Hypertrophy consists in muscle remodeling and
addition of cellular protein structures after a bout of strenuous exercise and
muscle damage. As a consequence muscle fibers grow in cross-sectional area and
the muscle becomes thicker. Several factors regulate this adaptive response,
including hormones, genetics and protein synthesis.
Hormones
Hormones as IGF-1, testosterone, and growth hormone
play a major role in this response (1,2,3). When these hormone levels are
reduced as in elderly populations the hypertrophic response is blunted (4,5).
However it must be noted that acute short-term rises in these hormones after training have a negligible effect on hypertrophy (6-13). It’s only in the case of supraphysiological levels that these hormones make a difference (9,50,51,52,53).
However it must be noted that acute short-term rises in these hormones after training have a negligible effect on hypertrophy (6-13). It’s only in the case of supraphysiological levels that these hormones make a difference (9,50,51,52,53).
Skeletal-muscle adaptation is an intrinsic process. McMaster’s University has
done much of this work. For example, in one study the same subjects performed
both resistance and endurance exercise on each leg and showed different
adaptations for each leg. Resistance exercise stimulated both myofibrillar
and mitochondrial protein synthesis, while endurance exercise stimulated mitochondrial
protein synthesis but not myofibrillar protein synthesis (37).
Exercise programs should not be centered on the
manipulation of acute exercise variables and multi-joint exercises seeking to
induce a favorable ‘anabolic’ hormonal milieu.
Genetics and hyper-responders
Genetics is a key factor in the variability
between individuals (6,14,15,18,43,44), in fact subjects can be stratified as low,
moderate and high responders (16,17,18,45). High responders can have 4
to 5 times greater hypertrophic response compared to low responders (18),
and interestingly some subjects are in fact non-responders and can even lose
muscle mass despite proper training and nutrition.
In one paper the hypertrophic range in
cross-sectional area (CSA) for type I and Type 2 fibers was between -22 to 106%
and -4 to 67% respectively (6). In another cluster analysis the range
for nonresponders was -16 ±99 µm2 for CSA (17). In another study the
lowest responders gained about 1 kg while the highest responders gained 5 to 6
kg of LBM, in 12 weeks (18).
In another study results ranged from -2 to +59% (-0.4 to +13.6 cm) in biceps muscle size, with
the exercise training program leading to an average of 18.9% gain in biceps
CSA size in 12 weeks (14)!
Even with 3 different programs (volume load equated) there is great variability between trained (>4 years) individuals in hypertrophy ((1.7–13.3%) and strength after 12 weeks (55).
See those 4 subjects in the NP group above +2kg, and those 2 up there above +4 kg? What about in the HP
group those 3 up there around +6kg LBM
in 8weeks? Same with the body fat individual data.
Here is another study with creatine and creatine nitrate for only 28 days (56). See those subjects above 4kg LBM and the ones at 7-9 kg LBM? Obviously some of these gains are attributed to water and glycogen via creatine, but...
This variability is related to changes in microRNA androgen expression (6,18,19), satellite cell number for remodeling (20,21,22,23,24,25,26,27,28), intramuscular anabolic signaling protein activation (29), protein synthesis (30,31), and genetic variation (32,41).
Even with 3 different programs (volume load equated) there is great variability between trained (>4 years) individuals in hypertrophy ((1.7–13.3%) and strength after 12 weeks (55).
Another study with trained subjects either getting normal or higher protein also show
great variability between subjects (54). For the normal protein group (2.3g/kg) and also the higher protein group
we can see a mean change in FFM of +1.5kg in 8 weeks, but thankfully we have individual data which is more telling
of what can happen:
Here is another study with creatine and creatine nitrate for only 28 days (56). See those subjects above 4kg LBM and the ones at 7-9 kg LBM? Obviously some of these gains are attributed to water and glycogen via creatine, but...
This variability is related to changes in microRNA androgen expression (6,18,19), satellite cell number for remodeling (20,21,22,23,24,25,26,27,28), intramuscular anabolic signaling protein activation (29), protein synthesis (30,31), and genetic variation (32,41).
In one study investigating the systemic
correlates of resistance training-induced hypertrophy (16wk), the change
(increase) in androgen receptor protein content and the magnitude of the
protein kinase p70S6K phosphorylation (a target of mTOR) after 5h, accounted for
46% of the variance in the hypertrophic response (6). Some of the subjects had
a 1.5-2.5 fold increase in AR protein content, suggested to account for about
25% of the variability.
Some subjects show little to no gain, and others show profound changes, increasing size by over 10 cm2 and doubling their strength. There is also variability between men and women; men had only a slight advantage in relative size gains compared with women, whereas women outpaced men considerably in relative gains in strength (46).
Some subjects show little to no gain, and others show profound changes, increasing size by over 10 cm2 and doubling their strength. There is also variability between men and women; men had only a slight advantage in relative size gains compared with women, whereas women outpaced men considerably in relative gains in strength (46).
Some
individuals even lose strength and muscle mass. Another
study collected data of untrained
healthy men and women (age 19 to 78 years, n =
287 with 72 controls) from ten 20–24 weeks RT
interventions. Muscle size changed during RT had a range from −11
to 30 % (47).
From
the total group of 287 training subjects, the response of 35 subjects (12.2 %)
were defined as high responders with
increased muscle size gains between
10% to above 30% of muscle size (47).
Now if this high-responder gains in the untrained continue over time, if they continue to respond 4-5x better compared to moderate or low responders is unknown from a scientific perspective.
Protein synthesis
The muscle protein synthesis acute response from
exercise is a dose-response depending upon exercise intensity and workload.
After a latent period after exercise of about 45 minutes to an hour (33), MPS
rises sharply (2-3 fold) between 45 and 150 min.
This increase in MPS may be sustained for up to 4h in the fasted state after exercise (33), and in the presence of increased AA availability up to 24-48h after exercise (34,35) or even 72 (42) before returning to baseline.
This increase in MPS may be sustained for up to 4h in the fasted state after exercise (33), and in the presence of increased AA availability up to 24-48h after exercise (34,35) or even 72 (42) before returning to baseline.
Remarkably, even training after fasting
(overnight) the rate myofibrillar protein fractional synthetic rate is
still elevated over breakdown (36). This means that we are not catabolic in the
fasted state. The increased synthesis over breakdown appears to come from
non-myofibrillar proteins (i.e. collagen, sarcoplasmic, and/or mitochondrial
proteins), because muscle protein breakdown is also elevated after exercise
(36). The exercise stimulus is therefore the greatest anabolic signal.
However, acute measures (1-6h post exercise) of
MPS following an initial exposure to RE in novices are not correlated with
muscle hypertrophy following chronic resistance training (39). There’ also a
review on the relationship between acute of muscle protein synthesis response
and changes in muscle mass (40).
Muscle protein breakdown is also important for the regulation of muscle hypertrophy on the long term, and the chronic (positive) balance between MPS and MPB is more important than considering acute rises in MPS.
Muscle protein breakdown is also important for the regulation of muscle hypertrophy on the long term, and the chronic (positive) balance between MPS and MPB is more important than considering acute rises in MPS.
Keep also in mind that mRNA translation is thought
to be the rate-limiting step in protein synthesis (48,49).
There are many ways and mechanisms of
hypertrophy, as summarized by Schoenfeld (38): mechanical tension,
muscle damage and metabolic stress. There is no “one-size fits all”, and
some will simply respond better or worse than others. Despite all this
inter-individual variability, there are some general evidence-based
recommendations for hypertrophy, regarding exercise programs.
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