Post by John A. Casler on May 23, 2009 8:38:59 GMT -8
This is from Jamie Carruthers as posted to SuperTraining
To visit SUPERTRAINING FORUM
health.groups.yahoo.com/group/Supertraining/?yguid=44276758
The signaling underlying FITness1
Keith Baar
High load leads to muscle hypertrophy and
increased strength
article.pubs.nrc-cnrc.gc.ca/ppv/RPViewDoc?issn=1715-5312&volume=34&issue=3&startPage=411
With regard to understanding what drives the endurance or strength response, the stimulus for the strength adaptation is better understood. In 1988, Wong and Booth (1988) performed the definitive experiment, showing that load on the muscle was the primary determinant of muscle growth. In this study, they used field stimulation to maximally excite all of the muscles of the distal hindlimb of rats. By using field stimulation, they guaranteed that all of the muscles received the exact same electrical stimulus; therefore, the metabolic stress and the flux of calcium were identical. Since the muscle mass is greater in the plantar flexors than in the dorsi flexors, when all of the muscles were maximally
stimulated, the foot plantar flexed. During the plantar flexion, the dorsi flexors underwent lengthening contractions (at a force greater than maximal isometric force (Po)), while the plantar flexors shortened (at a force less than Po). One set of animals performed the exercise without external weights, while another group performed the training against resistance that increased the force on the plantar flexors (close to Po). The weight was progressively increased over the 10 weeks of training to keep the plantar flexors close to Po. The results of the study are summarized in Fig. 1. Briefly, in both the unweighted and weighted groups, the tibialis anterior muscle (a dorsi flexor) hypertrophied ~17% over the 10-week training period. This occurred because the lengthening muscles were always under the same load (that produced by the plantar flexors). In the plantar flexors, the results were very different. The gastrocnemius, soleus, and plantaris muscles (the plantar flexors)
hypertrophied only when an external weight was used, even though the electrical stimulation was exactly the same. This experiment clearly shows that if all the other parameters are equal, increasing the load on a muscle causes muscle hypertrophy. While the work of Wong and Booth (1988) showed that high active forces were required to increase muscle mass and strength, a number of experimental models have shown that passive stretch may be enough to drive muscle growth.
However, the experimental models that show that passive stretch stimulates muscle hypertrophy have either used developmentally immature muscle cell culture models or in situ stretch (Vandenburgh and Kaufman 1979, 1982; Vandenburgh et al. 1989; Hornberger et al. 2006). Developmentally immature muscle and muscle cells in culture release calcium from the sarcoplasmic reticulum when they are stretched (Mutungi et al. 2003), which means that in vitro stretch results in release of calcium and contraction. As a result, stretch in tissue culture will increase active force within the myotubes. For in situ stretch models, these systems apply a 15% stretch to isolated muscles using servo motors (Hornberger et al. 2006). While a 15% stretch across a muscle tendon unit in vivo is within physiological limits, stretch in vivo is much different. In vivo, the majority of this stretch would occur within the tendons, not the muscle fibers themselves. Even when a muscle is undergoing lengthening
contractions, muscle fibers are not actually stretched (Griffiths 1991). Instead, during a lengthening contraction, the tendon lengthens while the muscle fibers contract isometrically. In the in situ models of passive lengthening, applying the 15% stretch in the absence of functional tendons means that the stretch across the muscle fibers is significantly greater than would occur in vivo. Interestingly, when in vivo passive stretch is performed using intact tendons, the same signaling pathways are not activated (Lockhart et al. 2006), suggesting that extreme passive stretch is required to produce the same effects as high-load active contractions.
High-load active contractions have been used extensively to study the cellular and molecular response to resistance exercise. What is clear from these studies, and is supported by studies in human subjects, is that the activation of protein synthesis is the primary response to high-load muscle contractions (Wong and Booth 1990a, 1990b; Chesley et al.
1992; Phillips et al. 1997; Tipton et al. 1999). The rate of protein synthesis is, in turn, controlled by a series of phosphorylation events, which are governed by the mammalian target of rapamycin complex (mTORC) 1. As would be expected, there is a direct relationship between the load on the muscle, muscle hypertrophy, and the activation of mTORC1 (Baar and Esser 1999; Terzis et al. 2008). Therefore, exercise against a high load with low metabolic stress results in the activation of mTORC1, through a currently unknown mechanism. When the resistance exercise is repeated at a sufficient frequency to allow optimal immune response (Novak et al. 2009) and recovery, the result is muscle hypertrophy and an increase in muscle strength.
While confusion over the exact mechanisms still exist, it is
becoming clear how different types of exercise signal different
cellular responses. This is most clear for resistance training,
where high loads are required for the activation of
mTORC1 and muscle hypertrophy. While the endurance response
remains harder to define because overlapping signaling
pathways are used, metabolic stress and calcium likely
are the primary determinants of this response. In highintensity
endurance exercise, the load is likely too small
and the metabolic cost too high to activate the strength response,
allowing the endurance paradigm to predominate.
========================
Jamie Carruthers
Wakefield, UK
To visit SUPERTRAINING FORUM
health.groups.yahoo.com/group/Supertraining/?yguid=44276758
The signaling underlying FITness1
Keith Baar
High load leads to muscle hypertrophy and
increased strength
article.pubs.nrc-cnrc.gc.ca/ppv/RPViewDoc?issn=1715-5312&volume=34&issue=3&startPage=411
With regard to understanding what drives the endurance or strength response, the stimulus for the strength adaptation is better understood. In 1988, Wong and Booth (1988) performed the definitive experiment, showing that load on the muscle was the primary determinant of muscle growth. In this study, they used field stimulation to maximally excite all of the muscles of the distal hindlimb of rats. By using field stimulation, they guaranteed that all of the muscles received the exact same electrical stimulus; therefore, the metabolic stress and the flux of calcium were identical. Since the muscle mass is greater in the plantar flexors than in the dorsi flexors, when all of the muscles were maximally
stimulated, the foot plantar flexed. During the plantar flexion, the dorsi flexors underwent lengthening contractions (at a force greater than maximal isometric force (Po)), while the plantar flexors shortened (at a force less than Po). One set of animals performed the exercise without external weights, while another group performed the training against resistance that increased the force on the plantar flexors (close to Po). The weight was progressively increased over the 10 weeks of training to keep the plantar flexors close to Po. The results of the study are summarized in Fig. 1. Briefly, in both the unweighted and weighted groups, the tibialis anterior muscle (a dorsi flexor) hypertrophied ~17% over the 10-week training period. This occurred because the lengthening muscles were always under the same load (that produced by the plantar flexors). In the plantar flexors, the results were very different. The gastrocnemius, soleus, and plantaris muscles (the plantar flexors)
hypertrophied only when an external weight was used, even though the electrical stimulation was exactly the same. This experiment clearly shows that if all the other parameters are equal, increasing the load on a muscle causes muscle hypertrophy. While the work of Wong and Booth (1988) showed that high active forces were required to increase muscle mass and strength, a number of experimental models have shown that passive stretch may be enough to drive muscle growth.
However, the experimental models that show that passive stretch stimulates muscle hypertrophy have either used developmentally immature muscle cell culture models or in situ stretch (Vandenburgh and Kaufman 1979, 1982; Vandenburgh et al. 1989; Hornberger et al. 2006). Developmentally immature muscle and muscle cells in culture release calcium from the sarcoplasmic reticulum when they are stretched (Mutungi et al. 2003), which means that in vitro stretch results in release of calcium and contraction. As a result, stretch in tissue culture will increase active force within the myotubes. For in situ stretch models, these systems apply a 15% stretch to isolated muscles using servo motors (Hornberger et al. 2006). While a 15% stretch across a muscle tendon unit in vivo is within physiological limits, stretch in vivo is much different. In vivo, the majority of this stretch would occur within the tendons, not the muscle fibers themselves. Even when a muscle is undergoing lengthening
contractions, muscle fibers are not actually stretched (Griffiths 1991). Instead, during a lengthening contraction, the tendon lengthens while the muscle fibers contract isometrically. In the in situ models of passive lengthening, applying the 15% stretch in the absence of functional tendons means that the stretch across the muscle fibers is significantly greater than would occur in vivo. Interestingly, when in vivo passive stretch is performed using intact tendons, the same signaling pathways are not activated (Lockhart et al. 2006), suggesting that extreme passive stretch is required to produce the same effects as high-load active contractions.
High-load active contractions have been used extensively to study the cellular and molecular response to resistance exercise. What is clear from these studies, and is supported by studies in human subjects, is that the activation of protein synthesis is the primary response to high-load muscle contractions (Wong and Booth 1990a, 1990b; Chesley et al.
1992; Phillips et al. 1997; Tipton et al. 1999). The rate of protein synthesis is, in turn, controlled by a series of phosphorylation events, which are governed by the mammalian target of rapamycin complex (mTORC) 1. As would be expected, there is a direct relationship between the load on the muscle, muscle hypertrophy, and the activation of mTORC1 (Baar and Esser 1999; Terzis et al. 2008). Therefore, exercise against a high load with low metabolic stress results in the activation of mTORC1, through a currently unknown mechanism. When the resistance exercise is repeated at a sufficient frequency to allow optimal immune response (Novak et al. 2009) and recovery, the result is muscle hypertrophy and an increase in muscle strength.
While confusion over the exact mechanisms still exist, it is
becoming clear how different types of exercise signal different
cellular responses. This is most clear for resistance training,
where high loads are required for the activation of
mTORC1 and muscle hypertrophy. While the endurance response
remains harder to define because overlapping signaling
pathways are used, metabolic stress and calcium likely
are the primary determinants of this response. In highintensity
endurance exercise, the load is likely too small
and the metabolic cost too high to activate the strength response,
allowing the endurance paradigm to predominate.
========================
Jamie Carruthers
Wakefield, UK