TREN A and endurance

[Cravenmorehead]

Since Tren increases RBC.........why the decrease in cardio performance???

[PK-V]

The prostaglandin release from tren can lead to a shortness of breath, couple that with increased blood pressure and you will be putting a major strain on your cardiovascular system


>Cardio bunny

>Weightlifter

Pick one!

[redz]

I never experienced any decrease from Tren myself but most say it affects them.

[Cravenmorehead]

Maybe a beta-blocker combined with a dose of Cialis or Viagra would help.

[Sgt. Hartman]

Maybe a beta-blocker combined with a dose of Cialis or Viagra would help.

Seems like a vasodilator like cialis or viagra would further increase BP.

In addition to what pk-v posted about tren directly affecting cardio by prostaglandin causing bronchial constriction, many people find it very difficult to do cardio on tren b/c of the massive pumps/cramps you get from performing a repetetive movement like running, cycling, etc.

[Bonaparte]

The prostaglandin release from tren can lead to a shortness of breath, couple that with increased blood pressure and you will be putting a major strain on your cardiovascular system

Correct, because it can cause bronchioconstriction.

Maybe a beta-blocker combined with a dose of Cialis or Viagra would help.

No. You would want a beta-2 agonist like Clen or Albuterol.

Seems like a vasodilator like cialis or viagra would further increase BP.

In addition to what pk-v posted about tren directly affecting cardio by prostaglandin causing bronchial constriction, many people find it very difficult to do cardio on tren b/c of the massive pumps/cramps you get from performing a repetetive movement like running, cycling, etc.

Vasodilation (an increase in blood vessel diameter) reduces blood pressure.
But BP is not the issue, since plenty of compounds increase BP and do not hinder endurance.

[Cravenmorehead]

Albuterol raises the HR.......perhaps something like Advair before a workout......Cialis and Viagra have been shown to be performance enhancers at altitude for sure

[trenbo100]

i ran 75mg ed tren ace i could rep had no shortness of breath, my endurance weight wise went through the roof! i could rep and rep and rep without losing my breath so i just think it depends on the person. everybody has different sides.

[Wakalito1]

great stuff

[Bonaparte]

Albuterol raises the HR.......perhaps something like Advair before a workout......Cialis and Viagra have been shown to be performance enhancers at altitude for sure

Salmetrol (found in Advair) also increase HR, as it is just another B2 agonist (and slower acting than albuterol).
And Fluticasone is a corticosteroid and isn't going to do shit for our purposes.

And again, the endurance issue has nothing to do with BP.

[PK-V]

Seems like a vasodilator like cialis or viagra would further increase BP.

In addition to what pk-v posted about tren directly affecting cardio by prostaglandin causing bronchial constriction, many people find it very difficult to do cardio on tren b/c of the massive pumps/cramps you get from performing a repetetive movement like running, cycling, etc.

Anyone know what causes these muscle specific pumps when there are subjected to endurance work

A lot blame gets put on glycogen retention, but how on a fundamental level does having excessive glycogen store compromise the ability of our slow twitch fibers to carry out excessive repetition?

[MR10X]

[QUOTE=Bonaparte;5807671]Correct, because it can cause bronchioconstriction.



No. You would want a beta-2 agonist like Clen or Albuterol.



Vasodilation (an increase in blood vessel diameter) reduces blood pressure.
But BP is not the issue, since plenty of compounds increase BP and do not hinder endurance.[/QUOTE

I found that out when i took cialis in the afternoon ,then took 50mg of viagra an hour before sex. I thought i was going to pass out,i checked my blood pressure and it was EXTREAMLY LOW.When they say it can cause an unsafe drop in blood pressure they mean just that.

[PK-V]

Anyone know what causes these muscle specific pumps when there are subjected to endurance work

A lot blame gets put on glycogen retention, but how on a fundamental level does having excessive glycogen store compromise the ability of our slow twitch fibers to carry out excessive repetition?

bump

[NewMuscle83]

Interesting thread. Bumping.

[Cravenmorehead]

Possibly the increased glycogen causes an increase of lactic acid buildup and associated nitric oxide. The excess fuel combined with not enough aerobic capacity results in the intolerable pumps??

[Sgt. Hartman]

I don't think it's lactic acid build up as i get a painful shin pump within 5min of walking fast or jogging on the treadmill.

Bump for Bonaparte.

[Cravenmorehead]

Shin Splints are essentially compartmentaliztion syndrome.......

[Sgt. Hartman]

They're not shin splints. I've had shin splints before and this is different. It starts out as a pump and then becomes so painful I have to stop. I get the same thing on the stairmill but in my teardrop muscle.

[Bonaparte]

Shin Splints are essentially compartmentaliztion syndrome.......

I'm still trying to fully understand the cause behind these pumps.
And yeah, it does involve some sort of compartment syndrome caused by excess bloodflow to a muscle. But it is mainly caused by AAS that promote heavy glycogen storage (orals).
Unfortunately, the medical/scientific community doesn't have answers for us on this (that I know of).

Taurine helps a lot in large doses (5-10g). But while the traditional explanation for this is that it is a vasodilator (which would allow the excess trapped blood to escape more efficiently from target areas), no other vasodilators seem to help. Hmmm...

[Far from massive]

I get crazy pumps in the front of my legs where the tensor fasciane latus (spell check) inserts at the top. Particularly when I get up from sitting in the morning I can feel it tightening and if I touch it then it contracts even worse...although its a really neat feeling, kinda like working out without doing anything.

[Cravenmorehead]

Chronic Exertional Compartment Syndrome

Pathophysiology
The pathology of CECS is not well established and is still debated; a general discussion follows.

CECS is associated with increased pressure in muscles at rest. Transient increases in compartmental pressure have been demonstrated experimentally as a normal response to exercise. Repetitive muscle contraction alone can increase intramuscular pressure to levels that may cause transient ischemia.

Elevated pressures usually normalize within 5 minutes after cessation of exercise. In CECS, however, the pressure between successive contractions remains high and impedes blood flow. As the pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping.[8] Pressures may remain elevated for 30 minutes or longer in persons with CECS.

Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure. This is also stated by the following formula:

LBF = (PA - PV)/R

In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance.

Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.[9]

When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

With myocyte necrosis, myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood. One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure.

When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate. Changes in local vascular resistance (autoregulation) can compensate for some reduction in the local AV gradient. However, compartment tamponade occurs as arterial blood flow is occluded.

Shrier and Magder questioned this traditional hypothesis for the pathophysiology of CS and postulated that a critical closing pressure exists within muscle compartments (similar to West zone II in lung physiology).[10] These authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow.

The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures that exceed 30 mm Hg and persist for 6-10 hours result in muscle infarction, tissue necrosis, and nerve injury. For unclear reasons, compartment syndrome that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.[11, 12]

Pressure-induced functional deficits are likely due to decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion.

In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis (acute compartment syndrome); conversely, rhabdomyolysis may result in compartment syndrome.[13, 14]


In other words.....be cautious with the huge pumps........this may be the answer to the TREN reports of renal issues........just a theory

[ScotchGuard02]

Interesting thread.

[Bonaparte]

Thanks. I missed this post until just now.