13. Blood flow restricted resistance exercise and reductions in oxygen tension attenuate mitochondrial H 2 O 2 emission rates in human skeletal muscle
14. Skeletal Muscle Fiber Adaptations Following Resistance Training Using Repetition Maximums or Relative Intensity
15. High-Frequency Resistance Training Is Not More Effective Than Low-Frequency Resistance Training in Increasing Muscle Mass and Strength in Well-Trained Men
16. Lower-Load is More Effective Than Higher-Load Resistance Training in Increasing Muscle Mass in Young Women
17. The acute effects of resistance exercise on affect, anxiety, and mood – practical implications for designing resistance training programs
18. The Role of Inflammation and Immune Cells in Blood Flow Restriction Training Adaptation: A Review
19. A comparison of the acute physiological responses to BODYPUMP™ versus iso-caloric and iso-time steady state cycling
20. Microvascular adaptations to resistance training are independent of load in resistance-trained young men
21. Effects of different intensities of resistance training with equated volume load on muscle strength and hypertrophy
22. The Role of Blood Flow Restriction Training to Mitigate Sarcopenia, Dynapenia, and Enhance Clinical Recovery
23. Physical Exercise and Aging
24. Strength and Hypertrophy Adaptations Between Low- vs. High-Load Resistance Training: A Systematic Review and Meta-analysis
25. Muscle Hypertrophy: A Narrative Review on Training Principles for Increasing Muscle Mass
26. The Effect of Different Resistance Training Load Schemes on Strength and Body Composition in Trained Men
27. Training to Fatigue: The Answer for Standardization When Assessing Muscle Hypertrophy?
28. Effects of BodyPump and resistance training with and without a personal trainer on muscle strength and body composition in overweight and obese women—A randomised controlled trial
29. Körperliches Training in Prävention und Therapie – Gestaltung und Effekte
30. Impact of high versus low fixed loads and non-linear training loads on muscle hypertrophy, strength and force development
31. Protein metabolism and physical training: any need for amino acid supplementation?
32. The impact of repetition mechanics on the adaptations resulting from strength-, hypertrophy- and cluster-type resistance training
33. Acute Anabolic Response and Muscular Adaptation After Hypertrophy-Style and Strength-Style Resistance Exercise
34. Effects of resistance training with moderate vs heavy loads on muscle mass and strength in the elderly: A meta-analysis
35. Upper body muscle activation during low-versus high-load resistance exercise in the bench press
36. Unique activation of the quadriceps femoris during single- and multi-joint exercises
37. Greater Strength Gains after Training with Accentuated Eccentric than Traditional Isoinertial Loads in Already Strength-Trained Men
38. Muscular adaptations in low- versus high-load resistance training: A meta-analysis
39. Blood flow restricted and traditional resistance training performed to fatigue produce equal muscle hypertrophy
40. Individual Responses for Muscle Activation, Repetitions, and Volume during Three Sets to Failure of High- (80% 1RM) versus Low-Load (30% 1RM) Forearm Flexion Resistance Exercise
41. Muscle activation during three sets to failure at 80 vs. 30 % 1RM resistance exercise
42. Effects of Low- vs. High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men
43. Investigation of Fatigability during Repetitive Robot-Mediated Arm Training in People with Multiple Sclerosis
44. Low-load resistance training promotes muscular adaptation regardless of vascular occlusion, load, or volume
45. Nutritional Supplements in Support of Resistance Exercise to Counter Age-Related Sarcopenia
46. Intramuscular anabolic signaling and endocrine response following high volume and high intensity resistance exercise protocols in trained men
47. Optimizing the Physical Conditioning of the NASCAR Sprint Cup Pit Crew Athlete
48. Pelvic floor and exercise science
49. Muscle activation during low- versus high-load resistance training in well-trained men
50. Effects of Different Dietary Proteins and Amino Acids on Skeletal Muscle Hypertrophy in Young Adults After Resistance Exercise
51. Is There a Minimum Intensity Threshold for Resistance Training-Induced Hypertrophic Adaptations?
52. miRNA Analysis for the Assessment of Exercise and Amino Acid Effects on Human Skeletal Muscle
53. Feasibility Study Evaluating Four Weeks Stochastic Resonance Whole-Body Vibration Training with Healthy Female Students
54. Blood flow-restricted exercise in space
55. Exercise and Amino Acid Anabolic Cell Signaling and the Regulation of Skeletal Muscle Mass

View Options

View options

Full Text

Open Full Text


Download PDF

Get Access

Login options

Check if you access through your login credentials or your institution to get full access on this article.


Click on the button below to subscribe to Applied Physiology, Nutrition, and Metabolism

Purchase options

Purchase this article to get full access to it.

Restore your content access

Enter your email address to restore your content access:

Note: This functionality works only for purchases done as a guest. If you already have an account, log in to access the content to which you are entitled.





Share Options


Share the article link

Share with email

Share on social media