Medical Advice On Muscle?

Training Bodybuilding
41

[quote]Lorisco wrote:
tveddy wrote:
playmaker08 wrote:

LDL is important. LDL transports triglycerides and cholesterol from our liver to our tissues. If our tissues could not get cholesterol then our cell membranes would become more rigid, as cholesterol maintains the fluidity of cells. Also triglycerides are used as energy by our body. Some recent studies have shown very low cholesterol levels to be a cancer risk, but then again what isnt a cancer risk?

Come to think of it, testosterone is cholesterol based, does this mean that it is transported through our blood stream and to the target tissues via LDL?

OK, so the question that I was leading up to…

I had my Cholesterol check a while back when I gave blood and my Total was 74. My HDL’s were in the 60’s I don’t remember how hi. So would that mean anything other than I just need to have it checked again?

Total cholesterol 74? That can’t be right. Don’t you mean your LDL was 74 and your HDL 60?

And if this is true, that is very good.
[/quote]

I remember for sure that my total was 74. I need to just give blood again and find out the exact numbers.

42

Totat=74? That seems insanely low?

Either way like the above posters indicated, cholesterol isn’t bad per se. Only thru oxizidation or glycation.

Eat your eggs and red meat, and veggies and good carbs, do your ESW/cardio and hit the weights hard. What else can you do? That’s about it.

43

[quote]greekdawg wrote:
Either way like the above posters indicated, cholesterol isn’t bad per se. Only thru oxizidation or glycation.

[/quote]

This is somewhat true, however, the presence of higher concentration of LDL implies, all else being equal, a greater absolute number of LDL exposed to radical oxigen species or glycation. Also, the increase in LDL also generates a higher degree of macrophage and foam cell LDL uptake with increased plaque formation.

So non-oxydized, non-glycated LDL is much less atheromatous than the oxydized/glycated versions, it is still not particularly healthy in terms of endothelial function or atheroma formation.

Statins act both in decreasing the absolute amount of LDL produced, increased the concentration of scavenger HDL and act as anti-oxydants for cholesterol. Some high dose regimen of newer generation statins can even stop or minimally reverse plaque formation, which is pretty impressive (considering we are building plaques in our arteries since we’re basically fetuses).

A few agents one might consider prior to or as adjuvant to statin therapy.

Exerpt from
Lipoprotein classification; metabolism; and role in atherosclerosis

UpToDate 15.2

Treatment with lipid lowering drugs that reduce the susceptibility of LDL to oxidation may reverse some of these changes, resulting in an improved vasomotor response to acetylcholine [48,56,60]. Endothelial function can also be improved by the administration of the NO precursor L-arginine in hypercholesterolemic rabbits [61] and, in patients with hypercholesterolemia, vitamin C, folate, and 5-methyltetrahydrofolate, the active form of folic acid; improvement occurs without changes in plasma lipids [62-64]. Vitamin C and folate may prevent the degradation of NO.

AlexH

44

[quote]Dandalex wrote:
greekdawg wrote:
Either way like the above posters indicated, cholesterol isn’t bad per se. Only thru oxizidation or glycation.

This is somewhat true, however, the presence of higher concentration of LDL implies, all else being equal, a greater absolute number of LDL exposed to radical oxigen species or glycation. Also, the increase in LDL also generates a higher degree of macrophage and foam cell LDL uptake with increased plaque formation.

So non-oxydized, non-glycated LDL is much less atheromatous than the oxydized/glycated versions, it is still not particularly healthy in terms of endothelial function or atheroma formation.

Statins act both in decreasing the absolute amount of LDL produced, increased the concentration of scavenger HDL and act as anti-oxydants for cholesterol. Some high dose regimen of newer generation statins can even stop or minimally reverse plaque formation, which is pretty impressive (considering we are building plaques in our arteries since we’re basically fetuses).

A few agents one might consider prior to or as adjuvant to statin therapy.

Exerpt from
Lipoprotein classification; metabolism; and role in atherosclerosis

UpToDate 15.2

Treatment with lipid lowering drugs that reduce the susceptibility of LDL to oxidation may reverse some of these changes, resulting in an improved vasomotor response to acetylcholine [48,56,60]. Endothelial function can also be improved by the administration of the NO precursor L-arginine in hypercholesterolemic rabbits [61] and, in patients with hypercholesterolemia, vitamin C, folate, and 5-methyltetrahydrofolate, the active form of folic acid; improvement occurs without changes in plasma lipids [62-64]. Vitamin C and folate may prevent the degradation of NO.

AlexH[/quote]

It is irresponsible to advocate medical treatment over the internet. Statins are actually HMG-CoA reductase inhibitors and not free of side effects. Typically these kinds of medications are only prescribed with patients with lipid profiles that are considered in the high risk range. Advocating Statins to those with normal lipid profiles is not appropriate. Do you work for a drug company?

Side effects of Statins: constipation, diarrhea, hepatitis, cholestatic jaundice, fatty changes in the liver, myopathy and rhabdomyolysis, hemolytic anemia, thrombocytopenia, and leukopenia, headache and weakness, acute renal failure secondary to rhabdomyolysis, hypospermia, gynecomastia, and thyroid dysfunction, peripheral edema, and chest pain, etc.

45

[quote]Lorisco wrote:
It is irresponsible to advocate medical treatment over the internet. [/quote]

Kinda odd considering that you told the OP that the recommendations of a person legally designed to provide medical advice earlier in the thread were simply misapplied knowledge – i.e. you were offering medical advice over the internet.

FWIW, I agree that the knowledge was likely misapplied and misunderstood by the nurse – but – giving her/him the benefit of the doubt would lead me to believe that s/he may basically be right (but there is no absolute proof). The US Cancer Prevention II Study determined that BMI was the single greatest predictor of death across all ages from all causes.

Some will holler, “but those were fat people!” Well, the study does not differentiate how the BMI became elevated and it can be assumed that some of those million+ participants were resistance trainers and massive in the good way. So, the prudent thing to recommend when confronted with a patient whose weight places them in the >25 BMI range would be to recommend that they cut their weight.

I don’t think there is an officially accepted verdict on high LBM but high BMI types but the general evidence is pretty strong. It falls to prudence. What do you want your health care professionals telling you -

How to be safe or how to try to skirt the edges of damaging behavior? Do you want the Health Department telling 18 year old guys that they probably don’t have much to fear AIDS wise from having a heterosexual 1-night-stand? (odds were roughly 1-in-500 with an infected partner by one study)

There are also tons of theories on life extension that involve calorie restriction, free radical damage, ect… all of which equate to greater consumption shortening life span. These, IMO, are all still in the realm of speculation and don’t necessarily warrant any actionable response.

When thinking about what is the best behaviors to prolong health span it is important to remember that some people - including doctors and nurses will get swallowed up in any kewl theory like coffee enemas, drinking urine, and fecal transplants.

Your health is ultimately your responsibility – 20 years from now some standard practices accepted and advocated by just about every respected authority will be considered bunk. The trick is knowing which ones. Still, I don’t see many iron bunny cardiologists with 21" guns, most (around here anyway) are compact and trim - body by cardio.

What does it mean? Probably nothing.

46

Duhhh, If you’re bigger your heart has to work harder. Are you people actually arguing this? Being a lean 275 is not as bad as being a fat 275 but your heart still has to work a lot harder than if you are 175.

When I was in the best shape of my life, in the low 190s, my heart rate was barely under 60. At the worst shape of my life, at about 156 lbs (really), my heart rate was under 50. That’s all the proof I need.

47

[quote]Moreau wrote:
Lorisco wrote:
It is irresponsible to advocate medical treatment over the internet.

Kinda odd considering that you told the OP that the recommendations of a person legally designed to provide medical advice earlier in the thread were simply misapplied knowledge – i.e. you were offering medical advice over the internet.
[/quote]

There is a big difference between offering medical opinion vs. actually advocating specific treatment. If you don’t know the difference you should not be posting.

48

[quote]on edge wrote:
Duhhh, If you’re bigger your heart has to work harder. Are you people actually arguing this? Being a lean 275 is not as bad as being a fat 275 but your heart still has to work a lot harder than if you are 175.

When I was in the best shape of my life, in the low 190s, my heart rate was barely under 60. At the worst shape of my life, at about 156 lbs (really), my heart rate was under 50. That’s all the proof I need.[/quote]

And if I run or exercise in anyway my heart has to work harder as well. Funny thing is that my heart gets used to the activity and gets stronger. As a result, my resting heart rate lowers because my heart is stronger and more efficient. So it can produce the output with one beat that it used to need two beats to produce.

So when you are bigger (muscle) your heart gets stronger to accommodate the extra tissue it needs to support. However, as weight training is anaerobic in nature, the heart compensates by becoming larger. When you do aerobic activity your heart compensates by getting stronger and more efficient contractions, but not larger.

This is why comparing fat mass to lean body mass in terms of heart function is so tricky. The mechanism your body uses to compensate is much different with fat tissue verses muscle tissue.

Muscle tissue is very physiologically active and requires much more support or accommodation than fat. So the level of adaptation for increases in muscles vs. fat is very different. This is the piece the average medical community misses because they are not trained in exercise physiology or sport medicine.

As for your heart rate actually lowering when you were in worse shape, sounds like you were over-trained. Rises in resting heart rate are often associated with over-training. Also the time of day. To check this accurately you need to check your heart rate first thing in the morning upon waking and still in bed.

49

[quote]on edge wrote:
Duhhh, If you’re bigger your heart has to work harder. Are you people actually arguing this? Being a lean 275 is not as bad as being a fat 275 but your heart still has to work a lot harder than if you are 175.

When I was in the best shape of my life, in the low 190s, my heart rate was barely under 60. At the worst shape of my life, at about 156 lbs (really), my heart rate was under 50. That’s all the proof I need.[/quote]

That’s just proof to you. My heart rate and blood pressure has dropped with increased LBM over the years. No, I’m not 275, but it seems that my workouts have done nothing but good to my body.

50

[quote]Lorisco wrote:
on edge wrote:
Duhhh, If you’re bigger your heart has to work harder. Are you people actually arguing this? Being a lean 275 is not as bad as being a fat 275 but your heart still has to work a lot harder than if you are 175.

When I was in the best shape of my life, in the low 190s, my heart rate was barely under 60. At the worst shape of my life, at about 156 lbs (really), my heart rate was under 50. That’s all the proof I need.

And if I run or exercise in anyway my heart has to work harder as well. Funny thing is that my heart gets used to the activity and gets stronger. As a result, my resting heart rate lowers because my heart is stronger and more efficient. So it can produce the output with one beat that it used to need two beats to produce.

So when you are bigger (muscle) your heart gets stronger to accommodate the extra tissue it needs to support. However, as weight training is anaerobic in nature, the heart compensates by becoming larger. When you do aerobic activity your heart compensates by getting stronger and more efficient contractions, but not larger.

This is why comparing fat mass to lean body mass in terms of heart function is so tricky. The mechanism your body uses to compensate is much different with fat tissue verses muscle tissue.

Muscle tissue is very physiologically active and requires much more support or accommodation than fat. So the level of adaptation for increases in muscles vs. fat is very different. This is the piece the average medical community misses because they are not trained in exercise physiology or sport medicine.

As for your heart rate actually lowering when you were in worse shape, sounds like you were over-trained. Rises in resting heart rate are often associated with over-training. Also the time of day. To check this accurately you need to check your heart rate first thing in the morning upon waking and still in bed.
[/quote]

Except for the last paragraph I agree with you… to an extent.

While the heart gets stronger as a person trains and gets bigger, it seems to lag the body with it’s metabolic adjustments. Sure, if you’ve got a 150 pound couch potato who decides to get in shape and puts on 50 pounds over a few years, his RHR is probably going to be lower. But, if you take a fit, active 150 pounder who decides to take up weights and he puts on 50 lbs over the same time period, his heart will get stronger but not strong enough to make up for the weight gain. Even if it’s all lean weight.

Your last paragraph is horrible. Can you also tell what color my cats eyes are based on my post? In my post I’m talking periods of years. Do you think I took my pulse randomly once when I was 195 and then once again at 155? Do you think I was consistently over-trained during the years I was over 190?

51

[quote]BigRagoo wrote:
on edge wrote:
Duhhh, If you’re bigger your heart has to work harder. Are you people actually arguing this? Being a lean 275 is not as bad as being a fat 275 but your heart still has to work a lot harder than if you are 175.

When I was in the best shape of my life, in the low 190s, my heart rate was barely under 60. At the worst shape of my life, at about 156 lbs (really), my heart rate was under 50. That’s all the proof I need.

That’s just proof to you. My heart rate and blood pressure has dropped with increased LBM over the years. No, I’m not 275, but it seems that my workouts have done nothing but good to my body.[/quote]

While your LBM has gone up, what has happened to your total weight?

I’m sure your workouts have done your body nothing but good. I don’t think a low heart rate is the only indicator of fitness. I did describe myself as being in the best shape of my life in the 190s with a higher heart rate.

52

Interestingly enough, and contrary to what might have been interpreted by some, my post does not advocate medical treatment to anyone, merely stating that how one of the only well studied, effective and well tolerated pharmacological agent works at reducing hypercholesterolemia through various mecanism and even presented other more benign agents that can be used.

Also, statements such as ''Do you work for a drug company?
‘’ how frankly inappropriate and do nothing but highlight one’s bias against an industry in a capitalist context that does not apply to other people such as myself living in Quebec in a system of socialized medicine where medications constitute a marginal expense to patients compared to other contriesw and where medication costs are negotiated by the goverment to be significantly lower that what they would be in say, a country such as the U.S.

There are vast majority of the people, if not to say largely all the medical and scientific community worldwide that agrees, based on the current research, in the mortality/morbidity benefits of agents such as statins.

Clearly thers is no interest in making this thread into one of the heated and hated cholesterol debate forum.

Lastly, I would say that presenting cholesterol as a largely benign molecule is not a much more appropriate behaviour.

AlexH

[quote]Lorisco wrote:

It is irresponsible to advocate medical treatment over the internet. Statins are actually HMG-CoA reductase inhibitors and not free of side effects. Typically these kinds of medications are only prescribed with patients with lipid profiles that are considered in the high risk range. Advocating Statins to those with normal lipid profiles is not appropriate. Do you work for a drug company?

Side effects of Statins: constipation, diarrhea, hepatitis, cholestatic jaundice, fatty changes in the liver, myopathy and rhabdomyolysis, hemolytic anemia, thrombocytopenia, and leukopenia, headache and weakness, acute renal failure secondary to rhabdomyolysis, hypospermia, gynecomastia, and thyroid dysfunction, peripheral edema, and chest pain, etc.

[/quote]

53

In terms of cardiovascular changes associated with resistance training and aerobic training, one must think in terms of forces the heart faces.

In aerobic exercice, the heart increases its heart rate, its stroke volume and oxygen uptake. Therefore the stress faced is in aerobic exercise is volume-load. The compensatory mechanism being improved mechanical coupling at a molecular level for myofiber contraction, improved preload (initial stretching of the fibers like a spring, generating more force when it contracts) and asymetric hypertrophy (the ventricular wall enlarges more than the septum (the wall between the right and left ventricules). This leads the the heart to be a more physiologically efficient pump. Since Cardiac Output (in Liters of blood pumped per minute) = Heart Rate X Stroke Volume, a heart with increased stroke volume secondary to improve coupling/ asymetric hypertrophy requires a lower heart rate to maintain a same output.

Therefore, lowered heart rates are expected in aerobically more fit individuals since the heart has been trained.

In resistance training, the general human habit is to generate muscular force while performing a Valsalva manoever (trying to push air out without breating out), both these actions increase intrathoracic pressure which reduce venous return (pressure in the thorax is too great for blood to come back to the heart). This can be strong enough for people to loose consciousness momentarily when defecating. To combat this the heart increases heart rate (to maintain cardiac output) and increase vasoconstriction to maintain blood pressure. Once you let the air out and stop contracting (racking to bar and breathing after a squat) the venous blood ‘‘blocked’’ in the abdomen and lower body returns to the heart (which is beating faster) and is pushed toward a vasoconstricted system which increases the pressure that the heart must fight against to push blood through the system. This can take a few minutes to return to baseline.

Therefore resistence training is a pressure-load on the heart which leads to symetric hypertrophy with no changes in the diameter of the ventricules. So the heart here adapts to fight against pressure and not volume, therefore a drop in baseline heart rate is not expected as physiological adaptations to increase cardiac output where not present. However, the heart is not adapted to deal with higher pressures therefore, in subsequent bouts of submaximal resistance training, the HR needed to maintain cardiac output in a higher pressure system is lower and blood pressure is also slighlty lower.

So basically, type of training affects the heart physiology as a function of the forces it faces.

In terms of cardiovascular health, aerobic exercice increase cardiac pump efficiency the most.

Resistance training tends to ‘‘keep’’ up with muscle mass with either no benefits to cardiovascular fitness (outside of those that are secondary to reduced bodyfat, improved metabolism and so on) or minimal benefits, more importantly though, is that there is no adverse effects to that physicological hypertrophy induced hypertrophy.

Caveat: This would not apply to someone using AAS with resistance hypertrophy as AAS have a tendency to increase BP for relatively long periods of time, as opposed to the short bouts of elevated BP facing the non-AAS using athlete. This is simply because the heart has a very hard time adapting to chronic pressure-load and does so in a pathological manner (eccentric hypertrophy with loss of efficient contractility (leading to heart failure) and eventual difficulties wiht cardiac tissue oxygenation (leading to MI or ischemic cardiomyopathy.)

Hum, this was supposed to be short.

Basically, I’ll have to go with Lorisco on this one, one who is cardiovascularly fit would have a lower heart rate.

You might look fit, but it does not imply that the cardiovascular system is particularly trained ((I look much more fit when I weight train then when I run marathons, but my HR and my BP say otherwise).

Also, we can’t rule out other reasons why you HR might have been lower prior.

AlexH