Gym & Misc General Health and Fitness Thread

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Why can’t the rest of my body grow like my calves do. I DON’T EVEN WORK THEM. It’s like I move 10cm and they expand 1m :unamused:
 
vonn said:
Why can’t the rest of my body grow like my calves do. I DON’T EVEN WORK THEM. :(
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You’d be surprised how much work they do on lower body exercises like squats etc
They’re also our primary means of locomotion throughout the day so they get a crap tonne of volume.

Oh . . . And genetics lol
 
Aeglos said:
You’d be surprised how much work they do on lower body exercises like squats etc
They’re also our primary means of locomotion throughout the day so they get a crap tonne of volume.

Oh . . . And genetics lol
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:'(
 

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Out of curiosity - does ‘big’ equal ‘strong’, or mean I have a higher base than someone?

As in, my calves are huge (relative to my body) with barely any fat, so does that mean I can go on calf press and move higher weight than someone with smaller calves? And/or does that mean my base is higher than someone with naturally less muscular/smaller calves?

I knew that I would work them indirectly, but I didn’t even realise anyone ever felt it until I read that some people get sore calves after squats.
 
vonn said:
Out of curiosity - does ‘big’ equal ‘strong’, or mean I have a higher base than someone?

As in, my calves are huge (relative to my body) with barely any fat, so does that mean I can go on calf press and move higher weight than someone with smaller calves? And/or does that mean my base is higher than someone with naturally less muscular/smaller calves?

I knew that I would work them indirectly, but I didn’t even realise anyone ever felt it until I read that some people get sore calves after squats.
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A larger muscle has a greater potential for strength, but that doesn’t necessarily guarantee it will be stronger or that you can display that strength well in a certain movement/action.
 
vonn said:
Why can’t the rest of my body grow like my calves do. I DON’T EVEN WORK THEM. It’s like I move 10cm and they expand 1m :unamused:
Click to expand...

As you brother from another mother (lol jokes) I say its genetics. I know us China southerners are smaller and stockier traditionally hence more weight down below the hips, thus the calves. Aren't you (heritage wise) from the north though where lean and tall are commonplace?
 
peternorth said:
As you brother from another mother (lol jokes) I say its genetics. I know us China southerners are smaller and stockier traditionally hence more weight down below the hips, thus the calves. Aren't you (heritage wise) from the north though where lean and tall are commonplace?
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Correct, Southern stalker, I am from the North.

My parents are both taller than me (at 5’5), but they seem to gain and retain muscle easily, so maybe this is why.
 
Aeglos said:
A larger muscle has a greater potential for strength, but that doesn’t necessarily guarantee it will be stronger or that you can display that strength well in a certain movement/action.
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So you’re saying if I directly targeted them, I could obtain the title of ‘World’s Biggest and Strongest Calves’?
 
vonn said:
Correct, Southern stalker, I am from the North.

My parents are both taller than me (at 5’5), but they seem to gain and retain muscle easily, so maybe this is why.
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I have notifications anytime calves are mentioned on bigfooty
 

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Been drop-setting leg press/curl with alternating single leg and the burn is 50x better. Definitely noticed quad growth.
 
showdownhero said:
A really good family friend (younger than my Dad) dropped dead of a heart attack not long ago, I found it so strange that a reasonably healthy man who looks after himself (in terms of regular doc checkups and exercise) could have such serve undiagnosed atherosclerotic plaque/cardio vascular disease.

Gonna watch this doco tonight, goes into some detail about test that can be done to check for CVD before you die

http://www.imdb.com/title/tt3470838/
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free on youtube, well the hour long "tv" version. The full version is 95 minutes long

 
Love this section and everyone posting btw. Good to read what others do and know there's many alike. It's motivating and reinforces on why I/we train.


Good stuff.
 
Bazzar said:
Fact, more people die of CVD with lower cholesterol than higher cholesterol.
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This is patently false.

Total Cholesterol = HDL (good) + LDL (bad) + other stuff(very dense and very bad)

TC is only part of the picture. One can have TC within reference ranges, but invariable LDL will be high (concomitantly with low HDL) - but generally not.

Average age of first MI in Australia is 64, primary prevention should be focus from >35 yo with reviews every 3 years thereafter, 30 if known family history (not just of CVD, but other covariates, e.g. FH, and associated events e.g. stroke, PE, etc.)

The demarcation between normal and abnormal in Australia is 5.5 mmol/L. Most Australian adults are above this cutoff. Drug intervention is typically indicated at 7.5 mmol/L, often lower depending on absolute risk. Meeting a patient following an MI with a TC of <5.5 is rare.

All the major long-term epidemiological Heart Health studies (Framingham to name just one) demonstrate a very strong association between elevated TC at first and recurrent MI's.

If you want to stave off CVD, consume less animal meats, eggs and diary, maintain a healthy body weight, regularly see your GP and exercise more.
 
Tsongkie said:
This is patently false.

Total Cholesterol = HDL (good) + LDL (bad) + other stuff(very dense and very bad)

TC is only part of the picture. One can have TC within reference ranges, but invariable LDL will be high (concomitantly with low HDL) - but generally not.

Average age of first MI in Australia is 64, primary prevention should be focus from >35 yo with reviews every 3 years thereafter, 30 if known family history (not just of CVD, but other covariates, e.g. FH, and associated events e.g. stroke, PE, etc.)

The demarcation between normal and abnormal in Australia is 5.5 mmol/L. Most Australian adults are above this cutoff. Drug intervention is typically indicated at 7.5 mmol/L, often lower depending on absolute risk. Meeting a patient following an MI with a TC of <5.5 is rare.

All the major long-term epidemiological Heart Health studies (Framingham to name just one) demonstrate a very strong association between elevated TC at first and recurrent MI's.

If you want to stave off CVD, consume less animal meats, eggs and diary, maintain a healthy body weight, regularly see your GP and exercise more.
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False

Just get your HDL to Triglyceride ratio to be at least 4:1. Statins are useless and do so much more harm with their side-effects. All your crap about animal meats, eggs and dairy is wrong and outdated, same with exercising more. Eat real, unprocessed nutrient dense food, high in omega 3 and low in omega 6. You need to exercise smarter. HIIT and resistance training.
 
Big Cox 88 said:
False

Just get your HDL to Triglyceride ratio to be at least 4:1. Statins are useless and do so much more harm with their side-effects. All your crap about animal meats, eggs and dairy is wrong and outdated, same with exercising more. Eat real, unprocessed nutrient dense food, high in omega 3 and low in omega 6. You need to exercise smarter. HIIT and resistance training.
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yeah I love how they have pretty much proven that sat fats are not the problem they used to believe they were but the first thing anyone says is don't eat eggs, go low fat for yoghurt cheese etc
 
Tsongkie said:
This is patently false.

Total Cholesterol = HDL (good) + LDL (bad) + other stuff(very dense and very bad)

TC is only part of the picture. One can have TC within reference ranges, but invariable LDL will be high (concomitantly with low HDL) - but generally not.

Average age of first MI in Australia is 64, primary prevention should be focus from >35 yo with reviews every 3 years thereafter, 30 if known family history (not just of CVD, but other covariates, e.g. FH, and associated events e.g. stroke, PE, etc.)

The demarcation between normal and abnormal in Australia is 5.5 mmol/L. Most Australian adults are above this cutoff. Drug intervention is typically indicated at 7.5 mmol/L, often lower depending on absolute risk. Meeting a patient following an MI with a TC of <5.5 is rare.

All the major long-term epidemiological Heart Health studies (Framingham to name just one) demonstrate a very strong association between elevated TC at first and recurrent MI's.

If you want to stave off CVD, consume less animal meats, eggs and diary, maintain a healthy body weight, regularly see your GP and exercise more.
Click to expand...

100% agree TC is only part of the picture, that was my point, and by the way who said LDL is bad? more to the point can high LDL be good?
 
Watching a Catalyst expose on statins hardly makes one a subject matter expert.

As someone who deals with cardiac patients every day, I can safely and confidently say you have no idea what you're talking out.

Here's some data for you across the life-span - for 'low'-risk cardiac patients, statin use extends life by an average of 7-8 months. For 'high' risk cardiac patients, the average life extension is 6-7 years. Statins associated muscle soreness (SAMS) is indeed a problem, which is why any good Dr would weigh up the pro/cons of administration on a case by case basis.

To the casual readers following this thread, please disregard any 'medical advice' conferred by BigFooty resident 'experts' and see your GP if you have any questions. Please don't ask BigCox.
 
As an aside, statins block HMG-CoA Reductase, the rate-limiting enzyme involved in the creation of cholesterol.

Interestingly, there is sine waveform variation across the day (i.e diurnal or circadian variation), typically from low (AM) to high (AM) expression, peaking at 8-8.30PM and bottoming-out at 6.30AM. Some newer studies show that shifting dinner forward a few hours, can affect conversion of cholesterol and thus improve lipid levels. Why? Because the cholesterol is consumed when the HMG-CoA reductase levels are naturally lower and thus convert less.

Trials are on-going in Tokyo, and they're getting good outcomes.

That's enough from me. How shit was the umpiring in the WCE/SYD game last week?!
 

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