Muscle Hypertrophy & Applications to RT

Muscle Hypertrophy & Applications to RT

1. 'Simple' Definitions

   • Muscle Hypertrophy
     • The enlargement of contractile elements of muscle, with corresponding extracellular matrix expansion (Vierck et al., 2000)
       • Vierck, J, O'Reilly, B, Hossner, K, Antonio, J, Byrne, K, Bucci, L, and Dodson, M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 24: 263-272, 2000.
       • Generally an adaptive process targeted by resistance training, resulting from 'microtears' & subsequent repair
         • Many factors mediate the hypertrophic process
       • Can occur either in series or parallel to direction of fibres - though most are in parallel (Paul & Rosenthal, 2002)
         • Paul, AC and Rosenthal, N. Different modes of hypertrophy in skeletal muscle fibers. J Cell Biol 18: 156: 751-760, 2002.
         • Increase in series leads to shortening of sarcomere length - commonly seen when a muscle is immobilised for extended periods at long lengths (Toigo and Boutellier, 2006)
           • Toigo, M and Boutellier, U. New fundamental resistance exercise determinants of molecular and cellular muscle adaptations. Eur J Appl Physiol 97: 643-663, 2006.
           • Animal studies have demonstrated this in training, where repeated eccentric-only loading led to increased number of sarcomeres in series (Lynn and Morgan, 1994)
             • Lynn, R and Morgan, DL. Decline running produces more sarcomeres in rat vastus intermedius muscle fibers than does incline running. J Appl Physiol 77: 1439-1444, 1994.
     • When muscle has overload stimulus, a chain of events is set off which ultimately increases size & number of actin-myosin filaments
   • Muscle Hyperplasia
     • The increase in total muscle fibre count within a muscle
       • Evidence that this occurs in humans has generally come from erroneous data, and it is unlikely to occur beyond the embryonic phase of development
         • Kelley, G. Mechanical overload and skeletal muscle fiber hyperplasia: A meta-analysis. J Appl Physiol 81: 1584-1588, 1996. Paul, AC and Rosenthal, N. Different modes of hypertrophy in skeletal muscle fibers. J Cell Biol 18: 156: 751-760, 2002.

2. Why do we want hypertrophy?

   • For health - numerous reasons not central to performance discussion but still highly useful
   • For Performance
     • Muscle CSA is strongly correlated to strength (Maughan, Watson & Weir, 1983)
       • Maughan, RJ, Watson, JS, and Weir, J. Strength and cross-sectional area of human skeletal muscle. J Physiol 338: 37-49, 1983.
       • Greater fibre size allows for a greater number of cross bridges to form, which can generate greater mechanical tension
         • This generally improves performance in sporting actions, allowing us to lift heavier loads and generate greater forces - when combined with rapid rate of cross bridge cycling, this can lead to improved power and velocity

3. Training for hypertrophy

   • General observations
     • Timescale:
       • Within untrained subjects, hypertrophy is generally not observed in the first weeks of training - with neural adaptations much more rapid - contributing to 'beginner strength gains'. Hypertrophy is generally delayed by several weeks/months (Mulligan et al., 1996). The Upper body tends to experience hypertrophy before the lower body (Tesch, 1988)
         • Mulligan, SE, Fleck, SJ, Gordon, SE, and Koziris, LP. Influence of resistance exercise volume on serum growth hormone and cortisol concentrations in women. J Strength Cond Res 10: 256-262, 1996. Tesch, PA. Skeletal muscle adaptations consequent to long-term heavy resistance exercise. Med Sci Sport Exerc 20(5 Suppl.): S132-S134, 1988.
     • Specificity
       • The principle of specificity dictates that some routines should be superior to others, (Bickel et al., 2005) though many varied routines have been shown to be highly effective. This debate mostly revolves around what the 'most effective' and efficient method is.
         • Bickel, CS, Slade, J, Mahoney, E, Haddad, F, Dudley, GA, and Adams, GR. Time course of molecular responses of human skeletal muscle to acute bouts of resistance exercise. J Appl Physiol 98: 482-488, 2005.
     • Large interindividual variation
       • There are many factors which mediate the hypertrophy response to resistance training - including age, ethnicity, gender etc... This will likely lead to a vast array of 'optimisations' for different populations

4. Repeated eccentric-only contractions could lead to hypertrophy in series

   • Rat study using either incline or decline treadmill running, demonstrated shorter sarcomere length post-intervention (Lynn & Morgan, 1994)
     • Lynn, R and Morgan, DL. Decline running produces more sarcomeres in rat vastus intermedius muscle fibers than does incline running. J Appl Physiol 77: 1439-1444, 1994.
     • Shorter sarcomere lengths shifts force-velocity relationship, allowing for greater force production at greater contraction velocity
       • Sarcomere contractile filaments are able to generate more force with slower cycling (or when isometric) than when rapidly cycling - similar to pedaling on a bike, spinning too fast generates little acceleration
         • Sarcomere contraction speed sums throughout the muscle length however, so by having more, shorter sarcomeres in series, we can increase force output at higher muscle contraction velocities

5. The internal physiology of Hypertrophy

   • Satellite Cells
     • A group of myogenic stem cells - residing between the basal lamina and sarcolemma - which become active when sufficient mechanical stimulus is imposed upon skeletal muscle (Vierck et al., 2000). Their activity is thought to mediate hypertrophy (Rosenblatt et al., 1994)
       • Vierck, J, O'Reilly, B, Hossner, K, Antonio, J, Byrne, K, Bucci, L, and Dodson, M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 24: 263-272, 2000. Rosenblatt, JD, Yong, D, and Parry, DJ. Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Mus Nerve 17: 608-613, 1994.
       • Once active, satellite cells proliferate and fuse to existing cells to create new myofibers, providing the precursor needed for repair and growth of new muscle tissue (Vierck et al., 2000; Toigo and Boutellier, 2006)
         • Vierck, J, O'Reilly, B, Hossner, K, Antonio, J, Byrne, K, Bucci, L, and Dodson, M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 24: 263-272, 2000. Toigo, M and Boutellier, U. New fundamental resistance exercise determinants of molecular and cellular muscle adaptations. Eur J Appl Physiol 97: 643-663, 2006.
         • During hypertrophy, the muscle mass to nuclei ratio appears to remain constant - The concept of myonuclear domain proposes that the myonucleus regulates mRNA production for a finite sarcoplasmic volume - as such increase in volume must be accompanied by supply of myonuclei.
           • Satellite cells meet this need, donating extra nuclei from their proliferation - essentially acting as a pool of myonuclei to support muscle growth, by increasing ability of muscle to to synthesize new contractile proteins (Moss and Leblond, 1970; Barton-Davis et al., 1999)
             • Moss, FP and Leblond, CP. Satellite cells are the source of nuclei in muscles of growing rats. Anat Rec 170: 421-435, 1970. Barton-Davis, ER, Shoturma, DI, and Sweeney, HL. Contribution of satellite cells to IGF-I induced hypertrophy of skeletal muscle. Acta Physiol Scan 167: 301-305, 1999.
             • Satellite cells also coexpress a number of myogenic regulatory factors that aid in muscle repair, growth and regeneration (Cornelison and Wold, 1997)
               • Cornelison, DD and Wold, BJ. Single-cell analysis of regulatory gene expression in quiescent and activated mouse skeletal muscle satellite cells. Adv Dev Biol 15; 191: 270-283, 1997.
   • Myogenic Pathways
     • A series of signaling pathways which use molecular signaling to shift muscle protein balance from degradation to synthesis in response to mechano-stimulation
     • Mammalian Target of Rapamycin (mTOR)
       • While not fully understood, is though to act as a master anabolic network
         • When activated, Akt signals mTOR, which exerts downstream effects to promote hypertrophy (Nader, 2005; Toigo & Boutellier, 2006)
           • Nader, GA. Molecular determinants of skeletal muscle mass: Getting the “AKT” together. Int J Biochem Cell Biol 37: 1985-1996, 2005.
           • Rapamycin seems to prevent downstream actions which stimulate muscle protein synthesis (essentially it has catabolic effects) - mTOR acts specifically to block actions of rapamycin, stimulating hypertrophy
           • Nutritional interactions - MPS relies upon: 1. mechanical stimulation, 2. positive energy balance, 3. available amino acids
             • But there is evidence for a 'leucine trigger hypothesis', whereby leucine interacts with mTOR pathway to lower threshold needed. Leucine may also inhibit AMNPK phosphorylation (a negative upstream regulator of mTOR) - Leucine interaction may be specific to post-exercise though? (Phillips, 2014; Drummond & Rasmussen, 2016)
               • Milk has a near-optimal whey-casein ratio of 80/20 and is high in leucine (plus high calorie) so could be an optimal post-exercise recovery drink (choccy milk phenomenon)
     • Mitogen Activated Protein-Kinase (MAPK)
       • MAPK has been shown to modulate growth and differentiation via myocytes (Roux & Blenis, 2004)
         • Roux, PP and Blenis, J. ERK and p38 MAPK-activated protein kinases: A family of protein kinases with diverse biological functions. Microbiol Mol Biol Rev 68: 320-344, 2004.
         • JNK is most responsive to mechanical tension, particularly to eccentric exercise - leading to rapid rises in mRNA transcription for cell proliferation and repair (Aronson et al., 1998; 1997)
           • Aronson, D, Boppart, MD, Dufresne, SD, Fielding, RA, and Goodyear, LJ. Exercise stimulates c-Jun NH2 kinase activity and c-Jun transcriptional activity in human skeletal muscle. Biochem Biophys Res Comm 251: 106-110, 1998. Aronson, D, Dufresne, SD, and Goodyear, LJ. Contractile activity stimulates the c-Jun NH2-terminal kinase pathway in rat skeletal muscle. J Biol Chem 272: 25636-25640, 1997.
     • Calcium-dependent pathways
       • Skeletal muscle uses calcium as a messenger to respond to external stimuli. Elevated intracellular Ca activates Calcineurin, leading to expression of genes involved in growth, repair and remodeling of muscle tissue (Sakuma & Yamaguchi, 2010)
         • As a result, post-exercise elevations in intracellular calcium are generally considered to be anabolic
           • However...
             • Excessive/chronic elevations in Ca (where the mitochondria cannot sufficiently sequester 'leaked' Ca) can activate proteases, leading to apoptosis of muscle cells - animal studies demonstrate significant anti-inflammatory response after 6 week High reps, high force protocol (Hadrevi et al., 2019)
               • Calcium Fluxes in Work-Related Muscle Disorder: Implications from a Rat Model
               • BUT
                 • There are no studies directly linking training which brings about excessive/chronic intracellular Ca to impaired hypertrophy in humans, but evidence points to risk factors
                   • Essentially, calcium is a key hypertrophic messenger, but there is a fine balance - where high volume training could contribute to damage and impaired function
         • In addition, elevated intracellular Ca post-exercise can signal mTOR and MAPK pathways (ito et al., 2018)
           • ATP-Induced Increase in Intracellular Calcium Levels and Subsequent Activation of mTOR as Regulators of Skeletal Muscle Hypertrophy - PMC
   • Hormones and Cytokines
     • Both serve as upstream regulators of hypertrophic responses - many of which facilitate satellite cell binding to damaged fibers (Toigo and Boutellier, 2006; Vierck et al., 2000)
       • 187. Vierck, J, O'Reilly, B, Hossner, K, Antonio, J, Byrne, K, Bucci, L, and Dodson, M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 24: 263-272, 2000.
       • IL-5, IL-6, fibroblast growth factor, leukemia inhibitory factor promote anabolism
         • IL-6 - as a myokine
           • Skeletal muscle releases IL-6 in response to contractions (not muscle damage as previously thought - there are specific intramuscular effects, not just systemic inflammation), activating AMPK, enhancing glucose uptake and fat oxidation - with systemic effects on hepatic glucose production and adipose lipolysis
             • Increased insulin sensitivity - activates PI3K-Akt, increasing insulin sensitivity and stimulating GLUT4 translocation
               • Hypertrophic effects - promotes mTOR and satellite cell signaling and proliferation
                 • Interleukin‐6 myokine signaling in skeletal muscle: a double‐edged sword? Pura Muñoz‐Cánoves
                 • IL-5 - Indirect myokine role
                   • IL-5 partially recruit eosinophils - mice lacking eosinophils show impaired regeneration - suggesting that IL-5 has a role in muscle repair and regeneration
                     • Insulin? - May help to limit proteolysis - but not increase MPS
                       • These generally appear to be non-modifiable factors - only need to be considered in a detrimental light with poor fueling or significant overtraining and chronic inflammation
         • Insulin-like growth factor, testosterone and growth hormone as most closely linked with hypertrophic signalling
           • IGF-1 - a peptide hormone, whose receptors are found in satellite cells, adult myofibers and Schwann cells
             • Thought to provide the main anabolic response and shows enhanced effects in response to mechanical loading (IGF-1Ec in particular)
               • Muscle produces and utilises IGF-1 during exercise, with availability controlled by binding proteins
                 • Levels of IGF-1 remain elevated in muscle for up to 72 hours post-exercise (with derivative MGF particularly sensitive to muscle damage)
                   • IGF-1 both directly promotes anabolism through elevated myofiber MPS and indirectly through satellite cell activation & calcium channel gene expression (and calcium-dependent pathways)

6. Hypoxia

   • Hypoxia contributes to hypertrophy in absence of exercise - vascular occlusion can attenuate muscular atrophy in bed rest patients (Takarada et al.,)
     • Hypoxia may also have additive hypertrophy effects in lower intensity RT (~50% 1RM) - comparable to high intensity exercise gains
       • WHY? - And use of Blood Flow Restriction
         • Increased lactate accumulation and reduced clearance rate may increase swelling, upregulating MPS (Takarada et al., 2000)
           • 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.
           • ROS may promote (seen in cardiac & smooth) skeletal muscle hypertrophy (Takarada et al., 2000) (oxidative stress drives adaptation by causing repair response) - with ROS activity thought to increase in hypoxic training - ROS have been shown to mediate satellite cell proliferation (Kawada et al., 2005) and activate MAPK signaling post RT (Kefaloyianni et al., 2006)
             • 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. Kawada, S and Ishii, N. Skeletal muscle hypertrophy after chronic restriction of venous blood flow in rats. Med Sci Sport Exerc 37: 1144-1150, 2005. Kefaloyianni, E, Gaitanaki, C, and Beis, I. ERK1/2 and p38-MAPK signalling pathways, through MSK1, are involved in NF-kappaB transactivation during oxidative stress in skeletal myoblasts. Cell Signal 18: 2238-2251, 2006.
             • Reactive hyperemia (sudden restoration of blood flow, increasing shear forces) - may help to deliver anabolic endocrine agents and growth factors to damaged tissue activating anabolic pathways (Takarada et al., 2000; Vierck et al., 2000) - which is otherwise unable to bring this about through forceful contractions - highlighting usefulness in injury rehab
               •  Vierck, J, O'Reilly, B, Hossner, K, Antonio, J, Byrne, K, Bucci, L, and Dodson, M. Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 24: 263-272, 2000. 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.

7. Cell Swelling

   • Cell swelling can stimulate MPS and reduced proteolysis - though not entirely clear why
     • 1. Increased pressure against membrane is perceived as threat to cell integrity - signals reinforcement; 2. hydrated cells initiate processes such as protein-kinase signaling pathways
       • RT can induce changes in intra/extracellular water balance - maximised by glycolysis reliance & resulting lactate accumulation
         • Cell swelling may also be augmented by regimens leading to increased glycogen storage

8. Exercise-induced initiation of hypertrophy

   • Mechanical Tension
     • Produced by force generation and stretch - considered essential to muscle growth - a combination of each has additive effects (periods of unloading conversely cause atrophy)
       •  Vandenburgh, HH. Motion into mass: How does tension stimulate muscle growth? Med Sci Sport Exerc 19(5 Suppl.): S142–S149, 1987. Goldspink, G. Gene expression in skeletal muscle. Biochem Soc Trans 30: 285–290, 2002.
       • Process is controlled by MPS during protein translation
         • Tension associated with RT causes myofibrillar and satellite cell responses
           • Upstream signaling - growth factor, cytokines, stretch-activated channels
             • Downstream signaling - mTOR pathway (direct or indirect - phosphaditic acid)
       • Eccentric Contractions - passive tension augments active tension from contractile elements - enhancing hypertrophic response
         • HOWEVER - Passive tension effect is fiber-type specific - with only fast-twitch fibers seeing increased hypertrophy
           • Slow-twitch fibers exhibit lower passive tension in titin filaments than fast-twitch fibers (Prado et al., 2005)
             •  Prado, LG, Makarenko, I, Andresen, C, Kru¨ger, M, Opitz, CA, Linke, WA. Isoform diversity of giant proteins in relation to passive and active contractile properties of rabbit skeletal muscles. J Gen Physiol 126: 461–480, 2005.
             • Mechanical tension alone can produce hypertrophy - but is unlikely to be the sole mechanism, with many other implicated pathways
               • Evidence has even shown that routines with high degrees of mechanical tension may elicit primarily neural adaptations, not structural (Vissing et al., 2008)
                 • Vissing, K, Brink, M, Lønbro, S, Sørensen, H, Overgaard, K, Danborg, K, Mortensen, J, Elstrøm, O, Rosenhøj, N, Ringgaard, S, Andersen, JL, and Aagaard, P. Muscle adaptations to plyometric vs. resistance training in untrained young men. J Strength Cond Res 22: 1799–1810, 2008.
   • Muscle Damage
     • RT can cause localised damage, which in some circumstances can create a hypertrophic response
       • Evans, WJ. Effects of exercise on senescent muscle. Clin Orthopaed Rel Res 403(Suppl.): S211–S220, 2002.  Hill, M and Goldspink, G. Expression and splicing of the insulin like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage. J Physiol 549: 409–418, 2003.
       • Damage can be limited to a few filaments or to large tears in muscle tissue (sarcolemma, basal lamina, connective tissue etc.) - Any damage which significantly impairs following training will have an overall atrophy response however
         • The popping sarcomere dictates that the weakest part of the structure will be the first to rupture - as the weakest sarcomeres are not uniformly located in myofibrils, nonuniform lengthening causes shearing
           • T-tubules and membrane damage leads to calcium homeostasis and subserquent damage
             • Allen, DG, Whitehead, NP, and Yeung, EW. Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: Role of ionic changes. J Physiol 567: 723–735, 2005.
             • The following inflammatory response (neutrophil migration & signalling of macrophages & lymphocytes) removes cellular debris & produce cytokines which activate myoblasts
               • Resulting release of growth factors regulate satellite cell proliferation and differentiation, stimulating remodeling and hypertrophy
   • Metabolic Stress
     • There is a wide body of evidence supporting the role of exercise-induced metabolic stress (with disputed over whether this or high force is more important for hypertrophy)
       • Does not appear to be essential for muscle growth - but has significant additive effects
         • A result of anaerobic glycolysis for ATP production, with buildup of lactate, H ions, creatine etc. (BFR/ischemia can contribute to this)
           • Cell swelling, altered hormonal environment, oxidative stress all cited as drivers of hypertrophy - in addition to acidic environment increasing muscle damage & subsequent repair response

9. Modifiable Training Variables

   • Intensity (or load)
     • Massively important - dictates mechanical tension & plays directly into damage & metabolic stress
       • If we assume intensity as a % of 1RM, we can then equate it to the number of repetitions we carry out:
         • 1 - 5 reps: low rep range, can achieve higher relative intensity
           • 6 - 12 reps: moderate rep range
             • 15+ reps: high rep range
               • High rep ranges have proved inferior at causing hypertrophy - likely due to a lack of mechanical tension and muscle damage (and not sufficient to activate larger MUs) - though we can achieve high metabolic stress (1/3 key components)
                 • A load <65% 1RM is not enough to promote hypertrophy
                   • BUT - we can combine low load, high reps with BFR during injury to prevent the worst of atrophy we might experience
                     • Low vs Moderate Rep Ranges
                       • Both elicit significant gains in muscle bulk
                         • The case for moderate ranges
                           • Moderate repetitions rely heavily on anaerobic glycolysis - resulting in metabolite buildup and metabolic stress
                             • Robergs, RA, Ghiasvand, F, and Parker, D. Biochemistry of exercise induced metabolic acidosis. Am J Physiol. Reg Int Comp Physiol 287: R502-R516, 2003.
                             • Also maximises acute anabolic hormonal response of exercise (both testosterone & GH) beyond that seen in low rep ranges - increasing downstream regulation of muscle remodeling
                               • Häkkinen, K and Pakarinen, A. Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes.&nbsp;J Appl Physiol&nbsp;74: 882-887, 1993. Kraemer, WJ, Fleck, SJ, Dziados, JE, Harman, EA, Marchitelli, LJ, Gordon, SE, Mello, R, Frykman, PN, Koziris, LP, and Triplett, NT. Changes in hormonal concentrations after different heavy-resistance exercise protocols in women.&nbsp;J Appl Physiol&nbsp;75: 594-604, 1993. McCaulley, GO, McBride, JM, Cormie, P, Hudson, MB, Nuzzo, JL, Quindry, JC, and Travis Triplett, N. Acute hormonal and neuromuscular responses to hypertrophy, strength and power type resistance exercise.&nbsp;Eur J Appl Physiol&nbsp;105: 695-704, 2009.
                               • Moderate rep ranges also appear to create a 'pump'. Where arterial delivery is unaffected, but venous return is inhibited by compressed veins. This leads to a buildup of fluid into interstitial spaces, and increased cell swelling - altering downstream MPS regulation
                                 • Muscle Damage may be increased with moderate ranges due to increased time under tension. Microtrauma and metabolic stress are elevated, and there may be more fatigueability across a range of fiber types (slow-twitch are fatigue-resistant, so need more TUT for metabolic fatigue)
                                   • For hypertrophy, moderate rep ranges seem to be king: still reach sufficiently high tension; increase total time under tension; increased metabolic stress & resulting signaling; increased GH and testosterone levels post-exercise; increased metabolic stress of slow-twitch fibers; increased cell swelling (But still need to exceed 65% 1RM
                                   • In Summary:
               • Why High rep ranges are rubbish for hypertrophy
   • Volume
     • Higher volume, multi-set protocols have long been associated with increased hypertrophy for a multitude of reasons
       • E.g. testosterone is not significantly elevated until after the fourth set of squatting (Schwab et al., 1993)
         • Schwab, R, Johnson, GO, Housh, TJ, Kinder, JE, and Weir, JP. Acute effects of different intensities of weight lifting on serum testosterone.&nbsp;Med Sci Sport Exerc&nbsp;25: 1381-1385, 1993.
         • Smilios et al., - compared a 4x5 reps @88% 1RM & 4x 10 reps @75% 1RM protocol (tested GH post set 2 & 4). GH was significantly elevated between set 2 & 4 in 4x10 reps protocol alone. I.e. there is evidence that higher volume & metabolic stress is key to GH release
           • Smilios, I, Pilianidis, T, Karamouzis, M, and Tokmakidis, SP. Hormonal responses after various resistance exercise protocols.&nbsp;Med Sci Sport Exerc&nbsp;35: 644-654, 2003.
           • 'Overreaching' - achieved by increasing training volume or intensity over a short period (days or weeks?). Can lead to supercompensation, particularly if followed by prolonged rest. Can increase hypertrophy response, but minimal effect for moderate to highly trained athletes
             • Fry, AC. The role of resistance exercise intensity on muscle fibre adaptations.&nbsp;Sport Med&nbsp;34: 663-679, 2004.
             • Overtraining - has significant catabolic effects on muscle (especially with insufficient feeding). Characterised by chronic decreased testosterone & LH, and increased cortisol. Repetitive trauma to MSK system - particularly with excessive volume (Chronic Volume considerations - we need sufficient rest, feeding and recovery to adapt to load)
               • Häkkinen, K and Pakarinen, A. Serum hormones in male strength athletes during intensive short term strength training.&nbsp;Eur J Appl Physiol&nbsp;63: 191-199, 1991. Raastad, T, Glomsheller, T, Bjøro, T, and Hallén, J. Changes in human skeletal muscle contractility and hormone status during 2 weeks of heavy strength training.&nbsp;Eur J Appl Physiol&nbsp;84: 54-63, 2001. Häkkinen, KA, Pakarinen, A, Alen, M, Kauhanen, H, and Komi, PV. Relationships between training volume, physical performance capacity, and serum hormone concentrations during prolonged training in elite weight lifters.&nbsp;Int J Sport Med&nbsp;8(Suppl.): 61-65, 1987.
               • Within-session volume consideration: the longer a session lasts, the greater the loss of intensity of effort and motivation. We can even observe alterations in immune response. 1 hour cap may be suitable to maintain sufficient intensity throughout
                 • Kraemer, WJ, Gordon, SE, Fleck, SJ, Marchitelli, LJ, Mello, R, Dziados, JE, Friedl, K, Harman, E, Maresh, C, and Fry, AC. Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females.&nbsp;Int J Sport Med&nbsp;12: 228-235, 1991. Zatsiorsky, VM.&nbsp;Science and Practice of Strength Training. Champaign, IL: Human Kinetics, 1995.
   • Exercise Selection
     • There is potentially infinite nuance to exercise selection - with muscle architecture and innervation highly complex
       • E.g. during bench press - sternal head of pec major is more active in a decline then flat bench, and clavicular head (& triceps) more active in narrow grip than wide grip
         • Multi joint vs single joint exercises
           • Hormonal changes seem to respond to total active muscle mass - Multi joint movements produce larger post exercise increases in both testosterone & GH vs single joint
             • Multijoint exercises also incorporate synergists, stabilisers and fixators which might otherwise not be active - increasing workload of more target muscles & potentially hypertrophy response
               • BUT, this conflict may be disadvantageous. Competition for total nervous stimulus between prime movers & assisting muscle
                 • Single joint muscles may allow for targeted development of target muscles. Increased stability & points of contact may also increase ability to maximise force (use of unstable surfaces is not supported by literature on hypertrophy)
                   • Antonio, J. Nonuniform response of skeletal muscle to heavy resistance training: can bodybuilders induce regional muscle hypertrophy?&nbsp;J Strength Cond Res&nbsp;14: 102-113, 2000.
                   • Single joint exercises may also allow us to exploit muscle architecture & principles of movement - such as biceps brachii long & short head
                     • On the discussion of stability - unstable surfaces reduce peak force & rate of force development by 40-60%, in all muscle groups & multijoint movements, with the exception of some core muscle groups & exercises
                       • Anderson, KG and Behm, DG. Maintenance of EMG activity and loss of force output with instability.&nbsp;J Strength Cond Res&nbsp;18: 637-640, 2004. McBride JM, Cormie, P, and Deane, R. Isometric squat force output and muscle activity in stable and unstable conditions.&nbsp;J Strength Cond Res&nbsp;20: 915-918, 2006. Sternlicht, E, Rugg, S, Fujii, LL, Tomomitsu, KF, and Seki, MM. Electromyographic comparison of a stability ball crunch with a traditional crunch.&nbsp;J Strength Cond Res&nbsp;21: 506-509.

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