 Brad Pilon

  This is a review of

the collection of the available research regarding inflammation and muscle growth. conclusive, but rather a theory based on my personal interpretation of the available evidence. Finally, it should be obvious, but just in case – This document should not be mistaken for medical advice.

  It is by no means complete or

 

  Latin: inflammare, to set on fire   Two main types Acute and
Chronic stimuli

  biological response to harmful   removes the injurious stimuli and
initiates the healing process

  Without inflammation, wounds

and infections would never heal is associated with disease.

  However, long term inflammation

.

Theory of Muscle growth is as follows:   As this presentation will show. inflammation plays an important role in regulating muscle growth. the   Simply put the Inflammation . ‘Signal and Noise’ theory of inflammation’s role in regulating muscle growth attempts to explain how many lifestyle factors can prevent optimal muscle growth.  Other than the obvious health reasons (prevention of disease).

The Inflammation Theory of Muscle growth .

. Below: The Same Acute Inflammation Response to periods of Resistance Training in a person WITH chronic inflammation. The Spikes are hidden by the ‘noise’ and thus muscle growth is not initiated.Above: The Acute Inflammation Response to periods of Resistance Training in a person with no chronic Inflammation. The “Spikes” are large enough to initiate muscle growth.

  Chronic inflammation is the body’s response to the chronic harmful stimuli. our bodies cannot get rid of the fat with the inflammation response and thus will stay inflamed as long as the extra fat is still present. (Peterson 2005)   Low grade chronic inflammation is   In the case of Obesity the extra fat is the ‘harmful stimuli’ that is causing the inflammation. . such as excess body fat or other chronic metabolic ‘insults’. IL-6 and CRP . characterized by a 2 to 3 fold increase in the systemic concentrations of cytokines such as TNF-alpha.

.

.

IL-6   TNF-Alpha is proposed as the main driver of chronic low grade inflammation (Brandt. and CRP   3 Common types: TNF-Alpha.acute-phase . 2009) protein. 2010) exercise after exhaustive exercise (Levinger. such as interleukins and interferons. elevated in inflammation and illnesses such as cancer   IL-6 increases several fold post-   C-Reactive Protein .  Cytokines are small cell-signaling protein molecules   The term "cytokine" has been used to refer to the immunomodulating agents.

Bruunsgaard 2003. Schlitt 2004. 2007) . Sriwijitkamol 2006. atherosclerosis.  This type of prolonged whole body (systemic) inflammation is associated with many disease states including:   Rheumatoid arthritis.   Fatty liver   Asthma   Insulin resistance and diabetes   Cardiovascular disease   Alzheimer Disease   And even the aging process itself. (Arend 2001. Finch CE.   hypertension.

this inflammation- cancer link was suggested as far back as the late 1800’s when German Pathologist Rudolf Virchow stated: “Chronic irritation which is manifested by a chronic inflammation is a key promoter of cancer. Aggarwal BB.  Chronic Inflammation is a process that seems to be an underlying mechanism in many forms of cancer (Bharat 2009.” . 2006)   Surprisingly.

  Chronic inflammation is widely observed in obesity (Kershaw.   Leptin   IL-18 (Loffreda S 1998. Esposito K 2002). elevated markers of inflammation including: . 2004).   Insulin.   CRP.   TNF-Alpha.   The obese commonly have many   IL-6.   Blood glucose.

(Rogowksi.  Waist circumference significantly influences the inflammatory response. and increasing levels of inflammation. 1997) increasing levels of obesity. and this production increases with increasing adiposity (Mohamed-Ali V.   Thus there is a link between . 2010)   Adipose tissue has been shown to produce 10-35% of IL-6 in a resting individual.

.

.

  High Sat Fat containing meals and   This is an acute response however . Blackburn P 2006. it may become chronic if the overeating is chronic. (Hotamisligil. 2009). . 2006) even large mixed meals have also been associated with increased markers of inflammation (Zimmerman MB 2008.  Hyperglycemia induces IL-6 production from endothelial cells and macrophages. Van Dijk SJ.

.

acute inflammation is to remove the injurious stimuli and damaged tissue and to initiate the healing process .  The bodies response to insult and injury (Think Bee sting)   It Involves the mobilization of   Role of Cytokines and other immune molecules to protect the body.

research using:   Cross Sectional Area   Fractional Synthetic Rate  Amino Acid Markers  Increases in Muscular Strength   Increases in Muscular Weight  This has been shown in . From the available research we know that muscular contraction is the signal for workinduced muscle growth.

  There is a known relationship

between inflammation and muscle growth. (Toth MJ, 2005) response to muscular contractions seems to be necessary for muscle growth (Marimuthu 2010).

  Acute localized inflammation as a

  Muscles can synthesize cytokines
in response to contractions (Lang CH, 2003; Frost RA, 2002; Pedersen BK 2009; Bruunsgaard H. 1997 ) anti-inflammatory medicines are able to blunt muscle growth (Mikkelsen UR, 2009; Trappe TA 2001.)

  High doses of

  The inflammation response plays

a role in the degeneration and regeneration process of muscle and surrounding connective tissue after exercise induced muscle damage. contractions the acute inflammatory response initiates the breakdown and removal of damaged muscle tissue (Cannon J, 1998) and IL-6 are expressed in skeletal muscle up to 5 days after exercise (Cannon J, 1989; Fielding R 1993)

  As a response to muscular

  The Cytokines Il-1B and TNF-A

Louis E.  IL-6 is released by muscle cells as a response to muscular contraction. intensity etc) (Phillips. (Hiscock 2004) fold above resting levels. 2007)   The IL-6 increase associated with . 2009)   This increase can be up to 100   IL-6 responds differently to different workloads and intensities of training. but this seems to be training protocol dependent (volume. 2001. training increases about 4 hours after resistance training and remains elevated for up to 24 hours. 2010. MacIntyre. (Pedersen.

.

.

Hawke TJ 2001) up to 100% more satellite cells than untrained controls (Kadi F 1977. (Serrano AL. 2008) providing new myonuclei and repair damaged segments of mature myofibers for successful regeneration following injury or exercise induced muscle damage. 2002. (Grounds MD. 2005)   They contribute to hypertrophy by   High level power-lifters can have . Eriksson A.  Satellite cells are crucial for skeletal muscle adaption to exercise. Hawke TJ 2005.

  A rapid and transient localization of the IL-6 receptor and increased IL-6 expression occurs in satellite cells following contractions (McKay 2009) hypertrophic muscle growth both in vitro and in vivo (Serrano AL. 2007. Mikkelsen UR 2009) and exercise induced protein synthesis (Trappe TA. 2008) increase IL-6 by up to 6 fold at 5 hours post exercise and 3 fold 8 days after exercise (Mikkelssen UR 2010) Drugs can decrease satellite cell response to exercise (Mackey AL. 2002)   IL-6 has been shown to mediate   Unaccustomed exercise can   Non-Steroidal Anti-inflammatory .

.

.

2007)   The cytokine response to resistance exercise and running occur differently with running causing a more pronged response. especially at the 12-24 hour mark (Louis E. 2007) . (Louis E.  The increase in Cytokines after resistance exercise coincides with the decrease in myostatin levels.

  Even a small increase in chronic inflammation can increase the risk of muscle strength loss and cause a decrease in your ability to build muscle. Jansen. 2005) anabolic effects of IGF-1 (Frost RA 2007. (Toth. Juraniski CV 1995)   Chronic inflammation has been   Increased protein levels of   Increased levels of   Cytokines may antagonize the . 2005. 2007. Visser M. 2002) myostatin have been described in patients with diseases characterized by chronic low-grade inflammation (Reardon. implicated as part of the cause of the muscle loss that occurs with aging (sarcopenia). Garcia-Martinez 1993. 2001) TNF-Alfa can suppress the AKT/mTOR pathway and increase muscle catabolism (Lang CH.

.

2010)   Sepsis is able to prevent leucine   In animal models when .  Sepsis is an extreme whole body inflammatory state that is able to inhibit the synthesis of both myofibrillar and sarcoplasmic proteins preferentially in muscles composed of fast twitch fibers. Lang 2007) from stimulating muscle protein synthesis (Lang 2005) inflammation is created mTOR loses it’s ability to be stimulated by muscle growth (Lang. (Vary. 1992.

.

.

.

Loffreda S. 1994) 2010)   Lack of Sleep (Mullington JM. 2001. Ershler. 2010.  Chronic Exhaustive Exercise (Gleeson M. 2003. 2002)   Obesity (Monterio R. 2006)   Stress (Carpenter LL.   Overeating (Vozarova B. 1998) . Esposito K. 2000. Rogowski O. 2010)   Aging (Bruunsgaard. 2010.

.

.

. The “Spikes” a large enough to initiate muscle growth. Below: The Same Acute Inflammation Response to periods of Resistance Training in a person WITH chronic inflammation. The Spikes are hidden by the ‘noise’ and thus muscle growth is not initiated.Above: The Acute Inflammation Response to periods of Resistance Training in a person with no chronic Inflammation.

  Research has shown that there is a strong trend towards reduced post absorptive muscle protein synthesis associate with aging. Payette H 2003. 2003)   Evidence suggests that this is   High levels of . IL-6 and CRP (Toth MJ. Roubenoff R. related to increased circulating levels of inflammatory cytokines TNF-Alpha. 2005) circulating IL-6 can predict muscle atrophy in the elderly (Ferrucci L 2002.

.

  There are as many as 100 original scientific reports concerning exercise and cytokines (Suzuki K. 2002) between exhaustive exercise and chronic low grade inflammation (Suzuki K. (Suzuki K. 2003) IL-6 levels as much as 100 times over normal and increases total leuckocyte count and neturophil mobilization. 2003)   There is a strong relationship   Marathon running may enhance .

.

.

(Smith JK. Pedersen 2000) may help reduce chronic low grade inflammation (Ploeger HE. 2005)   Baseline measurements of circulating inflammatory markers do not seem to differ greatly between healthy trained and untrained adults (Gleeson M. 2006. 2009) . McFarlin BK 2005. 1999.  Regular physical activity is reported to decrease markers of inflammation. 2009)   However long-term chronic training   Levels of inflammatory markers (IL-6) remained elevated longer into the recovery period following and acute bout of exercise in patients with inflammatory diseases as opposed to healthy controls (Ploeger HE. Stewart LK.

.

Mackinnon LT 2000) . 2008. 2008. Gleeseon M.Timmerman KL.  Low intensity training can reduce resting pro-inflammatory markers (CRP IL-6) .   Moderate exercise can have some   Strenuous or exhaustive exercise can increase inflammation. 2006. (Niclas BJ. anti-inflammatory benefits.

.

specifically IL-6 and Leptin (Reed JL. 2010)   Short term fasting may have anti  Calorie restriction is anti-   Weight loss is effective at reducing . 2009) inflammatory (Morgan TE 2007.  Weight Loss achieved through different diet programs in combination with or without exercise resulted in decreases of markers of low grade inflammation by 7 to 48%. 2006) inflammatory benefits (Varaday K. (Basu. Fontana L 2009) inflammatory markers.

.

.

D’agostino P 1999. Li ZG. IL-1B and TNF-Alpha (Hatakeyama H. 2008) the expression IL-6.  Testosterone injections result in profound declines in markers of inflammation (Glitay EJ. 2002. 1993) the production of antiinflammatory IL-10 (liva SM. 2001)   Testosterone is able to suppress   Testosterone can also stimulate .

.

.

  Overeating has been purported to add in the muscle building process in young. leading to speculation that the slow build up of inflammation eventually reaches a point where muscle growth is blunted.   This time course would depend on . non-steroid using athletes.   However this effect seems to decrease with time. the degree of overeating and speed of fat gain in the individual.

and exhaustive exercise may blunt muscle growth signals form both exercise and diet may allow for a return to proper anabolic signaling.  Low grade chronic inflammation brought about by any combination of overeating. obesity. lack of sleep. aging.   Decreasing chronic inflammation   However. stress. it seems wiping out inflammation completely also prevents the acute local inflammation needed for muscle growth (as evidenced by high does NSAID Studies) .

get lots of sleep. body fat low. .   Train consistently. and avoid excessive use of exhaustive exercise for optimal muscle growth and long term health.  Utilizing the signal/noise theory of the role of inflammation in muscle growth it seems very plausible that the best course of action for long term muscle growth is the opposite of what we have been lead to believe.   Keep Calories low. and match strenuous exercise with periods of light exercise.

.

com/references .  References available at: Inflammationtheory.

Sign up to vote on this title
UsefulNot useful