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The purpose of this article is to explore the available data concerning the protein needs of anaerobic athletes and to explain these needs in a metabolic context. It is important to keep in mind that the words "need" or "requirement" as they appear in this article do not simply refer to the minimum amount of dietary protein necessary to sustain health, but to the amount of protein necessary for optimum athletic performance or physique enhancement.

The intent of several studies has been not to determine precisely how much protein anaerobic athletes require, but merely to establish that amino acid metabolism is altered to some extent in these individuals. Tarnopolsky and his colleagues reported that 1 hour of circuit weight training did not affect leucine (an amino acid) turnover immediately after activity or for several hours afterward (Tarnopolsky, Atkinson, MacDougall, Senor, Lemon, and Schwarcz 1991). In agreement, acute weight lifting exercise was not found to increase urinary levels of 3-methylhistidine (Hickson, Wolinski, Rodriguez, Pivarnik, Kent, and Shier 1986; Horswill, Massey, Layman, Boileau, and Williams 1988), an indicator of lean tissue –and especially contractile protein– catabolism (Young and Munro 1978).

In contrast to the findings of studies regarding the acute effects of weight training, studies monitoring the effects of chronic weight training have revealed increased protein degradation. Pivarnik and others documented increased urinary levels of 3-methylhistidine in untrained subjects after the third day of resistance training, suggesting that skeletal muscle was being degraded as a result of resistance training (Pivarnik, Hickson, and Wolinsky 1989). The phenomenon of increased 3-methylhistidine excretion was substantiated by several other teams of researchers (Frontera, Meredith, and Evans 1988; Hickson and Hinkelmann 1985).

Several studies have attempted to determine the protein requirement for maintaining nitrogen balance during resistance training. Nitrogen balance is an indicator of lean body mass growth, maintenance, or atrophy. A positive nitrogen balance denotes an increase in lean tissue; a zero nitrogen balance indicates maintenance of existing lean tissue; a negative nitrogen balance represents the wasting of lean tissue.

Despite the findings of Pivarnik and Hickson which showed increased excretion of 3-methylhistidine, neither researcher reported evidence of increased protein requirements. Hickson further commented that the RDA of .8 g/kg/day for protein is sufficient for resistance-trained athletes. Tarnopolsky recently suggested that a value of .9 g/kg/day is sufficient to maintain nitrogen balance (Tarnopolsky, Atkinson, MacDougall, Chesley, Phillips, and Schwarcz 1992). This value modestly exceeds the RDA. In a study examining the first month of training for novice male body builders, Lemon, Tarnoplosky, MacDougall and Atkinson (1992) reported that nitrogen balance could be achieved with a minimum of 1.4 – 1.5 g/kg/day.

The real issue for the anaerobic athlete, of course, is not simply maintaining a neutral nitrogen balance, but achieving a positive nitrogen balance for long periods of time. In one of the first studies to address protein needs of weightlifters, Celejowa and Homa (1970) demonstrated a negative nitrogen balance in at least four out of ten weight lifters who consumed protein in the amount of 2 g/kg/day. Another study on weight lifters suggested a protein intake of 1.3 to 1.6 g/kg/day is sufficient to create a positive nitrogen balance (Laritcheva, Yalovaya, Shubin, and Smirnov 1978). Consolazio and colleagues observed greater nitrogen retention (32.4 vs 7.1 g) in resistance-trained athletes over a forty day training regimen when protein intake was 2.8 g/kg/day versus 1.4 g/kg/day (Consolazio, Johnson, Nelson, Dramise, and Skala 1975). Tarnopolsky published an abstract reporting that a high protein diet of 1.05 g/kg/day resulted in a slightly positive nitrogen balance in body builders, while an even higher protein diet of 2.77 g/kg/day resulted in a more positive nitrogen balance (.62 g/day vs 10.9 g/day) (Tarnopolsky, MacDougall, Atkinson, Blimkie, and Sale 1986). Also supportive of these findings is a study which followed for four weeks two groups of novice weight lifters (Fern, Bielinski, and Schutz 1991). One group consumed their normal protein dietary intake of 1.3 g/kg/day while the higher protein group consumed this amount plus a protein powder supplement of 2g protein/kg/day, giving a total of 3.3 g/kg/day. Nitrogen balance was determined to be .01g N/day and 3.4g N/day, respectively. Similarly, the recent study by Lemon, Tarnopolsky, et al. found enhanced nitrogen retention at 2.62 g/kg/day as opposed to 1.35 g/kg/day (8.9 ± 4.2 and 3.4 ± 1.9g N/day, respectively). Likewise, it has been shown in heavily training body builders consuming a hypoenergetic diet that negative nitrogen balance occurred at 0.8 g/kg/day, but a positive balance was achieved at 1.6 g/kg/day (Walberg, Leedy, Sturgill, Hinkle, Ritchey, and Sebolt 1988). Under milder training conditions in older adults, it was demonstrated that a negative nitrogen balance was achieved at 0.8 g/kg/day, whereas a positive nitrogen balance resulted at 1.62 g/kg/day (Campbell, Crim, Young, Joseph, and Evans 1995).

Interestingly, Oddoye and Margen (1979) illustrated that it is possible to maintain a highly positive nitrogen balance for up to fifty days in the complete absence of resistance exercise. These researchers administered protein in the amount of 3.0 g/kg/day to three subjects, and monitored nitrogen balance for one hundred days total. Although nitrogen retention peaked at fifty days, the nitrogen balance remained positive throughout the remainder of the experiment. This phenomenon is particularly intriguing because prior to this study it was always assumed that excess dietary nitrogen would simply be excreted (Lemon 1991).

Also of interest is the Fern study, which was the first study to show a ceiling for protein intake of resistance-trained athletes by employing labeled metabolic tracers (Fern et al.). The high-protein group, consuming 3.3 g/kg/day, displayed a 150 percent increase in amino acid oxidation, which suggests that the optimal protein intake had been exceeded. Lemon later determined an overload at 2.4 g/kg/day (Lemon, Tarnopolsky, et al.).

Using 40K measures (an alternative to nitrogen balance assessment), Torun and his co-investigators measured a decreased cell mass during six weeks of strength training when protein consumption was equal to the RDA. In this study, it is noteworthy that two of the five subjects continued to train for an additional six weeks while consuming an increased protein intake equal to 1.6 g/kg/day, which is twice the RDA. At this increased protein intake, the cell mass of these subjects increased (Torun, Scrimshaw, and Young 1977). Surprisingly, this metabolic demand for protein was caused by isometric exercise or static contractions, which do not damage muscle tissue as severely as the negative or lowering component of isotonic or dynamic contractions. In the Consolazio study previously described, the higher protein group (2.8 g/kg/day) experienced nearly three times the increase in lean body mass as compared to the lower protein group (1.4 g/kg/day). In this study, changes in lean body mass were measured by densitometry (3.28 vs 1.21 kg). Dragan, Vasiliu, and Georgescu (1985) observed a 6 percent increase in lean body mass over several months, as assessed by skin fold measures, among Romanian weight lifters when protein consumption was increased from 2.2 to 3.5 g/kg/day. Utilizing computerized axial tomography (CAT scan), Frontera et al. reported enhanced hypertrophy in the quadriceps of participants in a twelve week study who consumed a daily protein supplement of .33g protein/kg body weight/day in addition to the RDA amount of protein. Urinary creatinine, an index of whole body muscle mass, further substantiated this increase in muscle mass. In a study consisting of two exercise bouts, Morin and Clarkson (1990) failed to find a difference in the circumference of eccentrically trained forearm muscles of females receiving a daily protein supplement containing 37.5 g of high quality protein. A study found leg hypertrophy to be similar between two groups of previously untrained males consuming protein at either 1.30 g/kg/day or 2.94 g/kg/day over the course of thirteen weeks of resistance training (Weideman, Flynn, Pizza, Coombs, Boone, Kubitz, and Simpson 1990). In agreement is the Lemon study (Lemon, Tarnopolsky, et al.) which found similar increases in muscle mass between groups consuming 1.35 g/kg/day and 2.62 g/kg/day. This study is very convincing because changes in muscle mass were assessed via three means: densitometry, creatinine excretion, and CAT scan. In sharp contrast, however, is the Fern research which reported an average of 1.5 kg in the moderate protein group (1.3 g/kg/day) and 2.8 kg in the high protein group (3.3 g/kg/day). Lean body mass was estimated through skin fold measurement and underwater weighing (Fern et al.). Most recently, a group of Brazilian researchers showed an impressive 3.28 kg muscle increase in one month using body builders consuming an average of 2.0 g/kg/day (Maestá, Cyrino, Corrêa, Bicudo, Angeleli, Tsuji, and Burini 1998).

Studies measuring the effects of high protein diets on strength are few. The Dragan study described above reported a 5 percent increase in strength over several months when the subjects increased their protein intake (Dragan et al.). In contrast, the Frontera study previously described failed to find an increase in leg strength in the high protein group when compared to training alone (Frontera et al.). Likewise, the Morin and Clarkson study found no significant increase in strength in the forearm flexors of the protein-supplemented group. Strength gains were not significantly different between moderate and high protein groups in the Weideman study or in the most recent Lemon study (Lemon, Tarnopolsky, et al.). Maestá et al. documented an 11.8 percent increase in strength over one month in experienced body builders.

There are several factors that can confound the results of experiments to assess protein needs of anaerobic trainees. For example, there is an inverse relationship between energy intake and protein requirements in resistance-trained individuals (Lemon 1995). This issue especially presents problems in the study of recreational and competitive body builders who, in an attempt to minimize body fat, often establish a caloric deficit.

Other extraneous variables exist that make design, execution, interpretation, and comparison of studies assessing the adequacy of protein intake among anaerobic participants difficult. These include the age and sex of the subjects, possibility of anabolic androgenic steroid use, variation in the quality (biological value) of the protein consumed, timing of the protein consumption relative to the strength-training bout, and differences in the training regimens regarding frequency, intensity, and duration. It is quite true that the training strategies employed were highly variable and would account largely for discrepancies between studies.

Studies which show increased turnover of certain amino acids as a result of resistance exercise provide evidence that at least certain amino acids may be required by anaerobic athletes in amounts greater than those required by a sedentary population. However, there is disagreement as to whether this increase in need can be applied to all amino acids. Lemon (1987) warns that 3-methylhistidine data must be carefully examined because of variability introduced by time of collection, exercise duration and intensity, and 3-methylhistidine contributed by the gastrointestinal tract.

Nitrogen balance studies, besides being quite difficult to employ due to their requiring collection of all urine, feces, sweat, etc., possess inherent errors that favor underestimation of nitrogen losses (Lemon and Proctor 1991). Thus, individuals may appear to be in a positive nitrogen balance when they are not. Energy deficits can further complicate nitrogen balance techniques. Even with these well-known short-comings, nitrogen balance studies have overwhelmingly supported the usefulness of high protein diets in increasing nitrogen retention. Additionally, the variability in nitrogen retention study results is often such that although perhaps the subjects were on average in a positive nitrogen balance, a few subjects were actually in a negative nitrogen balance. It must also be remembered that the objective of resistance training for most individuals should not be simply attaining a positive nitrogen balance, but attaining the most positive nitrogen balance possible while not compromising other dietary or health aspects.

A common misconception regarding nitrogen balance studies is that muscle hypertrophy is impossible when an individual is in negative nitrogen balance. In fact, muscle growth can occur when protein intake is insufficient by the stealing of amino acids from other organs. However, this process cannot continue indefinitely and a higher protein diet would likely prove superior (Lemon 1995).

Muscle growth alone, as observed through CAT scan or circumferential measurements, is not sufficient to determine dietary protein adequacy due to the body’s ability to hypertrophy muscle tissue at the expense of other tissues. Likewise, strength alone cannot be used as a sole indicator of dietary protein sufficiency for this very same reason.

In regards to the effect of additional protein on strength, the author feels that the test samples were not appropriate for the testing of that parameter. All of the studies which failed to find a statistically significant positive effect of additional dietary protein on strength used untrained individuals and measured strength over a relatively short period of time (Frontera et al. 1988; Morin and Clarkson 1990; Weideman et al. 1990; Lemon et al. 1992). It is well-documented that the grand strength increases that occur in the initial stages of a strength training regimen are primarily due to neurological adaptations, which are independent of protein accretion, rather than muscle hypertrophy (Sale 1986, p. 290). Therefore, it would be more appropriate for researchers to measure strength increases in experienced athletes in whom strength increases are more likely to reflect muscle hypertrophy, a process dependent on protein assimilation. The chances of finding a significant difference between groups would be increased because strength improvements in experienced athletes are much more modest than those that occur in neophytes. To account for confounding neurological changes, it has recently been recommended that strength testing should be performed via electromuscular stimulation which would bypass the individual’s own central neural input (Lemon, 1997), but still not account for the possibility of muscle borrowing amino acids from other tissues.

I propose that the paradoxical increase in hypertrophy without a significant increase in strength reported by Frontera et al. could be attributed to muscle growth by means other than augmentation of contractile proteins. It is thought that the delayed onset muscular soreness (DOMS) that results from initial training is brought about partially by a disruption of the structural protein called a Z-disk and possibly damage to the surrounding connective tissue (Armstrong, Warren, and Warren 1991). After just a few training sessions, individuals apparently become resistant to this disruption, because generation of soreness becomes more difficult. Therefore, it seems possible that initial protein assimilation during training may increase the size of the structural proteins and connective proteins as opposed to the contractile proteins. This phenomenon would account for an increase in muscle mass devoid of an accompanying increase in strength. Another possible cause of muscle hypertrophy without a concomitant strength increase is an increase in muscle glycogen content. Muscle glycogen stores have been shown to increase rapidly in untrained subjects (MacDougall 1986, p. 279). For each gram of glycogen stored in muscle tissue, 2.7g of water are attracted and held intracellularly (McCardle, Katch, and Katch 1995, p. 472). An increased muscle glycogen content could therefore cause a volumizing effect independent of protein synthesis. As stated previously, observation of more experienced subjects over a longer period of time may be appropriate if electromuscular stimulation is not employed.

Studies that focus on the first few weeks of training for a neophyte have their place in the literature, for they suggest that protein needs are increased at the beginning of an exercise regimen. However, it appears that a leveling off occurs after a few weeks or months as the body learns to conserve protein. While this information may be helpful for those individuals just beginning a program, Butterfield suggests that these studies may partially account for inflated estimates of protein needs among athletes of various levels of experience. Butterfield expresses a need for long-term studies so that true protein needs may be accurately assessed (McCarthy 1989).

So, how much protein do you need to maximize your muscle? You’ll have to tune in to the next installment, in which we’ll also tackle the pesky issue of protein cycling as well as the results of my own statistical analysis. Until then, train hard!

Dr. Greg Bradley-Popovich holds dual master's degrees in Exercise Physiology and Human Nutrition from West Virginia University as well as a doctorate in Physical Therapy from Creighton University. He is the Director of Clinical Research at Northwest Spine Management, Rehabilitation, and Sports Conditioning in Portland, Oregon.

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