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A Model for Exercise Induced Hypertrophy in Muscle Using Drop Sets

guss

guss

MuscleHead
Aug 11, 2010
380
179
#1
Most bodybuilders rest between sets. They perform a given exercise until muscular failure and then rest for anywhere from less than 30 seconds to three or four minutes or more. The question is, why do bodybuilders rest between sets? Perhaps the single most important reason that bodybuilders believe they should rest between sets is to allow fatigued muscle fibers a chance to recover their force-generating capacity Indeed, this simple tenet is not only strictly adhered to in conventional training circles, but it's also upheld by numerous members of the scientific community.

So, if you were to create a training approach based solely on this conventional sentiment, you'd plan on taking enough rest between sets to be able to maintain muscular force over time. This, presumably, stimulates the greatest degree of hypertrophy. Obviously, this is not the case. As many, if not most, bodybuilders will agree, such routines are more conducive to developing strength-that is, neural adaptations-than muscle hypertrophy, despite the fact that they enable you to perform considerably more work while lifting far heavier loads. Even so, most bodybuilders rest between sets. Hence we have the paradox of bodybuilding, the resolution of which is long overdue.

The Missing Link

In order to use resistance exercise to stimulate muscle hypertrophy, you must understand the relationship between the two at the molecular level. The catch is that this relationship is anything but firmly established. Fortunately, though, patterns are beginning to emerge. Recently, it has become apparent that active tension-that is, the force developed by contraction-in the muscle fibers is a major regulator of growth in skeletal muscle. Though the molecular mechanism by which this physical stimulus actually causes the biochemical alterations associated with muscle hypertrophy is unknown, there are some distinct possibilities. For instance, substances that scientists call second messengers could be involved in causing that force to alter muscle turnover rates. Two substances that scientists have included in this group are the prostaglandins and calcium.

Calcium and Prostaglandins in Muscle Protein Synthesis

Calcium plans a critical role in regulating a variety of biological functions in response to cellular signals. Perhaps its best known function involves regulating muscle contraction. Stored inside the muscle fiber in a saclike structure known as the satcoplasmic reticulum, calcium is released into the region surrounding the contractile filaments, the actin and myosin, in response to a nerve impulse. This is the green light for muscle contraction. Actin and myosin can't associate, or combine, with each other in the absence of calcium, but when the calcium level rises in the fiber following neural stimulation, it attaches to the actin molecules, which enables myosin to hind to actin and the muscles to contract.

When the neural stimulation ends, energy-dependent proteins rapidly pump calcium back into the sarcoplasmic reticulum for safekeeping until the next contraction, the actin and myosin filaments can then disassociate and slide apart so that the fiber can relax and return to its resting length. Higher physiological concentrations of calcium may exert very different effects on a muscle fiber. It may be involved in the effects that hormones like insulin have on growth factors and in the activation of the prostaglandin synthetic pathway, all of which could play a role in the fiber's hypertrophic response.

Increasing the concentration of calcium has been shown to stimulate the synthesis of RNA and protein in cardiac muscle tissue slices and in the skeletal muscle of rats. The calcium-to-muscle growth connection may explain at least one reason why stretching helps induce muscle growth: because it causes an in crease in protein synthesis, possibly by opening stretch-sensitive calcium channels in the muscle cell membrane, increasing calcium influx from the sarcoplasmic reticulum.

As suggested above, scientists believe that calcium might mediate a muscles' hypertrophic response by increasing the activity of the prostaglandin synthetic pathway in the muscle fibers. The prostaglandins are a class of hormone-like compounds derived from the 20- carbon polyunsaturated fatty acid arachidonic acid, a component of the plasma membrane of skeletal muscle fibers. Many of the enzymes involved in freeing arachidonic acid from the membrane structure are calcium-sensitive in that a slight elevation in intracellular calcium leads to an increase in intracellular arachidonic acid levels and so an increase in prostaglandin synthesis. Prostaglandins regulate the muscle hypertrophic response to insulin and force development, and they appear to be involved in the stretch-induced increase in protein synthesis in skeletal muscle described above.

The Bad News About High Calcium Levels

Despite the benefits of calcium discussed above, excessive levels of the mineral can have devastating effects on muscle. Recent research shows that this can cause a decrease in the number of internally bound enzymes involved in &ycolysis, the process in which ATP is synthesized in the cell. This, in turn, causes the APT supply to be depleted, which leads to muscle damage. Under pathological conditions cells can accumulate enough calcium to actually stop the exudative process that resynthesizes ATP, a situation somewhat analogous to putting your car's automatic transmission in neutral and one that is observed in approximately 95 percent of cdl deaths.

The Importance of Stretch

As suggested above, stretch plays a critical role in the stimulation of muscle hypertrophy. But is it likely to be much help to you as a bodybuilder? Probably not. There are several reasons for this. To begin with, any stretching of a muscle is unlikely to be significant under normal conditions. This is due to what is called the stretch reflex and to the anatomical limits set by the muscle's origin and insertion points. Some researchers have suggested that stretch hypertrophyis probably the least applicable model for the study of exercise-induced skeletal muscle hypertrophy in humans.

The response topography is different; the magnitude of muscle enlargement is greater; and the adaptations in muscle length, fiber composition and connective tissue composition are all different from the strength-training situation. Basically, while passive stretch of a muscle will result in increases in amino acid uptake and protein synthesis, it takes a more chronic stimulus-say, 18 hours or more-to make that happen, rather than the brief stimulus of Less than one minute per day that you get from lifting heavy weights.

What's more, unhiNe what happens with weight training, in which the magnitude of training-induced hypertrophy is closely linked to the magnitude of the load, the size of the amino acid uptake response is not directly related to the magnitude of the stretch. It's also been shown that the stretch-induced growth response of muscle doesn't rely on electrical activity. Nevertheless, there does appear to be a common theme to the observations made by many of the studies on stretch-induced hypertrophy-calcium, prostaglandins and increased protein synthesis. The question is, what role, if any, might these two factors play in exercise-induced hypertrophy?

A Model for Exercise-Induced Hypertrophy

I came upon my first clue to this riddle while studying the myotonic myopathies, a group of conditions characterized by abnormally slow relaxation after voluntary muscle contraction. Ask patients who have myotonia to squeeze a tennis ball, for instance, and their clenched fists can only relax very slowly after exer tion In other words, their muscle fibers have higher-than-normal calcium levels after contraction, which leads to a slowed relaxation of the contractile elements. The cause of this condition is unknown.

Research on the subject of myotonia congenita, or Thomsen's disease, a rare form of rnyotonia, turned up a side effect that I found rather interesting: normal muscular hypertrophy. That got me wondering, what's common to both myotonia congenita and resistance training that might stimulate muscular hypertrophy? My answer: prolonged relaxation. Apparently, the elevated calcium levels associated with prolonged relaxation initiate a hypertrophic response in the muscle of patients with that condition. The affected fibers hypertrophy to the extent that the same workload is less likely to elevate calcium levels in the fiber as dramatically the next time. This led to my next question, How can I maximize the intracellular calcium content of my muscle cells during a workout?

Prolonged Relaxation and Muscular Fatigue

In mathematical terms pH refers to the negative logarithm of the effective hydrogen ion concentration of a solution. The higher the hydrogen concentration, the lower the pH, and the more acidic the solution is said to be. The term pH is used to express acidity and alkalinity on a scale that runs from 0 to 14, with 7 representing neutrality, numbers less than 7 showing increased acidity and numbers greater than 7 increased alkalinity.

The major source of acid production in contracting skeletal muscle is the anaerobic production of lactic acid from glucose and glycogen. At physiological pH that lactic acid breaks down into lactate and hydrogen. In general, the higher the exercise intensity, the greater the decline in p1-I; that is, the higher the hydrogen content. During high-intensity exercise such as resistance training, the intracellular p1-I of skeletal muscle can fall to values as low as 6.2, which can have a dramatic effect on a fiber's ability to regulate calcium levels.

Fatigued muscle requires a prolonged relaxation time, and research indicates that the slowed relaxation is due to an increase in intracellular hydrogen content. The observation of a significant correlation between intracellular pH and half-time of relaxation during the recovery from fatigue supports this hypothesis, as does the observation that a decreased pH in the cell fluid maintains an increased calcium concentration.

Many of you have undoubtedly felt the effects of prolonged relaxanon while training, particularly when you were working your abdominals. If you don't take much rest between sets, the pH continues to drop, hindering the ability of the individual cells to resequester calcium between repetitions. Thus, maments begin to have trouble dissociating, and the muscle may actually begin to cramp, or stiffen as you continue.

So here's the theory: During resistance training the intracellular pH of the working muscle fibers drops and calcium levels inside the fibers remain elevated. Following the workout, the prostaglandin synthetic pathway is initiated as a result of the increased calcium content, ultimately leading to a hypertrophic response- Thus, the muscle fibers increase in both size and functional capacity to the extent that the same workload is less likely to elevate calcium levels as easily the next time.

The Drop Set

If maximizing calcium levels in the muscle fibers is going to be your objective at each workout, you'll need a yardstick by which to measure them; that is, to ensure that the pH of the working muscle fibers is depressed as low as possible. Fortunately you've got one, and it's simple to use. The yardstick is force-specifically the decline of force. By reducing the force- generating capacity of the working muscle as completely as possible, you ensure that calcium levels are high in the cell and that your exercise will stimulate a maximum hypertrophic response.

Since testing between sets will enable the force-generating capacity of the muscles to recover-for example, the pH will return to pre-fatigue values-the only logical training technique to use would be the drop set. To perform drop sets, you choose an initial load, and when you hit muscular failure, you reduce the weight-for example, by 20 to 25 percent-and continue the set, going down the rack, as it's called, and dropping the weight until you can reduce the force no further. Assuming you have reduced the force as low as possible, a second drop set will be unnecessary.

Fatigue will simply force you to begin subsequent drop sets with lighter loads, letting you reach that physiological limit sooner but no better off. Consequently, in most circumstances you'll only need one drop set per muscle group, and you can fully stimulate the muscle in only a few minutes.
 
Austinite

Austinite

Member
Sep 21, 2013
40
11
#2
I've noticed several articles that have not been linked to the original source. Am I missing it somewhere?
 
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