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Physicaltherapyscience.com- News - Effects of exercise on skeletal muscles and tendons

Effects of exercise on skeletal muscles and tendons

In this review from Minetto et al, the reactions of skeletal muscles and tendons to exercises were investigated and possible implications with regard to development of positive and negative effects associated with acute and chronic exercises such as muscle function changes, muscle pain and hypertrophy of muscles and tendons. The understanding of these effects is said to be essential to provide clinical recommendations for prescribing exercise in healthy and pathological individuals.

Acute muscle reaction to physical activity consists of microdisruption and disarrangement of myofibrils and cytoskeleton structures. This is a condition known as 'exercise-induced muscle damage'. This is mainly due to the execution of non-usual exercise. Its severity is modulated by training intensity, duration and, in particular, the type of muscle contraction. The greatest damage to muscle tissue is observed after eccentric (i.e., extension) muscle actions.

Muscle damage implies the extracellular outflow of myocellular proteins, the loss of skeletal muscle function (ie, strength and range of movement decreases) and the development of muscle pain that usually occurs a few days after the training period ('delayed muscle pain'). The physiological mechanisms that underlie muscle function loss and delayed muscle pain are thought to be different. Muscle function changes have a neural origin while muscle pain is caused by an inflammation reaction to intramuscular fluid and electrolyte shifts caused by microtrauma.
A number of indirect markers of muscle damage that are currently being extensively investigated are the muscle size and structure variables derived from ultrasound. In fact, it has been shown that edema-induced muscle swelling associated with muscle damage increases the variables of muscle size (ie, thickness and cross-section [CSA]), as well as the intensity of muscle echo and contrast correlation. However, it remains to be seen whether these increases can be useful in predicting the extent and/or duration of muscle damage.
The most interesting insights into the acute response of skeletal muscle to exercise were obtained through another indirect marker for muscle damage: the increased circulating levels of skeletal muscle proteins. Previous studies have shown that heavy muscle contractions cause CK to leak into interstitial fluid and increase its circulation level. The accumulation of serum CK in response to exercise has the following main characteristics: (I) exercise must exceed an intensity threshold to cause substantial increases in CK levels; (II) the CK level increases within a few hours after exercise and peaks 24 - 96 hours after exercise; (III) a more modest increase in CK values ​​after exercise often (but not always) indicates a less traumatic training session (although interpreting minimal variations in muscle proteins is a challenge); and (iv) individuals classified as "high responders" have a much higher rise in CK levels after exercise than those classified as average or normal responders. However, there is currently no consensus on a clinical definition of raising the CK level to establish an individual as a high responder.

The neural mechanisms underlying the injury-associated loss of muscle function have been extensively investigated in experimental studies by electromyography (EMG). Surface EMG studies have shown that non-uniform muscle adjustments occur in response to harmful exercises: these adjustments are attributed to the variation in morphological and architectural characteristics of muscle fibers, depending on their location in a skeletal muscle and the uneven activation of muscle areas during exercise damage.

It is not easy to draw conclusions from multiple heterogeneous epidemiological and experimental studies. It is currently reasonable to conclude that tendons only become larger than their normal load after exercise. However, there are conflicting results in longitudinal studies of more than 12 months. In older adults, Eriksen et al. Concluded after one year an increased CSA with no difference between high and moderate resistance resistance training, while Massey et al. Concluded that CSA remained unchanged after four years of resistance training despite significant differences in muscle strength and size. Variations in longitudinal study results may be the result of a speed limiting effect on tendon adjustments caused by exercise. Total stiffness continues to increase to four years with consistent high-intensity training; however, the rate of improvement begins to decline after two to three months. Conversely, in endurance training exercises, the speed of tendon adjustments is more linear and increases with a more consistent speed over many years. These behaviors and the respective weighted effect sizes of Young's modulus (0.69) and CSA (0.24) suggested that increases in tendon stiffness are mainly due to changes in material properties (Young's modulus) and secondary to changes in morphological properties (CSA).
Although the latest technological developments have made progress in the study of tendons possible, the heterogeneity of the data regarding their response to stress and exercise does not yet allow definitive conclusions to guide clinical recommendations for training prescriptions in healthy subjects and athletes. Conversely, exercise training is highly recommended for improving pain and function in patients with tendinopathies of the upper and lower limbs. Also because the effects of exercise can be enhanced by a wide range of other treatments, including nutritional supplements, patient information and physiotherapy.

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