Physiological Changes in Skeletal Muscle as a Result of Strength Training

Abstract

The picture of training that emerges is of a process that can be divided into a number of phases. In the first phase there is a rapid improvement in the ability to perform the training exercise such as lifting weights which is the result of a learning process in which the correct sequence of muscle contractions is laid down as a motor pattern in the central nervous system. This phase is associated with little or no increase in the size or strength of individual muscles. The learning process appears to be very specific in that lifting weights makes better weight lifters but not better sprinters. The second phase is an increase in the strength of individual muscles which occurs without a matching increase in the anatomical cross‐section. The mechanism for this is not clear but could be a result of increased neural activation or some change in the fibre arrangement or connective tissue content. The third phase starts at a point where scientific studies usually end, at about 12 weeks when non‐athletic subjects are beginning to tire of the repeated training and testing. After this point, if training continues, there is probably a slow but steady increase in both size and strength of the exercised muscles. The stimulus for these changes remains enigmatic but almost certainly involves high forces in the muscle, probably to induce some form of damage that promotes division of satellite cells and their incorporation into existing muscle fibres. Our information on the effect of long‐term training comes primarily from observations on elite athletes whose physique may well be the result of genetic endowment or the use or abuse of drugs. For the athlete or patient hoping to increase muscle size by weight training the best combination of intensity, frequency and type of exercise still remains a matter of individual choice rather than a scientific certainty.

Changes in agonist neural drive, hypertrophy and pre-training strength all contribute to the individual strength gains after resistance training

“…The increased QEMG MVT amplitude following training in the current study was likely a result of increased motor unit firing rate (Kamen and Knight 2004;Knight and Kamen 2008). It is also possible that recruitment of additional motor units (Jones et al 1989;Folland and Williams 2007) and/or increased motor unit synchronization (Milner-Brown et al 1975;Semmler and Nordstrom 1998) could also enhance EMG amplitude, although it is unclear if the later can contribute to an increase in contractile force (Lind and Petrofsky 1978). The observation of agonist activation being the largest contributor to the strength changes after RT (30.6% of the total variance explained) is consistent with the apparently much larger cohort level changes in agonist activation (+29.1%) than muscle hypertrophy (+5.6%) in the current investigation.…”

Changes in paraspinal muscles and their association with low back pain and spinal degeneration: CT study

“…Several studies evaluated the association between CT-evaluated paraspinal muscles density and LBP [14,15,19,28,29,34,40]. Muscle density is an expression of degeneration of the muscles and reflects the number of muscle fibers, the area of the individual muscle fiber, and the packing of the contractile material [22], whereas the CSA is mainly determined by the total number of muscle fibers, to a lesser degree, the size of the fibers [35,36], and the quantity of fat in the muscle [6,9]. Laasonen [34] more than two decades ago described the decrease in CT-evaluated density of sacrospinal muscles after spinal surgery.…”

Polymorphisms in PTK2 are associated with skeletal muscle specific force: an independent replication study

“…Although it remains unclear how an increased costamere density corresponds to an increase in specific force, it could be achieved via enhanced lateral transmission of force (Jones et al 1989;Street 1983). An increased costamere density is likely to result in more intermediate connections between the ECM, myofibres and aponeurosis, effectively splitting serial sarcomeres into numerous force-generating units whilst also reducing functional muscle fibre length (Jones et al 1989).…”

“…Thus, a pathway of force transmission exists by which force can be transmitted laterally across adjacent myofibres and the sarcolemma to the extracellular matrix (ECM) (Flück et al 1999;Patel and Lieber 1997;Bloch and GonzalezSerratos 2003), via these regular connections. Given the location of costameres, they could effectively split the serial sarcomeres of a myofibre into multiple force-generating units to enable this pathway of force transmission to the muscle fascia, although this hypothesis is speculative (Jones et al 1989;Huijing 1999). Costamere formation and turnover is regulated by FAK activity, which is known to increase in hypertrophying muscle (Flück et al 1999).…”