Just work hard damnit!

       It's humorous how often people warn me that the way I train (very basic without much accessory work) will lead me to sub-par performance on the platform and a huge set of injuries. It's impossible, they tell me, to adequately train and prepare the muscular system for athletic exertion without a massive list of special exercises and corrective drills, and without isolating motor patterns around joints, I'll be hurting myself regularly.

       The fact is, as I've transitioned over the years to a low-variety system based on specificity, many nagging injuries have cleared up. I've PR'ed in 2 weight classes in powerlifting and expanded the number of federations I hold titles and records in by over 100% with no new major injuries. I've attained my largest size yet at a leanness I haven't matched in years.

       My hiking performance has benefitted too. It's the other sport I participate in with serious interest. Times and recovery intervals have decreased while my capacity for long hikes and hard trail runs in a given time span has gone up. I'll add that I sustained no hiking-specific injuries last season either.

       My hamstrings haven't exploded because of a lack of knee flexion in my program. In fact, both hamstrings have old injuries that have improved since removing the fluff from my training to go harder on what works.My pec tendons haven't shortened into unmoveable cords because I don't do deep dumbbell presses and my bench lockout hasn't gone to hell over a lack of triceps extensions. My back requires me to let the seams out on my shirts, even though I haven't done anything for it besides chins and rows since I moved to Portland. Neither ankle has been devastated by the rampaging injuries supposedly common to those who don't train calves, and my calves push on the legs of my pants hard enough to rub all the hair off. And, oh yeah, doing absolutely zero cardio training hasn't affected my conditioning. At all. (Clearly hiking is endurance training and this specificity has been enough to prepare me for the rigors of the sport.) My training is a lifting template so boring you'd have to be in love with powerlifting just to do it and as many hikes in a week as I can fit when the season to hike approaches.

       You'd be surprised how much of an impact proper, basic strength training will have on every single aspect of your athleticism if you give it a chance. Clearly, there is more than one way to train. I'm all for individualizing programming to meet specific needs and I'm all for doing the corrective work and special training that carries over to your athletic endeavors. But I often ask people to look critically at their training and ask what the purpose and result of every lift they do is. If you can't identify a purpose, and the movement doesn't result in a measurable performance or rehabilitative improvement then why are you doing it? Isn't it a waste of time? Many times, athletes are shocked to learn that a large portion of their training falls into the category of lifts without clear purpose or effect. If this describes you, consider going back to basics. It's okay not to be fancy, especially if it allows you to finally train as hard as you always should have been.
     

Testosterone and Your Heart

       Testosterone receives much more than its fair share of bad press. A few seconds on a search engine reveals it will shrink your penis, make you permanently sterile, cause multiple forms of cancer, destroy your heart, weaken your connective tissues, and make you go insane. But what does the data say? If you've looked, you'll know that testosterone has classically been considered a major cardiac risk but that attitudes are changing as we learn more about the pathologies of various cardiac issues and diseases.

       Recently, the media is piling on accusations of extreme cardiac risk associated with testosterone following the publication of a recent study and article. It's too bad for these sensationalists that the study was one of the worst designed ever and was roundly dismissed by most authorities. I won't link it here, but you can find it easily if you want it. Instead, lets look at studies designed to look at the issue in more detail.
    
       Fair warning: This post, in its entirety, is going to be a thick read. Skip it or skim it if you have not yet delved into the murky world of PED research. It's essentially a collection of hard data that I've been working through for a research project for my work. I'm not going to go into heavy detail on most since the papers themselves are satisfactory to explain the data. For the more research-minded among you I strongly urge at least a cursory skimming of the provided literature to get up to date on the current understanding of risk. For those of you just looking for broad summaries and interpretation, stick to the synopsis sections.

http://cardiovascres.oxfordjournals.org/content/57/2/370.short

Not much more to say here: "We found no evidence for cardiac toxicity of T administration despite a 10-fold increase in T levels after testosterone undecanoate administration compared to placebo administration. Neither infarct size nor procedure-related mortality was influenced by T status. In contrast, there was a tendency to an improved hemodynamic outcome..."

http://www.ncbi.nlm.nih.gov/pubmed/12800107

Visceral Abdominal Fat is a major risk factor for myocardial infarction, linking and perhaps superceding other risk factors and "linking" them for a larger effect. Estradiol is emerging as a major risk factor for myocardial infarction in men as well. This study concluded: "(1) VAT in men may largely explain the correlations of sex hormones, insulin, and obesity with the risk factors for MI measured, (2) VAT may be the principal factor in men, independently of other measures of adiposity, that links risk factors for MI to form the constellation, and (3) estradiol may play a more important role in the sex hormone-insulin relationship in men than has generally been considered."

http://circ.ahajournals.org/content/102/16/1906.short


Again, pretty clear: "Low-dose supplemental testosterone treatment in men with chronic stable angina reduces exercise-induced myocardial ischemia."


http://www.pnas.org/content/74/4/1729.short


Glucose metabolism dysfunction and estrogen elevations continue to be seen as primary cardiac risk factors. "The hypothesis is presented (i) that in men who have had a myocardial infarction, an abnormality in glucose tolerance and insulin response and elevation in serum cholesterol and triglyceride concentrations are all part of the same defect (glucose-insulin-lipid defect), (ii) that this glucose-insulin-lipid defect when glucose intolerance is present is the "mild diabetes" commonly associated with myocardial infarction but is based on a mechanism different from that of classical diabetes, (iii) that this glucose-insulin-lipid defect is secondary to an elevation in E/T, and (iv) that an alteration in the sex hormone milieu is the major predisposing factor for myocardial infarction."


http://www.ncbi.nlm.nih.gov/pubmed/3573299


http://www.sciencedirect.com/science/article/pii/S0140673676929688


Both of the two links above show estrogen elevations, with the second of these two having this to say:


"These results suggest that the hyperœstrogenæmia preceded the myocardial infarction and that hyperœstrogenæmia may be an important risk factor for myocardial infarction in men."


http://archinte.jamanetwork.com/article.aspx?articleid=601660


More about estrogen as a risk factor.


http://circ.ahajournals.org/content/99/13/1666.short


Reduction in exercise-induced ischemia with supplemental testosterone.


http://circ.ahajournals.org/content/100/16/1690.short


Testosterone induces coronary dilation and is shown to improve bloodflow in men with coronary artery disease.


http://cardiovascres.oxfordjournals.org/content/57/2/370.short


Reduced stress on the cardiac wall with testosterone doses sufficient to cause anabolism in diseased populations.


http://atvb.ahajournals.org/content/14/5/701.short


Low T hypothesized to be a risk factor for coronary atherosclerosis.


http://biomedgerontology.oxfordjournals.org/content/60/11/1451.short


Notable for it's conclusion that T did not significantly affect likelihood of cardiac events.


http://journals.lww.com/co-endocrinology/Abstract/2010/06000/Testosterone_and_heart_failure.14.asp


"Anabolic deficiency is a major component of the CHF syndrome and testosterone replacement therapy has been subject to recent trials."


There can never be enough research. We need much more to assemble a proper understanding of testosterone and associated cardiac risk. But here is a summary of what we know about it:


1. Obesity and metabolic syndrome are considered over-arching risk factors.


2. Elevated estrogen levels are beginning to be seen as primary instigators of cardiac issues in men, despite physiologic doses exerting positive effects.


3.Testosterone is being studied for its potential therapeutic uses in cardiac patients.


        There is and should be concern for health if you use PED's. These drugs carry risk and that should not be ignored. But when we look at the data, it’s easy to see that much of the fear mongering about testosterone and cardiac risk is just that. While some studies do highlight risk, it’s important to note that methodology and design alters the appearance of the data in many cases. The pieces above, and many more, support the idea that testosterone is not as dangerous to cardiac tissues, in most cases, as is often claimed. In fact, lifestyle factors such as metabolic syndrome and other hormones, estrogen and insulin chief among them, carry much more risk and affect cardiac tissue much more negatively. Until a full picture is assembled, continue to focus e on staying healthy via exercise and diet to maintain cardiac health, and be aware of how estrogen levels might affect your heart. It appears at this point that cardiac risk from testosterone has been overstated. The American Heart Association says TRT improves quality of life and carries minimal cardiac risk. Enough said.