Re: Muscle growth paradox

[Guest guest]

>

>

> > Growth with and without Damage

> >

> > In other words, genetic mechanisms can remodel tissues either to

> > facilitate normal growth, growth stimulated by mechanical effort

or

> > growth to repair damage. The above example, therefore, suggests

> that

> > one should be cautious before implicating damage as a central and

> > necessary process which can explain all hypertrophy. After all,

it

> > would appear to be unnecessarily inefficient and stressful for

the

> > training athlete always to be in a state of damage. Does it

sound

> > logical that damage should be the primary stimulus for all

> biological

> > growth? Would it not be preferable to implicate cellular

> > restructuring orchestrated by genetic programmes in response to

> > environmental and endogenous stresses (such as increase in tissue

> > tension).

> >

> > Then, again, the frequent occurrence of macroscopic tissue

injuries

> > (manifesting as partial or complete tissue ruptures or lesions)

> among

> > sports competitors would seem to corroborate the theory that

> > accumulating micro-injuries and damage are the fundamental cause

of

> > many injuries which are not caused by traumatic impact or

accident.

> >

> > Possibly we need to distinguish carefully between several

different

> > categories of growth and abandon the hypothesis that all growth

is

> > stimulated by damaging tissue through exercise:

> >

> > . Growth occurring as part of the normal maturation process

> > . Growth to replace tissues depleted by daily living and ageing

> > . Growth regulated by the mechanical stimulation of effort

> > . Growth to repair damage caused by excessive levels of tissue

> stress

> > . Growth to repair damage caused by disease or disuse

****

Relevant to the above

Exercise-Induced Muscle Damage

in Humans

ABSTRACT

son PM, Hubal MJ: Exercise-induced muscle damage in humans.

Am J Phys Med Rehabil 2002;81(Suppl):S52–S69.

Exercise-induced muscle injury in humans frequently occurs after

unaccustomed exercise, particularly if the exercise involves a large

amount of eccentric (muscle lengthening) contractions. Direct

measures of exerciseinduced muscle damage include cellular and

subcellular disturbances, particularly Z-line streaming. Several

indirectly assessed markers of muscle damage after exercise include

increases in T2 signal intensity via magnetic resonance imaging

techniques, prolonged decreases in force production measured during

both voluntary and electrically stimulated contractions (particularly

at low stimulation frequencies), increases in inflammatory markers

both within the injured muscle and in the blood, increased appearance

of muscle proteins in the blood, and muscular soreness.

Although the exact mechanisms to explain these changes have not

been delineated, the initial injury is ascribed to mechanical

disruption of the fiber, and subsequent damage is linked to

inflammatory processes and to changes in excitation-contraction

couplingwithin the muscle. Performance of one bout of eccentric

exercise induces an adaptation such that the muscle is less

vulnerable to a subsequent bout of eccentric exercise.

Although several theories have been proposed to explain this " repeated

bout effect, " including altered motor unit recruitment, an increase

in sarcomeres in series, a blunted inflammatory response, and a

reduction in stress-susceptible fibers, there is no general agreement

as to its cause. In addition, there is controversy concerning the

presence of sex differences in the response of muscle to damage-

inducing exercise. In contrast to the animal literature, which

clearly shows that females experience less damage than males,

research using human studies suggests that there is either no

difference between men and women or that women are more prone to

exercise-induced muscle damage than are men.

Key Words: Eccentric Exercise, Skeletal Muscle, Creatine Kinase,

Magnetic Resonance Imaging, Repeated Bout, Inflammation, Muscle

Weakness

Excerpts:

In 1981, Fride´n et al.3 provided some of the first evidence of

muscle fiber damage in humans after exercise. Subjects performed

repeated stair descents, and biopsies of the soleus muscle were taken

2 and 7 days later. The biopsy analysis showed myofibrillar

disturbances and Z-line streaming. In a follow-up study, Findings of

Newham et al.5 concurred with those of Fride´n et al.4 in that biopsy

samples taken 24–48 hr after exercise showed greater damage than

those taken immediately after exercise.

Force Loss

Prolonged strength loss after eccentric exercise is considered to be

one of the most valid and reliable indirect measures of muscle damage

in humans.2 Decrements in force immediately after exercise that does

not produce damage (e.g., concentric contractions) are restored in

the next few hours and are generally considered to be to due to

metabolic or neural fatigue.19 Concentric protocols are typically

associated with strength losses of 10–30% immediately after exercise,

with strength returning to baseline within hours after exercise.20,21

Eccentric-biased downhill running protocols that produce minimal

damage typically generate approximately 10–30% force loss immediately

after exercise, with a recovery period longer (up to 24 hr

postexercise) than that associated with concentric protocols.22

CK Activity in the Blood

Many studies have assessed the appearance of muscle proteins in the

blood after eccentric exercise to provide indirect evidence of muscle

damage. The muscle enzymes lactate dehydrogenase, aspartate

aminotransferase, carbonic anhydrase isoenzyme II, and CK have been

assessed.51

FACTORS THAT CAUSE OR EXACERBATE DAMAGE

Eccentric contractions clearly cause more muscle damage than either

concentric or static contractions. Greater damage with eccentric

contractions is not related to metabolic fatigue but due to a

mechanical insult.73 This has been attributed to the fact that, as

muscle lengthens, the ability to generate tension increases and a

higher load is distributed among the same number of fibers, resulting

in a higher load per fiber ratio.74,75 However, the fact that

soreness peaks 24–48 hr postexercise and swelling becomes pronounced

several days after exercise suggests that damage may be exacerbated

in the days after exercise. The inflammation occurring after the

initial insult is likely responsible for the continued damage and may

also function in the regeneration process.

Inflammation.

Inflammation after muscle injury occurs to clear debris from the

injured area in preparation for regeneration. This inflammation

response is thought to be activated by the initial mechanical trauma

and is characterized by infiltration of fluid and plasma proteins

into the injured tissue and increases in inflammatory cell

populations.87–89 The proliferation of inflammatory cells is thought

to amplify the initial muscle injury through increased release of

reactive oxygen species and activation of phospholipases and

proteases in the tissue at the injury site.87

SUMMARY

Eccentric contractions produce damage to muscle fibers as documented

by morphologic analysis of muscle biopsy samples, although some

questions have been raised over the accuracy of this technique to

assess muscle damage. Changes in MRI signal intensity have been found

after eccentric exercise and are taken to indicate muscle edema, yet

these changes, which can last up to 1 mo, are not fully understood.

Prolonged force loss seems to be a reliable indicator of damage and

may be explained by damage to contractile elements, impairment in

excitation-contraction coupling, and inflammation. Analysis of muscle

proteins in the blood provides only a qualitative indicator of

damage, and the changes observed demonstrate a large intersubject

variability. The level of any protein in the blood is a function of

both what is being released from the damaged tissues and what is

being cleared from the blood. Muscle soreness accompanies muscle

damage and may be caused by a combination of factors, including

swelling, increases in noxious chemicals, and byproducts of

inflammation. Muscle damage is initially caused by mechanical strain

on the muscle, and this damage is exacerbated by the inflammatory

response in the days after the exercise.

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Carruthers

Wakefield, UK