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In order of importance:
1) Satellite cells must be activated, differentiated, and fuse with existing fibers, donating their nuclei.
2) Mechanical stress must be transmitted to the sarcolemma (mechanotransduction) and contractile protein structures within the sarcomeres. This will trigger focal adhesion kinases (FAK) that in turn initiate the downstream signaling events leading to an increase in the contractile and cytoskeletal protein expression/synthesis.
3) pH and oxidative stress must be acutely increased within the muscle fiber.
Focusing just on the workout, this pretty much sums it up. If #1 doesn’t happen, you will not grow…ever. If number two doesn’t happen, you will grow a little, but you will soon reach the limits of the sarcoplasmic/nuclear ratio and growth will stop. If #3 doesn’t happen, you will still grow quite significantly, but the rate of growth might be enhanced or facilitated if #3 is achieved.
#1 is achieved when a certain level of microtrauma is experienced by the fibers. This is brought about by load, eccentric contractions, and to a much lesser extent, hypoxia (A.K.A. #3) When load, eccentric contractions and #3 occur, each fiber will produce and release muscle specific-IGF-1 (sometimes called mechano-growth factor) The IGF-1 in turn seeps out of leaky sarcolemmas and acts on nescient satellite cells to initiate #1. Microtrauma is rapidly reduced from workout to workout (Repeated bout effect) thereby limiting the effectiveness of any given load to induce further hypertrophy.
#2 is achieved by loading a muscle that is actively contracting.
#3 is achieved by contracting a muscle (doing reps) until you create an oxygen deficit and subsequent hypoxic byproducts (e.g. lactate and oxygen radicals).
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Skeletal muscle is a dynamic tissue that responds adaptively to both the nature and intensity of muscle use. This study tested the hypothesis that a damaging bout of exercise is pre-requisite for muscle hypertrophy. Although this hypothesis has been widely accepted, there is surprisingly scant evidence that muscle damage, accompanied by an inflammatory response, is a necessary precursor to muscle hypertrophy. Subjects were divided into two experimental populations: (PT) pre-trained (n=7) and (NA) naïve (n=7). Muscle damage was avoided in the pre-trained group by a 3 week gradual "ramp-up" program before both groups were subjected to an 11 week high force eccentric cycle ergometry program (20min, 3x/week). Work totals throughout the 11 week session were the same for both groups. The naïve group experienced damage, whereas the pre-trained group did not, as indicated by: >5 times higher plasma CK levels and self reporting of perceived soreness, fatigue and exertion. The observed increase in mean cross sectional area (and total muscle volume) was significant for both groups (p<0.01) but not different between groups (NA=7.0% and PT=6.1%). Strength increases were also observed for all subjects in the study (PT=20% and NA=24% improvement) again, no significant difference was found between the groups. Independent of any initial muscle damage, muscle volume increases and quadriceps strength increases were found to be the same for both groups indicating that a damaging bout may not be a prerequisite to muscle hypertrophy. Arizona Technology and Research Initiative Fund.
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Disruption to proteins within the myofibre after a single bout of unaccustomed eccentric exercise is hypothesized to induce delayed onset of muscle soreness and to be associated with an activation of satellite cells. This has been shown in animal models using electrical stimulation but not in humans using voluntary exercise. Untrained males (n = 8, range 22–27 years) performed 210 maximal eccentric contractions with each leg on an isokinetic dynamometer, voluntarily (VOL) with one leg and electrically induced (ES) with the other leg. Assessments from the skeletal muscle were obtained prior to exercise and at 5, 24, 96 and 192 h postexercise. Muscle tenderness rose in VOL and ES after 24 h, and did not differ between groups. Maximal isometric contraction strength, rate of force development and impulse declined in the VOL leg from 4 h after exercise, but not in ES (except at 24 h). In contrast, a significant disruption of cytoskeletal proteins (desmin) and a rise of myogenic growth factors (myogenin) occurred only in ES. Intracellular disruption and destroyed Z-lines were markedly more pronounced in ES (40%) compared with VOL (10%). Likewise, the increase in satellite cell markers [neural cell adhesion molecule (N-CAM) and paired-box transcription factor (Pax-7)] was more pronounced in ES versus VOL. Finally, staining of the intramuscular connective tissue (tenascin C) was increased equally in ES and VOL after exercise. The present study demonstrates that in human muscle, the delayed onset of muscle soreness was not significantly different between the two treatments despite marked differences in intramuscular histological markers, in particular myofibre proteins and satellite cell markers. An increase in tenascin C expression in the midbelly of the skeletal muscle in both legs provides further evidence of a potential role for the extracellular matrix in the phenomenon of delayed onset of muscle soreness.
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1. It adds to the mounting evidence pool that DOMS is not indicative of muscle damage. Something that still seems to permeate the internet bodybuilding lore.
2. As I've said previously the response seen with this study shows us that the satellite cell activation is more atuned to a repairing type response that soley a purely hypertrophic response (conferred from other work).
3. In light of 2 above I still have to wonder if indeed damage is a prerequisite to hypertrophy.
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Abstract:Volitional animal resistance training constitutes an important approach to modeling human resistance training. However, the lack of standardization protocol poses a frequent impediment to the production of skeletal muscle hypertrophy and the study of related physiological variables (i.e., cellular damage/inflammation or metabolic stress). Therefore, the purposes of the present study were: (1) to test whether a long term and low frequency experimental resistance training program is capable of producing absolute increases in muscle mass; (2) to examine whether cellular damage/inflammation or metabolic stress is involved in the process of hypertrophy. In order to test this hypothesis, animals
were assigned to a sedentary control (C, n=8) or a resistance trained group (RT, n=7). Trained rats performed 2 exercise sessions per week (16 repetitions per day) during 12 weeks. Our results demonstrated that the resistance training strategy employed was capable of producing absolute mass gain in both soleus and plantaris muscles (12%, p<0.05). Furthermore, muscle tumor necrosis factor (TNF-a) protein expression (soleus muscle) was reduced by 24% (p<0.01) in trained group when compared to sedentary one. Finally, serum creatine kinase (CK) activity and serum lactate concentrations were not affected in either group. Such information may have practical applications if reproduced in situations where skeletal muscle hypertrophy is desired but high mechanical stimuli of skeletal muscle and inflammation are not. Copyright 2010 John Wiley & Sons, Ltd.
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Reps do not have to be performed consecutively to be effective in creating hypertrophic change.
Metabolic acidosis (accumulation) in this study did not seem to be additive to signaling processes involved in hypertrophy.
Damage was not evident in this study.
Training frequency of 2 or 3 times per week may be equally effective in creating a hypertrophic response.
Assuming that damage isn't necessary for hypertrophy, does this call the HST model into question?