Benefits of RT

Benefits & Adaptations to Resistance Training

Benefits of Resistance Training

Neurological
Adaptations

Muscular

Adaptations

Endocrine Responses

The aim of this section is to provide the reader with relevant evidence from early pioneering research (experimental and theoretical) that has shaped our current understanding regarding the underlying mechanism for muscular strength. The effects RT program design has on the adaptational responses of the neurological, muscular and endocrine systems towards muscular strength development. Evidence suggests that careful manipulation of acute RT program variables has a significant effect on neural adaptations, signalling pathways and hormone responses that may influence protein synthesis and therefore gradual protein accretion leading to increased muscle strength and size. RT appears to influence T, GH, and IGF-1 with studies reporting an association with favourable outcomes related to muscle strength. Most research concerning RT conforms to maximising hormonal responses to promote muscular strength and hypertrophy.

Consequently, examining muscular strength responses to manipulated RT variables (daily and weekly set-volume, loading and frequency) is necessary. The optimal stress response should, therefore, be determined relative to the volume of sets, loading and frequency for specific muscle groups. In practice, this information will aid in designing time-efficient strategies for RT to maximise muscular strength while improving training consistency and training compliance.

Why do athletes and non-athletes resistance train

There are numerous benefits of performing resistance training, and individual’s train for different reasons including health and fitness-related goals. Most individuals engage in resistance training solely for recreational purposes where the overriding goals are to increase muscle size, improve endurance and to a lesser extent improve strength. Other individuals may have specific goals to enhance their muscular power, strength, size or endurance, whereas some engage in resistance training for rehabilitation. Rehabilitation suggests an individual has an injury or disease that has ensued which pose some physical constraint and now they engage in training to strengthen the weakened area. Furthermore, many individual’s perform prehabilitation where the primary goal is injury prevention ensuring muscles are balanced. Performance-based athletes engage in resistance training to increase athletic performance. During the competitive season, athletes engage in maintenance training, ensuring that off-season gains and adaptations are maintained as best as possible within the competition. The training modality shifts towards more sports specific conditioning, practice, and competition. This phase is temporary until the competitive season is concluded.

Maintenance training is not solely reserved for athletes and many non-athletes may participate in this training depending on their circumstances. Many non-athletes engage in resistance training to elicit positive health adaptations to their body (i.e. muscle, nerve, skeletal and cardiorespiratory systems). Finally, individuals do not have to explicitly need to train for one goal; rather, many individuals train with multiple goals. This is often referred to as integrative training where multiple goals are pursued for training purposes.

Benefits of resistance training

As indicated earlier there are numerous health and performance benefits of resistance training (Table 1). Several studies have demonstrated the positive effects resistance training has on improving multiple aspects of an individuals health and sporting performance. Collectively, these studies have been performed on a range of population groups ( clinical, older adults, children and athletes), and it has been suggested that resistance training is a safe and effective mode of exercise for most individuals. These ramifications are critical to enhancing the performance of activities of daily living and optimal athletic performance.

Table 1. Benefits of Resistance Training.

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Neurological adaptations to RT

Muscle adaptations to RT

Physiological Adaptations to Resistance Training

Resistance training has a profound effect on various biological systems. Careful manipulation of acute RT program variables by strength and conditioning coaches and exercise practitioners can therefore promote positive alterations in muscular strength and hypertrophy. Therefore, it is essential to overview the main physiology mechanisms and adaptational responses that occur due to the RT stimuli. The modification or alteration to any RT program variable provokes a different RT stress stimulus and can lead to an increase or decrease in muscular strength (Figure 1). Therefore, an overview of three areas will be examined, namely: (1) the neurological adaptations to RT; (2) muscle adaptations; and (3) the endocrine responses to RT.

Figure 1. Resistance training stress continuum and muscle adaptation. Within the parameters of training theory, three possible outcome pathways following resistance training stress.

Neurological adaptations to resistance training

Training for increased muscular strength not only affects muscle tissue but also results in changes in the central nervous system. Unfortunately, early evidence on neurological adaptations has been generated [in part] from indirect observations and inferences drawn from techniques that were applied to animal studies. However, evidence over the last 20-years suggests that neural adaptations result from alterations in coordination and learning that aid in improved recruitment and activation of muscles during RT. This evidence has transpired due to non-invasive methods that capture electrical and twitch responses of muscle.

Motor unit recruitment, rate coding, and synchronisation

Early observations on muscular strength reported that when performing a RT program, the muscle responds to the demands of increasing amounts of resistance lifted (Hellebrandt and Houtz, 1956). This increase in muscle strength results from the ability of the nervous system to recruit motor units (MU) involved in the activation of the muscle and the adaptations at the muscle fibre (Sale, 1988; Tesch, 1988). These alterations in the nervous system following RT have been referred to in scientific literature as neural adaptations (Sale, 1988). Studies have reported increases in strength with no or minimal changes in the cross-sectional area of the muscle (Moritani and deVries, 1979; Tesch, 1988).

Motor unit recruitment

Henneman and Olson (1965) developed the selective recruitment theory, which states that MU’s are composed of the same fibre types and are innervated by motor neurons with different thresholds for each fibre type. The MU is considered the functional unit of the muscle and consists of a motor cell, the axon and terminal branches and all the individual muscle fibres supplied by the axon (Freund, 1983). A skeletal muscle, together with the motor neurons controlling it, comprises several hundred MU of different sizes (Figure 2). A single motor unit can innervate a few to several hundred muscle fibres with each specific muscle containing ten to several hundred MU. For example, muscles involved in eye movement have an innervation ratio of 1:4 (the number of motor axons divided by the total number of muscle fibres). Large muscles that do not require the same degree of motor control have an innervation ratio as large as 1:300 (i.e. gastrocnemius muscle) (Garnett et al., 1979). The force output of a muscle is determined by the sum of the force outputs of the active MU (Senn et al., 1997). An increase in force production is, therefore, a result of the systematic activation of a greater number of MU being recruited and an increased frequency of activation (rate coding) (Figure 7)

Figure 2. Muscle innervation by the motor neurons. The ventral horn of the spinal cord contains motor neurons that innervate skeletal muscle fibres.

The size principle and the application to resistance training

The Henneman size principle (Figure 3) states that when the central nervous system recruits MU for a specific activity, it initiates smaller, easily excited MU’s and proceeds to the larger more difficult to excite MU’s (Henneman et al., 1974). This orderly recruitment of MU provides smooth graduation of force (Guyton, 1991). If the input to a pool of MU’s exceeds the excitation threshold of the motor neuron, the neuron will generate nerve impulses (action potential) to activate the innervated fibres (Guyton, 1991; Senn et al., 1997). Cope and Pinter (1995) specified that the motor neuron recruitment threshold is determined by the interaction between the strength and organisation of the synaptic inputs and motor neuron responses. Depending on the muscle, studies have suggested that maximal recruitment occurs between 30-to-90% of maximal voluntary contraction (Enoka and Fuglevand, 2001; DeLuca, Foley and Erim, 1996). Linnamo et al., (2003) reported that the threshold for maximal recruitment was higher in static compared to dynamic muscle actions. Most peer-reviewed evidence suggests that there are no functionally significant violations of the size principle (Cope and Pinter, 1995).

Figure 3. The size principle. Each circle denotes a motor unit made up of different types and numbers of fibres. The blue outlined circles are Type I motor units and the blue circles are Type II motor units, with larger circles depicting larger motor units containing more fibres. As one goes up the line of orderly recruitment, heavier and heavier resistances recruit more motor units and their associated muscle fibres.

Until recently, the body of scientific evidence on neurological adaptations was derived indirectly with varied techniques used to evaluate neural adaptations. However, recent technological advancements have more accurately defined the specific neural mechanisms contributing to RT induced increases in maximal strength. Folland and Williams (2007) stated that neural adaptations are positive alterations in coordination and learning that enable better MU recruitment and activation of the muscles involved during a specific strength task. This is apparent, particularly in the early stages of when untrained individuals perform strength training, as there are disproportionately larger increases in muscle strength than muscle size (Figure 4).

Figure 4. Neuromuscular interplay to resistance training stimulus over time.

However, there are several morphological and neurological factors that contribute to increased strength following RT. Typically, the increased size of an exercised muscle is regarded as the long-term adaptation, although this varies to the exposure to the training stimulus. The body of indirect evidence suggests substantial neurological adaptations may be due to learning and changes in the intermuscular co-ordination of agonist and antagonist interactions. During the early stages of RT, strength is associated with greater neural adaptations (within several weeks). This is in contrast with trained and elite individuals as the extent of the adaptations are within the muscles, promoting an increase in muscle mass (hypertrophy) (Figure 5).

Figure 5. Short-term to long-term neural and muscle adaptations to strength training.

Rate coding and synchronisation

As discussed previously, to activate and deactivate MU requires structured sequencing based on the size principle (Henneman et al., 1974). This sequence depends on the size of the MU with the smallest motor neurons recruited first and deactivated last, and MU with the largest motor neurons recruited last and deactivated first. According to Henneman and colleagues (1974), the order of MU recruitment is encoded by size and is not directly organised by the brain. The production of muscle force depends on the number of active MU and the rate at which the MU discharge action potentials. There are two kinds of rate coding with evidence suggesting that muscle force exerted during a voluntary contraction is dependent on the number of MU and the rates and frequency in which these MU discharge action potentials (Milner-Brown et al., 1973). These properties are known as recruitment and rate coding with early studies suggesting that recruitment is a more significant factor for low forces, whereas rate coding is more responsible for changes in muscle force at intermediate and high forces. Milner-Brown et al., (1973) introduced electromyography measurements that quantified MU synchronisation by measuring MU activity. This six-week resistance study indicated increased MU synchronisation in the first dorsal interosseous muscle of the hand. Milner-Brown, Stein and Lee (1975) performed a further cross-sectional study comparing weightlifters to a control group. Results from this study observed that all seven weightlifters showed a significant degree of synchronisation. Semmler and Nordstrom (1998) indicated that athletes possess greater MU synchronisation than untrained individuals with heavy RT, increasing synchronisation.

Muscle adaptations to resistance training

RT promotes structural and functional changes in the body as indirect observations made on the muscular size and strength of highly trained strength athletes. The magnitude of these muscular adaptations is directly proportional to the physical stress placed on the body (training volume, loading and frequency) and the recovery period necessary to produce favourable changes.

Muscle fibre types

Humans comprise varying percentages of muscle fibres, with fibre composition varying between muscles and individuals (Gollnick and Matoba, 1984). Several classifications have been used to distinguish different fibre types established from biochemical, histochemical, and physiological evidence (Morris, 1969; Morris, 1970; Peter et al., 1972; Sale et al., 1983). Early researchers developed physiological techniques that assessed the contractile properties of muscle and the speed at which fibres can generate peak tension (Table 2). Two fibre types (slow-twitch [ST] and fast-twitch [FT]) were identified (Morris, 1969). These fibres developed different tension characteristics with ST developing tension more slowly than FT fibres but were resistant to fatigue. Morris (1969) reported that ST fibres are recruited for the long term, low-intensity work and FT for a short duration, high-intensity work (i.e. resistance training).

Early studies on RT programs demonstrated that FT and ST fibre ratio increased and selective hypertrophy of individual fibres following heavy progressive loading and explosive jump training (Thorstensson et al., 1976; Häkkinen Alen and Komi, 1985). Thorstensson et al., (1976) examined the effects of progressive strength training on eight healthy male subjects (22-to-31 years) leg extensor muscles over eight weeks. Thorstensson and colleagues reported that no or minor alterations were observed in anthropometrics, muscle enzyme, and fibre composition. However, the muscle fibre ratio suggested a specific effect of ST on fast-twitch muscle fibres. Häkkinen and colleagues (1985) examined 11 male subjects performing 24-weeks of high-load ST. It was reported that subjects increased maximal isometric strength by 26.8%. The increases in strength correlated with significant increases in neural activation of the leg extensor muscles during an intensive period of training. Häkkinen et al., (1985) suggested that selective RT induced hypertrophy contributed to strength gain. Other researchers have also reported that heavy RT can influence hypertrophy on FT fibres, with Prince, Hikiia and Hagerman (1976) and Tesch et al., (1988) suggesting that weightlifting increases FT fibre area more than ST. Research suggests that resistance-trained athletes possess hypertrophied FT fibres, while endurance athletes have more hypertrophied ST fibres.

However, the development of staining techniques and electron microscopy measurements led to additional fibre classifications (Brooke and Kaiser, 1970; Burke et al., 1971). Researchers identified a third fibre type in addition to ST and FT fibres (Peter et al., 1972; Brooke and Kaiser, 1970; Burke et al., 1971). Rose and Rothstein (1982) combined the different classification schemes and described muscle fibres based on biochemical, histochemical, and physiological. The three muscle fibre types were reclassified:

Type I (slow oxidative, ST) fibres
Type IIA (fast oxidative glycolytic, FT-fatigue resistant) fibres
Type llB (fast glycolytic, FT-fast fatigable) fibres

Staron et al., (1984) applied this fibre type classification and performed a cross-sectional investigation on weightlifters, distance runners and sedentary individual’s fibre type ratios. The authors observed that weightlifters had a significantly larger type IIA area than the other two groups (distance runners [aerobically trained] and untrained [control] subjects).

Table 2. Overview of the evolution of identifying muscle fibre types.

Muscle fibre adaptations to resistance training

As detailed previously the progressive overload of the muscle produced by the RT (stress) stimuli has been shown to increase the cross-sectional area (CSA) of the muscle (Håggmark, Jansson and Svane, 1978; MacDougall et al., 1977; Young et al., 1983). The relationship between increased CSA and strength gain has been demonstrated frequently within the scientific literature. However, the debate continues as to whether the CSA of the muscle is a result of hypertrophy (increased fibre size) or hyperplasia (increased number of fibres) (Figure 6).

Figure 6. Hypertrophy versus hyperplasia.

Muscle hypertrophy

Muscle hypertrophy has been a frequently reported response to exposure to long-duration RT and is characterised by an increase in the individual muscle fibre diameter (Lüthi et al., 1986; Håggmark, Jansson and Svane, 1978; MacDougall et al., 1977; Young et al., 1983). Morpurgo (1887) first demonstrated that muscle fibres respond to an exercise stimulus by fibre enlargement without an increase in fibre number. Early studies performed pre-to-post strength measurements with subjects repeating strength testing to indirectly examine changes in measurable hypertrophy (Bowers, 1966; Coleman, 1969; deVries, 1968; Hellebrandt, Parrish and Houtz, 1947). Indirect evidence from dissection of rats suggested that the number of muscle fibres in skeletal muscle is permanent and that increases in muscle mass were the result of fibre hypertrophy not because of increased fibre number (Goldspink, 1970; Gollnick et al., 1981).

Evidence from human studies also supported the premise of changes to CSA because of RT. Delorme and Watkins (1948) proposed that increases in strength were due to motor learning and muscle hypertrophy. Moritani and deVries (1979) demonstrated that neural factors account for the greatest part of strength gains in the first three to five weeks in young untrained subjects. MacDougall et al., (1977) reported hypertrophy in human muscle after five months of RT. Håggmark, Jansson and Svane (1978) evaluated the CSA of weight lifters compared to sedentary subjects. Håggmark and colleagues observed that weightlifters had greater CSA compared to sedentary subjects, with the weightlifters having an increase in the size of the individual muscle fibre. MacDougall et al., (1984) examined the CSA of professional bodybuilders, intermediate bodybuilders and sedentary subject’s bicep brachii muscles. Using computerised tomography and muscle biopsy techniques, MacDougall and colleagues observed significantly greater CSA in both bodybuilding groups compared to sedentary subjects. However, no significant differences were reported between all three groups in the number of muscle fibres. The authors concluded that heavy RT increased the CSA of the muscle fibre and not the increased muscle fibre numbers. Longitudinal evidence by Lüthi et al., (1986) reported an 8.4% increase in CSA of the vastus lateralis muscle in humans after six weeks of heavy resistance training.

Muscle hyperplasia

Early RT research theorised that heavy RT might produce muscle fibre splitting (hyperplasia) in humans (Fleck, Deschenes and Kraemer, 1988). This hyperplasia hypothesis was supported by the observations made of longitudinal fibre splitting in the muscle fibres of rats (Edgerton, 1970), chickens (Sole and Christensen, 1984) and cats (Gonyea, Erickson and Bonde-Peterson, 1977; Gonyea and Erickson, 1980; Gonyea and Sale, 1983). The pioneering work of Gonyea and Erickson (1976) suggested that after maximal muscle hypertrophy was obtained additional strength development could only occur via the addition of new muscle fibres when existing muscle fibres are divided (Figure 6).

Additional research performed during the 1980s studied the existence of hyperplasia in humans through cross-sectional studies comparing the muscle strength of athletes and bodybuilders with inactive subjects (Larson and Tesch, 1986; MacDougall et al., 1984). Both Larson and Tesch (1986) studies reported that hyperplasia was more evident in bodybuilders than sedentary individuals. MacDougall et al., (1984) further reported that bodybuilders did not have more muscle fibres than untrained subjects. Evidence of human muscle hyperplasia following RT is sparse. Moreover, research produced from animal studies has been criticised due to methodological errors associated with fibre number estimations from histological sections (Gollick et al., 1981). Most researchers agree that increased CSA of muscles following long term RT is primarily a result of muscle hypertrophy (Lüthi et al., 1986; Håggmark, Jansson and Svane, 1978; MacDougall et al., 1977; Young, Stokes and Round, 1983).

Endocrine systems response to resistance training

The endocrine environment has an essential influence on acute and long-term adaptational responses to RT (Häkkinen, 1989; Kraemer and Ratamess, 2004) (Figure 7). The human endocrine system adapts to the repeated stimulus of RT by increasing or decreasing hormone secretion depending upon the acute resistance training variables (ACSM, 2009). This is achieved by increasing or decreasing the number of circulating proteins that bind the hormone and protect it from degradation while rendering it biologically inactive and changing the number of cellular hormone receptors.

Figure 7. Physiological and biochemical responses to resistance training in relation to muscular strength and hypertrophy.

The performance of RT stimulates anabolic hormonal responses, including Testosterone (T), Growth Hormone (GH) and Insulin Growth Factor one (IGF-1) but also a catabolic hormone (C) (ACSM, 2009). Stone et al., (1988) indicated that alteration to acute RT program variables dictates the extent of this hormonal response. Training protocols (high set volume, moderate to high resistance load and short inter-set recovery) that recruit large muscle groups (i.e. squats, deadlifts, bench press) appear to produce the greatest endocrine response (Stone et al., 1988). Additionally, Staron et al., (1994) reported that changes in fibre type are due to hormonal adaptations in previously untrained men. Researchers have also observed that changes in muscular strength and power in competitive Olympic weightlifters have been correlated to chronic hormonal adaptations (Häkkinen et al., 1987; Fry et al., 2000).

Testosterone

T is a male anabolic sex hormone that is secreted from the Leydig cells of the testes under hypothalamic and pituitary-gonadal axis control (Viru and Viru, 2005). The primary role of T in RT is to promote protein synthesis of contractile proteins involved in muscle tissue, resulting in increased muscle mass and strength (Kraemer et al., 1993). Exercise can acutely increase or decrease circulating T and is conditional on the mode and intensity of exercise (Schmid et al., 1982). Increases in circulating T increases during relatively short, high-intensity activities (i.e. resistance exercise), while the decline in T is associated with increased duration including marathons and other ultra-running events (Kuoppasalmi et al., 1980; Schurmeyer et al., 1984).

Ahtiainen et al., (2003) reported that T plays an important factor in strength development with a relationship between changes in isometric strength and T. Intriguingly, Ahtiainen and colleagues also indicated that subjects who exhibited acute increases in T after training had a CSA increase of muscle more than those with lower T. Spiering et al., (2008) reported that T causes an upregulation of androgen receptors with elevated muscle protein synthetic response for approximately 48-hours, although this period is reduced with training. The hormone response to RT has been frequently studied with the concept of endogenous T and androgen receptors interacting during the recovery period that stimulates protein synthesis, muscle hypertrophy and strength (Wilkinson et al., 2006; Crewther et al., 2009). This is further reinforced by Sinha-Hikim et al., (2002) who reported that when exogenous T (by supplementation) is combined with RT, significantly increases muscle mass and strength. However, a decrease in T may cause an increase in fat storage due to reduced fat oxidation, diminished resting energy expenditure, and increased adiposity (Zitzman and Nieschlag, 2003).

Growth Hormone

GH has been associated with the promotion of anabolism in both muscle and connective tissue. The anterior pituitary gland secretes GH polypeptides molecules from the acidophilic cells and enhances cellular amino acid uptake and protein synthesis in muscle, resulting in hypertrophy (Crist et al., 1991). The most frequently studied GH is the 22-kDa isoform molecule that consists of 191 amino acids with other isoforms functioning similarly in promoting tissue anabolism (Kimball, Farrell and Jefferson, 2002). Kraemer et al., (2017) suggest that a superfamily of different GH mediate biological actions during recovery to exercise stress and not merely the 22-kDa monomer. The GH receptor is abundant in various cells and tissues, and the understanding of recovery response patterns to RT is not fully understood (Kraemer et al., 2017). The release of GH in the blood during recovery involves a multitude of GH that aggregate during recovery (Hymer et al., 2001).

Florini, Ewton and Coolican (1996) suggested that concentrations of GH in the blood depend on the specific exercise stimuli. RT has been shown to acutely elevate many GH variants and promote muscle anabolism (Spiering et al., 2008). Kraemer et al., (1993) indicated that post-exercise GH levels are elevated 30-minutes’ post-RT. However, the magnitude of GH level depends on the amount of muscle mass recruited, volume, intensity and rest periods (Kraemer et al., 1991; Gotshalk et al., 1997; Smilios et al., 2003). GH appears to be highly influenced by the volume of the RT protocol. A further study by Kraemer et al., (2010) suggested that short inter-set recovery periods and RT stimulate higher concentrations of immunoreactive GH in both men and women. However, alterations to the recovery period and increased resistance loading resulted in significantly lower levels of immunoreactive GH (Kramer et al., 2010).

Insulin-Like Growth Factor-1

IGF-1 (originally termed somatomedin C) is produced in many tissues, primarily the liver and is secreted in response to GH-stimulated somatic growth, and as a mediator of GH-independent anabolic responses in many cells and tissues (Fry, Kraemer and Ramsey., 1998). RT has been shown to increase concentrations of circulating and muscle IGF-1, although several studies have reported no change (Chandler et al., 1994; Bamman et al., 2001). Studies suggest that RT changes the concentration of IGF binding proteins that affect the biological activity of IGH-1 (Bamman et al., 2001; Nindle et al., 2000). In response to mechanical overload initiated by RT, mechanogrowth factor stimulates satellite cell activation with IGF-1 increasing the proliferation and differentiation of satellite cells that aid in muscle hypertrophy (Hather et al., (1991).

Resistance training variables and the endocrine system

RT has been recognised as an effective method for strengthening muscles, connective tissue, and enhancing physical functioning associated with sporting performance. It is also acknowledged that these adaptive responses result from careful manipulation of acute training variables including load, volume, frequency, inter-set recovery, contraction velocity of movement, the range of motion, selection and order of exercise (ACSM, 2009). Altering the resistance volume and load affects several acute responses, including neural, hormonal, metabolic, and cardiovascular responses (Häkkinen, Alen and Komi, 1985; Ratamess et al., 2007).

Manipulation of acute RT program variables stimulates anabolic hormonal responses including T, GH, and IGF-1, but also C (ACSM 2009). Typical strength and hypertrophy protocols (high volume, moderate to high resistance loading and short inter-set recovery periods) have been reported to produce the greatest endocrine response (Stone et al., 1988). Schoenfeld (2010) has suggested that increased RT volume stimulates extensive metabolic stress and mechanical tension that produces greater metabolite accumulation, substrate depletion and muscle damage (Figure 7). These factors activate anabolic responses during the recovery phase that leads to adaptational responses (Helms et al., 2015).

Subsequently, controlling the RT volume and loading (altering the number of sets per exercise, the number of repetitions per set and the number of exercises per session) can affect metabolic and hormonal responses to RT (Borst et al., 2001; ACSM, 2009). For example, Willoughby et al., (1991) reported significantly greater GH and T responses with multiple sets compared to one-set programs. Borst et al., (2001) observed that long term RT that uses multiple sets per exercise is superior compared to single sets for strength development. However, it is unclear whether an RT dose-response exists between volume, loading, and RT adaptations. There have been reports of similar strength increases when two and four sets and two and three sets (Housh et al., 1992; Staron et al., 1994; Kraemer, 1997). In contrast, others have reported that three sets were superior to two sets for strength development (Berger, 1962; Ostrowski et al., 1997).

Over recent years there have been several reviews and meta-analyses have examined the effects of set-volume and resistance loading on muscular strength and hypertrophy. This has generated varied debate and opinions on the optimal RT required to produce optimal strength gains. The use of higher set volume has been promoted in recommendations (ACSM, 2009; NSCA, 2008), review (Wernborn et al., 2007) and several meta-analyses (Rhea et al., 2003; Peterson et al., 2004; Wolfe et al., 2004; Peterson et al., 2005; Krieger, 2009). Unfortunately, the association between endocrine signalling and androgen receptor expression is (partially) elusive regarding strength and hypertrophic responses (Schroeder et al., 2013). However, it is essential to appreciate the fundamental role the endocrine system plays in muscle regeneration and adaptational responses. Damas et al., (2016) reported that the increased magnitude of micro-damage to the muscles might be caused by either higher RT volume or loading, with myofibrillar synthesis associated with changes in muscle size. Equally, Ostrowski et al., (1997) reported that if RT volume is excessive, then it may limit optimal endocrine responses (T: C ratio). Ratamess and colleagues (2005) also observed that increased RT volume had been associated with a reduction in the number of androgen receptors, which may mediate muscular strength and hypertrophy development.

Endocrine system & RT