Most people would agree that more muscle equates to more strength, but if it were that simple then why do bodybuilders so often post significantly weaker strength levels compared to powerlifters of similar or even smaller size?
Are All Muscles Created Equal?
Most of us have seen someone visibly smaller or weaker display greater strength abilities than someone of larger or seemingly stronger stature. Why is that? Did the smaller person have better form? Was the bigger one not feeling well? It just doesn’t make sense that someone with less muscle would be stronger than someone with more muscle. Or does it?
This counterintuitive phenomenon isn’t smoke and mirrors. It is actually two forms of muscular hypertrophy at work: sarcoplasmic and myofibrillar. While there is a lack of physical evidence at the microscopic level (not too many athletes want to donate their muscle tissue for cross-sectional observation), the best explanation for this observable difference is that certain resistance training stimulates a strength adaptation, while others trigger less strength but more size.
If you think about these training styles and the physiological changes that occur in the muscle during training sessions, it’s easy to see how exercise scientists arrived at the conclusion of there being two types of muscular hypertrophy. One stresses the fluid capacity of tissue by forcing larger volumes of blood into the muscle, causing it to stretch and expand. The other generates maximum neuromuscular activation and contractional tension, overloading both the nervous system and the actual sarcomeres that are responsible for force production (strength).
Muscular hypertrophy stimulated by the influx of fluid into the tissue, causing microdamage to the tissue walls due to the excessive blood volume is referred to as sarcoplasmic hypertrophy. The sarcoplasm is the fluid surrounding myofibrils which contiain the sarcomeres (which contain the actual contraction components of muscle tissue: the actin and myosin). When muscles are forced to contract against increasingly difficult resistance, blood rushes to deliver nutrients for the muscles so they can continue operating effectively. The more work the muscle is forced to perform, the more fluid is delivered. By maximizing tension of each muscle contraction, the many membranal linings within the muscle belly incur small tears. These tears (with proper nutrition) are repaired by proteins that fill in this gaps, resulting in more muscle volume. Multiply the microexpansion in muscle size by weeks and over time you have significant, visible improvements in muscle size and definition.
Hypertrophic changes in muscle tissue as a result of an increase in the number of contractile components (myofibrils, sarcomeres, etc.) is known as myofibrillar hypertrophy. This form of hypertrophy produces a much slower increase in muscle size because less cellular damage occurs during training and buildiing entirely new cellular structures takes signficantly more time. However, improvements in force production are drastically enhanced by training for this form of hypertrophy. This is largely due to the Central Nervous System adaptation that coincides with the hypertrophic response.
When muscles activate with an intensity within 80% (this number is debatable) or more of their maximum contractile potential (commonly known as the 1 Rep Max), the connection from the brain to the muscle via the nervous system also reaches its maximum signal capacity. The more frequently this signal is sent, the stronger it can get and the more receptors the body will want to build to deliver that signal to the muscular fibers. It is for this very reason that not everyone is certain that myofibrillar hypertrophy exists the way we understand it. Some believe it is soley the CNS adaptation that is responsible for improvements in muscle recruitment and therefore increases in strength. This idea isn’t without merit, but seems to avoid an explanation for the hypertrophic response that accompanies this adaptation.
Whether or not continual research shows these two hypertrophic variations to be equivalent to that of current understanding, observational evidence within the exercise science community all but confirms their validity. Keep in mind that neither of these are likely to ever be mutually exclusive. One will always produce some of the other, and vice versa. This further complicates the decision for selecting the various hypertrophic variables within your strength or size program, especially during plateaus.