Bodybuilding - Size Means Strength? Sarcoplasmic hypertrophy vs. Myofibrillar hypertrophy

Sarcoplasmic hypertrophy (common in bodybuilding) involves the growth of the sarcoplasm (fluid like substance) and non-contractile proteins that do not directly contribute to muscular force production. Filament area density decreases while cross-sectional area increases, without a significant increase in strength.

Myofibrillar hypertrophy occurs due to an increase in myosin-acting filaments. Contractile proteins are synthesized and filament density increases (Zatsiorsky 1995). This type of hypertrophy leads to increased strength production. Sarcoplasmic Hypertrophy Muscle fibers adapt to high volume training by increasing the number of mitochondria (organelles in the cell that are involved in ATP production) in the cell. This type of training also leads to the elevation of enzymes that are involved in glycolytic and oxidative pathways. The volume of sarcoplasmic fluid inside the cell and between the cells is increased with high volume training. This type of training contributes little to maximal strength while it does increase strength endurance due to mitochondria hypertrophy. Growth of connective tissue is also present with sarcoplasmic hypertrophy.

Myofibrillar hypertrophy occurs due to increases in the number of myosin/actin filaments (sarcomeres) inside the cell. This leads to increased strength and size of the contractile unit of muscle. Ultimately this means greater force production. This is often referred to as functional muscle, while sarcoplasmic hypertrophy is referred to as non-functional muscle. ATP and Muscular Growth as we said earlier, increasing the number of mitochondria in the cell means increased ATP production. ATP is required for protein synthesis to occur. Low levels of ATP will halt muscular growth as well as inhibit other metabolic functions that take place inside the muscle cell. Siff and Verkhoshansky have shown that it is possible to increase your muscles contractile unit faster than the mitochondria’s ability to compensate for this growth. When actin/myosin filaments out grow the number of mitochondria, growth of elements besides the sarcomere is inhibited. The insufficient quantity of ATP results in the body’s inability to promote protein synthesis.

You actually can get large muscles from lifting light weights. Here’s how:

It turns out that lifting a weight that’s 90% of the maximum weight you can lift until you can’t lift any more (failure) is less effective at muscle building than lifting a weight that’s 30% of the maximum weight you can lift until you can’t life any more (failure). It turns out you lift the lighter weight a lot more times and that builds more muscle. here is that study: via

We report for the first time that low-load high volume resistance exercise (30FAIL) is more effective at increasing muscle protein synthesis than high-load low volume resistance exercise (90FAIL). Specifically, the 30FAIL protocol induced similar increases in MYO protein synthesis to that induced by the 90FAIL protocol at 4 h post-exercise but this response was sustained at 24 h only in 30FAIL. …  There were three groups: 90% 1RM to failure (90FAIL), 30% 1RM which matched the external work to the 90FAIL group (30WM), and 30% 1RM to failure (30FAIL). 

The fact is that most people when lifting a light weight don’t lift it enough times to reach failure, so that’s probably why this study is a bit counter intuitive.
The reality is if you push yourself to near failure any weight and rep combination, you’ll likely get results.