Case study essay 4
Delayed Onset Muscle Soreness
Regular exercise is one of the best things we can do for our health. It has
many benefits, including improving our overall health and fitness as well as reducing our risk for
many chronic diseases. When we exercise, we put our muscles to work and by working harder
than we used to, we tend to cause microscopic damage to our muscle fibers resulting to muscle
soreness or stiffness. The muscle pain experienced during and after strenuous activity is due to
inflammation within the muscle, which is one of the main triggers for muscle soreness.
Soreness is a typical and often expected side effect of any moderate level of physical
activity. However, there are many different types of soreness which are a result of strenuous
activities. For example, the soreness that occurs during or immediately after exercise (acute
soreness) or delayed Onset Muscle Soreness which occurs 24-72 hours after the exercise is over.
Acute soreness typically develops within a couple of minutes of the muscle contraction and
dissipates within anywhere from a few minutes to several hours after the contractions have
ended. It is widely accepted that this soreness is a result of the accumulation of chemical by-
products, tissue edema, or muscle fatigue. Since Sara complained of soreness that lasted from 24
to 72 hours, this indicates that she is suffering from delayed onset muscle soreness and not acute
soreness.
Delayed Onset Muscle Soreness typically develops between 12-24 hours after muscle
contractions end, with peak soreness being experienced 24-72 hours after the exercise is over. It
is classified as a type I muscle strain injury and present with tenderness or stiffness to palpation
or movement. The sensations experienced with this injury can vary from slight muscle stiffness,
which rapidly disappears during daily routine activities, to severe debilitating pain which
restricts movement. Tenderness is concentrated in the distal portion of the muscle and becomes
progressively diffuse by 24–48 hours post exercise. This localization of pain can be attributed to
a high concentration of muscle pain receptors in the connective tissue of the myotendinous
region. The myotendinous junction is characterized by a membrane which is continuous,
extensively folded and interdigitated with the muscle cells. The oblique arrangement of the
muscle fibers just prior to the myotendinous junction reduces their ability to withstand high
tensile forces. As a result, the contractile elements of the muscle fibers in the myotendinous
junction is vulnerable to small/microscopic damage.
Delayed Onset Muscle Soreness is usually associated with unfamiliar, high-force
muscular work and is precipitated by eccentric actions. Eccentric activity is characterized by an
elongation of the muscle during simultaneous contraction which causes small-scale damage to
the muscle fibers. This is because the external load exceeds the muscle’s ability to actively resist
the load, and thus the muscle is forced to lengthen, and active tension is generated. Cross bridges
formed during eccentric actions must also be separated with greater force due to the disruption of
the actin-myosin bonds prior to relaxation. As a result, greater tension per active motor unit is
developed and there is an increased risk of injury to the vulnerable myotendinous junction.
Delayed onset muscle soreness occurs due to structural damage in sarcomeres,
particularly to the z-disks and contractile filaments. Z-disks provide the structural support for the
contractile filaments of the sliding filament mechanism. Damage to the sarcomeres (membrane
damage and breakdown of muscle protein) causes an influx of white blood cells, leading to
inflammation, which is itself associated with increased plasma enzyme concentration,
myoglobinemia, and abnormal muscle structure and histology. A further response to sarcomere
damage is necrosis following damage to the mysium, which peaks about 48 hours following
exercise. The structural damage to sarcomere such as damage to sarcoplasmic reticulum will
cause calcium to leak out and collects in the mitochondria which inhibits ATP production
resulting to no energy supply and thus halts force production within the muscle.
Hyperplasia is the increase in number of muscle fibers. Since Sara is experiencing
delayed onset muscle soreness, hyperplasia is not one of the reasons for her soreness. This is
because, Delayed onset muscle soreness is primarily caused by a type 1 muscle strain (a minor
fiber damage) which is not too serious . She is sore because she is not accustomed to strenuous,
tasks of an eccentric nature. The pain she is experiencing is due to nociceptors responding to the
damaging stimuli by sending pain signals to the brain. In the muscle tissue, these receptors can
sense chemical stimuli such as inflammation. For hyperplasia to occur, Sara must severely
exercise muscle fibers which will in turn activate satellite cells. The satellite cells will undergo
cell division and give rise to new myoblast. These myoblast cells will then fuse together to form
to form a new fiber. Hyperplasia do occur in human beings due to number of causes such as
proliferation of basal layer of epidermis to compensate skin loss, chronic inflammatory response,
hormonal dysfunctions, or compensation for damage muscle tissues. To have hyperplasia, Sara
must have a major fiber damage to initiate cell division and for this reason her soreness was not
due to hyperplasia.
The best way to relieve the muscle soreness is by performing gentle exercises, like
walking or light stretching. This may seem counter intuitive, but the more you move, the faster
the discomfort will go away. A heating pad will also help to ease the discomfort temporarily, but
ice is a better treatment in the long run because it helps to decrease the swelling and
inflammation in the muscles .Moreover, during the few days of experiencing muscular soreness,
it is advisable to consider performing alternate exercise activities in order to give the sore
muscles an opportunity to recover while strengthening other muscles. Warming up before
participating in sports and activities is another important thing to do. Also follow an exercise
programs aimed at stretching and strengthening the muscles, increasing the intensity of your
training program gradually (never push yourself too hard, too soon) as well as using the correct
technique when lifting heavy weights. In addition, slowly begin an exercise for a certain period
such as 5 to 10 weeks. The slow progression allows the exercised muscle to adapt to the exercise
stress. Also, it is advisable to use compression clothing because they improve recovery from
exercise induce muscle soreness, massage, rest, ice, elevate as well as using anti- inflammatory
drugs.
In conclusion, Delayed Onset Muscle Soreness occurs due to participation in strenuous,
unaccustomed tasks of an eccentric nature. Symptoms of Delayed Onset Muscle Soreness
include, tenderness or stiffness to palpation particularly at the musculotendinous junction, a loss
of range of motion, flexibility, force production and mobility. Greater perception of muscle
soreness tends to be associated with high intensity exercise, of any exercise, although duration
also has a contributing effect. Numerous theories of Delayed Onset Muscle Soreness have been
proposed in the literature, with most criticism directed at the lactic acid theory and muscle spasm
theory. Treatment mechanisms are also plentiful, however only limited success has been
reported.
