The human body has succeeded and survived due to its ability to respond to its environment. This is most evident when observing modern day sport, in particularly athletics where the extremes of muscle mass in lightweight efficiency driven marathon runners are in sharp contrast to the powerful and explosive bodies of sprinters.
This ability to dynamically respond to environmental stimulus by shifting levels and distribution of muscle mass has obvious evolutionary advantages but has a physiological basis that can and should underpin personal fitness and the focus of training techniques.
There are several biological mechanisms that dictate the boundaries of a humans ability to deposit protein as muscle mass. Variations in genetics, hormonal profiles, anatomical variation and environment are all essential components that explain why certain training techniques are more effective in some than others. It is self-explanatory that a maximal muscle deposition with minimal muscle breakdown is key to achieving the greatest net muscle mass gain. We have known for a long time that increased rates of protein breakdown as a result of strenuous exercise are a necessary accompaniment to muscle growth due to the mechanism by which myofibrils (muscle fibres) proliferate (Millward et al. 1975). However, we also know that there are limits to how positive large amounts of muscle breakdown can be. This is never more apparent that in the potentially fatal medical condition of rhabdomyolysis. Rhabdomyolysis is excessive pathological muscle breakdown, often occurring in individuals who push their limits too far after being out of physical activity for a time. This zero to maximal shift in activity doesn’t allow the body to compensate or react in time resulting in huge muscle breakdown that’s waste products can potentially result in kidney failure and a long recovery period. From this we can conclude that the aim for maximal muscle mass gain must be to create enough muscle breakdown to stimulate myofibril proliferation, but not too much as to push the capabilities of the system too far resulting in more muscle breakdown than it is possible to synthesize. This translates into formulating training programmes that are appropriate to the individual and balance pushing physical limits with rest periods.
Returning to the variables that dictate muscle mass it is an unfortunate fact that there is very little we can do nothing to change our genetic limits. This inability for muscle expansion beyond our phenotypic (genetic trait) size is partly because protein mass is limited by the connective tissue matrix that defines muscle fibre volume (Millward et al. 1995). Essentially muscle is contained within an unmoveable box of connective tissue that defines how large the muscle can become. Other genetic components that cannot be changed legally or safely is the level of muscle synthesis stimulating hormone we produce. This leaves the at times controversial and complex role of nutrition in developing muscle mass. It is surprising but true that science is still uncertain as to how nutrition and specifically protein supplementation affects muscle development, or indeed if it affects it at all. The evidence is divided with some pro-supplementation studies suggesting that the efficacy of protein supplementation is dependent on the timing of ingestion in relation to exercise (immediate post-exercise consumption being better), composition of amino acids and the type of protein (Tipton et al. 2004). Others researching this area are opposed to supplementation and argue that a normal diet provides an excess of protein that meet all muscle synthesis demands. A classic text by Chittenden published in 1907 even showed that in a group of elite University of Yale athletes who were persuaded to reduce their protein intake by 50% over 5 months resulted in their strength being increased on average by 35%. It is likely that the truth may lie somewhere in the middle of these seemingly opposed pieces of evidence where there is a role for periods of decreased protein intake and specific times of protein consumption.
What is clear is that developing effective training programmes relies upon responding effectively to the dynamic changes and demands of the individual’s body, while keeping in mind the basic biological mechanisms that underpin muscle mass adaptation.
R. H Chittenden. (1907). The Nutrition of Man. London: Heinemann.
D. Millward et al (1995). A Protein-Stat Mechanism For Regulation of Growth and Maintenance of the Lean Body Mass. Nutrition Research Reviews, 93-150.
D. Millward et al. (1975). Skeletal-Muscle Growth and Protein Turnover. Biochem. J. 150, 235-243.
K. Tipton et al. (2004). Protein and amino acids for athletes. Journal of Sports Sciences. 22, 65-79.
Soldiers often struggle to gain type II muscle fibers, they tend to develop more type I
muscle fibers due to the having a heavily aerobic training program. Three major factors
heavily influence the development of both mentioned muscle fibers; rest nutrition and
training. Though muscle fiber type is genetically predisposed this can be harnessed from the
type of training done. Type I fibers tend to be more prominent within endurance athletes and
Type II more in explosive athletes i.e. sprinters.
Anabolism and Catabolism is a set of metabolic pathway, anabolic is to build up of organs and
tissues (muscle) using energy, whilst catabolic is the breakdown creating energy. Soldiers when on
exercise or operations tend to predominantly be in a catabolic state due to having limited and
irregular sleep, basic nutrition and highly taxing aerobic activity. On the other hand, when soldiers
return home or ‘in camp’ they can freely return to an anabolic state. This will allow them to have
regular rest in order to recover, consume more proteins and carbohydrates having easier access,
and do more resistance/anaerobic training.