Hers Starter's Guide 2016 - Dumbbell Bentover Row
My old training partner and I stumbled on the muscle magic of dietary salt purely by chance. We used to train at a gym in a suburb of upstate New York called Yorktown Heights. The name of the gym was Bob Baff’s, and it was the first serious gym I ever trained at. In those days, we would spend stupid hours overtraining in the gym. It was a labor of love and an addiction that, to date, has had no equal in either of our lives.

Back then it was eat, train, eat, sleep, eat, grow, sleep, train, grow, eat, sleep, and chase girls. At any rate, part of our routine was to occasionally meet early in the parking lot and, despite a sizable breakfast, we’d need to eat more just to get through our utterly moronic two- to four- hour training routine. As a prelude 
to pumping iron, once or twice each week (that’s all we could afford back then) we’d walk over to this crummy Chinese restaurant located in the same strip mall as the gym. While it was certainly convenient, the food honestly wasn’t very good. But it did have one major “attribute”—it was salty as hell. It seemed like they had some kind of cooking philosophy that if they just added enough salt out of there and hit the weights,
 our muscles would pump like crazy. At times it was absolutely freakish to the point that we thought they jacked their food! Not only were the pumps bigger and more dramatic, but the salt-enhanced pump lasted far longer than usual. For some time we figured it was just a matter of all the extra calories. Then, after trying some other food options, we quickly realized that there was no substitute for the Chinese salt torture.


Of course, when you even mention an excess salt intake story like this to almost anyone, the first thing they do is have a heart attack! The result is absolute disbelief. At the mere mention of dietary salt, many begin to cringe as negative connotations swirl endlessly around
the subject. But the fact is that we need dietary salt to live. The body 
is dependent on salt intake since 
the body has no significant means by which it can store large amounts of salt for later use. Athletes know this all too well, as there is little debate that dietary salt deficiency results in a significant attenuation of athletic performance.(1) So why do so many believe that this logic, albeit at a more physiologic extreme, has no application to the general populous? Perhaps it all started with shortsighted physicians spreading their misinformation about salt to their hapless patients. Combine that with the seemingly endless media thumping that has jaded nearly all of us, and it’s no wonder society found another proverbial witch to burn at the stake.

The systematic mass convincing that table salt is evil likely stemmed from early medical evidence in patients with salt-sensitive hypertension or kidney problems who
saw their conditions get worse with higher salt intake. But these are the relatively rare exceptions that occur only under conditions of illness and most certainly are not reflective of the state of the general population, let alone the athlete or bodybuilder. The honest truth is that, in otherwise normal physiology, dietary salt certainly does not cause kidney failure. In fact, as stated, salt is absolutely essential to the human body. Dietary salt governs countless reactions and functions in the body including, but by no means limited to, nerve conduction, muscle contraction, membrane stability, osmotic gradient, kidney and fluid transport, molecular transport systems at the cellular level, and serving as an enzymatic co-factor in countless reactions throughout the body.


To further the point, the latest research has gone so far as to not only challenge the efficacy of a low salt diet but also actually indicate that it may be harmful to many. One recent hotly debated but very comprehensive review article showed that a low-versus high-sodium diet barely decreased blood pressure in people with normal blood pressure (1%) while at the same time it produced a significant increase in plasma cholesterol (2.5%) and plasma triglycerides (7%).(2) These controversial results refuted the long-standing mainstream belief that dietary salt restriction has a significant benefit in the general population. Moreover, in a society where heart disease is the No. 1 killer, such an overzealous demonizing of salt may in fact be problematic over the long haul for many.

Bodybuilders have fallen into the same trap of misguided conventional wisdom. As far as I’m concerned, dietary salt intake is one of the most powerful yet underestimated pump enhancers and cheap anabolic substances readily available to each and every one of us. There is little doubt from the available published research that all of us, including the salt haters, must now accept the fact that dietary sodium plays
a direct role in the action potential required for muscle contraction.(3) But the real shocker is that animal studies are now coming in show
ing us that a bolus of salt infusion literally nearly doubles blood flow to skeletal muscles.(4)

Meantime, my training partner and I had already discovered the pump-enhancing benefits of dietary salt loading and performed our
 own “animal study” on ourselves nearly 30 years ago! As to how much sodium we were consuming in one sitting, I can’t really say with much certainty. What I can say is that it must have been at least 5 grams of sodium at a single sitting. Perhaps it seems like a huge amount, especially when you consider the American Heart Association recommendation that salt intake should not exceed 2,400 milligrams day. Then again, there are other countries that regularly ingest up to 8 grams or more of salt each day and have no significant increases in the same so-called salt-related illnesses. But the truth is that we luckily did not do our salt-load every day. That’s not to say that we would not have gladly pushed the limits, but simply that we were busted flat most of the time and could afford only once a week most of the time. But therein lies another thing we may have inadvertently done correctly. While the bolus of salt certainly blew us up in the gym, it seems it would have gone in the opposite direction if we kept pushing the limits of the response. That’s because modern clinical research now tells us that excessive long-term high-salt usage will actually lead to a decrease in blood flow to the muscles. Over time (four or more weeks), daily high-salt intake actually impairs arteriolar responses to oxygen smooth muscle responsiveness.(5) Fortunately due to our youthful mutually impoverished dispositions, we were unable to test these limits, which we surely would have done if finances allowed.


So what exactly is going on in the body that causes an acute, orally ingested sodium bolus to produce such a radical muscle pump? To understand this better, we first need to consider the role of sodium in activating a muscle to contract. Before a muscle cell contracts, the inside of each cell maintains a negative electric charge compared with the positive exterior of the cell. This state of “polarization” is not achieved passively and is maintained using “pumps” powered by cellular energy (adenosine triphosphate, or ATP). This active process involves higher concentrations of positively charged sodium molecules (Na+) outside the cell, while keeping negatively charged chloride molecules (Cl-) inside each muscle cell. The concentration of sodium outside the muscle cell is about 10 times greater than the inside. This charge-gradient results in a net negative “resting muscle cell potential” of about -75 millivolts (mV) relative to the surrounding charge. So basically each muscle cell sits there waiting to contract with a negative charge as a result of this electrical gradient. Then when the muscle cell is stimulated to contract, sodium channels in the membrane of the muscle cell open and sodium rushes into the cell to balance out and neutralize the charge and concentration gradient. As the sodium floods into the muscle cell, the electrical signal to contract is propagated throughout the muscle cell, and a full muscle contraction begins. The entry of sodium into the muscle cell is balanced by the exit of potassium molecules (K+). Potassium concentration inside the muscle cell is maintained at a level of about 20 times that outside the cell. As contraction subsides, sodium channels close and these potassium channels open. Sodium molecules are then once again actively moved out of the cell by the work of the sodium pumps, while potassium molecules are pumped back in to restore the gradient. Since a vigorous contraction is dependent on a high concentration of sodium molecules outside the muscle cells, logic tells us that a higher exterior sodium concentration would potentiate a forward reaction resulting 
in a brisker muscle contraction and greater resultant perfusion. To put it another way, augmenting this gradient with orally ingested salt may set off a more rigorous influx of sodium molecules into the muscle cells, resulting in a more efficient contraction. I call it a “contraction potential” and it’s akin to having more water built up behind a damn. When you open the floodgates and water careens through, the more you have behind the damn, the greater the flooding forces.


Finally, I wouldn’t want you to think this is any kind of commentary on good behavior for general health. Excess salt can in fact be dangerous and even fatal in the wrong person. Although you might choose to experiment with acute salt loading, I wouldn’t suggest drowning yourself in it or doing it repetitively over the long haul. Try to be smart about self-experimentation…and don’t order the egg foo yong.


REFERENCES: 1) V. Valentine, Curr Sports Med Rep., 6(4):237–40, 2007. 2) A. Niels, Am J Hypertens., 25(1):1–15, 2012. 3) Scientific Opinion on the substantiation of health claims related to sodium and maintenance of normal muscle function (ID 359) pursuant to Article 13(1) of Regulation (EC) No 1924/2006, EFSA J., 9(6):2260 [14 pp],2011. 4) J.F. Liard, Am J Physiol – Heart Circ Physiol., 240 (3):H361-67, 1981. 5) P.J. Marvar et al., Am J Physiol – Heart Circ Physiol., 292(3):H1507-15, 2007.