The changes that take place in adolescents during the development, affect the muscles, bones, tendons, and ligaments in ways that predispose the pediatric population to injuries less commonly seen in adults. Tendons and ligaments are relatively stronger and more elastic compared to the epiphyseal plates; therefore, growth plate damage is more common in this group [3]. Those changes, along with structural abnormalities related to genetic or birth defects, can also predispose to injuries to the musculoskeletal system.

Chronic compartment syndrome has also been shown to occur in young athletes due to muscle hypertrophy and is commonly seen while running [3]. Pain, numbness, and tingling, associated with athletic activity, are often the presenting symptoms. Compartment syndrome can be both acute and chronic with acute development raising the potential of a medical emergency.

Pain in the lower limbs of a growing child can be a common complaint with a multitude of etiologies. A very common diagnosis, yet one of exclusion, for lower limb pain in children is growing pains . Growing pains usually begin in children aged 4–12 years [11, 12] and are described as bilateral musculoskeletal pains affecting the lower limbs, primarily the calf and thigh muscles. The etiology of growing pains is not known, and although they occur in growing children, they are not caused by growth. Pains do not occur at the sites of growth, do not affect the growth of children, and do not overlap with periods of growth [11]. Parents have commented on increasing episodes of pain after periods of increased physical activity. Other etiologies including fatigue, postural abnormalities related to orthopedic abnormalities, overuse, and restless leg syndrome have been proposed. Pains are described as crampy or restless in legs of older children aged 6–12 years [11]. Pains usually occur during the evenings and may interrupt sleep, being severe enough to induce crying in young children. Symptom-free periods range from days to months. Pains are generally relieved by massage, heat, or analgesics such as acetaminophen or ibuprofen. The pains do not alter normal activity or movement and are not specifically linked to joints. The differential diagnosis for pains in the lower extremity is extensive; it is important to rule out all other possibilities before designating calf and thigh pain as growing pains . Serious conditions that must be ruled out when considering a diagnosis of growing pains include but are not limited to trauma, tumor, infection, osteonecrosis, and vascular pathology [11]. The natural history of growing pains is a benign one. The pain is treated symptomatically and will subside eventually within a year or two of onset as the child matures [11]. If symptoms progress to a point that they affect movement or activity, or involve worsening pain, pain during the day or activity, or if the child becomes ill, it is important to get a full workup to either exclude or diagnose a more serious cause of the pain .

Relative to other populations, the pediatric population can be more susceptible to viral myositis. There have been cases of myositis during outbreaks of influenza A and B [7]. Viral myositis is a benign, self-limiting illness that presents with muscle pain, tenderness, and sometimes swelling. The calf muscles of the lower limb are most commonly affected. Children will present with refusal to walk on their toes, and their calf muscles will be tender to palpation. It is possible for muscle enzyme to elevate up to 20–30 times the normal; however, myoglobinuria and acute renal failure have not been reported [7]. Muscle biopsy is not needed to diagnose viral myositis, but it does reveal evidence of muscle necrosis and muscle fiber regeneration. As stated previously, viral myositis is self-limiting, and recovery is seen in 3–10 days with resolution of the elevated muscle enzymes within 3 weeks [7].

Cerebral palsy (CP) is a neurological disorder causing lesions of the brain during development that can lead to impairments of the neurological and musculoskeletal system, usually manifesting as spasticity, dystonia, muscle contractures, bony deformities, incoordination, and muscle weakness [13]. Spastic muscles undergo significant changes during development, often undergoing shortening to create muscle contractures, leading to joint contractures, decreased range of motion (ROM), and increased tone and stiffness [14, 15]. This sequence can lead to loss of function of the affected skeletal muscles and limb movement with declining functional ability over time. The lower limbs of children with CP and the muscles responsible for locomotion are often affected.

Duchenne muscular dystrophy (DMD) is a fatal, X-linked muscle-wasting disease seen in male patients caused by the absence of the membrane-associated cytoskeletal protein dystrophin, due to mutation of the dystrophin gene. DMD is characterized by the progressive loss of contractile function, muscle weakness, and progressive degeneration of muscle tissue with replacement by noncontractile fat and connective tissue [17]. DMD onset is usually around 3–5 years and usually presents with intellectual impairment, in addition to speech and motor delays. Fast-twitch fibers are particularly susceptible to myopathy with DMD [18]. The muscle involvement is bilateral and symmetrical and normally affects the lower limbs first. A common finding is pseudohypertrophy of the gastrocnemii, in which they appear to be larger than normal but exhibit progressive muscle weakness [17]. DMD generally affects the proximal muscles more than the distal ones; however, the gastrocnemii are normally involved. Affected muscles are more prone to injuries occurring with repeated strain, including repeated lengthening, or eccentric contractions of sufficient load and frequency to induce fatigue injury in skeletal muscles. The load magnitude required to induce muscle damage with repeated eccentric contractions in DMD patients is much lower than that of typical normal muscles [18]. The absence of dystrophin renders muscle cells more vulnerable to damage by mechanical stress, possibly through a more injury-susceptible sarcolemma [17]. Along with increased susceptibility to injury, muscle repair in DMD patients is ineffective. One theory is that multiple rounds of degeneration and regeneration deplete the satellite cell pool responsible for muscle regeneration [17]. Therefore, patients diagnosed with DMD are at higher risk for muscle injury and damage than the general population, including distally affected muscles such as the gastrocnemii. Clinicians should be aware of the possibility of DMD in pediatric patients who present with calf complaints, including bilateral hypertrophy associated with delays or difficulty in ambulation.

Estrogen has been shown to influence many aspects of muscle physiology and function, along with potentially influencing muscle damage, inflammation, and repair [20]. There have been a number of mechanisms thought responsible for the ability of estrogen to have such an influence, including antioxidant properties, possible membrane stabilization, and inhibition of neutrophil and leukocyte infiltration during the post-damage inflammatory response [20].

It has been shown that female athletes with sports-induced amenorrhea or oligomenorrhea have decreased serum levels of estradiol [22]. Therefore, this population of females may not benefit from the protective influence that estrogen may have on skeletal muscles, thereby increasing their risk for muscle damage and impaired muscle regeneration.