In this QT, we’ll look at the latest research on heavy lifting and heart health.

Intense Resistance Training and Cardiac Hypertrophy

For decades, the Morganroth hypothesis has ruled the roost of exercise and heart health. Put simply, it states that endurance exercise enlarges the volume of the heart’s left ventricle without making the muscle thicker (a good thing) while the high internal body pressure created by lifting weights makes the heart grow thicker, which reduces ventricular volume (a bad thing).

A joint Aussie/UK team decided to revisit the hypothesis. They reasoned that the inaccurate tools of the time (1970s echocardiography) and the lack of subsequent longitudinal studies might have skewed the results. The researchers solved both these problems by creating a 24-week study with MRI-determined results.

They also created a good exercise protocol, which is often lacking in research like this. A cohort of untrained men (roughly 25–30 years of age) was split into endurance and weightlifting groups. Each group followed a periodized training plan that had them at the gym three times a week. Intensities were determined by heart rate and VO2 max for the endurance group and percentage of 1RM for the lifters. Most impressively, the lifters followed a linearly periodized Olympic routine that used the clean and jerk and snatch as the main lifts and squats, deadlifts, presses, and other movements as accessory lifts.

The endurance athletes improved as expected—better heart function, more ventricle volume, and lower resting heart rate. The lifters showed improvements and flat trends in the expected areas. Though contrary to Morganroth, they didn’t have thickened ventricle walls. The research team actually expected this trend based on invasive, short-term studies investigating the mechanics of blood flow and the Valsava maneuver; the research found that aortic pressure didn’t excessively rise during lifts.

This study isn’t the last word on big weights and the heart by any means. The results might be different in longer frames and bigger studies with trained subjects or women. Still, it’s a far sight better than what’s come before it.

Reference

  • Spence AL, et al (2011) A prospective randomized longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise training in humans. Journal of Physiology 589(22):5443–52.

AAS and Cardiac Hypertrophy

You can’t get much more longitudinal than death, as a team of Swedes demonstrated when they dug into the autopsy reports of confirmed AAS users versus non-users. Controlling for factors like age, body mass, and other drug use, the men with steroids in their systems still had larger hearts than the control group. In fact, a third of the AAS users were noted by their coroners as having enlarged hearts.

I think a few details are also of interest. For one, there’s no way of knowing if the larger hearts had an effect on lifespan because most of the AAS users died from drug overdoses, homicide, suicide, and accidents. Also, there seemed to be a connection between steroid use and increased blood loss.

More interesting might be the study’s limitations. One of these limitations actually preceded the study—the toxicology screens only tested for steroids if the deceased had unusually high muscle mass. On the one hand, this is sampling bias of a sort. On the other, it likely excluded new users and very low dose users from the AAS group, meaning that the data is probably most relevant to people who would be most concerned about it.

Now, this study doesn’t prove a blessed thing on its own. HGH would’ve been undetectable and the data sets are messy. But taking into account other data gathered over the years (including the earlier piece refuting the Morganroth hypothesis), it seems that the usual strength pharmacology can come with unwanted side effects.

Reference

  • Hamid RMF, et al (2012) Cardiac hypertrophy in deceased users of anabolic androgenic steroids: an investigation of autopsy findings. Cardiovascular Pathology 21(4):312–16.

Get Under the Bar to Convert Your Cholesterol

We’ve come a long way from the days of just worrying about triglycerides, LDL-C, and HDL-C. The particulars of fatty acid profiles seem to change by the week. LDL-C and HDL-C have been segmented into types, and apolipoproteins are on the radar.

Whether you’re a proponent of the lipid hypothesis or not, worrying about “good cholesterol” and “bad cholesterol” just doesn’t cut it. Yet another example is that HDL-C can actually turn bad and help cause atherosclerosis and that people with heart disease often have this dysfunctional HDL. A more nuanced way of saying this is that under specific instances of trauma, HDL-C will promote inflammation as part of the healing process. It seems that certain body states can cause HDL-C to remain chronically inflammatory in a way that promotes oxidation of LDL-C and lessens cholesterol efflux.

Researchers at UCLA have been at the forefront of research into dysfunctional HDL-C. One of their latest studies sought to show just why high fitness levels seem more cardio-protective than low body weights. They thought that fitness might promote healthy HDL-C. Turns out, they might be right.

The study looked at three groups of young men—individuals with a BMI less than 25 who lifted weights at least four times a week, trained individuals with a BMI over 27 who lifted weights at least four times a week, and untrained individuals with a BMI over 27. They found that the two groups of lifters had similar levels of normal HDL-C and that higher levels of strength/muscle were correlated with better HDL-C profiles.

Assuming the concept of dysfunctional HDL-C holds up, one caveat is that this isn’t exactly license to adopt the "gallon of peanut butter milkshake a day" protocol. The average BMI for the hefty groups was about 30. The trained subjects had about 18 percent body fat while the untrained group had about 28 percent. If you’re five feet, eleven inches tall and weigh 250 pounds, your BMI of 35 would put you outside of the results, as would your age if you’re over thirty.