Strength training does not result in muscle growth

There are two schools of thought when it comes to bodybuilders’ training. According to one, muscles grow faster if you push them hard during a workout. This philosophy says you have to surprise muscles or, even better, push them to the limit. The sorer the muscles afterwards, the better. If it hurts, it works, the saying goes. The other philosophy says that strength athletes should push their muscles, but they’ll grow faster if they are not pushed to the limit. Always leave a little bit in the gas tank. According to a Brazilian study, the latter training philosophy is probably the right one.

The researchers got ten young men, all of whom had not touched a barbell for at least six months, to train their legs by doing leg presses and leg extensions twice a week for 10 weeks.

In week 1 [T1], 3 [T2] and 10 [T3] the researchers took a small sample of muscle tissue from the vastus lateralis muscle just before, and 24 and 48 hours after the workout and studied it under the microscope. The researchers also took blood samples at the same time, measured the strength in the participants’ legs and asked the men to indicate how sore their muscles were feeling on a scale of 0-10.

The figure below shows that the muscle fibres in the vastus lateralis only showed growth in week 10. Nevertheless, the synthesis of muscle proteins [FSR] was higher in the first week, when the muscles were overcome by stimuli they weren’t used to, than in weeks 3 and 10. This is shown in the second figure below.

The men had more creatine kinase in their blood after doing the workout in week 1 and 3 than in week 10. A high level of creatine kinase is a sign of muscle damage.

The men reported more muscle soreness in week 1 than in weeks 3 and 10, as the figure above shows. In addition, the men lost a considerable amount of muscle strength after their workout in week 1. The figure below shows this.

The cells in the men’s leg muscles only started to grow when the men had become used to the training stimuli. Hypertrophy in the muscle tissue only started to occur once the men did not have sore muscles after working out, and once their creatine kinase levels were not spiralling high.

Of course strength training stimulates muscle growth, the Brazilians concluded. But not if the stimulus is too intense.

Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage

Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown.
We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post-RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3.

Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3.
When muscle damage was the highest, so was the integrated MyoPS (at T1), but neither were related to hypertrophy; however, integrated MyoPS at T2 and T3 were correlated with hypertrophy.
We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.


Skeletal muscle hypertrophy is one of the main outcomes of resistance training (RT), but how hypertrophy is modulated and the mechanisms regulating it are still unknown. To investigate how muscle hypertrophy is modulated through RT, we measured day-to-day integrated myofibrillar protein synthesis (MyoPS) using deuterium oxide and assessed muscle damage at the beginning (T1), at 3 weeks (T2) and at 10 weeks of RT (T3). Ten young men (27 (1) years, mean (SEM)) had muscle biopsies (vastus lateralis) taken to measure integrated MyoPS and muscle damage (Z-band streaming and indirect parameters) before, and 24 h and 48 h post resistance exercise (post-RE) at T1, T2 and T3. Fibre cross-sectional area (fCSA) was evaluated using biopsies at T1, T2 and T3. Increases in fCSA were observed only at T3 (P = 0.017). Changes in MyoPS post-RE at T1, T2 and T3 were greater at T1 (P < 0.03) than at T2 and T3 (similar values between T2 and T3). Muscle damage was the highest during post-RE recovery at T1, attenuated at T2 and further attenuated at T3. The change in MyoPS post-RE at both T2 and T3, but not at T1, was strongly correlated (r ≈ 0.9, P < 0.04) with muscle hypertrophy. Initial MyoPS response post-RE in an RT programme is not directed to support muscle hypertrophy, coinciding with the greatest muscle damage. However, integrated MyoPS is quickly ‘refined’ by 3 weeks of RT, and is related to muscle hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent changes in MyoPS post-RE in RT, which coincides with progressive attenuation of muscle damage. Source: