Research Update #13

by Hypertrophy

As we approach the new millennium we find the science of building muscle progressing faster than ever before. Long gone are the days of simple trial and error when it comes to building muscle. The modern bodybuilder demands more than just "hear say" if they are to adopt a new training routine or nutritional supplement. This column was created to keep today’s bodybuilder on the cutting edge of scientific research that might benefit them in their quest for body perfection.

Title: Effects of resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body mass and resting metabolic rate.

Researchers: Bryner RW, Ullrich IH, Sauers J, Donley D, Hornsby G, Kolar M, Yeater R; Department of Human Performance and Applied Exercise Science, West Virginia; University, Morgantown 26506, USA.

Source: Journal of the American College of Nutrition 1999 Apr;18(2):115-21

Summary: The purpose of this study was to examine the effect of intensive, high volume resistance training combined with a very low calorie diet (VLCD) on weight loss, lean body weight loss (LBW), and resting metabolic rate (RMR). METHODS: Twenty subjects (17 women, three men), mean age 38 years, were randomly assigned to either standard treatment control plus diet (C+D), n = 10, or resistance exercise plus diet (R+D), n = 10. Both groups consumed 800 kcal/day liquid formula diets for 12 weeks. The C+D group exercised 1 hour four times/week by walking, biking or stair climbing. The R+D group performed resistance training 3 days/week at 10 stations increasing from two sets of 8 to 15 repetitions to four sets of 8 to 15 repetitions by 12 weeks. Groups were similar at baseline with respect to weight, body composition, aerobic capacity, and resting metabolic rate. RESULTS: Maximum oxygen consumption (Max VO2) increased significantly but equally in both groups. Body weight decreased significantly more in C+D than R+D. The C+D group lost a significant amount of LBW (~ 4 kg or 8.8 pounds). No decrease in LBW was observed in R+D. In addition, R+D had an increase in RMR O2 ml/kg/min (2.6 to 3.1). The 24 hour RMR decreased in the C+D group. CONCLUSION: The addition of an intensive, high volume resistance training program resulted in preservation of LBW and RMR during weight loss with a VLCD.

Discussion: When caloric expenditure is greater than caloric intake (e.g. while dieting), the body converts it’s tissues into burnable forms of energy such as glucose, amino acids and free fatty acids. This is carried out in response to heightened activity of catabolic hormones. These hormones are able to mobilize energy buy causing cells to disassemble proteins, sugars and fats that make up the cells enzymes and internal structures.

With an increase in catabolic hormones it is only natural that the body will begin to lose mass and get smaller. When calories are restricted the body not only draws upon fat stores but also upon tissues such as muscle, blood and even your internal organs in order to get amino acids used in gluconeogenesis.

Due to the central nervous systems’ constant need for glucose, gluconeogenesis increases sharply when calories are restricted. This means that protein is broken down to make key amino acids available to be converted into glucose as well as for other essential functions. All this is done at the expense of protein rich tissues such as muscle and internal organs.

During starvation diets as much as 50% of the total amount of weight lost has been observed to come from lean tissue. This is disastrous for anyone trying to lose fat! Imagine that you have a car and your goal is to use up all of the gas in the gas tank. The catch, is that the more gas you use, the smaller the engine gets, and the less gas it requires. (It must be one of those foreign jobs.) This illustrates the impact of losing lean tissue as you try to lose fat. Muscle tissue, through its own metabolic activity as well as it’s relation to thyroid output, is almost 90% responsible for the number of calories that you burn in a day. As you lose muscle it becomes harder and harder to continue to lose weight because fewer calories are needed by the body. The usual response is to cut calories even further which only exacerbates the situation. This predicament is the result of normal metabolic adaptations to caloric restriction.

Although the effects of weight training on the preservation of lean mass during caloric restriction is very old knowledge to bodybuilders, the medical community must once again try to feel responsible for making the discovery. In the study above we see subjects put on what has previously been considered a dangerous very low caloric intake of 800 liquid Kcals per day. Some of the people on the diet were put on a resistance training program. This group performed resistance training 3 days/week at 10 stations increasing from two sets of 8 to 15 repetitions to four sets of 8 to 15 repetitions by the end of 12 weeks. The control group used the same diet but performed aerobics or endurance exercise. The result? As expected the weight training group held on to their muscle while the aerobics group lost almost 9 pounds of theirs.

A couple of issues need to be brought up while interpreting these results. First, these were regular non-weight training, non-athletic people. The anabolic stimulus created by their meager attempts at pumping iron was sufficient to completely counter the catabolic effects of an 800 Kcal per day liquid diet. They were not holding on to any hypertrophied lean tissue before dieting. This being the case, their muscle was already somewhat resistant to catabolism when compared to some one who must bust their butt most days of the week just to keep from getting "small".

The second issue that must be recognized is that they adhered to a very important principle of resistance exercise, namely the principle of progressive resistance. This means that over the period of their diet, the amount of resistance as well as the volume lifted increased steadily. This seems to be problematic for most bodybuilders. In fact it is common practice to actually decrease the poundages for most lifts over the course of a pre-contest diet. This happens because they make no effort to cycle their training to accommodate the diet. Starting a diet at the peak of a strength plateau is not the best method to keep your size for an upcoming show. A period of "strategic deconditioning" during which size is maintained while intensity and volume slowly decrease is necessary to prepare for dieting. Then, the diet begins at the same time a progressive resistance cycle is begun. This simulates the conditions under which a novice experiences significant muscle gains at the onset of a weight training program and is more conducive to keeping, if not increasing, lean mass while dieting. Of course this is a simplification yet the principle is sound and the results reproducible.

Claims About the Dangers of Creatine May Be Overstated.

Title: Long term oral creatine supplementation does not impair renal function in healthy athletes.

Researchers: Poortmans JR., & Francaux M.

Source: Medicine and Science in Sports and Exercise 31(8): 1108-1110, 1999

Summary: Side effects have been postulated from the use of creatine supplements yet no thorough investigations have been conducted to support these assertions. The purpose of this study was to determine if indeed long term creatine use was detrimental to the kidneys of healthy individuals. METHODS: Creatinine, urea, and plasma albumin clearances were measured in oral creatine consumers (taken regularly for 10 months to 5 years) and in control subjects (never used creatine). RESULTS: There were no statistical differences between the control group and the creatine consumers group for plasma contents and urine excretion rates for creatinine, urea, and albumin. Clearance of these compounds did not differ between the two groups. Thus glomerular filtration rate, tubular reabsorption, and glomerular membrane permeability were normal in both groups. The authors conclude that neither short-term, medium-term, nor long-term oral creatine consumption induce detrimental effects on the kidney of healthy individuals.

Discussion: Any time something good comes from the supplement industry (a rare yet highly anticipated occurrence) there will be nay sayers quick to declare the evils of the new super supplement. Creatine was not immune to such opponents of progress. Add to this rumors of kids peeing blood after loading the stuff for football practice and you have a full blown controversy. There has even been a published case study detailing the dangers of creatine on kidney function (Pritchard, 1998). Upon closer examination you will find that their one subject had a pre-existing kidney disease for the last 8 years. Not only that but the subject had been taking drugs that are toxic to the kidney for the last 5 years prior to their case study. Not surprisingly, their subject experienced kidney dysfunction after 7 weeks of creatine supplementation. This subject would probably have experienced kidney dysfunction after 7 weeks of mother’s milk!

The subjects in this study did not have any pre-existing kidney problems. Nine athletes were chosen to represent "long term" creatine supplementation. Eighty five subjects served as controls. Those who consumed creatine regularly did so in the following manner. Individual doses from 1 - 20 grams of creatine were taken from 1 to 4 times per day. Total daily doses ranged from 1 to 80 grams per day taken 7 days per week for a period ranging from 10 months to 5 years.

As you are aware from the above summary of the study, long term creatine supplementation does not appear to cause any kind of kidney dysfunction. All of the parameters looked at by these researchers showed no difference between the experimental group and the control group. There is one thing that I can promise you, you will not here about this study on the morning news. They only focus on sensationalizing supplements in the context that they are dangerous and their use is akin to drug abuse. Rest assured they will have someone with no actual knowledge of supplements or science extolling the dangers of supplements. All of this misinforms the general public making the work of actual experts in the field of nutritional supplementation all the more difficult as they have to go back and try to undo all of the hysteria. I’m afraid this is turning into some sort of rant. That’s a sure sign that I have said enough on this subject.

When It Comes to Building Tendons, Not All Steroids are Created Equal.

Title: Stimulation of collagen synthesis by the anabolic steroid stanozolol.

Researchers: Falanga V, Greenberg AS, Zhou L, Ochoa SM, Roberts AB, Falabella A, Yamaguchi Y; University of Miami School of Medicine, Department of Dermatology, Miami, Veterans Affairs Medical Center, Florida, USA.

Source: J Invest Dermatol 1998 Dec;111(6):1193-7

Summary: In this report, we measured the effect of the anabolic steroid stanozolol on cell replication and collagen synthesis in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5 micrograms per ml) had no effect on fibroblast replication and cell viability but enhanced collagen synthesis in a dose-dependent manner. Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and alpha1 (III) procollagen and, to a similar extent, upregulated transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels. There was no stimulation of collagen synthesis by testosterone. The stimulatory effects of stanozolol on collagen synthesis were blocked by a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and in dermal fibroblast cultures derived from TGF-beta-1 knockout mice. We conclude that collagen synthesis is increased by the anabolic steroid stanozolol and that, for the most part, this effect is due to TGF-beta-1. These findings point to a novel mechanism of action of anabolic steroids.

Discussion: I must first acknowledge that the commonly held belief is that anabolic steroids predispose an athlete to tendon rupture. This conclusion is drawn from animal studies showing that some steroids produce a larger, stiffer tendon in rats and that these steroid-induced tendons "fail" before the tendons from the control animals. The term fail refers to the breaking point.

The interesting thing about the present study is that the steroid stanozolol (Winstrol) had a different effect than testosterone. If you are a regular reader of Mesomorphosis you should be well aware that not all steroids act in the same manner. And that because of subtle differences in there molecular structure they are able to elicit different responses. For example, Deca seems to act primarily through the androgen receptor (AR) where as Dianabol has effects beyond those associated with the AR.

Because synthetic steroids have differ in their chemical properties it should not be surprising that testosterone did not have the same effect as Winstrol. Winstrol increased collagen synthesis as opposed to testosterone which did not in this study. Interpreting the results of this study are more difficult than simply describing them. Other researchers have suggested that steroids cause a rapid increase in protein synthesis within tendon fibroblasts which results in fibroids or fibrous nodules within the tendon (Michna,1988). These fibroids alter the mechanical properties of the tendon perhaps predisposing it to rupture. It is also noted that during short term use of steroids there is an alteration in the alignment of collagen fibers which may also lead to rupture. Interestingly these alterations in collagen metabolism are transient with markers of collagen turnover returning more or less to baseline after 3-4 weeks of steroid administration (Karpakka,1992). These same researchers noted that low dose anabolics effect primarily muscle collagenous tissue with tendon being effected only at higher doses (i.e. 5 times the therapeutic dose) which would more closely represent what is needed by bodybuilders to put on mass.

The question remains, dose this mean that Winstrol will actually help prevent tendon injury or will it lead to bigger yet stiffer tendons prone to injury? It is difficult to take animal research and extrapolate the results to humans. Stanozolol is used therapeutically in humans to treat a variety of connective tissue and vascular disorders and its clinical effects suggest that it can modulate connective tissue breakdown in people. Despite being labeled as "ineffective" by many bodybuilders it is very popular among athletes. As with most hormones, dosage plays a role in what effects are seen, be they positive or negative. Hopefully future studies will shed light on the therapeutic effects of different steroids on tendons in humans.