Resistance training is an excellent way of building muscle mass (hypertrophy) and preventing muscle loss (atrophy) following forced or desired immobilization, or due to age. To optimize gains in muscle hypertrophy, it is often recommended to use loads whose intensity can vary from 30 to 85% of 1RM. In the scientific literature, several hypotheses have been put forward to explain the growth of muscle tissue. Hypertrophy could be stimulated by mechanical tension, metabolic stress and/or muscle damage occurring during exercise, activating pathways that promote the accumulation of muscle proteins in the muscles involved.
Metabolic stress is characterized by an accumulation of metabolites during exercise. And it is assumed that these metabolites have a direct or indirect effect on hypertrophy. What's more, metabolic stress is often associated with muscle congestion (the "pump"). When muscles are gorged with blood, particularly during sets with a high number of repetitions and short rest periods, this leads to an accumulation of metabolites, such as lactate, which draw more fluid into the muscle cells. This acute cellular swelling affects the muscle's water balance. During intense muscle contractions, the veins would be compressed, increasing the concentration of blood plasma in the muscles. The plasma would then flow into the spaces between the cells, causing a pressure gradient that draws plasma back into the muscles, a process known as "reactive hyperemia".
Muscle congestion is generally temporary. It's often used by bodybuilders before competitions to make muscles look bigger and denser. Most bodybuilders often seek to maximize this effect during their workouts for immediate swelling and the feeling of pleasure it brings. Some recent research suggests that congestion may also contribute to long-term muscle growth. Indeed, cellular swelling has been shown to increase protein synthesis and decrease protein degradation in various tissues, including muscle. These signalling pathways may be activated in response to the stretching of the cell membrane caused by swelling. To protect its integrity, the cell would send signals to strengthen itself. Although congestion is associated with the presence of large quantities of metabolites, and therefore with the use of relatively light loads, what happens when high loads are used?
To find out more, researchers compared the acute effects of two weight training protocols of equivalent volume on muscle congestion, in 8 experienced resistance-trained men (6.7 ± 2.8 years of practice; 1RM unilateral biceps curl: 29.4 ± 6.8 kg). To do this, they compared two protocols on the dominant arm, one week apart: a low-load session with 4 sets at 50% of 1RM until muscle failure; and a high-load session with 10 sets at 85% of 1RM until muscle failure. In both cases, the rest period between each set was set at 90 seconds. Both protocols were equivalent in volume, that is, they involved lifting the same total load (sets x repetitions x load).
To compare the effects of the two protocols, the researchers measured the thickness of the elbow flexor muscles (biceps brachii and brachialis) using ultrasound, arm circumference and blood lactate concentration. All these measurements were taken before and 10 minutes after each protocol. To assess acute cell swelling, many studies have used variations in muscle thickness or cross-sectional area. Ultrasound is a relatively inexpensive and non-invasive method for assessing skeletal muscle and can be used immediately after exercise.
The main results of this study show that low-load and high-load resistance training lead to similar and significant increases in muscle thickness and blood lactate concentration. Low-load training led to a greater increase in muscle thickness of 18.9% (from 42.08 to 50.06 mm), while high-load training led to an increase of 11.53% (from 41.04 to 45.81 mm). However, the researchers observed no statistically significant difference between the two conditions.
In terms of blood lactate concentration, for low-load training, blood lactate concentration increased by 163.6% (from 1.61 to 4.08 mmol/l), and for heavy-load training, by 105.48% (from 1.85 to 3.5 mmol/l). Again, no statistically significant interaction was observed between conditions. However, this adds to the evidence suggesting that the low-load resistance training protocol potentially stimulates a more favorable environment for acute cell swelling.
Whether with light or heavy load, both protocols elicit significant lactate production and a significant increase in elbow flexor muscle thickness after a session with equal volume load. This suggests that muscle congestion, and by extrapolation cellular swelling, can be stimulated by a wide range of external load intensities. However, it would seem that a session involving longer times under tension would tend to have a greater impact on congestion.
Most importantly, however, the precise role of cell swelling on long-term muscle hypertrophy remains to be elucidated. Cellular swelling occurs when there is an increase in the water content inside a cell, causing it to expand. Some studies hypothesize that the muscle nucleus is a mechanoreceptor and therefore actively participates in mechano-transduction. The larger volume would apply stress to the nucleus, triggering a series of biochemical events, such as the stimulation of protein synthesis to strengthen muscle fibers, and the inhibition of protein degradation. This process could lead to cell growth and repair, and could contribute in part to muscle growth. Finally, bear in mind that cell swelling is associated with both metabolic stress and muscle damage, in the form of an inflammatory response. Thus, the relative role of congestion on muscle hypertrophy has yet to be precisely defined, and it should not be the focus of your sessions. There are other more important variables to focus on, such as training volume and exercise choice.
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