In humans, skeletal muscle mass can be increased in two primary ways: muscle hypertrophy and muscle hyperplasia. These two processes, while being intimately linked with one another, represent distinct biological mechanisms for muscle growth. A comprehensive understanding of these mechanisms, their differences, and the evidence supporting the occurrence of muscle hyperplasia in humans is vital to effectively advancing the study of muscular physiology as well as the development of targeted conditioning and strength training protocols.
Muscle Hypertrophy and Hyperplasia: A Deeper Dive
The term muscle hypertrophy describes an increase in the size – that is to say, both the diameter and the volume – of an existing muscle fiber. It is a term that is well known to anyone who exercises with the goal of increasing muscle mass. In contrast, an enlargement of muscle mass due to muscle hyperplasia involves an increase in the sheer number of fibers within a muscle. Muscular hypertrophy, a process triggered by an array of factors such as strength training and resistance exercise, results primarily from an increase in protein synthesis exceeding that of protein degradation within muscle cells. Hypertrophy, in essence, stems from localized micro-damage to muscle tissue leading to a process of cellular repair and adaptation. What about hyperplasia?
Muscle hypertrophy refers to the increase in size or volume of existing muscle fibers. It occurs as a result of resistance training or other forms of exercise that cause muscle fibers to adapt and grow. Hypertrophy is primarily driven by an increase in the size of individual muscle fibers, rather than an increase in their number. This means that the existing muscle fibers become larger and thicker, leading to an overall increase in muscle size. Hypertrophy is a well-documented phenomenon in humans and is commonly observed in individuals who engage in regular strength training exercises.
Muscle hyperplasia refers to an increase in the number of muscle fibers. Unlike hypertrophy, hyperplasia involves the formation of new muscle fibers through the division of existing ones. This process is more commonly observed in animals, particularly during early development or in response to certain physiological conditions. However, the evidence for muscle hyperplasia in humans is limited and controversial.
Is Muscle Hyperplasia Really Possible in Humans? Scientific research?
The possibility of hyperplasia occurring in humans has been a topic of controversy and unanswered questions. The often-cited supporting evidence for hyperplasia stems primarily from research involving animal models, with divergent results and interpretations blurring the clear-cut conclusion. In human studies, the evidence, some would argue, is rather thin. This begs a critical question: Despite the fact that robust and undisputed evidence for hyperplasia in humans remains elusive, can we categorically rule out the potential role this biological process may play in human muscle growth?
Those positioned in the affirmative camp argue that the prevalence of muscle fiber splitting, often witnessed in response to extreme physiological stressors (such as intensive resistance training or significant muscle damage), could be indicative of hyperplasia. They propose that the existence of new, smaller muscle fibers could potentially be a consequence of parent fibers splitting, hence leading to an absolute increase in fiber number.
The team arguing against it, however, believes this concept is built on shaky grounds. They argue that the increase in fiber number could equally be attributed to satellite cells, undifferentiated myogenic cells that reside in skeletal muscle tissue, coming to the rescue in response to muscle damage. The satellite cells may donate their nuclei to the damaged muscle fibers, increasing the overall protein synthesis rate and facilitating more significant repair and growth.
This seeds doubt about the roles of hypertrophy and hyperplasia in muscle growth and highlights the important need for further research to explore this dichotomy.
Moving from empirical observations to experimental evidence, it is important to remember that controlled human studies on muscle hyperplasia are incredibly sparse, and those that exist are fraught with methodological limitations. The most tangible evidence comes from an early study conducted by Tamaki et al. (1992).
This highly cited study found that, after an intensive resistance training program, the cross-sectional area of the muscle increased while the size of individual fibers remained mostly unchanged, hinting at an increased number of fibers. However, later examinations and critiques of this study concluded that the observed increase in cross-sectional area could be attributed to enhanced muscle density or an increase in non-contractile elements, rather than purely an increase in muscle fiber number.
In our pursuit of an empirical understanding of the major mechanisms driving skeletal muscle growth, we must bear in mind that the science of muscle hypertrophy and hyperplasia, unlike other mature fields, is still in its relative infancy. The interpretation of existing research findings and theories should be approached with caution and a recognition of the many unknowns that persist.
In conclusion, although human muscle hyperplasia remains under speculation due to the lack of irrefutable scientific evidence, dismissing its occurrence would be premature. The field at large recognizes that our understanding of these mechanisms is far from complete, and as such, researchers continue to explore this lesser-known frontier of muscle biology. Nevertheless, the bottom line is that if hyperplasia does occur, it likely only accounts for a small portion (e.g., 5 percent) of the increase in muscle size. Therefore, hypertrophy is the primary mechanism for muscle growth in humans.