Hard Cardio while on AAS? Ally/Enemy/Indifferent?

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There quite a bit of discussion online about how intense cardio should be while on AAS or even high levels of TT/fT. This thread is intended to discuss HIIT/intense cardio while using AAS. Net benefit or detriment to your cardiovascular system?

Given the considerable literature hinting that too much cardio can be detrimental to heart's electrical and plumbing, are we hurting ourselves doing more intense cardio while on AAS?
 
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Before bringing AAS into the equation, I think it is better to set context and point out that extended cardio above one's level of aerobic fitness is likely a bad idea for everyone no matter what. There has been lots of study and writing on this from people like Phil Maffetone, Mark Sisson, and various cardiologists who point out that extended high-intensity cardio clearly produces blood markers of CV damage without any offsetting benefit in comparison to correct training. This is a huge topic, but as Mark Sisson sums it up, "Make your long easy workouts longer and easier, and your short hard workouts shorter and harder". Introducing AAS into the topic is just another opportunity to unfairly bash AAS when in fact the problem is the training modality. Additionally, AAS could include a lot of different scenarios and could be beneficial in some cases. For example, if someone was going to do something they knew was not ideal from a cardiac conditioning standpoint where they could be overworked (a charity bike ride for example), I would be very interested to know if something like Boldenone, which increases EPO and is well-known to support enhanced endurance, could in fact be cardio-protective in such a situation. or if it could promote more rapid adaptation to a high cardiac load that would partially last after the drug cleared. Or as other threads have described, if nandrolone makes the difference between someone be basically immobile and being able to do appropriate cardio, the cardio benefits could very well be a net positive even if there are theorized/unproven cardiac negatives to the compound. So...I suggest either eliminating AAS from the question or clarifying specifically how they might help since we know "hard cardio" is bad by itself.
 
First off let clarify the benefits of HIIT on the cardiorespiratory system etc. According to the studies below:

1. Data show that HIIT significantly enhanced VO2max and O2 pulse and power output in active men and women.
2. Eight weeks of HIIT performed at 100% peak power output is more effective than long slow distance training in improving performance and aerobic characteristics in well-trained rowers.
3. Improved neuromuscular characteristics that were transferred into improved muscle power and work economy.

So Vo2 max is increased O2 pulse, power output. So HIIT increases the cardiorespiratory output and also seems to effect muscular performance over low intensity long duration exercise.

Astorino TA, Allen RP, Roberson DW, Jurancich M. Effect of high-intensity interval training on cardiovascular function, VO2max, and muscular force. J Strength Cond Res. 2012 Jan;26(1):138-45. doi: 10.1519/JSC.0b013e318218dd77. PMID: 22201691.

Ní Chéilleachair NJ, Harrison AJ, Warrington GD. HIIT enhances endurance performance and aerobic characteristics more than high-volume training in trained rowers. J Sports Sci. 2017 Jun;35(11):1052-1058. doi: 10.1080/02640414.2016.1209539. Epub 2016 Jul 20. PMID: 27438378.

García-Pinillos F, Cámara-Pérez JC, Soto-Hermoso VM, Latorre-Román PÁ. A High Intensity Interval Training (HIIT)-Based Running Plan Improves Athletic Performance by Improving Muscle Power. J Strength Cond Res. 2017 Jan;31(1):146-153. doi: 10.1519/JSC.0000000000001473. PMID: 27172268.
 
There quite a bit of discussion online about how intense cardio should be while on AAS or even high levels of TT/fT. This thread is intended to discuss HIIT/intense cardio while using AAS. Net benefit or detriment to your cardiovascular system?

Given the considerable literature hinting that too much cardio can be detrimental to heart's electrical and plumbing, are we hurting ourselves doing more intense cardio while on AAS?
Any chance you can link to some of these discussions? would love to dig in.
 
Given the considerable literature hinting that too much cardio can be detrimental to heart's electrical and plumbing,

Before bringing AAS into the equation, I think it is better to set context and point out that extended cardio above one's level of aerobic fitness is likely a bad idea for everyone no matter what.
Thank you for the discussion and feedback.

I thought I made that clarifying point that very intense and long duration cardio can be a problem even before introducting AAS into the picture. Hence, the u-shaped/j-shaped relationship between cardiac risk and exercise training volume/METs.

Nevertheless, let's start there.


A sample of the literature:







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1659963364492.png
 
First off let clarify the benefits of HIIT on the cardiorespiratory system etc. According to the studies below:

1. Data show that HIIT significantly enhanced VO2max and O2 pulse and power output in active men and women.
2. Eight weeks of HIIT performed at 100% peak power output is more effective than long slow distance training in improving performance and aerobic characteristics in well-trained rowers.
3. Improved neuromuscular characteristics that were transferred into improved muscle power and work economy.

So Vo2 max is increased O2 pulse, power output. So HIIT increases the cardiorespiratory output and also seems to effect muscular performance over low intensity long duration exercise.

Astorino TA, Allen RP, Roberson DW, Jurancich M. Effect of high-intensity interval training on cardiovascular function, VO2max, and muscular force. J Strength Cond Res. 2012 Jan;26(1):138-45. doi: 10.1519/JSC.0b013e318218dd77. PMID: 22201691.

Ní Chéilleachair NJ, Harrison AJ, Warrington GD. HIIT enhances endurance performance and aerobic characteristics more than high-volume training in trained rowers. J Sports Sci. 2017 Jun;35(11):1052-1058. doi: 10.1080/02640414.2016.1209539. Epub 2016 Jul 20. PMID: 27438378.

García-Pinillos F, Cámara-Pérez JC, Soto-Hermoso VM, Latorre-Román PÁ. A High Intensity Interval Training (HIIT)-Based Running Plan Improves Athletic Performance by Improving Muscle Power. J Strength Cond Res. 2017 Jan;31(1):146-153. doi: 10.1519/JSC.0000000000001473. PMID: 27172268.
Thanks @BigTex . Excellent points and I was mentioning the original Tabata protocol to someone the other day:
 
Let me constrain the discussion to athletes or those that are putting out FTPs above say 300 W. That addresses @Guided_by_Voices 's concern that I will end up bashing AAS and ignoring their therapeutic potential.

Are AAS users deluding themselves thinking that vigorous cardiovascular exercise is cardioprotective or confers some protective benefit while using AAS? Should intense cardiovascular exercise be avoid while on AAS or supraphysiologic levels of Test?

Example of this type of reasoning...


 
I just had to link this. This dude is an overachiever:


Case report​


A 53-year-old, otherwise healthy bodybuilder was seen in the emergency department with 3 months of progressive dyspnoea, palpitations, headache, and an episode of syncope. He admitted to a history of fatigue, decreased libido, and erectile dysfunction for which he had been prescribed topical androgen and sildenafil. He is employed as a firefighter, does not smoke tobacco, and uses <6 oz of alcohol per week. He is married with two children and denies any family history of cardiomyopathy. He enjoys 60–90 min of vigorous exercise daily, which predominantly involves heavy weightlifting.


Vital signs were remarkable for a regular heart rate of 90 b.p.m. and a blood pressure of 167/95 mmHg. The physical examination demonstrated a muscular man, elevated central venous pressure (12 cm H2O), normal symmetric pulses, a slightly enlarged and laterally displaced cardiac point of maximal impulse, a grade 3/6 holosystolic murmur at the apex, and a positive third heart sound. Chest X-ray revealed cardiomegaly, and a Doppler echocardiogram demonstrated a dilated left ventricle (6.9 cm) with severe global hypokinesis, left ventricular septal thickness in diastole (LVSthd) of 1.0 cm (normal < 1.2 cm), and a calculated left ventricular ejection fraction (LVEF) of 15% (Figure 1A). Colour Doppler images demonstrated severe mitral regurgitation (Figure 1B); myocardial speckle tracking showed a severely abnormal global longitudinal strain pattern (Figure 2). Of note, 3 years prior, his LVEF had been 57%.


The patient was admitted for diagnosis of new-onset heart failure, and subsequent evaluation revealed normal coronary angiogram, iron panel, and thyroid studies and negative blood viral panel (human immunodeficiency virus, Lyme disease, and hepatitis) and urine toxicology panel for illicit drugs. B-type natriuretic peptide was 303 pg/mL (normal < 100 pg/mL), and high-sensitivity troponin was 0.05 ng/mL (normal < 0.05 ng/mL) on initial presentation.


The patient was referred to the Advanced Heart Failure Therapy program at Aurora St. Luke's Hospital, Milwaukee, WI. Upon further questioning, the patient admitted to a 3 year history of routine intramuscular androgen administration for bodybuilding. A testosterone level was obtained and documented at 30 160.0 ng/dL (normal 280–1100 ng/dL). The patient was counselled extensively about the cardiovascular risks associated with AAS use. AAS use was discontinued, and he was started on guideline-directed medical therapy (GDMT) with comprehensive neurohormonal blockade with a focus on maximum tolerated doses of carvedilol; final doses of therapy were lisinopril 5 mg daily, spironolactone 25 mg daily, and carvedilol 25 mg twice daily. Subsequent outpatient care documented resolution of the patient's symptoms by 3 months. A repeat Doppler echocardiogram at 6 months indicated a normal LV dimension (4.5 cm) with improved cardiac function (LVEF of 53%) and LVSthd of 0.9 cm (normal < 1.2 cm), resolution of mitral regurgitation (Figure 3A,B), and improvement in, but not normalization of, the global longitudinal strain pattern (Figure 4). Subsequent clinical testing revealed testosterone level of 603.7 ng/dL and normalization of B-type natriuretic peptide (19 pg/mL).
 

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I wanted to throw this study in the mix before I start reading all f the rest of this information


Readalot, is this what you are talking about?

 
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Thanks @BigTex . Excellent points and I was mentioning the original Tabata protocol to someone the other day:
One clarification I wanted to make is, while . Tabata is a form of HIIT Tabata is a higher intensity and for longer duration and much shorter rest period. Hit is usually about 80 Max HR, short duration and longer rest periods.

Here is a typical HIIT program I used with athletes

Traditional Sprints (Track or Treadmill)​

  • Warm-up
    • 2 min brisk walk then 25% jog (30 sec)
    • 2 min brisk walk then 50% run (20 sec)
    • 2 min brisk walk then 90% sprint (15 sec)
    • 3 min walk
  • Workout
    • Sprint 100% (5 to 10 sec) then 4 minute walk
    • Repeat multiple times
    • 4 min walk cool down
Malmo V, Nes BM, Amundsen BH, Tjonna AE, Stoylen A, Rossvoll O, Wisloff U, Loennechen JP. Aerobic Interval Training Reduces the Burden of Atrial Fibrillation in the Short Term: A Randomized Trial. Circulation. 2016 Feb 2;133(5):466-73. doi: 10.1161/CIRCULATIONAHA.115.018220. Epub 2016 Jan 5. PMID: 26733609.

Not sure why they refer to it as aerobic when it is anaerobic and uses the anaerobic glycogen cycle.

Conclusions: AIT for 12 weeks reduces the time in AF in patients with nonpermanent AF. This is followed by a significant improvement in AF symptoms, o2peak, left atrial and ventricular function, lipid levels, and QoL.
 
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View attachment 24561



Cardiac remodeling, I am living proof. From my last US HEART W CONTRAST AND 3D ANALYSIS IF........Concentric left ventricular remodeling. In 2010 the guy doing an ultra sound on my hear noticed the left ventricle. They did not want to do surgery on my knee. A meeting of cardiologist determined this was related to powerlifting and was a normal adaptation to the heavy weight I was lifting. Again in 2020 the same finding. I don't compete but still do weight training
 
One clarification I wanted to make is, while . Tabata is a form of HIIT Tabata is a higher intensity and for longer duration and much shorter rest period. Hit is usually about 80 Max HR, short duration and longer rest periods.

Here is a typical HIIT program I used with athletes

Traditional Sprints (Track or Treadmill)​

  • Warm-up
    • 2 min brisk walk then 25% jog (30 sec)
    • 2 min brisk walk then 50% run (20 sec)
    • 2 min brisk walk then 90% sprint (15 sec)
    • 3 min walk
  • Workout
    • Sprint 100% (5 to 10 sec) then 4 minute walk
    • Repeat multiple times
    • 4 min walk cool down
Malmo V, Nes BM, Amundsen BH, Tjonna AE, Stoylen A, Rossvoll O, Wisloff U, Loennechen JP. Aerobic Interval Training Reduces the Burden of Atrial Fibrillation in the Short Term: A Randomized Trial. Circulation. 2016 Feb 2;133(5):466-73. doi: 10.1161/CIRCULATIONAHA.115.018220. Epub 2016 Jan 5. PMID: 26733609.

Not sure why they refer to it as aerobic when it is anaerobic and uses the anaerobic glycogen cycle.

Conclusions: AIT for 12 weeks reduces the time in AF in patients with nonpermanent AF. This is followed by a significant improvement in AF symptoms, o2peak, left atrial and ventricular function, lipid levels, and QoL.


The link to original Tabata paper was in thread I linked above but I'll just put it here:





Abstract


This study consists of two training experiments using a mechanically braked cycle ergometer. First, the effect of 6 wk of moderate-intensity endurance training (intensity: 70% of maximal oxygen uptake (˙VO2max), 60 min·d-1, 5 d·wk-1) on the anaerobic capacity (the maximal accumulated oxygen deficit) and ˙VO2max was evaluated. After the training, the anaerobic capacity did not increase significantly(P > 0.10), while ˙VO2max increased from 53 ± 5 ml·kg-1·min-1 to 58 ± 3 ml·kg-1·min-1 (P < 0.01) (mean± SD). Second, to quantify the effect of high-intensity intermittent training on energy release, seven subjects performed an intermittent training exercise 5 d·wk-1 for 6 wk. The exhaustive intermittent training consisted of seven to eight sets of 20-s exercise at an intensity of about 170% of ˙VO2max with a 10-s rest between each bout. After the training period, ˙VO2max increased by 7 ml·kg-1·min-1, while the anaerobic capacity increased by 28%. In conclusion, this study showed that moderate-intensity aerobic training that improves the maximal aerobic power does not change anaerobic capacity and that adequate high-intensity intermittent training may improve both anaerobic and aerobic energy supplying systems significantly, probably through imposing intensive stimuli on both systems.



Experiment 2. Subjects exercised for 5 d·wk-1 for 6 wk. For 4 d·wk-1, they exercised using exhaustive intermittent training. They were encouraged by the supervisor to complete seven to eight sets of the exercise. Exercise was terminated when the pedaling frequency dropped below 85 rpm. When they could complete more than nine sets of the exercise, exercise intensity was increased by 11 W. One day per week the subjects exercised for 30 min at an intensity of 70% ˙VO2max before carrying out four sets of the intermittent exercise at 170%˙VO2max. This latter session was not exhaustive. The anaerobic capacity was determined before, at 2 wk, and 4 wk into the training, and after the training. ˙VO2max was determined before, at 3 wk, 5 wk, and after the training.



So experiment 2 is 4 days/wk doing 20s on / 10s off (7-8 sets, estimated 170% VO2max extrapolation) plus another day doing 30 min at 70% VO2max then 20/10 for 4 sets.

Thanks for sharing the protocol above!
 
From what I know about using HIIT. that intensity with such briefs rest periods is way too high, I would think that the body does not have the time to clear the metabolites used at those intensities. I know short rest period in weight training have been shown to not be beneficial to growth for the same reason. Also, not sure #1 went 5 days a week?
 
I wanted to throw this study in the mix before I start reading all f the rest of this information


Readalot, is this what you are talking about?

Yep, that second one you linked and the one I linked above are good primers. Thanks for the first study on immune function and intense exercise. Interesting conundrum...you may live longer but have to deal with the AF that may come along for the ride. Oh well.
 
Chronic HIIT + AAS a recipe for disaster?



Myocardial fibrosis or scar is characterized by the accumulation of collagen in the extracellular matrix as a result of myocardial damage from a range of pathologies. The patterns of fibrosis can be broadly classified as reactive or replacement fibrosis.1 Reactive fibrosis is characterized by the synthesis of collagen by myocytes in response to cardiac stress from aging, pressure or volume overload, reactive oxygen species, or the renin-angiotensin aldosterone system and beta-adrenergic system. In replacement fibrosis, myocytes damaged by ischemia or viral infection are replaced by collagen. Reactive fibrosis may progress to replacement fibrosis.1 Replacement fibrosis can be localized as in myocardial infarction or can be more diffuse following systemic conditions such as viral myocarditis.

Myocardial fibrosis reduces ventricular compliance, the downstream effects of which include heart failure with preserved or reduced ejection fraction, atrial enlargement, atrial fibrillation, and ventricular arrhythmias. Replacement myocardial fibrosis can be easily identified using magnetic resonance imaging (MRI) after the injection of gadolinium-based contrast agents (late gadolinium enhancement [LGE]). The presence of myocardial LGE is an emerging risk factor for future cardiac events and mortality in multiple pathologic states in the non-athletic population.2 Reactive fibrosis, on the other hand, is a more diffuse process and may not be easily detected using LGE. Recent developments in nonparametric cardiac MRI techniques such as T1 mapping (myocardial T1 and extracellular volume [ECV] measurements) allow for identification and quantification of diffuse reactive fibrosis. T1 relaxation time varies in relation to the composition of the myocardium and rises with any increase in fibrotic tissue. T1 maps can depict even relatively small variations of T1 within the heart to highlight tissue pathology. T1 mapping performed before and after the injection of a contrast agent allows measurement of ECV, which quantifies the relative expansion of extracellular matrix as a result of diffuse reactive fibrosis.3

Emerging data in athletes suggest that prolonged, high-intensity exercise may also cause cardiac damage and fibrosis even in the absence of predisposition to cardiac disease.4 One animal study looking at rats that were forced to run for 16 weeks (equivalent to 10 years of endurance exercise training in humans) demonstrated the development of eccentric cardiac hypertrophy, myocardial fibrosis and inducible ventricular tachycardia in 42% of the rats. Interestingly, the fibrotic changes were reversed after an 8-week exercise cessation.5 Not all studies, however, support this hypothesis.6,7 Athletes with LGE tend to be older than athletes without LGE. The prevalence of LGE also increases with years of competitive exercise training and the number of completed endurance events.8
 


 
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