One more thing - All my Eth is unstaked. I go through an quarterly exercise looking at my entire portfolio and any edges to maximize revenue. So, with regard to ETH, just looking at possibly of staking - seems staking yield is less than 2% pa now. Am I correct?

Are you fucking kidding me?

What in the holy Goodrum assfuck is this phaggotry?

For fucks sakes some of you bedwetting pansies need to kill yourselves.

Mechanisms of Muscle Growth

The two primary mechanisms proposed for muscle growth are hypertrophy and hyperplasia.

Hypertrophy

Muscle hypertrophy is the most well-established and significant mechanism for increasing muscle mass in humans. It involves an increase in the cross-sectional area of individual muscle fibers, primarily due to an increase in the number and size of myofibrils within the fiber (Physiology of Sport and Exercise). This process is stimulated by mechanical tension, muscle damage, and metabolic stress, which trigger a cascade of cellular events leading to increased protein synthesis and decreased protein degradation (Strength and Conditioning: Biological Principles and Practical Applications). Satellite cells, quiescent myogenic stem cells located between the basal lamina and sarcolemma of muscle fibers, play a crucial role in hypertrophy. Upon activation by exercise, these cells proliferate, differentiate, and fuse with existing muscle fibers, donating their nuclei to support the increased protein synthesis required for fiber growth (The Oxford Handbook of Exercise Science).

Hyperplasia

Hyperplasia refers to an increase in the number of muscle fibers. While well-documented in some animal species, particularly birds and certain mammals in response to extreme overload, its occurrence in adult human skeletal muscle is far less clear and remains a subject of considerable debate (ACSM's Advanced Exercise Physiology).

Evidence for and Against Hyperplasia in Humans

The evidence for hyperplasia in humans is largely indirect and often based on observations that are difficult to definitively attribute to new fiber formation rather than other adaptive processes.

Arguments for Hyperplasia

Some researchers have proposed that hyperplasia might contribute to extreme muscle growth observed in elite bodybuilders or in response to very high-intensity, long-term resistance training.

Animal Studies: Studies in animals, particularly avian models (e.g., stretch-induced growth in the patagialis muscle of quail), have shown clear evidence of hyperplasia. When muscles are subjected to extreme overload, new fibers can be observed to form, often through longitudinal splitting of existing fibers or the differentiation of satellite cells into new fibers (Textbook of Work Physiology: Physiological Bases of Exercise). However, extrapolating these findings directly to humans is problematic due to significant physiological differences.
Cross-Sectional Studies: Some cross-sectional studies comparing highly trained athletes (e.g., bodybuilders) with untrained individuals have reported a higher number of muscle fibers in the trained group. However, these studies are correlational and do not prove causation. Differences could be due to genetic predisposition (individuals with more fibers might be more likely to excel in bodybuilding) or methodological limitations in fiber counting (Essentials of Strength Training and Conditioning).
Longitudinal Splitting: One proposed mechanism for hyperplasia in humans is the longitudinal splitting of existing, hypertrophied muscle fibers. As a fiber grows to a very large size, it might split along its length, effectively creating two smaller fibers from one larger one. This could be a mechanism to maintain an optimal surface-to-volume ratio and diffusion distances within the fiber. Some histological studies have reported observations consistent with fiber splitting in human muscle biopsies after intense training (Exercise Physiology: Theory and Application to Fitness and Performance). However, distinguishing true splitting from artifacts of tissue preparation or the presence of very small, regenerating fibers can be challenging.
Satellite Cell Differentiation: Another hypothesis is that satellite cells, in addition to fusing with existing fibers, could differentiate and fuse to form entirely new, small muscle fibers. While satellite cells are crucial for repair and hypertrophy, their direct role in de novo fiber formation in adult human muscle under normal exercise conditions is not definitively established (The Sarcopenia Handbook).
Arguments Against Hyperplasia

The majority of the scientific consensus leans towards hypertrophy as the predominant mechanism for muscle growth in humans, with little conclusive evidence for significant hyperplasia.

Methodological Challenges: Accurately counting muscle fibers in human biopsies is technically challenging. The irregular shape of fibers, the presence of connective tissue, and the difficulty in obtaining representative samples make it hard to definitively determine changes in fiber number. Many studies that initially reported hyperplasia have been criticized for methodological flaws (Muscle: The Physiology of Contraction).
Lack of Direct Evidence: Despite decades of research, no definitive, universally accepted direct evidence of significant de novo muscle fiber formation in adult humans in response to exercise has been presented. Most observed increases in muscle mass can be fully accounted for by hypertrophy (Physiology of Sport and Exercise).
Genetic Predisposition: The number of muscle fibers in humans is largely established during fetal development and early childhood. While some minor adjustments might occur, a substantial increase in fiber number in adulthood through exercise is not widely supported by current evidence (Human Physiology: An Integrated Approach).
Focus on Hypertrophy: The vast majority of research on muscle adaptation to resistance training consistently demonstrates that hypertrophy is the primary driver of strength and mass gains. The cellular and molecular pathways involved in hypertrophy are well-understood, whereas those for hyperplasia in humans remain speculative (ACSM's Guidelines for Exercise Testing and Prescription).

Current Scientific Consensus

The prevailing scientific view is that while hyperplasia might occur to a very limited extent in humans under extreme and prolonged training conditions, it is not a significant contributor to overall muscle mass gains. The primary and most robust mechanism for increasing muscle size in response to exercise is hypertrophy. Any potential hyperplasia is likely to be minor and difficult to distinguish from other adaptive processes or methodological variations. The focus of exercise physiology research and practical training applications remains firmly on optimizing the stimuli for muscle fiber hypertrophy.

Conclusion

In summary, while the concept of creating new muscle fibers (hyperplasia) through exercise in humans has been explored, the overwhelming scientific evidence indicates that the primary mechanism for muscle growth is hypertrophy—the increase in the size of existing muscle fibers. While some animal studies and indirect human observations have suggested the possibility of limited hyperplasia, particularly through longitudinal fiber splitting, definitive and widespread evidence in adult humans is lacking. Therefore, for practical purposes and based on current scientific understanding, exercise primarily leads to an increase in the size, rather than the number, of muscle fibers.

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