DETRAINING IN RELATION TO SKELETAL MUSCLE

Detraining is partial or complete loss of training, physiological & performance adaptations as a consequence of training reductions or cessation.

1. DETRAINING IN RELATION TO SKELETAL MUSCLE

2. Detraining is partial or complete loss of training, physiological & performance adaptations as a consequence of training reductions or cessation. Throughout their careers, athletes of all sports will go through different periods of detraining, either during holiday periods or caused by injuries, which, although undesirable, are part of the athlete's life.

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4. Muscular atrophy due to injury Atrophy is characterized by the decrease or loss of total muscle mass or a set of muscle fibers. The most widely accepted cause of muscle atrophy today is t he inhibition of protein synthesis . The period of inactivity, which can include an added period of immobilization of the affected area, will mark the degree of muscular atrophy produced.

5. Structure of skeletal muscle

6. We must also consider that the process of atrophy can be increased by nutritional, neuro-muscular and gravitational components, and protein synthesis hormonal levels, among others.

7. Some studies about muscle atrophy Mujika and Padilla (2000a) establishes that periods of detraining not exceeding two weeks do not cause any change in the distribution of muscle fibers, neither in long distance runners, nor in athletes who base their performance on the application of strength. Decreases in the fibrillar cross-sectional area can be seen in soccer players and weight lifters, especially because there is a decrease in the area of FT-type fibers. There is tendency for the muscular cross-sectional area to decrease after short periods of detraining, although muscular strength, in the set of studies that these authors reviewed (Mujika and Padilla, 2000a), did not seem to be affected. According to a study by Wang and Pessin (2013) in general FT fibers are more vulnerable to a period of inactivity than ST oxidative fibers. Some fibrillar conversion from FTa fibers to FTb fibers has also been observed in long-distance runners and cyclists (Mujika and Padilla, 2000b).

8. Some studies about muscle atrophy In people who suffer a prolonged period of inactivity (due to injury or illness), during the first weeks of absolute rest, the anti-gravitational muscle groups and the extensor chain are affected first (Boonyarom and Inui, 2006), which is important to take into account when scheduling training aimed at mitigating the atrophy process, or even preventing it as much as possible when the situation allows. The initial period of inactivity does not result in a change in the fibrillar distribution of the muscle, although, within the first eight weeks of inactivity, the so-called oxidative fibers decrease in endurance athletes and increase in strength athletes. On the other hand, the muscle cross section decreases rapidly in strength athletes and sprinters, as well as in endurance-trained novices, while it may increase slightly in well-trained endurance athletes (Mujika and Padilla, 2001).

9. Training method used prior injury It has been observed that in highly trained athletes in period of injury (immobilization), the eccentric strength and specific power of the sport can decrease significantly. The above figure shows a combination of eccentric and concentric work, necessary to limit the atrophy processes caused by an injury. It is important for the athlete to maintain optimal levels of strength, not only with the intention of having optimal performance, but also to preserve as much musculature as possible in case of injury.

10. Older people atrophy Gao, Arfat, Wang and Goswami (2018) explain how the literature is quite clear in stating that older people suffer more significant losses of muscle mass from inactivity compared to younger subjects. It is recorded that both the production of dynamic contractile strength and maximum isometric strength decrease in greater proportion in elderly subjects compared to younger subjects after two weeks of inactivity (Hvid et al. in Gao, Arfat, Wang and Goswami, 2018). It is important to note that these differences correlate with the existing process in older people of age-associated muscle atrophy (concept of sarcopenia).

11. De-adaptation of the contractile component: the muscle The work of Boonyarom and Inui (2006) explains that the process of atrophy is established in the first weeks after hospitalization. This process, in subsequent weeks, causes not only an alteration in muscle function, but also morphological changes such as a reduction in muscle mass, a reduction in the diameter of muscle fibers and a reduction in the total number of muscle fibers. The effects of this process are mainly located in the extensor muscles in comparison to the non-antigravitational or flexor muscles, as mentioned above.

12. O xidative stress Skeletal muscle experiences a loss of muscle protein and strength during long periods of inactivity. Powers, Kavazis and DeRuisseau (2005) use the cell biology explanation of the factors that lead to muscle atrophy. It seems that oxidative stress plays a major role in the regulation of proteolytic pathways that lead to a decrease in muscle mass produced in a period of inactivity, and this is an important fact, even though we commented that the main cause of atrophy is the decrease in protein synthesis.

13. Effects of inactivity The figure shows how a long period of inactivity reduces titin levels, which leads to the formation of myofibrils with an altered structure of the sarcomere, both laterally and longitudinally, resulting in a decrease in muscle performance.

14. De-adaptation of the tendon The tendon, as discussed earlier in this course, is a connective tissue that is responsible for the transmission of mechanical energy from muscle to bone to allow movement. Lack of activity is also harmful to the tendinous part of the skeletal muscle. In this way, detraining caused by an injury will require (as much as possible) simultaneous and subsequent planning of the therapeutic and readaptation process, since the lack of physical activity causes modifications that affect tenocytes, morphology and tendon metabolism (Prizziero et al., 2016).

15. Studies about tendon and inactivity The work of de Boer et al. (2007) was based on the hypothesis that the synthesis of collagen at both the myofibrillar level and the patellar tendon would decrease with inactivity over time. Narici and Maganaris (2007) explain how ultrasound studies show the negative effects of inactivity on the mechanical properties of the human tendon. The work of Reeves, Maganaris, Ferreti and Narici (2002) showed how 90 days of bed rest led to a 60% decrease in gastrocnemius tendon stiffness, a result seen through the slope of the strength-elongation ratio during an isometric plantar flexion. In other words, if the tendon, during inactivity, is kept in a relatively elongated position, the loss of its properties will be attenuated if compared to a tendon that maintains its position in shortening. The decrease in the mechanical properties of the tendon after long periods of bed rest (ninety days according to Reeves, Maganaris, Ferretti and Narici, 2005) lead to a 58% reduction in the stiffness of the Achilles tendon, as well as a decrease in Young's modulus of 57%.

16. Muscular hypertrophy Muscle hypertrophy is a term for the growth and increase of the size of muscle cells. The most common type of muscular hypertrophy occurs as a result of physical exercise such as weightlifting. When you start exercising a muscle there is first an increase in the nerve impulses that cause muscle contraction. This alone often results in strength gains without any noticeable change in muscle size. As you continue to exercise, there is a complex interaction of nervous system responses that result in an increase in protein synthesis over months and the muscle cells begin to grow larger and stronger.

17. Muscular hypertrophy capacity Wilmore and Costill (1998) define hypertrophy as increasing the size of the musculature, with the aim of increasing strength capacity. The muscle might increase in size, as a result of the growth in the number of myofibrils and their respective increase in size. It should be noted that this hypertrophy effect not only occurs in the contractile area of the muscle, but also extends to the tendon and connective tissue of the musculoskeletal system (McDonagh and Davies, 1984, in Tous, 1999).

18. Studies related to hypertrophy capacity Mallinson and Murton (2013) observe that, if we want to make the most of protein synthesis, we must correctly distribute the volume and intensity of exercise to be done, within the design of recovery programs following a period of inactivity. Individuals who perform various strength training series develop an intensity of 70% of 1RM (maximum exercise strength, or ability to perform a maximum repetition) in a knee extension exercise, achieving a significant increase in protein synthesis 5 hours after the exercise, which remains heightened for the next 24 hours. It is important to consider high volumes of exercise with some intensity, in order to achieve the desired adaptations of hypertrophy.

19. Studies related to hypertrophy capacity During rehabilitation processes, exercise-induced myogenesis is partly responsible for skeletal muscle recovery, and we have already explained that exercise results in rapid and sustained myostatin suppression. This is important to produce an increase in muscle mass, in conjunction with the existence of myogenic proteins (Marimuthu, Murton and Greenhaff, 2011). In rehabilitation processes, it is essential to preserve the continuity of the stimuli activated through exercise, in order to maintain a high rate of myogenesis and thus recover muscle mass. This continuity of exercise, with the appropriate intensity and volume, results in the activation of satellite cells, which assist in the enhancement of skeletal muscle in the recovery process.

20. Studies related to hypertrophy capacity Such cells can be important in increasing muscle volume, but it is important to highlight the assistance they can provide by migrating to the area of injury when activated (Marimuthu, Murton and Greenhaff, 2011). These authors highlight eccentric exercise, under normal circumstances, as the type of activity that best causes the proliferation of satellite cells, compared to concentric exercise. We must also keep in mind that eccentric actions, to which the muscle is less accustomed, trigger a greater disruption of sarcomeres, followed by a response to the subsequent inflammation and an expected regenerative effect.

21. Studies related to hypertrophy capacity Rennie (2007) explains the sharp increase in post-exercise protein reduction. This occurrence highlights the importance of eating food high in carbohydrates and proteins after exercise, in order to facilitate protein synthesis. Mallison and Murton (2013) also note that the measure to be developed to counter the process of atrophy must be based on ideal exercise and a suitable. Both measures should aim to enhance the increase in protein synthesis. In terms of muscular atrophy that is caused by inactivity, it is important to note that exercise not only stimulates protein synthesis in the contractile zone, but it also has an effect on the tendon (Rennie, 2007).

22. The possibility of muscular hyperplasia Hyperplasia is defined as the growth of new muscle fibers. Hyperplasia is different from hypertrophy in that the adaptive cell change in hypertrophy is an increase in the size of cells , whereas hyperplasia involves an increase in the number of cells. Dankel, Kang, Abe and Loenneke (2019) based on the existing bibliography, and among these the often referenced work of McCall, et al. (1996), explains that this is a very rare phenomenon in humans.

23. DETRAINING IN RELATION TO SKELETAL MUSCLE