Metabolic Stress And Muscular Hypertrophy


What Is Metabolic Stress?

If your goal is to increase muscular hypertrophy then you have probably come across the term metabolic stress. Well, that is not a surprise because metabolic stress plays a large role in muscle gains so it is definitely something you should pay close attention to if more muscle is your goal. However, while many are aware of the term metabolic stress, many are unsure of what it actually is or how you go about effectively inducing metabolic stress in your training.

So, what is metabolic stress? Well, when you utilise your muscles during your training, your muscles need energy. WIthout sufficient energy, your muscles cannot produce sufficient force. The energy needed for optimal levels of force production, comes in the form of ATP. Really, you can think of ATP as stores of energy. Now, this ATP can be supplied from a number of energy systems in the body, but that is not all. As your body produces this ATP through these many energy systems, by-products are produced such as hydrogen ions, lactic acid and phosphate ions. All of which can accumulate over time in the muscle as more ATP is demanded and used up. The build-up of these by-products can lead to changes in the internal environment of the muscle ultimately leading to a stress response. It is this stress response which is thought to trigger a cascade of downstream physiological processes leading to eventual muscular hypertrophy. Which, kind of makes sense, right? If the muscle becomes stressed then it is going to initiate a protection response. How can it protect itself? Become bigger and stronger! Great news for you.

Don’t forget oxygen and cell swelling! It also plays a major role in metabolic stress. When oxygen levels in the muscle drop, a hypoxic environment is created. Lack of oxygen is likely to increase the activity of those energy systems which rely less on oxygen. What happens is that these energy systems which rely less on oxygen, also happen to produce high levels of lactic acid and phosphagen and hydrogen ions. As a result, lower levels of oxygen can lead to an accumulation of these products ultimately inducing stress within the muscle. What then? The hypertrophy process is set in motion! Cell swelling is also something to look at. Accumulation of waste products from ATP utilisation and intense, sustained muscular contractions can lead to an increase in fluid within the muscle. As this fluid builds up, so does the pressure. But, too much pressure is not good! Why? It places huge amounts stress on the structural machinery of the muscle. As a result, the muscle must do something to protect itself and so it is logical that hypertrophy kicks in so that the muscle can reinforce and strengthen its internal structure.

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Resistance Training And Metabolic Stress

An important question to ask is how can you best utilise resistance training in order to enhance the level of metabolic stress? Well, a study conducted by Gonzalez et al. (2015) of ten resistance-trained men, found that acute higher volume resistance training (70% 1RM, 10-12 repetitions, 1 minute rest intervals) induced greater levels of blood lactate, cortisol and growth hormone compared with those utilising high training intensities (90% 1RM, 3-5 repetitions, 3 minute rest intervals).

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Gonzalez et al. (2015). Figures show the acute elevations in IGF-1, Insulin, Testosterone, GH and Cortisol at various time points in response to high-intensity and high-volume training in resistance trained men. High-volume training induced significantly greater elevations in cortisol, GH and insulin over high-intensity training. 

Another study conducted by Tanimoto and Ishii (2006) looked to investigate the effects of low-intensity resistance training (knee extension work) with slow movement and tonic force generation in non-resistance trained men (50% of 1RM, 3 second eccentric and concentric, 1 second pause), on muscular size and strength over a 12-week training period. Two further experimental groups involved a group utilising high-intensity, normal speed work (80% 1RM, 1 second concentric and eccentric actions, 1 second pause) and, low-intensity, normal speed (50% 1RM, 1 second concentric and eccentric speeds and 1 second pause). Important to note is that the amount of work and intensity between the low-intensity, high speed and low intensity-normal speed group was matched. After 12 weeks it was found that low-intensity with slow movements and high-intensity with normal movements produced significant increases in muscular cross-sectional area and strength. But, there was no change with the low-intensity, normal speed group.

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Tanimoto and Ishii (2006). Figure shows the changes in cross-sectional area of the knee extensors in non-resistance trained men following low-intensity, slow speed (LST at 50% 1RM, 3 second eccentric and concentric and, 1 second rest pause), high-intensity, normal speed (HN, 80% 1RM, 1 second eccentric and concentric, 1 second rest pause) and low-intensity, normal speed (LN, 50% 1RM, 1 second concentric and eccentric, 1 second rest pause) resistance training. LST and HN produced significant increases in cross-sectional area of the knee extensors over LN, suggesting that the slower speed (aka increased time under tension) might have provided a hypertrophy signal similar in magnitude to that of the HN training.

Also, it was found that the low-intensity, low speed group exhibited the greatest levels of muscle deoxygenation. This suggested that slower movements allow for constant tension on the muscle, thus enhancing levels of hypoxia which could of lead to the significant improvements in muscular hypertrophy in this group.

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Tanimoto and Ishii (2006). Figure shows the level of oxygenation in the knee extensor muscles in response to LST, HN and LN resistance training. LST induced the greatest levels of reduction in oxygen of the knee extensor muscle. It is likely that this would lead to the greatest accumulation of metabolic waste products (e.g. lactate and hydrogen ions) in turn inducing the greatest degrees of metabolic stress and hence the accompanying hypertrophy response. This could potentially explain the results obtained for LST. 

Interestingly, studies have provided evidence that training to failure with lighter loads, might induce similar magnitudes of muscular adaptations as training with higher loads (but not to failure). A study by Schoenfeld et al. (2015) investigated the differences in muscular size and strength in resistance-trained men over an 8-week period. One group performed a low-load resistance training program (30-50% 1RM, 25-35 repetitions performed per set, per exercise), while the other group performed a high-load resistance training program (70-80% 1RM, 8-12 repetitions per set per exercise). Each group performed 3 sets of 7 different exercises to target all major muscle groups. After 8 weeks it was found that both groups exhibited significant increases in cross-sectional area of the elbow flexors and quadriceps femoris. Why the similarity in results? It is believed that training with lower loads to failure could have exerted higher levels of metabolic stress which in turn, could have allowed for a hypertrophic response similar to that produced in those training with much higher loads (although this has not been specifically proven, it sounds plausible!).

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Schoenfeld et al. (2015). Figures show the changes in cross-sectional area of the quadriceps and elbow flexors in response to low-load and high-load training. Both low-load (30-50% 1RM, 25-35 repetitions, 3 sets) and high-load (70-80% 1RM, 8-12 repetitions, 3 sets) training induced statistically similar increases in cross-sectional areas. It is likely that training to failure of the low-load resistance training group exhibited a hypertrophy response similar to that of the high-load group. Potentially through greater levels of metabolic stress caused through low-load training to failure. 

Training Recommendations?

Research suggests that lower load training with higher repetitions and shorter rest periods can provide a training signal strong enough to elicit muscular hypertrophy gains. It is likely that a combination of these training factors allows for the accumulation of high levels of metabolites which in turn set in motion a chain of events in the muscle leading to eventual hypertrophy. While mechanical tension induced through higher load training (approx. training loads of 75% 1RM and greater) is the main driver of hypertrophy, a level of metabolic stress can likely add to this in order to maximise it. Given that it is not good to always train with heavy loads due to potential recovery issues, adding in frequent low load, higher repetition work can not only aid in recovery, it can also generate the higher levels of metabolic stress needed to keep the hypertrophy process moving along.




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