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Topics - CoolColJ

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Injury, Prehab, & Rehab talk for the brittlebros / Tendinopathy resource
« on: September 06, 2021, 09:56:03 am »

Pics, Videos, & Links / 5'10" 200lbs , head to rim
« on: August 30, 2021, 08:57:44 am »
The guy recently squatted 505lbs, 2.5x BW, after 13 years of training  :ninja:
He follows the Jump Science approach, strength work, then back off completely after a few months and peak the jump

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MUSiC anD SHeeT! / JABBAWOCKEEZ dance crew
« on: August 25, 2021, 01:23:26 pm »
Not sure where to put this..
You may have seen them dance at halftime during many NBA finals over the years, wearing a mask and outfit as per their trademark

But anyway I can't get enough of this, them casually freestyling as they walk around as tourist sans mask) - so much flow

At 1:15 and 5:35
it's almost ends up like Bose speaker commercial  ;D
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I gotta learn that dance moves at 2:43... it's so smooth
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More free styles

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plenty more stuff on their channel

pretty interesting video and perspective

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see the difference in forces (x bodyweight) subjected to the soleus vs the gastroc at various running speeds

They also show that the total calf muscle volume is made of soleus mainly (43.7%), then medial gastroc (34.3%), then lateral gastroc (22.1%). This fits in withthe very high physiological cross sectional area of the soleus (Lieber 2011) and much higher forces (x bodyweight) in the soleus versus the gastroc in running (see table below showing predicted muscle forces in running at increasing speed, adapted from Dorn 2012) and


    This PDF is a free sample issue of MASS, the monthly research review by me (Greg Nuckols), Dr. Eric Trexler, Dr. Eric Helms, and Dr. Mike Zourdos made specifically for strength and physique athletes, coaches, and enthusiasts.

    Every article or video in the PDF breaks down a recent study that covers a topic relevant to strength, physique, or nutrition. It explains what the study found and what the results mean practically for you.

This PDF contains a preview of what each issue contains and is released in relation to their charity sale starting April 27th, details at the bottom.

Table of contents:

Improving Muscle Growth by Individualizing Training Volume
​by Greg Nuckols

Time to Reframe the Proximity to Failure Conversation
​by Michael C. Zourdos

A Progression Framework for Hypertrophy
by Eric Helms

Modest Glycogen Depletion May Impact Lifting Performance More Than You Think
by Eric Trexler

Ribosome Biogenesis Influences Whether High Volumes Cause More Growth
​by Greg Nuckols

Penalty: Reduction in Gains for Interference
​by Michael C. Zourdos

Protein Distribution Matters, To An Extent
​by Eric Trexler

Females Fatigue Slower than Males Largely Due to Differences in Blood Flow
​by Greg Nuckols

VIDEO: Volume Cycling
​by Michael C. Zourdos

VIDEO: Translating Nutrition Guidelines to Life
​by Eric Helms

Pics, Videos, & Links / 5'6" Anthony Height check
« on: March 01, 2021, 07:27:22 am »

Strength, Power, Reactivity, & Speed Discussion / Easy way to belt squat
« on: October 22, 2020, 01:16:37 am »
This is ingenius  8)

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I learned more from watching Alexander Bromley's videos in this playlist than various books I own on how to program workouts

He has many more useful videos in his Youtube as well, not in this playlist

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Not as much as you think

TL;DR (but please read the whole review, it's very interesting and it subverts your expectations on multiple occasions as you go through it):

    Your testosterone levels affect how much muscle you carry around, whether you train or not. Then, when you begin to train, your responsiveness to training is mostly similar regardless of whether you have low or high testosterone levels. It may be a bit less with lower testosterone, but the biggest impact is on your baseline.

    For example, let's say you have a baseline lean mass of 50 kg, and you have a testosterone level in the low end (say around 300 ng/dL). You [by training] gain 10% over 6 months, which is 5 kg.

    Now, take this same situation, but the person has a baseline testosterone to 600 ng/dL. Your baseline lean mass now may be 52 kg. You still gain 10% over 6 months, which is 5.2 kg. Thus, the relative gain is similar. However, the starting point, and the absolute gain, is larger because of the higher testosterone. [How larger?] The data suggests that fat-free mass will increase by 0.7 - 1.3 lbs (0.3 - 0.6 kg) for every 100 ng/dL increase in blood levels of testosterone within the physiological range. Thus, if you went from 300 ng/dL to 600 ng/dL, that would be 0.9 - 1.8 kg or about 2.1 - 4 lbs.

    Let's consider another example. Let's say a person goes on some type of testosterone replacement, boosting testosterone from 250 ng/dL to 500 or 600 ng/dL. That person will initially experience some higher-than-normal relative gains, as he moves towards his new baseline for his new testosterone level. It will feel like "newbie" gains. However, once that person has reached his new baseline, his relative gains will be similar to when he had lower testosterone.


Key Takeaways:

    We make the argument that the force production of a repetition is a vital and often underemphasized aspect to training specificity for maximal strength. Training with heavy loads and low intraset fatigue/velocity loss results in force production the most specific to a 1RM.
    For short to moderate term strength gains, performing sets to or close to failure doesn’t offer an additional training effect but can cause other detrimental changes. We also discuss the interplay between muscle growth and proximity to failure for long term strength gains.
    The available research suggests that when training with 65-85% of 1RM, staying far from failure allows for the accumulation of repetitions that provide the majority of the strength stimulus. This means that sets can be terminated before large decreases in bar velocity occur (roughly 10-20% velocity loss) while still maximizing the strength stimulus. We also recommend incorporating regular heavy top sets (>85% of 1RM) for skill practice at velocities similar to a 1RM.

Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage


According to our hypothesis, delayed onset muscle soreness (DOMS) is an acute compression axonopathy of the nerve endings in the muscle spindle. It is caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The acute compression axonopathy could coincide with microinjury of the surrounding tissues and is enhanced by immune-mediated inflammation. DOMS is masked by sympathetic nervous system activity at initiation, but once it subsides, a safety mode comes into play to prevent further injury. DOMS becomes manifest when the microinjured non-nociceptive sensory fibers of the muscle spindle stop inhibiting the effects of the microinjured, hyperexcited nociceptive sensory fibers, therefore providing the ‘open gate’ in the dorsal horn to hyperalgesia. Reactive oxygen species and nitric oxide play a cross-talking role in the parallel, interlinked degeneration–regeneration mechanisms of these injured tissues. We propose that the mitochondrial electron transport chain generated free radical involvement in the acute compression axonopathy. ‘Closed gate exercises’ could be of nonpharmacological therapeutic importance, because they reduce neuropathic pain in addition to having an anti-inflammatory effect. Finally, DOMS could have an important ontogenetical role by not just enhancing ability to escape danger to survive in the wild, but also triggering muscle growth.

6. Conclusions

According to our hypothesis, DOMS is an acute compression axonopathy of the nerve terminals in the muscle spindle caused by the repetitive superposition of compression with a coinciding cognitive demand, coupled with possible microinjury to the surrounding tissues and enhanced by immune-mediated inflammation. Our theory states that DOMS happens only if the superposition of compression reaches the muscle spindle and microinjures the nerve terminals under cognitive demand. The cornerstones of our hypothesis are as follows:

    DOMS could be an acute compression axonopathy of the nerve endings in the muscle spindle,

    The cause of DOMS could be the repetitive superposition of compression under cognitive demand and a resultant metabolic insult,

    DOMS could be initiated from the muscle spindle,

    The fluid cavity in the muscle spindle could play an important functional role in DOMS,

    Mitochondrial electron transport chain generated free radical involvement is suspected with a TAD-like lesion in the acute axonopathy of the sensory nerve endings in DOMS,

    Unaccustomed or strenuous eccentric exercise-induced SNS activity could be an essential underlying factor in DOMS initiation,

    DOMS could be initiated earlier than it is experienced, but at the beginning, it is suppressed by SNS activity,

    Delayed onset of soreness could be a result of the hypoalgesic state of the ‘closed gate’ caused by the enhanced firing of the microinjured Type Ia sensory fibers in addition to the initial SNS suppression,

    There could be a cross-talk on the PGE2 level between the pain pathways,

    Hyperexcited microinjured Type II sensory fibers in the muscle spindle could override, with the possible help of SNS, the conduction velocity reducing microinjured Type Ia sensory fibers’ inhibition with a delayed onset. The result will be an ‘open gate’ in the dorsal horn and the pathway to hyperalgesia in DOMS,

    Keeping a ‘closed gate’ with concentric exercise could have importance in non-pharmacological disease and neuropathic pain management by simultaneously alleviating pain and enjoying the positive anti-inflammatory characteristics of exercise; therefore, we call it a ‘closed gate exercise’,

    DOMS could cause a transient increase of the blood–spinal cord barrier and selective muscle spindle barrier permeability,

    DOMS could be a safety function in repetitive eccentric contractions as it resolves when the microinjury of the muscle spindle afferent sensory and motoneuron nerve endings are regenerated,

    Finally, we suspect that DOMS could play an important role in ontogenesis by triggering muscle growth and adapting the nervous system in the growth process.

The variability of timelines and symptoms of DOMS, after initiation, will depend on how pervasive the injury is to the surrounding tissues and what tissues are affected. The individual differences could be explained by the complexity of pathways and cross-talking of the microinjured tissues and immune systems. The type and duration of eccentric exercise, trained status, age, genetics, and underlying allergies and low-grade inflammation or diseases could also affect the timelines and the extent of symptoms in DOMS.

So I have been loading videos into this web app that allows you precisely tag takeoff and landing points of a video and calc hang time and vertical etc.!

And a lot of jump mat videos are so inflated it's crazy.
That 47.1 vertical vid from a football combine is only 41 or so inches based on hang time...

I wanted to measure a lot of popular vids, on Youtube and instagram but they tend to slow mo the jump after takeoff... blah...

Clarence's jump back when he was 80kg, with that 200kg squat is a legit 40 inches or so on the app. Not bad for a non vert training person.

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another vid I tried was Rugter's Dunker's vertical on a vertec, which was supposedly 40 inches, I only got 30 inches....

I think he is 5'9" 165lbs
40.5 inch vertical and 44 running jump - kinda weird that he jumps well off 1 leg :)

64 1/8th inches box jump

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