Best heart rate to increase HDL

redkiwi

New Member
Hey people,

I know the "burning fat zone" is between 55%-70% of your MHR (ie 220-age).

1) How about to increase HDL? What's the optimal heart rate?

2) Is there a threshold when you don't get any more benefits or the higher HR the better?

3) Which will work better? Moderate cardio/ high frequency or intense cardio/low frequency.

Let me know what you think.
 
It's a lot easier to decrease ldl than inceeasing hdl. Besides that there's a lot of medical research that showed no health benefits with increased hdl.

To answer your question, the aerobic training zone is great for both hdl and ldl.
 
It's a lot easier to decrease ldl than inceeasing hdl. Besides that there's a lot of medical research that showed no health benefits with increased hdl.

To answer your question, the aerobic training zone is great for both hdl and ldl.
Agree with this. Would love someone like @Type-IIx to chime in. Impact from statins? (I haven’t see much from Rosuvastatin, but I am on 10mg 3 days a week which is very low)

Cardio and diet has been the only definitive thing I’ve seen reliably impact HDL. Honestly, I think genetics (as usual) has a huge role to play here.

Perhaps especially so here. I and my wife hover around 180 total. That said while my HDL is low … my wife’s accounts for over HALF her number … good lord
 
Agree with this. Would love someone like @Type-IIx to chime in. Impact from statins? (I haven’t see much from Rosuvastatin, but I am on 10mg 3 days a week which is very low)

Cardio and diet has been the only definitive thing I’ve seen reliably impact HDL. Honestly, I think genetics (as usual) has a huge role to play here.

Perhaps especially so here. I and my wife hover around 180 total. That said while my HDL is low … my wife’s accounts for over HALF her number … good lord
HDL-C is a strong independent predictor of cardiovascular disease risk despite its causality not being established. LDL-C, unlike HDL-C, is actually a firmly established causal factor in dyslipidemia. Since HDL-C in plasma reflects factors beyond cholesterol efflux capacity (CEC), including net production and catabolism, metabolism of different particles like HDL3 (a smaller subfraction more prone to breakdown vs. HDL2), merely increasing HDL-C in plasma does not seem to reduce cardiovascular disease risk significantly.

Cholesterol Efflux Capacity (CEC) is the capacity of HDL particles to accept cholesterol from macrophages, engulfing (phagocytosis) oxidized LDL particles that would otherwise tend to accumulate in the arterial wall (i.e., artherosclerosis). Cholesterol efflux, then, is the process of macrophagal-phagocytotic removal of these oxidized LDL from the arterial wall to the liver (protecting arteries from deterioration). This is the function of HDL-C that we care about.

A more meaningful target for reducing cardiovascular disease risk is to lower Apo B / Apo A1 ratio (or increase Apo A1 / Apo B ratio).

Apo A1 is associated with HDL & chylomicrons that transport lipids absorbed by intestines to rest of body (reflecting CEC). Apo B-100 is associated with VLDL & gives insight into LDL actually in bloodstream circulation (reflecting atherosclerotic risk).

There are not any currently available safe drugs that increase CEC (cardarine, e.g., is highly carcinogenic). Statins are a great way to reduce LDL. The efficacy of treatments like LXR agonists, miR-33 inhibitors, LCAT enhancers, etc. to reduce cardiovascular disease risk have not been established.

But beyond all that, an easy way to improve Apo B / Apo A1 ratio is to refrain from AAS ([link]) & insulin use (directly stimulates liver VLDL synthesis). Relatively, testosterone confers some protection against dyslipidemia by aromatization to E2 (estrogens are protective), nandrolone somewhat less, and on the extreme opposite end are potent 17AA orals that do not aromatize. Obviously, losing body fat & eating a low calorie, low saturated fat/cholesterol diet, is an effective means to reduce CVD risk.
 
Ldl and hdl levels have nothing to do with cardio. They are produced and regulated by the liver and diet. And determined largely by genetics.
 
HDL-C is a strong independent predictor of cardiovascular disease risk despite its causality not being established. LDL-C, unlike HDL-C, is actually a firmly established causal factor in dyslipidemia. Since HDL-C in plasma reflects factors beyond cholesterol efflux capacity (CEC), including net production and catabolism, metabolism of different particles like HDL3 (a smaller subfraction more prone to breakdown vs. HDL2), merely increasing HDL-C in plasma does not seem to reduce cardiovascular disease risk significantly.

Cholesterol Efflux Capacity (CEC) is the capacity of HDL particles to accept cholesterol from macrophages, engulfing (phagocytosis) oxidized LDL particles that would otherwise tend to accumulate in the arterial wall (i.e., artherosclerosis). Cholesterol efflux, then, is the process of macrophagal-phagocytotic removal of these oxidized LDL from the arterial wall to the liver (protecting arteries from deterioration). This is the function of HDL-C that we care about.

A more meaningful target for reducing cardiovascular disease risk is to lower Apo B / Apo A1 ratio (or increase Apo A1 / Apo B ratio).

Apo A1 is associated with HDL & chylomicrons that transport lipids absorbed by intestines to rest of body (reflecting CEC). Apo B-100 is associated with VLDL & gives insight into LDL actually in bloodstream circulation (reflecting atherosclerotic risk).

There are not any currently available safe drugs that increase CEC (cardarine, e.g., is highly carcinogenic). Statins are a great way to reduce LDL. The efficacy of treatments like LXR agonists, miR-33 inhibitors, LCAT enhancers, etc. to reduce cardiovascular disease risk have not been established.

But beyond all that, an easy way to improve Apo B / Apo A1 ratio is to refrain from AAS ([link]) & insulin use (directly stimulates liver VLDL synthesis). Relatively, testosterone confers some protection against dyslipidemia by aromatization to E2 (estrogens are protective), nandrolone somewhat less, and on the extreme opposite end are potent 17AA orals that do not aromatize. Obviously, losing body fat & eating a low calorie, low saturated fat/cholesterol diet, is an effective means to reduce CVD risk.
Exogenous insulin significantly impacts cholesterol?
 
Our lipid system is complicated
I think much more still needs to be studied..
I crashed my lipids panel with arimidex.. supplements fixed it little bit but statins really brought it up like a magic pill..

On the other side I have my granny 70yo 3 heart attacks diabetic with broken knees barely moves much... (0 cardio or any physical activities)

Saw her blood work the other day..
Hdl 92
Ldl 32
TRIGLYCERIDES 15
Total Cholesterol 85

From what I know she's on BP meds , statins , insulin, and blood thinning meds I think a certain cocktail of meds can bring the lipid system to the best values without breaking a sweat..
 
Our lipid system is complicated
I think much more still needs to be studied..
I crashed my lipids panel with arimidex.. supplements fixed it little bit but statins really brought it up like a magic pill..

On the other side I have my granny 70yo 3 heart attacks diabetic with broken knees barely moves much... (0 cardio or any physical activities)

Saw her blood work the other day..
Hdl 92
Ldl 32
TRIGLYCERIDES 15
Total Cholesterol 85

From what I know she's on BP meds , statins , insulin, and blood thinning meds I think a certain cocktail of meds can bring the lipid system to the best values without breaking a sweat..
Interesting. What supplements/statins did you use to bring up HDL and lower LDL?
 
Interesting. What supplements/statins did you use to bring up HDL and lower LDL?
Nattokinase extract



@Type-IIx Did you have an opinion on natto extract ?
 
Here’s a meta- analysis of a dozen studies looking at the impact of aerobic and resistance training on cholesterol parameters.
Differential Effects of Aerobic Exercise, Resistance Training and Combined Exercise Modalities on Cholesterol and the Lipid Profile: Review, Synthesis and Recommendations

“The evidence suggests that a moderate-intensity exercise programme will be effective in increasing HDL cholesterol”

“To directly reduce LDL cholesterol and triglyceride levels, however, the intensity of aerobic exercise must be increased”


Unfortunately a lot of the studies are on previously sedentary individuals. You can read into the specific training methods, HR %, and time periods if you’d like.
 
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Here’s a meta- analysis of a dozen studies looking at the impact of aerobic and resistance training on cholesterol parameters.
Differential Effects of Aerobic Exercise, Resistance Training and Combined Exercise Modalities on Cholesterol and the Lipid Profile: Review, Synthesis and Recommendations

“The evidence suggests that a moderate-intensity exercise programme will be effective in increasing HDL cholesterol”

“To directly reduce LDL cholesterol and triglyceride levels, however, the intensity of aerobic exercise must be increased”


Unfortunately a lot of the studies are on previously sedentary individuals. You can read into the specific training methods, HR %, and time periods if you’d like.
Haven't read but I'm wondering is this a case of exercise more eat better? Also I should assume that more exercise would reduce liver fat thus improving liver function thus improving chol.
 
They do say theirs is a dose dependent relationship.
Here’s their recommendation for healthy people
“Increase physical activity to >30 min/day 5 times weekly [16, 17]; prolonged moderate-intensity aerobic exercise at 70–80 % HRreserve[43], combined with low-intensity resistance training at 50 % 1 RM [23]”

I know you’re probably looking for a specific answer but we all already know what to do. Live a healthy lifestyle. Eat a clean diet, maintain BP, normal blood sugar, lift, and mix up aerobic exercise intensities and just move more throughout the day and prioritize sleep. Sitting on the couch for 23hrs a day when outside the weight room probably isn’t the best thing to do. Orals will have the biggest impact though regardless.
 
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