What should the protocols be on achieving the best possible lift when testing for a 1RM? Lets use bench press as an example with a PB of 385lb last time I tested and now looking to do 405lb. I personally believe that the least amount of lifts you do before your max the better; however, you still have to do a couple of single rep lifts as prescribed above. For example, when I hit my PB of 405lbs this is the sequence I used,
Glutamine for the macrocycle as well as Creatine (a little more on test day).
Carb loading for the 2 days prior to and including the day of the test.
10 min of cycling to warm up. Make sure to take lots of water and Gatorade.
BARx20 1min rest
135x10 3min rest
245x4 3min rest
275x1 3min rest
335x1 5min rest (Focus on Compensatory Acceleration)
405x1 NEW PB :eek: (Focus on Compensatory Acceleration)
Now some thoughts on what should be done. These are open to debate and not all of which do. Note some things can be taken out or rearranged. Some possiblities to include are,
Carb loading for the 2 days prior to and including the day of the test.
After 10min cyling. Make sure to take lots of water and Gatorade.
I would do a dynamic warm-up involving inch worms (definition below)
Then stretch the antagonist muscles the Lats & Biceps.
Then use the sequence noted above which is,
BARx20 1min rest
135x10 3min rest
245x4 3min rest
275x1 3min rest
335x1 3min rest (Focus on Compensatory Acceleration)
495 done Eccentrically loading muscles and preparing for Supercompensation.
3min rest
Then do 4 Plyo Pushups
2 min rest Make sure AC/DC is on & the song is Thunderstruck
Or Alternatively Rocky Soundtrack song is Eye of The Tiger
On the song selection there can be not debate.
405x1 NEW PB (Focus on Compensatory Acceleration)
Remember the stuff in bold above is not what I currently do but I things that I am debating on doing.
The defintion of an inch worm is an exercise where your hands and feet are on the ground and your body is in pushup position, then in this position you shift your body back and then down and forward doing a dip under an imaginary tipped over hurdle (or a stick 16 inches of the ground or like Catherine Zeta Jones in The Rock) all this time your feet and hands don’t come off the ground. To put it another way your rotating your shoulders in a counter clockwise manner if someone is looking at you sideways and the wt of the upperbody is on those joints. Do about 8 rotations. The next step is walking inch worms where after you do one rotation of shoulders you then bring your feet to your arms in a crawling like motion with one foot ahead of the other (your feet go in a straight parallel line in front of each) and once the feet reach the hands you swing your arms forward off the ground in front of you to the push up position and repeat the shoulder rotation.
The reason you don’t focus on Compensatory Acceleration before your last two sets is that you want to fire the least amount of MU and muscle fibers as possible until you get close to your 1 RM and the same goes for Plyo Pushups, you have to do it on the 335lb warmup bench press set so that you get them prepared for the 405lb lift. This I believe is very similar to CF’s massage techniques in order for the elite sprinter to run the best possible sprint in the final he has CF will do a massage on him so that the sprinter can get by the first two rounds by using the least amount of fibres before running the final. The reason I would do Plyo Pushups is to recruit MU and muscle fibres for the bench press to follow. The reason I included inch worms were to get the upper body really warmed up and increase blood flow/pump to the those muscles (remember the calve muscle acts like a second heart and pumps blood back upto the main heart). For reasons concerning why I would stretch the antagonistic muscles read my post below from another thread,
From: http://www.exploringspasticity.com/explore/muscle.html
What is Normal Muscle Control?
Normal Muscle Control
Despite its seeming simplicity, normal muscle control is actually very complex, involving several interacting regions of the brain and spinal cord. Voluntary movement of a muscle begins when electrical signals are generated in the outer layer of the brain. These electrical signals pass through the midbrain to the spinal cord along so-called upper motor neurons. Within the spinal cord, they connect to lower motor neurons, which convey the signals out of the spinal cord to the surface of the muscle involved. Electrical stimulation of the muscle causes contraction. The force of contraction pulling on the skeleton causes movement of the limb. Damage to the upper motor neurons or their connection to lower motor neurons is the cause of most spasticity.
Muscles are present in opposing groups, such as the biceps and triceps of the upper arm. Contraction of the biceps bends the elbow, while contraction of the triceps straightens it. When a muscle is being intentionally stimulated to contract, it is called an agonist. Opposing muscles are called antagonists. For instance, when you flex your biceps, it is the agonist, while the triceps is the antagonist. Note that any given muscle will be an agonist in one situation, but an antagonist in another. Also note that when an agonist contracts, the antagonist naturally gets stretched. The response to this stretching is what goes wrong in spasticity.
This natural stretching of antagonist muscles is necessary for movement, but too much stretching can damage the muscle. Two related signaling pathways help prevent too much, and too little, stretch of the antagonist. [1] First, while an agonist is contracting, the spinal cord sends inhibitory signals to the antagonist to prevent it from contracting while it is being stretched out. Second, the antagonist sends sensory signals back to the spinal cord to indicate how much it is being stretched. When the antagonist is stretched too far or too fast, these sensory signals override the inhibitory signals and set off protective contractions in the antagonist to prevent muscle damage. This protective contraction is seen in the stretch reflex that makes your knee jerk when the doctor hits a tendon with a rubber mallet. These two antagonist-regulating pathways help to ensure that the intended movement can occur, but cannot damage surrounding muscles.
Spasticity occurs when these two antagonist-regulating pathways are improperly controlled, usually due to upper motor neuron damage. First, the pathway that normally inhibits antagonist contraction becomes less active than normal, leading to unwanted co-contraction of antagonists during movement of an agonist. This prevents smooth movement and full range of motion in the agonist. Second, the stretch reflex becomes hyperactive, so that the antagonist is likely to contract even when stretched only slightly. As a result of loss of inhibition and hyperactive stretch reflexes, movement becomes difficult to control, and muscles may remain stiff and contracted for long periods of time.
Referring to the bold print up above I believe that the body sets these protective mechanisms at a point well before injury. I believe you can extend this point closer to the point of injury and therefore have bigger lifts but you do take on a greater chance of injury. You don’t want to overstretch and injure yourself, so this is a very tricky game of when is to little to produce the desired effect and when is to much that it causes injury?