Sports Medicine: Just the Facts

A chemical transmission occurs across the synapses

that generate electric potentials in the muscle mem-

branes. These electric potentials cause the sarcoplas-

mic reticulum to release calcium. The calcium binds

to troponin, which results in a conformational change

in tropomyosin that allows the interaction between the

myosin (thick) and actin (thin) filaments. These fila-

ments slide past each other to shorten or resist length-

ening. This process is powered by the hydrolysis of

ATP (Garrett and Best, 2000).

REPARATIVE PROCESS

• The pathophysiology of healing muscle is similar
  regardless of the type of injury. The reparative process
  involves both inflammatory cells (neutrophils,
  macrophages) and myogenic (satellite) cells.


• Inflammatory cell invasion of the damaged muscle
  tissue begins shortly after injury.
  
  
  1. Neutrophils initially infiltrate the injury site via
     cellular chemotaxis. The cellular mechanism
     responsible for attracting the neutrophils is not
     completely known but probably involves a com-
     plex signaling process. Mediators such as basic
     fibroblast growth factor(bFGF), platelet-derived
     growth factor(PDGF), and interleukin-1(IL-1)
     stimulate macrophages and fibroblasts within the
     muscle tissue, which in turn, attract and activate
     inflammatory cells (Tidball, 1995).
  
  
  2. Macrophages are the most prevalent inflammatory
     cells present in injured muscle. Distinct subclasses
     of macrophages have been identified and play spe-
     cific roles in the healing process. One subclass of
     macrophages is involved in the phagocytosis of
     damaged tissue and further stimulation of the
     inflammatory response. A second subclass of
     macrophages helps modulate the reparative process
     (Tidball, 1995).
  
  
  
  


• Satellite cells are myogenic mononuclear cells
  responsible for muscle fiber regeneration. Muscle
  injury stimulates these cells to differentiate into
  myoblasts, which fuse together and develop into mult-
  inucleated muscle fibers (Lehto and Jarvinen, 1991).


• Fibroblast proliferation and collagen matrix synthesis
  occur along with the inflammatory response and
  muscle regeneration. This connective tissue scar for-
  mation may inhibit the complete repair of injured
  muscle (Lehto and Jarvinen, 1991).

MUSCLE STRAIN INJURY

• Muscle strain is the most common injury sustained in
  sports. This type of muscle injury can range from

delayed muscle soreness (discussed below), to partial

muscle strain, to complete muscle disruption.

• These injuries occur most commonly during eccentric
  contraction in muscles that cross two joints (rectus
  femoris, biceps femoris, gastrocnemius). These mus-
  cles have a high proportion of type II (fast-twitch)
  fibers and these injuries occur most frequently during
  sprinting (Noonan and Garrett, Jr, 1999).

MECHANISM OFINJURY

• High forces are generated in relatively few muscle
  fibers during eccentric muscular contraction; how-
  ever, muscle contraction alone is insufficient to create
  muscle strain injury. Passive stretch of the muscle past
  its resting length is required to injure the muscle
  (Garrett et al, 1988). This increased strain disrupts the
  muscle fibers near the muscle-tendon junction.


• Cellular disruption results in the hydrolysis of struc-
  tural proteins and inflammation that further damages
  the muscle tissue (Nikolaou et al, 1987).


• Animal studies reveal that muscle tissue sustaining
  a nondisruptive strain injury demonstrates
  decreased load to failure when subjected to stress
  (Obremsky et al, 1994; Taylor et al, 1993). In addi-
  tion, these partially injured muscles generate signif-
  icantly less contractile force. This may explain the
  clinical observation that significant muscle strain
  injuries are frequently preceded by a minor injury.
  These studies also underscore the importance of rest
  and complete recovery prior to the resumption of
  athletic activities.

REPARATIVERESPONSE

• Similar to the general reparative response of muscle
  described above.


• The presence of inelastic fibrotic tissue (scar) may
  make the muscle more susceptible to additional
  injury.

TREATMENT ANDPREVENTION

• As mentioned above, reduced activity is key in the
  treatment of muscle strain injuries. This helps control
  inflammation and prevents further tissue damage.


• Immobilization can diminish pain, reduce inflamma-
  tion, and allow torn muscle ends to reapproximate.
  Prolonged muscle immobilization (greater than 7–14
  days) results in muscle that demonstrates lower loads
  to failure and should be avoided (Noonan and Garrett,
  Jr, 1999).

NONSTEROIDALANTI-INFLAMMATORYDRUGS

• Animal studies demonstrate that nonsteroidal anti-
  inflammatory drugs(NSAIDs) reduce the inflamma-
  tory response associated with muscle strain injury but

56 SECTION 1 • GENERAL CONSIDERATIONS IN SPORTS MEDICINE