Written by Dr. Tom Shurlock for and on behalf of GWF Nutrition Limited.

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When striated muscle undergoes high levels of work there is physical damage. Strength conditioning results in an increase in muscle size, which is largely the result of increased contractile proteins. Muscle contraction – concentric contraction – matches muscle elongation in a paired system and this is eccentric muscle contraction. This elongation produces ultrastructural damage and stimulates increased muscle protein turnover (Evans 1991).

Eccentric exercise and muscle protein breakdown is evidenced by increases in urinary 3-methylhistidine and creatine as well as interleukin levels (IL-1) and a general immunomodulatory response. This involved increases in neutrophils that migrate to the area of damage, phagocytize tissue debris and release lysozyme and free radicals, and these in turn further breakdown protein. This is indicated by an increase in leucine flux and oxidation.

There is also an increase in cytokines and tumour necrosis factors (TNF) both of which increase proteolysis, while IL-1 affects PGE2 production.

Within the overall context of regeneration there are three overlapping phases – inflammation, proliferation and maturation (Broadfoot, 2013). The inflammation phase is that of damage and this is followed by proliferation. It is this stage where nutrition can influence. Protein repair is heavily dependent on the formation of collagen; chronic inflammation stimulates scarring when growth factors and cytokines promote fibroblast proliferation and collagen synthesis. In excess, this leads to excessive collagen deposition and fibrosis. In terms of wound healing, this may be a favourable response but for muscular development a moderation of this process is required.

Anti-inflammatory parameters include relevant nutrients such as polyunsaturated fatty acids, antioxidant vitamins, flavonoids, prebiotics and probiotics.

PUFA have been well cited in their involvement in anti-inflammatory processes, Omega-3 are generally regarded as being more anti-inflammatory than omega-6, the latter involved in PGE2 production – but this may have an ameliorating affect to combat IL-1 inflammation. Supplemental arachidonic acid (C20:6) has been shown to enhance recovery from ischemic muscular damage in piglets (Jacobi et al, 2012). Omega-3 supplementation still appears to have a specific role in maintaining the neutral lipids of skeletal muscle and increased incorporation in membrane phospholipids (Otten et al, 1997).

Antioxidant vitamins also have a well-documented benefit in both muscle and general tissue repair. Vitamins A, C, D, and E have all been cited; although E is possibly the most researched. Vitamin effects are primarily concerned with restriction and its effect on marbling in muscle. Low levels of vitamin A induce intramuscular hyperplasia of the depot fat; retinoic acid inhibits adipocyte differentiation and high levels of A would inhibit building up of intramuscular fat depots (Gorocica-Buenfit et al, 2014). Although trials show no improvement in growth in production animals, there does appear to be an improvement of muscle mass possibly by diffusion of fat into the muscle matrix i.e. reduced marbling (Tous et al, 2014). In these trials the equivalent of 5000IU/kg were fed.

Although more associated with bone formation, vitamin D is involved in calcium homeostasis and is critical in both concentric and eccentric contraction. Additionally, it is known to modulate Genome Expression and modulate cellular health. High-intensity exercise, resulting in protein breakdown, has been associated with a reduction in DNA methylation – a reduction in cell development – although long term exercise can result in methylation of adipose tissue. B vitamins and biotin can support DNA methylation and help avoid protein breakdown (Broadfoot, 2013).

Vitamin C antioxidant properties are normally associated with heat stress (Barbour et al, 2010) but supplementation does improve muscle mass under these conditions (Toplu et al, 2014) and also maintains collagen synthesis at acceptable levels (Broadfoot, 2013). In combination with vitamin E, vitamin C reduces malondialdehyde, a marker for oxidative stress, in exercising athletes (Rabienejad, 2014). Exercise also generates high levels of creatine kinase which is associated with rhabdomyolysis (muscle breakdown). Vitamin E reduced both creatinine and creatine kinase in rhabdomyolysis induced rats leading to a reduction in muscle injury through its action on free radicals (Tajik et al, 2013). Increasing dietary vitamin E increases α-tocopherol in muscles and fat tissues (Alvarez et al, 2005), improved phosphocreatine, reduced lipid oxidation and improved conductivity – all indications of muscle growth (Lahucky et al, 2001). It was also shown that the muscles with the greatest oxidative capacity, the type I and IIa (slow twitch) muscles have the greatest stores of vitamin E. As these are the best supplied with vascular systems and mitochondria it makes sense to have the greatest antioxidative capacity. (Jensen et al, 1988).

Interactions between vitamin E and selenium are well documented and it has been shown that the combination significantly reduced malondialdehyde and increased superoxide dismutase activity in broilers (Harsini et al, 2012).

Selenium acts through selenoproteins to protect cells from damage, acts as an anti-inflammatory agent and stimulates the immune system (Zarcyet al, 2013). These activities help combat the protein breakdown of damaged muscle. Research in horses (Calamari et al, 2010) demonstrated that selenium yeast was the most efficient selenium source in combatting muscle damage.

Further antioxidant capability is observed from functional nutrients of some herbs. For example, curcumin has been demonstrated to improve antioxidant status in resisting heat stressed impaired muscle development and enhancing mitochondrial biogenesis – this is indicative of improved vascular supply and energy generation (Zhang et al, 2014). Reduction in oxidative stress and free radical induced damage as well as protein turnover has also been demonstrated with the use of plant extracts, increasing gene expression. (Zhu et al, 2011).

Trace element supplementation provides a non-specific improvement in muscle function, as they contribute to many co-factors and enzymes involved in protein synthesis and both concentric and eccentric contraction. Magnesium has been shown to reduce stress related lesions in loin muscle in pigs (Peeters et al, 2006), whilst manganese reduces malondialdehyde (Lu et al, 2007)

So far the inclusion of various antioxidants, nutraceuticals and vitamins all have an effect in combatting the catabolic/destructive effects of, mainly, eccentric contractions. By combatting the increase of free radicals, inflammatory and immunological cues, and moderating collagen synthesis; muscle damage and repair through scarring may be reduced. Beyond this there is a need to help maintain the anabolic processes of muscle development. Branched chain amino acids have been shown, in particular, to aid muscle growth (Brojer et al, 2012; Nostell et al, 2012; Ivy 2004; Ohtani et al. 2006), and arginine is well established as aiding microvascular development (Zhan et al, 2008), which is a critical step in muscle repair (Broadfoot 2013). It is also a prominent precursor for muscle protein synthesis, immune regulation, cell division and wound recovery (ShanMao & Yong, 2014).

As a significant proportion of regeneration of muscle (at least 10%) is composed of collagen additions the addition of collagen matrix will aid muscular development. In combination with those factors that resist muscle protein breakdown and so reduce leucine flux and restrain excessive collagen generation; supplementing with collagen and leucine is advisable.

Finally, although perhaps more associated with cartilage maintenance, glycosaminoglycans are associated with regulating connective tissue structure and permeability and as such will have a role in muscle maintenance (Broadfoot 2013).

As such the components of Muscle Maintenance have been collated to reduce the damage of eccentric contraction of muscle whilst supporting the anabolic processes of its regeneration.

References

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