The Zone Diet and Athletic Performance Contents1. What is the Zone Diet? 2. Efficacy of a 40/30/30 Diet Plan 3. Insulin, Glucagon and the Zone 4. Diet, Hormones and Eicosanoids 5. Eicosanoids and Exercise 6. Conclusion Acknowledgements Table I. Diet and hormonal factors affecting desaturase activities References Section: REVIEW ARTICLE Abstract
The Zone diet is the latest eating regimen marketed to improve athletic performance by opposing traditional high carbohydrate sports diets. The 40/30/30 diet is centred primarily on protein intake (1.8 to 2.2 g/kg fat free mass; i.e. total bodyweight -- fat weight) and promises a change in the body's insulin to glucagon ratio through its macronutrient alterations. Changes in the existing hormonal milieu are said to result in the production of more vasoactive eicosanoids, thus allowing greater oxygen delivery to exercising muscle. This favourable condition, known as the Zone, is anecdotally reported to benefit even the most elite endurance athletes.
Applying the Zone's suggested protein needs and macronutrient distributions in practice, it is clear that it is a low carbohydrate diet by both relative and absolute standards, as well as calorie deficient by any standard. Reliable and abundant peer reviewed literature is in opposition to the suggestion that such a diet can support competitive athletic endeavours, much less improve them.
The notion that a 40/30/30 diet can alter the pancreatic hormone response in favour of glucagon is also unfounded. The Zone is a mixed diet and not likely to affect pancreatic hormone release in the same way individual nutrients can. Although the postprandial insulin response is reduced when comparing a 40% with a 60% carbohydrate diet, it is still a sufficient stimulus to offset the lipolytic effects of glucagon.
Many of the promised benefits of the Zone are based on selective information regarding hormonal influences on eicosanoid biology. Contradictory information is conveniently left out. The principle of vasodilating muscle arterioles by altering eicosanoid production is notably correct in theory. However, what little human evidence is available does not support any significant contribution of eicosanoids to active muscle vasodilation. In fact, the key eicosanoid reportedly produced in the Zone and responsible for improved muscle oxygenation is not found in skeletal muscle. Based on the best available scientific evidence, the Zone diet should be considered more ergolytic than ergogenic to performance.
The practice of manipulating diet to improve athletic performance is a ritual as old as the Olympic Games themselves. According to legend, the first of these manipulations opposed the traditional vegetarian diet of Greek Olympians in favour of a meat diet, which long-distance runner Stymphalos declared was instrumental in his Olympic victories in the fifth century BC.[ 1] After over 2000 years of discovery, athletes continue to regularly experiment with new diet regimens aimed at optimising sports success. In fact, the recent explosion of sports nutrition research and information has come out of a renewed interest in nutritional interventions as a means of enhancing performance. As the list of banned substances in international competition grows, so too does the search for a 'natural' alternative to illegal drugs.
The myriad of available sports nutrition products promising ergogenic effects include combinations of macronutrient powders, micronutrient formulas, and various non-nutrient herb and root extracts to name a few. Numerous 'special' diets are also marketed to athletes and abound in local book stores. Although the consumption of more dietary carbohydrate remains the most widely accepted means by which modern athletes improve performance legally, a twentieth century revival of Stymphalos's diet is gaining popularity within the pages of 'The Zone'.[ 2]
1. What is the Zone Diet? According to its author, Dr Barry Sears, 'The Zone' is a physiological condition achieved by consuming food in the precise proportions of 40% carbohydrate, 30% protein, and 30% fat at each of 3 daily meals and 2 daily snacks. The ideal macronutrient distribution, and subsequent calorie requirement, in the Zone is determined primarily on the basis of protein intake. Athletes are given the recommendation to consume 1.8 to 2.2g of protein per kilogram (0.8 to 1.0g per pound) of lean body mass (actually, fat free mass). NFL American football offensive linemen, Olympic swimmers, competitive triathletes, and ordinary individuals alike have all reportedly benefitted from this type of protein-based dietary regimen.
Assuming that a typical male marathon runner weighs 64kg and is 7.5% body fat,[ 3] providing 2.2g of protein per kilogram fat free mass would result in a requirement of 130g of protein. Since protein should represent 30% of total calorie intake, the remaining macronutrient distribution would be 58g fat (30%) and 173g carbohydrate (40%). The sum total calorie requirement for such an athlete on the Zone diet is 1735 calories at the suggested 0.75 ratio of protein to carbohydrate. As a result of the recommended macronutrient ratio of the diet (0.75), a favourable glucagon to insulin balance is said to be achieved. Ensuing hormonal changes supposedly provide more energy and are also responsible for controlling the production of 'good' eicosanoids -- the 'key' to entering the Zone. Among the diet's performance promises are improvements in endurance, lean body mass, and reductions in body fat.
Given the popularity of the Zone diet and the conviction with which it opposes current sports nutrition wisdom, it is surprising that little has been formally written[ 4, 5] to evaluate the scientific basis for its claims, especially with regard to eicosanoids. Therefore, the purpose of this review is to provide a complete scientific evaluation of the Zone diet's potential effectiveness on exercise performance for competitive endurance athletes.
2. Efficacy of a 40/30/30 Diet Plan 2.1 Substrate and Dietary Carbohydrate Requirements for Exercise
The catabolism of muscle glycogen, as well as the uptake and oxidation of blood glucose into active muscle, provides energy (ATP) for muscle contraction. This has been clearly demonstrated by the observation that muscle glycogen content declines during physical work[ 6] and that stores are frequently near depletion at the point of physical exhaustion.[ 7] The inability to sustain power output following glycogen depletion is logically explained by the reduction in available substrate necessary for ATP production. One critical consideration of this observed phenomenon is the exponential relationship between exercise intensity and glycogen depletion. The fact that carbohydrate stores are preferentially oxidised at higher exercise intensities is evident not only from respiratory quotient (RQ) values and muscle biopsy data, but also from clinical interpretations. The genetic model of glycogen deficiency manifested in McArdle's Disease limits exercise intensity to only 40 to 50% of predicted maximal values.[ 8] In the case of exercise-induced glycogen depletion, it is agreed that prolonged work is only possible in exchange for a reduction in work intensity to below 70% of maximum intensity.[ 9] Since many competitive endurance athletes regularly train and compete at exercise intensities well above 70% of maximum capacity,[ 10-12] glycogen depletion remains a limiting factor in endurance sports.
In a classic study comparing the effects of diet on endurance, Bergstrom et al.[ 13] manipulated the macronutrient intakes of volunteers performing exhaustive exercise. Following a bout of glycogen depleting bicycle work on a mixed (normal) diet, volunteers were fed isocaloric (2800 kcal) diets of either 54% protein and 46% fat or 82% carbohydrate and 18% protein for 3 days prior to another exhaustive exercise bout at 75% of maximum oxygen uptake (VO2max). The volunteers then switched diets for another 3 days before being tested to exhaustion once more in the same manner. Bergstrom et al.[ 13] reported that when fed the high carbohydrate diet, the volunteers had 5 times and almost 2 times the starting glycogen values than when compared with the protein/fat diet and mixed diet, respectively. During the carbohydrate diet phase, the volunteers were shown to rely more on glycogen during exercise (higher RQs) and displayed more absolute glycogen utilisation (muscle biopsy). Exercise time to exhaustion on the carbohydrate diet averaged 189 minutes, compared with 126 minutes (mixed diet) and 59 minutes (protein/fat). It was concluded that muscle glycogen content could be manipulated by dietary intervention following glycogen depletion, and that muscle glycogen content is a limiting factor for sustaining work capacities above 70% VO2max.[ 13]
Thirty years later, a similar comparison between a mixed diet (40% carbohydrate) and a high carbohydrate diet (60%) on muscle glycogen levels and performance outcome in elite hockey players was undertaken.[ 14] The results confirmed the findings of landmark studies like those of Bergstrom[ 13] 3 decades before. The high carbohydrate diet resulted in higher pre-game muscle glycogen values and 30% greater skating distances, while demonstrating an overall linear relationship between glycogen levels and total distances skated.[ 14]
The importance of carbohydrates to endurance performance (events lasting longer than 60 minutes) may also be interpreted from the standpoint that purposeful carbohydrate loading before[ 15, 16] and glucose feedings during exercise[ 17, 18] delay exhaustion. The carbohydrate loading technique is an eating and training strategy designed to maximise muscle glycogen stores by relying on the mechanistic synergy between a high carbohydrate intake and a training taper several days prior to an event. This is meant to ensure that muscles are 'full' prior to exercise. Feeding carbohydrate during exercise is designed to act as an additional oxidative fuel source and potentially prevent hypoglycaemia associated with liver glycogen depletion late in prolonged exercise. One of the Zone's claims is that carbohydrate feedings themselves cause hypoglycaemia, thus impairing performance by evoking an insulin response which is exacerbated during exercise. Although the endocrine response of insulin to carbohydrate intake cannot be denied, controversy exists over whether this response to carbohydrate feedings before exercise impairs[ 19] or is of no consequence[ 20] to performance. It should be made clear that any disagreement concerning the benefits of carbohydrates to performance is only in regard to feedings in the 30 to 60 minutes prior to exercise. Large daily intakes, as well as consumption during and after exercise are clearly essential to endurance success.
The Zone contends there is no evidence that long term adherence (more than 9 days) to a high carbohydrate diet provides any performance advantage over an ordinary mixed diet. It can be inferred, however, that a high carbohydrate diet is needed daily as long as athletes train daily. Costill et al.[ 21] measured muscle glycogen levels in runners performing a 10 mile run at 80% VO2max on each of 3 successive days. The runners became progressively more glycogen depleted with each day while eating a mixed diet of 40 to 50% carbohydrate (250 to 350 g/day. After 5 days of rest on the same diet, 3 of 5 runners still had not replaced muscle glycogen levels to their pre-study values.[ 21]
Data collected in a similar study[ 22] providing varying amounts of carbohydrate ranging from 188 to 648 g/day showed that glycogen depleted muscles could be normalised within 24 hours when fed isocaloric diets (3000 kcal) containing 525 to 648g of carbohydrate. Therefore, the cumulative effects of daily glycogen depletion could only be reversed with a diet of 500 to 600g of carbohydrate. Although one long term ( 4-week) adaptation study providing a diet only 'moderate' (5 g/kg/day) in carbohydrate has been shown to maintain muscle glycogen levels in rowers training twice daily, the males in this study still averaged nearly 400g of carbohydrate per day.[ 23] It is therefore clear that athletes who train daily and compete regularly require large carbohydrate intakes as an integral part of their training programme.
Much of the Zone's claims are based on anecdotal evidence and non-peer reviewed data which was reportedly collected while working with collegiate swimmers at Stanford. The Zone diet is credited for carrying the team to a winning season and several individuals to Olympic medals. Published research with swimmers has shown that interval swim training at a velocity of 1.33 m/s can produce a 37% reduction in muscle glycogen levels.[ 24] In lieu of these findings, the performances of 2 groups of swimmers undergoing similar training have been compared after 9 days on diets consisting of either 43 or 80% carbohydrate.[ 25] This is one study quoted in the Zone to support a 40% carbohydrate diet. The original findings were that there were no significant differences between the performances of athletes on either of the 2 dietary protocols. However, because of the quantity of calories consumed, even the 43% carbohydrate group consumed an average of 502 g/day of carbohydrate versus 935 g/day in the 80% carbohydrate group. The Zone misleadingly reports the results of this Ohio State study as evidence that a 40% carbohydrate diet is as effective as an 80% carbohydrate diet without recognising that both groups of swimmers consumed more than 500g of carbohydrate.
Recent research comparing glycogen loading regimens in men and women have revealed findings consistent with the view that the absolute quantity of carbohydrate is important to exercise performance. When men and women consumed 75% carbohydrate diets for 4 days before an exercise trial to fatigue, only the men stored more glycogen and improved performance times. Because the men consumed more total calories, they averaged an intake of 614 g/day carbohydrate, while the women averaged only 370 g/day.[ 26] Therefore, athletes are advised to consume an absolute quantity of carbohydrates (500 to 600 g/day) rather than rely on a relative percent of carbohydrate calories in the diet. Obviously, the potential gender differences in the ability to store or synthesise glycogen have been set aside in interpreting these results. This criteria makes the Zone's recommended carbohydrate intake for the sample endurance athlete in this discussion less than one-third of that necessary for glycogen repletion.
Another attempt by the Zone to dismiss the importance of carbohydrate for endurance is made by quoting a published study[ 27] that demonstrated greater improvements in run time to exhaustion with a high fat diet than with a high carbohydrate diet. The truth is that scant evidence exists that suggests the habitual adaptation to a high fat diet can improve endurance, but only at submaximal exercise intensities (below 70% VO2max).[ 27, 28] The potential impact of such a diet on gastric emptying and cardiac health not withstanding, elite athletes frequently train and compete at exercise intensities above 70% VO2max. For further evaluation of the 'fat loading' concept, see Sherman and Leenders[ 29]
2.2 Caloric Requirements of Training and Competing
It has been suggested that the power outputs of distance runners during a marathon race approach 20 kcal/min.[ 30] Over the course of a 2- to 2.5-hour marathon performance, 2400 to 3000 kcal could therefore be expended. Confirmation of this estimate comes from measured energy expenditures ranging from 2414 to 2890 kcal for 12 males performing a treadmill marathon.[ 11] Add to this number the 30 to 40 kcal/kg/day necessary for the basal metabolic calorie needs of everyday life[ 31] and a 64kg marathon runner would require 4300 to 5600 kcal/day. In studying the affects of training on glycogen depletion in college swimmers, Costill et al.[ 24] observed and recorded that these athletes also required an average of 4400 kcal/day to maintain bodyweight. Finally, with regard to actual intakes, a 1989 nationwide survey of the nutritional habits of elite athletes suggests that female endurance athletes (runners, swimmers, cyclists and rowers) consume between 2100 and 3100 kcal/day, while male endurance athletes (runners and cyclists) consumed between 3100 and 5900 kcal/day.[ 32]
It therefore seems obvious that neither the carbohydrate content nor the calorie content of the Zone diet make it even close to optimal for competitive endurance sports. In addition, it seems intuitive that a precompetition meal consisting of 30% fat and 30% protein would likely delay gastric emptying, thus impeding maximum performance yet again. The explanation offered by the Zone for the success of such a diet is that the ratio of glucagon to insulin, achieved by the delicate macronutrient distribution, enhances lipolysis, thus sparing glycogen and providing a limitless source of fuel for exercise. These notions can be dismissed on several accounts.
3. Insulin, Glucagon and the Zone 3.1 Diet and Pancreatic Hormone Release
When studied as single nutrients, carbohydrates produce a marked increase in the release of insulin and a concomitant decrease in circulating glucagon levels, while protein consumed in the absence of carbohydrate elicits an increase in circulating glucagon levels with only a small increase in insulin.[ 33] These classic endocrine responses to single macronutrient intakes can only be vaguely generalised to the Zone's claims, however, since the Zone is still a mixed diet. Coulston et al.[ 34] compared insulin responses to a 60 or 40% carbohydrate diet (60/20/20 vs 40/20/40). Although insulin rose significantly less in response to the 40% carbohydrate diet, both diets elicited and maintained an insulin level over 40 μU/ml for 3 hours.[ 34] Since plasma insulin levels of 25 μU/ml[ 35] or lower[ 36] reduce glucagon mediated lipolysis, it is clear that even a 40% carbohydrate diet can stimulate an insulin response and impede the very lipolytic benefits such a diet is proposed to offer.
3.2 Glucagon, Lipolysis and Exercise Intensity
Because it has been demonstrated that lipolysis can be inhibited by even small elevations in circulating insulin,[ 35, 36] a diet much lower than 40% carbohydrate would probably be necessary to enhance fat mobilisation in this way. However, let us assume that a low carbohydrate, high protein diet might alter the ratio of glucagon to insulin in favour of glucagon. Although other highly lipolytic hormones predominate during exercise (catecholamines, glucocorticoids), elevated glucagon levels could, in theory, further enhance cyclic adenosine monophosphate (cAMP) stimulated hormone sensitive lipase activity. But a problem would still remain for well-conditioned athletes who often train and compete at exercise intensities approaching the lactate threshold. The accumulation of plasma lactate causes a direct inhibition of exercise mediated lipolysis in humans.[ 37]
The Zone also makes the claim that an exercise intensity of 60 to 80% of maximum heart rate (HR) improves eicosanoid balance, and thus is the intensity one should strive for when exercising on the Zone diet. On the basis of the linear relationship between heart rate and maximal oxygen consumption used in predicting VO2max from submaximal exercise,[ 38] a range of VO2 estimates between 42 and 70% of maximum could be expected for these respective heart rates when using the predictive equation of Hellerstein et al.[ 39] At the upper limit of the recommendation, exercise intensity would far exceed the lactate thresholds attainable in untrained and moderately active individuals.[ 40] It appears then that the proposed lipolytic benefits of a Zone diet could well be offset by the very exercise intensity it suggests for optimum eicosanoid balance. For competitive athletes regularly training and competing above the lactate threshold, the lipolytic theory again fails to gain favour as a reason to attempt dietary hormone manipulation.
3.3 Insulin, Glycogen and Recovery from Exercise
It has already been established that endurance training results in muscle glycogen depletion, for which a high carbohydrate diet is necessary for repletion. Mixed results have been gathered regarding differences in the rates of postexercise glycogen resynthesis when comparing simple to complex carbohydrates. Although simple and complex carbohydrates probably work equally well regarding overall recovery,[ 41] at least one study has shown that traditionally insulinaemic simple carbohydrates promoted faster glycogen resynthesis in the first 6 hours postexercise.[ 42] The Zone references a study by Zawadzki et al.[ 43] to dispute this traditional view.
After performing 3 bouts of exhaustive glycogen depleting cycle exercise, the participants in Zawadzki's study were given either 112g carbohydrate only, 40.7g protein only, or 112g carbohydrate and 40.7g protein. After the third exercise bout, muscle biopsies were taken immediately after and again 4 hours post exercise. The results of the study showed that the combination of carbohydrates and protein had a greater effect on insulin response than carbohydrate alone, thus improving glucose uptake and promoting faster muscle glycogen storage.[ 43] These results are not entirely surprising. In a study comparing the effects of various protein intakes on the insulin response to sugar (58g carbohydrate), progressively larger protein intakes (from 0 to 49.9g per test meal) stimulated insulin secretion in an incremental fashion.[ 44] The observed synergy between protein and carbohydrate taken together in this experiment might therefore be explained by an aminogenic insulin response. In any event, the ratio of protein to carbohydrate in this study is only 0.36 - much lower than the suggested 0.75 of the Zone. The carbohydrate feeding in the Zawadzki study also represents nearly an entire days carbohydrate allotment in the Zone. Recall that this allotment is supposed to be divided over 3 meals and 2 snacks. Finally, this example of a beneficial response to insulin production contradicts the bottom line message of the Zone diet which is clearly to avoid insulin production.
Several insulin-regulated metabolic steps stimulate glycogen synthesis on a molecular level. The important role of insulin-enhanced glycogen synthase activity is apparent from the observed insensitivity of this enzyme in type 2 diabetes mellitus (non-insulin-dependent diabetes mellitus; NIDDM).[ 45] Such a defect notably impairs the rate at which muscle glycogen synthesis occurs. DeFronzo et al.[ 46] have conducted controlled comparisons measuring muscle glucose uptake during an insulin clamp alone, exercise alone, and with combined hyperinsulinaemia and exercise. Their results have demonstrated an additional, distinct synergistic relationship between insulin and exercise on glucose uptake in humans. It has since been elucidated that insulin significantly enhances glucose uptake through a mediated intracellular translocation of glucose transporters (GLUT4) into the plasma membrane.[ 45, 47] While the Zone generally regards insulin as the enemy, it is quite clear that insulin is an ally in the quest to resynthesise the muscle glycogen necessary for optimal endurance performance.
4. Diet, Hormones and Eicosanoids The gateway to entering the Zone is said to ultimately depend on controlling the production of 'good' eicosanoids. Most critics of the Zone readily oppose the suggested connections it makes between diet, hormones and eicosanoid production. In general, they have been regarded as 'unknown' metabolic pathways. This is probably because the Zone offers little evidence to substantiate or dismiss its claims. However, a closer look at the evidence reveals that the biochemical pathways do exist and may be exogenously influenced. The real questions are: (i) to what degree, if any, can diet and hormones affect control over these pathways, and (ii) to what extent might control potentially impact exercise performance? A brief introduction to the synthesis and function of eicosanoids is important to adequately evaluate the following discussion. Because of the nature of the Zone's claims, the biochemistry of eicosanoid production will be made almost exclusively in reference to linoleic acid (18:2-6), an Ω6 fatty acid, and its metabolites. Mention of linolenic acid (18:3-6) and its Ω3 metabolites will only be made where appropriate.
4.1 Synthesis and Function of Eicosanoids
Eicosanoids are hormone-like derivatives of essential fatty acids (EFA) with notable and varied physiological activities. Formation (see fig. 1) begins with the desaturation of linoleic acid (LA) to ε-linolenic acid (GLA) via the Δ6 desaturase enzyme reaction. GLA is subsequently elongated to dihomo-ε-linolenic acid (DGLA - also known as DHLA). If Δ5 desaturase activity ensues, DGLA will become arachidonic acid. The family of compounds known as eicosanoids are made up of prostaglandins (PG), thromboxanes and leukotrienes. arachidonic acid is a precursor for the biosynthesis of eicosanoids with 2 double bonds in their structure (series 2), while DGLA acts as a substrate for eicosanoids characterised by one structural double bond (series 1). The Zone generally regards series 2 eicosanoids as 'bad'. This undoubtedly stems from the observation that series 2 thromboxanes promote platelet aggregation and vasoconstriction, a recognised potential contributing factor to cardiovascular disease.[ 48] Series 1 eicosanoids and prostacyclin (PGI2), a series 2 eicosanoid, promote vasodilation[ 49] and are purely antithrombotic,[ 50, 51] making them 'good'. It should be noted to eliminate later confusion that PGE1 and PGE2 manifest similar effects in most tissues, except in the case of platelets where they exhibit opposite effects.[ 52] For a more complete review of eicosanoid biology and metabolism, see Brenner[ 53] and Sprecher.[ 54]
The most significant eicosanoids for the purposes of the Zone and exercise performance are the prostaglandins, specifically PGE1, PGE2, and PGI2. Although all 3 prostaglandins act as potent vasodilators in humans,[ 48, 49, 55] PGE1 is the Zone's pristine prostaglandin. This is due to the nature of the Zone's proposed control of prostaglandin synthesis -- the inhibition of the Δ5 desaturase enzyme -- which would occur before the synthesis of arachidonic acid. As a result, inhibiting all 'bad' eicosanoids would also block PGI2 and PGE2 formation. While PGE1 is often considered as an equal[ 56] or more active[ 49] vasodilator than PGE2, it clearly remains a better inhibitor of sympathetically induced vasoconstriction.[ 57] PGE1 is also a known stimulator of adenylate cyclase activity,[ 58] and thus lipolysis. However, any benefit of this during exercise has already been dismissed (see section 3.2).
The basis for the Zone's claim of improved physical performance originates from the idea to consume more GLA, thus producing more DGLA, while simultaneously inhibiting the desaturation of DGLA to arachidonic acid (Δ5 desaturase). It is surmised that this would produce greater quantities of PGE1 and greater vasoactivity in the muscle microcirculation, thus ultimately improving oxygen-rich blood flow to working muscles. Theoretically, such a mechanism could be advantageous to any calibre of athlete.
4.2 Dietary Control of Eicosanoid Synthesis
In the war against cardiovascular disease, it has been demonstrated that the consumption of anti-aggregatory fish oil (Ω3 fatty acids) can reduce the production of thrombotic series 2 thromboxane by either displacing arachidonic acid from platelet phospholipid stores,[ 59] competitively inhibiting desaturation enzymes,[ 60] or by inhibition of the rate limiting cyclo-oxygenase enzyme.[ 61] Similarly, a more favourable platelet composition has been attempted with the oral administration of the less thrombotic prostaglandin precursor DGLA.
The arachidonic acid content of most tissues predominates over that of DGLA, with tissue phospholipid levels of the latter usually 20 times that of the former.[ 62] This is probably due at least in part to the scant availability of preformed GLA or DGLA in the diet, as well as the abundance of arachidonic acid in the typical western diet containing red meat.[ 63] If DGLA were to exert any antithrombotic effect in vivo, more than is typically consumed in a normal mixed diet would have to be made available to the body. With positive results already quantified in vitro and in animals,[ 64] it was next demonstrated in humans that DGLA consumption led to an increase in platelet levels of PGE1 and very little conversion to arachidonic acid.[ 65] Therefore, DGLA was not only actively taken up into membrane phospholipid pools, but also underwent conversion to its active prostaglandin form.
The same researchers confirmed their previous findings in a study providing the oral administration of DGLA in 1 to 2g doses.[ 52] After one dose, they observed measurable levels of DGLA in the bloodstream after 4 hours. When given the same dose each day over 28 consecutive days, it was again revealed that DGLA had penetrated membrane pools without platelet accumulation of arachidonic acid and that more PGE1 was produced. At no time, however, did DGLA tissue concentrations exceed those of arachidonic acid. It was concluded that DGLA was well absorbed, again displayed active uptake and conversion in membrane phospholipid pools, and that Δ5 desaturase enzyme activity in humans was apparently much lower than in other mammalian species.[ 52]
It would appear then that the synthesis of PGE1 is relative to the availability of DGLA in vivo, and that the degree of desaturation of DGLA to arachidonic acid is minimal in humans. This relationship probably explains the Zone's 'prescriptive' recommendation to consume 3 to 5 bowls of oatmeal weekly, which the book suggests is the only appreciable source of preformed GLA available in the diet besides breast milk. It deserves mention that this is not a solitary, nonscientific notion. The recommendation to consume recognised sources of preformed GLA like evening primrose oil or borage oil is known to patients with arthritis for its anti-inflammatory effects. Such effects may be produced through the potential elongation of GLA to DGLA and the production of anti-inflammatory series 1 eicosanoid products.[ 66, 67] With the measurably low activity of the Δ5 desaturase enzyme in humans and the commercial availability of GLA-containing oils, this theory makes sense. However, despite the positive observations by Stone et al.,[ 52] no alterations in the synthesis of PGE2 during the course of DGLA supplementation could be reported in the same study. In addition, observed PGE2 production rates were beyond that accountable by tissue arachidonic acid levels or Δ5 desaturase activity.[ 52] No explanation was offered for the idiosyncrasy except that 'something' other than traditional control factors must have been responsible for PGE2 production.
A similar lack of predictability for control over eicosanoid production has been observed in vitro. By incubating platelets with linoleic acid, researchers have demonstrated greater phospholipid concentrations of linoleic acid without the expected increases in tissue arachidonic acid or series 2 thromboxane synthesis.[ 68, 69] More recently, Dupont and Dowe[ 70] have determined that thromboxane synthesis actually decreases as the linoleic acid content of the diet approaches between 5 and 10% of calorie intake. It appears then that an undefined critical balance rather than an absolute quantity of exogenous eicosanoid precursors may determine the degree of potential prostaglandin synthesis. The relationship between dietary intakes of intact (linoleic acid) or derived (GLA/DGLA) eicosanoid precursors are well reflected in tissue levels both in vitro and in vivo. Unfortunately, neither seem to be a reliable means of controlling the desired eicosanoid outcome suggestive of known biochemical reactions. These relationships appear counterintuitive and promote intriguing questions, but are not illogical responses given the numerous negative feedback reactions inherent in the homeostatic human organism.
The consumption of eicosapentaenoic acid (EPA), an Ω3 fatty acid found in fish oil and responsible for series 3 eicosanoid synthesis, is also an integral part of the Zone diet regimen. The rationale for EPA consumption is said to be its inhibitory effects on the Δ5 desaturase enzyme. Recall that this would block the desaturation of DGLA to arachidonic acid, thus encouraging PGE1 production. More accurately, the effects of EPA on arachidonic acid metabolism are inhibitory only in the sense that it competes for the desaturase enzymes.[ 60] EPA also inhibits cyclo-oxygenase,[ 61] which is the rate-limiting enzyme responsible for the conversion of arachidonic acid to its series 2 metabolites. Under either circumstance, EPA would have little direct impact on the conversion of DGLA to arachidonic acid. Instead, the consumption and metabolism of EPA would result in greater series 3 prostaglandin synthesis -- a class of compounds which Dr Sears himself considers to be chemically unimportant in the Zone. Interestingly, sesame oil has been successfully used as a Δ5 desaturase inhibitor in Mortierella fungi for the mass production of DGLA.[ 71] To the knowledge of the author, any application to humans is unknown at the time of this writing.
4.3 Dietary and Hormonal Control of Eicosanoid Synthesis
The consumption of eicosanoid precursors GLA and EPA are meant to provide more usable substrate for and block enzymatic activity in favour of PGE1 synthesis. Furthermore, the diet-induced alteration in the insulin to glucagon ratio is believed to play a complementary role in PGE1 synthesis. According to the Zone, carbohydrates inhibit the Δ6 desaturase enzyme, while insulin is believed to accelerate its Δ5 desaturase counterpart. As previously stated, carbohydrates elicit an insulin response. Therefore, a diet low in carbohydrate would produce lower insulin levels resulting in more GLA production (active Δ6) and less DGLA desaturation to arachidonic acid (inactive Δ5).
Evidence is plentiful that carbohydrates do in fact have an inhibitory effect on Δ6 enzyme desaturation. Feeding studies with normal rats have demonstrated marked depressions in Δ6 enzyme activity when fed diets of 73%[ 72] and 50%[ 72, 73] carbohydrate. Similarly, the study of genetically diabetic Wistar rats by Mimouni et al.[ 74] have shown defective Δ5 and Δ6 enzyme activity under conditions of elevated blood glucose. The afore-mentioned research used in vitro microsomal liver preparations in their investigations, which makes in vivo extrapolation to humans doubtful. However, plausible indirect evidence has been published that suggests closely related patterns of enzyme sensitivity to insulin in humans as well. Prior to receiving insulin, newly diabetic humans were given deuterated DGLA, which was then largely incorporated into arachidonic acid only after insulin injection.[ 75] It may be concluded that the enzyme inhibition common to both the transient, postprandial elevation in blood glucose and the chronically elevated glucose levels of uncontrolled diabetes are evidence to support this facet of the Zone's theory.
When diabetic rats or humans are treated with insulin, Δ5 and 6 enzyme activities rapidly recover.[ 74, 75] This observation is only in partial agreement with the Zone. Insulin in the Zone is undesirable because it activates the Δ5 desaturase enzyme, stimulating series 2 eicosanoid production. Although this relationship is accepted, insulin stimulates the activity of the Δ6 desaturase also -- a positive occurrence in the Zone which is never considered. One important observation is that insulin treated normal rats show a much less pronounced activation response to insulin injections.[ 76] This may indicate that in a healthy population, carbohydrate feedings may play a larger role than insulin in controlling enzyme activity.
The Zone diet encourages a high protein intake, designed to elicit a larger glucagon response. It is said that glucagon will inhibit the Δ5 desaturase enzyme, thus promoting more PGE1 synthesis. Again, reliable evidence indicates that this is so. A high protein diet is correlated with higher glucagon levels,[ 33] and glucagon abolishes Δ5 desaturase activity.[ 77] Agreement is tentative here again, however, due to several apparent contradictions. Glucagon not only inhibits Δ5 activity, but Δ6 activity also.[ 78, 79] This would be unfavourable in the Zone, acting in the same way dietary carbohydrate acts on the Δ6 enzyme. Again, no mention of this fact is reported by the Zone. Additionally, the high protein intake of the Zone diet, necessary for the appropriate glucagon response, has been documented to stimulate both Δ5 and Δ6 enzyme activity in the same manner that insulin does. Protein intakes representing 73%,[ 72] 35%,[ 80] and as little as 20%[ 73, 77] of calorie intake have all been reported to have this effect.
It is clear that the enzymatic control of eicosanoid synthesis is complex and functions in intricate antagonistic fashion. Only the mechanism for glucagon Δ5 and Δ6 inhibition is well understood. It is known that glucagon stimulates cAMP accumulation, which in turn has demonstrated specific intracellular desaturase enzyme inhibition.[ 78, 79] It is speculated that insulin might exert its effects by enzyme induction.[ 81] Several theories abound for the direct effects of the macronutrients, while few definitive explanations are offered for the regulation or the predominance of obviously competitive reactions. The Zone assumes much by suggesting that dietary control over metabolism could ever be regulated so precisely. In addition, it fails to recognise multiple roles of hormones and macronutrients within closed systems to the point of making recommendations that contradict themselves (see table I).
5. Eicosanoids and Exercise The substance known as 'prostaglandin' has been recognised for its characteristic ability to lower blood pressure from the time it was first isolated in the 1930s.[ 82] As different classes of prostaglandin were discovered, relative comparisons of their vasoactive properties were made. Numerous biological preparations, including skeletal muscle, have been perfused[ 55, 82-85] or treated topically[ 49] with prostaglandin preparations to confirm vasoactivity in these tissues. The significant changes observed in blood flow and blood pressure resulting from prostaglandin treatment have raised questions regarding their potential effect in vasodilating the micro-circulation of 'active' muscle.
The regulation of blood flow during exercise represents a delicate balance between peripheral vasodilation and vasoconstriction. A portion of this control is regulated by the response of chemosensitive and mechanosensitive afferent nerve fibres to local tissue levels of metabolites within contracting muscle.[ 86-88] Sensitisation of these fibres during exercise produces local vasoactive effects on arterioles,[ 89] as well as systemic feedback to the central nervous system which modulates sympathetic control of blood flow between active and inactive tissues.[ 90] When blood flow to active muscle is restricted by way of static or dynamic contraction, prostaglandins are produced and have been shown to accumulate.[ 83, 91, 92] It is therefore a reasonable postulation that vasoactive prostaglandins could act as one class of metabolites responsible for regulating muscle blood flow in response to exercise-induced mechanical or sympathetic vasoconstriction.
5.1 Static Contraction in Animal Models
Stebbins et al.[ 93] have provided evidence that afferent nerve endings are sensitised by prostaglandins (PGE2) during static muscle contraction. It also appears that it is specifically the mechanoreceptors, formerly believed to respond only to purely mechanical stimuli, that are responsible for the observed prostaglandin-afferent connection. Rotto et al.[ 94] have reported a 265% increase in the sensitisation of mechanoreceptors to static contraction when cats were infused with 1 to 2mg of arachidonic acid. Specifically, arachidonic acid increased the discharge properties and potentiated the action of the receptor to chemical stimuli.[ 94] Despite the prostaglandin-enhanced afferent sensitivity, the Stebbins et al.[ 93] study indicated no significant blood flow inhibition to contracting muscle following indomethacin treatment. What they did demonstrate was that indomethacin attenuated mean arterial pressure (MAP) by 76% in the contracted cat hindlimb and that the pressor effects were attenuated with cyclo-oxygenase blockade. It would appear that during static muscle contraction, series 2 prostaglandins are involved more directly with the blood pressure portion of the exercise reflex without significantly affecting local arteriolar blood flow.
The majority of positive reports on the vasoactivity of prostaglandins have come from their measured effects in smooth muscle cells.[ 56, 57, 85] When making a direct comparison between smooth muscle and skeletal muscle under identical circumstances, Hedwall et al.[ 85] reported that infused PGE1 acted as a potent vasodilator in both tissue beds at rest. When canine gracilis muscle was statically contracted, however, only a small, but uniform inhibition of norepinephrine (noradrenaline)-induced vasoconstriction was observed. Studies of the same species under conditions of static muscle contraction, rest and during occlusion have also been reported. It was found that at rest arachidonic acid infusion into the canine hindlimb resulted in increased blood flow, which was attenuated by indomethacin injection.[ 83] This meant that skeletal muscle had the necessary eicosanoid producing enzymes and that PGE2 produced significant vasodilation of the muscle bed at rest.
Similar observations were made with arachidonic acid infusion during post-occlusion hyperaemia. The paradox in the study was that prostaglandin inhibition of the contracting muscle again had no effect on hindlimb blood flow.[ 83] Research using static contraction therefore denotes little or no improvement in muscle blood flow provided by prostaglandins. At least one author speculates that this may be the result of exercise-induced hyperaemia representing a more hypoxic condition, thus inhibiting the oxygen dependent conversion of arachidonic acid to PGE2 not evident post-occlusion or at rest.[ 83]
5.2 Dynamic Exercise in Humans
Perhaps the most compelling argument that prostaglandins must play a significant role in exercise performance can be inferred by the magnitude of their losses measured as urinary PGI2 metabolites ( 6-keto-PGF1α). Useful, but limited, data are available concerning the excretion rates of prostaglandins during different durations, intensities and using different modes of exercise. Long-distance runners asked to perform an exhaustive bout of cycling have been shown to produce a 1.5-fold rate of PGI2 metabolite excretion in as little as 7 minutes.[ 92] When cycling was performed over a 2-hour duration and at an intensity corresponding to a maximally achieved heart rate of 166 beats per minute, a 4-fold increase in PGI2 metabolite excretion was measured in normal healthy males.[ 95] 25 amateur marathon runners in the Helsinki City Marathon provided urine samples which revealed a 10-fold (women) and 30-fold (men) increase in PGI2 metabolite excretion for mean course completion times of 4 hours 12 minutes and 3 hours 45 minutes, respectively.[ 96] The results of these studies suggest that intensity, duration, mode of exercise, and even gender, have specific and currently ill-defined effects on prostaglandin production and excretion.
With some hesitation, it can be argued that elite or competitive endurance athletes, the concern of this review, probably experience a daily 5- to 20-fold greater loss of prostaglandin metabolites than would matched sedentary counterparts. Despite what appear to be considerable losses, the importance of absolute prostaglandin excretion rates seems negligible. Prostaglandins are derived from dietary fat (g) and ultimately tissue phospholipid stores (mg) of eicosanoid precursors (from arachidonic acid), making the threat of their depletion rather erroneous.
One proposed mechanism for the exercise-induced losses of PGI2 is cardiac shear stress. This suggestion stems from the observation that human PGI2 formation is limited largely to the vascular endothelium[ 51] and that increases in blood flow velocity appear to stimulate vasoactive prostaglandin release from arterioles.[ 97] Still another explanation stems from the observed correlation between plasma adrenaline and systemic PGI2 synthesis in response to heavy exercise.[ 95] However, since numerous confounding variables associated with exercise itself may affect such results, Riutta et al.[ 98] recently infused epinephrine into resting human volunteers at doses meant to mimic those of exercise. Their results still indicated a 2-fold increase in PGI2 synthesis and excretion, which lends support to earlier in vitro evidence gathered from rat aorta studies showing that catecholamines might directly stimulate the formation of PGI2 by an α-adrenoceptor-mediated event.[ 99]
5.3 Eicosanoids and Performance
Most of the evidence regarding vasoactive eicosanoids and exercise performance is speculative, but the estimated contribution of PGE2 and PGI2 to arteriolar vasodilation during exercise in humans is considered marginal. Wilson et al.[ 100] measured PG production and arteriolar resistance in twelve human volunteers performing an incremental forearm exercise protocol. PGI2 release from the forearm was 7.66 ng/L at the highest incremental intensity.[ 100] This represented an almost 5-fold increase in production over baseline; similar increases were observed also with PGE2. Despite an enormous reduction in PGI2 and PGE2 release following treatment with indomethacin, skeletal muscle blood flow was reduced only by a reported 10 to 20%. The conclusion was that prostaglandins did not play a dominant role in blood flow control.[ 100]
Staessen et al.[ 101] inadvertently provided the only 'true' performance data on vasoactive prostaglandins while studying the effects of prostaglandins inhibition on systemic haemodynamics. In their double-blind, placebo-controlled study, volunteers treated with indomethacin showed no decrement in VO2max or cycle time to exhaustion when compared with the control group.[ 101] Therefore, both indirect and direct evidence suggests that vasoactive prostaglandins have little impact on blood flow as it relates to performance outcome.
The Zone avidly opposes the synthesis of PGE2 and recommends dietary manipulations which would eliminate PGI2 synthesis as well. Despite the vasoactivity of the series 2 prostaglandins and the small positive role they play during exercise, the Zone narrowly labels them as 'bad' without consideration of their functions. According to the Zone, greater PGE1 synthesis is the ultimate performance benefit of a 40/30/30 diet. A small defence for this point can be made by recalling that the most important factor affecting blood flow is the radius of the blood vessel. According to Poiseuille's law, perfusion rate is related to the diameter of a vessel raised to the fourth power. Therefore, even small changes in a vessel's diameter can have a significant impact on blood flow. Now consider that Messina et al.[ 49] have shown that topically administered PGE1 vasodilates an arteriole almost 300% more than the same quantity of PGE2. Therefore, changes in the production of vasoactive prostaglandins from series 2 to series 1 prostaglandins could theoretically improve performance.
To understand why this proposed cause and effect relationship would be of no consequence to exercise, recall first that series 2 prostaglandin metabolites are excreted during exercise, indicating a lack of series 1 prostaglandin activity in the muscle microcirculation. Furthermore, all positive effects of PGE1 on skeletal muscle vasodilation have been observed only following topical administration or exogenous infusion.[ 49, 55, 82-85] Although prostaglandins are widely distributed among most mammalian tissues, the location of most PGE1 tissue precursor (DGLA) seems to be primarily in adrenal glands,[ 102] not skeletal muscle. This would seem to rule out any potential endogenous affects of PGE1 on muscle arterioles since prostaglandins of the E series appear to have only local physiological effects,[ 103] while any systemically active prostaglandins are metabolised and rapidly inactivated by the lungs upon entry into the bloodstream.[ 104, 105] In addition, previously stated scientific evidence profoundly disputes the notion that PGE1 production can be precisely controlled by either dietary or hormonal manipulation. It is also doubtful that any improvements in arteriolar blood flow, if it could be attained with greater levels of PGE1, would offset the clear performance disadvantages of a diet so low in carbohydrates and total calories.
6. Conclusion The claim that competitive and elite endurance athletes can improve performance by consuming a diet of 40% carbohydrates within the confines of less than 2000 daily calories is not substantiated by reliable scientific evidence. After nearly 60 years of corroborative findings, it is instead quite clear that measurable improvements in endurance can only be achieved by following a high carbohydrate diet. It therefore remains fundamental to the training programme of endurance athletes to follow the recommended high carbohydrate diet which profoundly opposes the Zone.
Although endurance athletes who neglect protein in order to maximise low fat, carbohydraterich food choices can benefit from consuming more dietary protein, the Zone diet recommendations (1.8 to 2.2 g/kg/day) exceed even the highest reported needs (1.2 to 1.4 g/kg/day) suggested in the literature.[ 106] In addition, any benefit of added protein would certainly be offset by the severe calorie and carbohydrate restrictions of the diet.
While the lipid biochemistry related to the Zone diet is factual, the connections made between nutrition, endocrinology, lipid metabolism, and exercise physiology are extremely oversimplified and sometimes paradoxical. Although the best available research profoundly disputes any performance benefit in adopting such a diet, its popularity continues to grow under a cloud of seemingly scientific 'facts'. When it comes to improving performance through diet, athletes would be well advised to steer clear of the Zone.
Acknowledgements The author wishes to thank two colleagues and mentors, Dr Jacqueline L. Dupont and Dr Robert J. Moffatt of the Department of Nutrition, Food and Movement Sciences, Florida State University, Tallahassee, Florida, for reading this manuscript and providing expert advice and guidance.
Table I. Diet and hormonal factors affecting desaturase activities Legend for Chart:
A - Hormone/macronutrientB - Δ6 DesaturaseC - Δ5 Desaturase
A B C
Glucagon Decreases activity Decreases activity(a)Insulin Increases activity Increases activity(a)Protein Increases activity(a) Increases activityCarbohydrate Decreases activity(a) Decreases activity
(a) The Zone misleadingly reports only these activities for eachrespective hormone and macronutrient.DIAGRAM: Fig. 1. Simplified classical and alternative pathways for the biosynthesis of series 1 and 2 prostanoids from n-6 polyunsaturated fatty acids (linoleic acid).
References [1.] Simopoulos AP. Opening address. Nutrition and fitness from the first Olympiad in 776 B.C. to 393 A.D. and the concept of positive health. Am J Clin Nutr 1989; 49 Suppl. 5: 921-926
[2.] Sears, B. The zone: a dietary road map. New York: Harper Collins, 1995
[3.] Costill DL, Bowers R, Kammer WF. Skinfold estimates of body fat among marathon runners. Med Sci Sports Exerc 1970; 2 (2): 93-5
[4.] Coleman EJ. Debunking the 'Eicotec' myth. Sports Med 1993; 15: 6-7
[5.] Coleman EJ. The biozone nutrition system: a dietary panacea? Int J Sport Nutr 1996; 6: 69-71
[6.] Bergstrom J, Hultman E. The effect of exercise on muscle glycogen and electrolytes in normals. Scand J Clin Lab Invest 1966; 18: 16-20
[7.] Bergstrom J, Hultman E. A study of the glycogen metabolism during exercise in man. Scand J Clin Lab Invest. 1967; 19: 218-28
[8.] Lewis SF, Haller RG. The pathophysiology of McArdle's Disease: clues to regulation in exercise and fatigue. J Appl Physiol 1986; 61: 391-401
[9.] Pernow B, Saltin B. Availability of substrates and compacity for prolonged heavy exercise in man. J Appl Physiol 1971; 31 (3): 416-22
[10.] Costill D, Coyle E. Energetics of marathon running. Med Sci Sports Exerc 1969; 1: 81-6
[11.] O'Brien M, Viguie CA, Mazzeo RS, et al. Carbohydrate dependents during marathon running. Med Sci Sports Exerc 1993; 25 (9): 1009-17
[12.] Williams C, Brewer J, Patton A. The metabolic challenge of the marathon. Br J Sports Med 1984; 18: 245-52
[13.] Bergstrom J, Hermansen L, Hultman E, et al. Diet, muscle glycogen, and physical performance. Acta Physiol Scand 1967; 71: 140-50
[14.] Akermark C, Jacobs R, Rasmusson M, et al. Diet and muscle glycogen concentration in relation to physical performance in Swedish elite hockey players. Int J Sports Nutr 1996; 6: 272-84
[15.] Karlsson J, Saltin B. Diet muscle glycogen and endurance performance. J Appl Physiol 1971; 31: 203-6
[16.] Sherman W, Costill DL, Fink WJ, et al. Effective exercise-diet manipulation on muscle glycogen and its subsequent utilization during performance. Int J Sports Med 1981; 2: 114-18
[17.] Coyle EF, Coggan AR, Hemmert MK, et al. Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate. J Appl Physiol 1986; 61: 165-72
[18.] Coyle EF, Hagberg JM, Hurley BF, et al. Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. J Appl Physiol 1983; 55: 230-5
[19.] Foster C, Costill DL, Fink WJ. Effects of preexercise feeding on endurance performance. Med Sci Sports Exerc 1979; 11: 1-5
[20.] Devlin JT, Calles-Escandon J, Horton ES. Effects of preexercise snack feeding on endurance cycle exercise. J Appl Physiol 1986; 60 (3): 980-5
[21.] Costill DL, Bowers R, Branam G, et al. Muscle glycogen utilization during prolonged exercise on successive days. J Appl Physiol 1971; 31 (6): 834-8
[22.] Costill DL, Sherman WH, Fink DJ, et al. The role of dietary carbohydrates in muscle glycogen resynthesis after strenuous running. Am J Clin Nutr 1981; 34: 1831-6
[23.] Simonsen JC, Sherman WM, Lamb DR, et al. Dietary carbohydrate, muscle glycogen, and power output during rowing training. J Appl Physiol 1991; 70 (4): 1500-5
[24.] Costill DL, Hinrichs D, Fink WJ, et al. Muscle glycogen depletion during swimming interval training. J Swimming Res 1988; 4: 15-8
[25.] Lamb DR, Rinehardt KF, Bartels RL, et al. Dietary carbohydrate and intensity of interval swim training. Am J Clin Nutr 1990; 52: 1058-63
[26.] Tarnopolsky MA, Atkinson SA, Phillips SM, et al. Carbohydrate loading and metabolism during exercise in men and women. J Appl Physiol 1995; 78 (4): 1360-8
[27.] Muoio DM, Leddy JJ, Horvath PJ, et al. Effect of dietary fat on metabolic adjustments to maximal VO2max and endurance in runners. Med Sci Sports Exerc 1994; 26: 81-8
[28.] Lambert EV, Speechly DP, Dennis SC, et al. Enhanced endurance in trained cyclists during moderate intensity exercise following two weeks adaptation to a high fat diet. Eur J Appl Physiol 1994; 69: 287-93
[29.] Sherman WM, Leenders N. Fat loading: the next magic bullet? Int J Sport Nutr 1995; 5 Suppl.: S1-12
[30.] Davies CTM, Thompson MW. Aerobic performance of female marathon and male ultramarathon athletes. Eur J Appl Physiol 1979; 41: 233-45
[31.] National Research Council. Recommended dietary allowances, 10th ed. Washington DC: National Academy Press, 1989: 29
[32.] van Erp-Baart AM, Saris WHM, Binkhorst RA, et al. Nationwide survey on nutritional habits in elite athletes: Part I. Energy, carbohydrates, protein, and fat intake. Int J Sports Med 1989; 10 Suppl. 1: S3-10
[33.] Muller WA, Faloona GR, Agullar-Parada E. Abnormal alpha-cell function in diabetes: response to carbohydrate and protein ingestion. N Engl J Med 1970; 283: 19-115
[34.] Coulston AM, Liu GC, Reaven GM. Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans. Metabolism 1983; 32 (1): 52-6
[35.] Lefebvre P, Luyckx A. Effect of insulin on glucagon enhanced lipolysis in vitro. Diabetologia 1969; 5: 195-7
[36.] Jensen MD, Caruso M, Heiling V, et al. Insulin regulation of lipolysis in nondiabetic and IDDM subjects. Diabetes 1989; 38: 1595-601
[37.] Boyd III AE, Glamber SR, Mager M, et al. Lactate inhibition of lipolysis in exercising man. Metabolism 1974; 23 (6): 531-42
[38.] Astrand PO, Ryhming I. A nomagram for calculation of aerobic capacity (physical fitness) from pulse rate during submaximal work. J Appl Physiol 1954; 7: 218-22
[39.] Swain DP, Abernathy KS, Smith CS, et al. Target heart rates for the development of cardiorespiratory fitness. Med Sci Sports Exerc 1994; 26 (1): 112-6
[40.] Davis JA, Frank MH, Whipp BJ, et al. Anaerobic threshold alterations caused by endurance training in middle-aged men. J Appl Physiol 1979; 46 (6): 1039-46
[41.] Roberts KM, Nobel EG, Hayden DB, et al. Simple and complex carbohydrate-rich diets and muscle glycogen content of marathon runners. Eur J Appl Physiol 1988; 57: 70-4
[42.] Kiens B, Raben AB, Valeur AK, et al. Benefit of dietary simple carbohydrates on the early postexercise muscle glycogen repletion in male athletes. Med Sci Sports Exerc 1990; 22 (2 Suppl.): S88
[43.] Zawadzki KM, Yaspelkis III BB, Ivy JL. Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise. J Appl Physiol 1992; 72 (5): 1854-9
[44.] Spiller GA, Jensen CD, Pattison TS, et al. Effect of protein dose on serum glucose and insulin response to sugars. Am J Clin Nutr 1987; 46: 474-80
[45.] Perseghin G, Price TB, Petersen KF, et al. Increased glucose transport-phosphorylation and muscle glycogen synthesis after exercise training in insulin-resistant subjects. N Engl J Med 1996; 335: 1357-62
[46.] de Fronzo RA, Ferrannini E, Sato Y, et al. Synergistic interaction between exercise and insulin on peripheral glucose uptake. J Clin Invest 1981; 68: 1468-74
[47.] Douen AG, Ramlal T, Rastogi S, et al. Exercise induces recruitment of the 'insulin-responsive glucose transporter.' J Biol Chem 1990; 265: 13427-30
[48.] Vane JR. Prostaglandins and the cardiovascular system. Br Heart J 1983; 49: 405-9
[49.] Messina EJ, Weiner R, Kaley G. Microcirculatory effects of prostaglandin E1, E2, and A1 in the rat mesentary and cremaster muscle. Microvasc Res 1974; 8: 77-89
[50.] Bild GS, Bhat SG, Axelrod B, et al. Inhibition of aggregation of human platelets by 8,15-dihydroperoxides or 5,9,11,13-eicosatetraenoic and 9,11,13-eicosatrienoic acids. Prostaglandins 1978; 16: 795-801
[51.] Moncada S, Higgs EA, Vane JR. Human arterial and venous tissues generate prostacyclin (prostaglandin X), a potent inhibitor of platelet aggregation. Lancet 1977; I: 18-20
[52.] Stone KJ, Willis AL, Hart M, et al. The metabolism of dihomo-gamma-linolenic acid in man. Lipids 1978; 14 (2): 174-80
[53.] Brenner R. The desaturation step in the animal biosynthesis of polyunsaturated fatty acids. Lipids 1971; 6 (8): 567-75
[54.] Sprecher H. Biochemistry of essential fatty acids. Prog Lipid Res 1981; 20: 13-22
[55.] Bergstrom S, Duner H, von Euler US, et al. Observations on the effects of infusion of prostaglandin E in man. Acta Physiol Scand 1959; 45: 145-50
[56.] Ryan MJ, Zimmerman BG. Effect of prostaglandin precursors, dihomo-gamma-linolenic acid and arachadonic acid on the vasoconstriction response to norepinephrine in the dog paw. Prostaglandins 1974; 6 (3): 179-92
[57.] Kadowitz PJ. Effect of prostaglandin E1, E2, A2 on vascular resistance and responses to noradrenaline, nerve stimulations, and angiotensin in the dog hindlimb. Br J Pharmacol 1972; 46: 395-400
[58.] Kather H, Simon B. Adenylate cyclase of human fat cell ghosts: stimulation of enzyme activity by prostaglandins. J Cyclic Nucleotide Res 1977; 3: 199-206
[59.] Herold PM, Kinsella JE. Fish oil consumption and decreased risk of cardiovascular disease: a comparison of findings from animal and human feeding trials. Am J Clin Nutr 1986; 43: 566-98
[60.] Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr 1991; 54: 438-63
[61.] Thomas LM, Holub BJ. Modification of human platelet phospholipids and agonist-stimulated phosoinositide phosphorylation by omega-3 fatty acids. In: Essential fatty acids and eicosanoids. Champaign: American Oil Chemists Society, 1992: 356-60
[62.] Lagarde M, Guichardant M, Dechavanne M. Human platelet PGE1 and diohomogamma linolenic acid. Comparison to PGE2 and arachidonic acid. Prog Lipid Res 1981; 20: 439-43
[63.] Willis AL. Unanswered questions in essential fatty acids and prostaglandin research. Prog Lipid Res 1981; 20: 839-50
[64.] Willis AL, Comai K, Kuhn DC, et al. Dihomo-gamma-linolenate suppresses platelet aggregration when administered in vitro or in vivo. Prostaglandins 1974; 25: 509-19
[65.] Kernoff PBA, Willis AL, Stone KJ, et al. Antithrombotic potential of dihomo-gamma-linolenic acid in man. BMJ 1977; 2 (6100): 1441-4
[66.] Fisher JM, Donegan DR, Leon H, et al. Effects of prostaglandins and their precursors in some tests of hemostatic function. Prog Lipid Res 1981; 20: 799-810
[67.] Tate G, Mandell BF, Laposata M, et al. Suppression of acute and chronic inflamation by dietary gamma linolenic acid. J Rheumatol 1989; 16 (6): 729-34
[68.] Needleman SW, Spector AA, Hoak JC. Enrichment of human phospholipids with linoleic acid diminishes thromboxane release. Prostaglandins 1982; 24: 607-22
[69.] Sato T, Nakao K, Hashizume T, et al. Inhibition of platelet aggregation by unsaturated fatty acids through interference with a thomboxane-mediated process. Biochim Biophys Acta 1987; 931: 157-64
[70.] Dupont J, Dowe MK. Eicosanoid synthesis as a functional measurement of essential fatty acid requirement. J Am Coll Nutr 1990; 9: 272-6
[71.] Shimizu S, Akimoto K, Shinmen Y, et al. Sesamin is a potent and specific inhibitor of delta-5 desaturase in polyunsaturated fatty acid biosynthesis. Lipids 1991; 26: 512-6
[72.] de Gomez Dumm INT, de Alaniz MJT, Brenner RR. Effect of diet on linoleic acid desaturation and on some enzymes of carbohydrate metabolism. J Lipid Res 1970; 11: 96-101
[73.] Peluffo RO, de Gomez Dumm INT, Brenner RR. The activating of dietary protein on linoleic acid desaturation. Lipids 1972; 7: 363-7
[74.] Mimouni V, Poisson JP. Spontaneous diabetes in BB rats: evidence for insulin dependent liver microsomal delta-6 and delta-5 desaturase activities. Horm Metab Res 1990; 22: 405-7
[75.] Boustani S, Causse J, Descomps B, et al. Direct in vivo characterization of delta-5 desaturase activity in humans by deuterium labeling: effect of insulin. Metabolism 1989; 38 (4): 315-21
[76.] Peluffo RO, de Gomez Dumm INT. Effect of protein and insulin on linoleic acid desaturation of normal and diabetic rats. J Nutr 1971; 101: 1075-84
[77.] Brenner R. Nutritional and hormonal factors influencing desaturation of essential fatty acids. Prog Lipid Res 1981; 20: 41-7
[78.] de Gomez Dumm INT, de Alaniz MJT, Brenner RR. Comparative effects of glucagon, dibutyryl cyclic AMP and epinephrine on the desaturation and elongation of linoleic acid by rat liver microsomes. Lipids 1976; 11 (12): 833-6
[79.] de Gomez Dumm INT, de Alaniz MJT, Brenner RR. Effects of glucagon and dibutyryl adenosine 3,5 -- cyclic monophosphate on oxidative desaturation of fatty acids in the rat. J Lipid Res 1975; 16: 264-8
[80.] Peluffo RO, Brenner RR. Influence of dietary protein on 6 and 9 desaturation of fatty acids in rats of different ages and in different seasons. J Nutr 1974; 104: 894-900
[81.] Brenner RR, Peluffo RO, Mercuri O, et al. Effect of arachidonic acid in the alloxan-diabetic rat. Am J Physiol 1968; 215 (1): 63-70
[82.] Horton EW, Main IHM. A comparison of the biological activities of four prostaglandins. Br J Pharmacol 1963; 21: 182-9
[83.] Beaty III O, Donald DE. Contribution of prostaglandin to muscle blood flow in anesthetized dogs at rest, during exercise, and following inflow occlusion. Circ Res 1979; 44: 67-75
[84.] Bergstrom S, Carlson LA, Oro L. Cardiovascular and metabolic response to infusions of prostaglandin E1 and to simultaneous infusions of noradrenaline and prostaglandin E1 in man. Acta Physiol Scand 1965; 64: 332-9
[85.] Hedwall PR, Abdel-Sayed WA, Schmid PG, et al. Vascular responses to prostaglandin E1 in gracilis muscle and hindpaw of the dog. Am J Physiol 1971; 221: 42-7
[86.] Rotto DM, Kaufman MP. Effect of metabolic products of muscular contraction on discharge group III and IV afferents. J Appl Physiol 1988; 64: 2306-13
[87.] Rowell LB, O'Leary DS. Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes. J Appl Physiol 1990; 69 (2): 407-18
[88.] Stebbins CL, Longhurst JC. Potentiation of the exercise pressor reflex by muscle ischemia. J Appl Physiol 1989; 66 (3): 1046-53
[89.] Bevegard BS, Shepherd JT. Regulation of the circulation during exercise in man. Physiol Rev 1967; 47: 178-213
[90.] Strange S, Secher NH, Pawelczyk JA, et al. Neural control of cardiovascular responses and of ventilation during dynamic exercise in man. J Physiol 1993; 470: 693-704
[91.] Rotto DM, Massey KD, Burton KP, et al. Static contraction increases arachidonic acid levels in gastrocnemius muscles of cats. J Appl Physiol 1989; 66: 2721-4
[92.] Viinikkia L, Vuori J, Ylikorkala O. Lipid peroxides, prostacyclin, and thromboxane A2 in runners during acute exercise. Med Sci Sports Exerc 1984; 16: 275-7
[93.] Stebbins CL, Maruoka Y, Longhurst JC. Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction. Circ Res 1986; 59: 645-54
[94.] Rotto DM, Schultz HD, Longhurst JC, et al. Sensitization of group III muscle afferents to static contraction by arachadonic acid. J Appl Physiol 1990; 68 (3): 861-7
[95.] Wennmalm A, Fitzgerald GA. Excretion of prostacyclin and thromboxane A2 metabolites during leg exercise in humans. Am J Physiol 1988; 255: H15-H8
[96.] Ronni-Sivula H, Malm H, Ylikorkala O, et al. Marathon run stimulates more prostacyclin than thromboxane synthesis and differently in men and women. Prostaglandins 1993; 46: 75-9
[97.] Koller A, Kaley G. Prostaglandins mediate arteriolar dilation to increase blood flow velocity in skeletal muscle microcirculation. Circ Res 1990; 67: 529-34
[98.] Riutta A, Kerttula T, Sievi E, et al. Adrenaline infusion increases systemic prostacyclin production in man. Prostaglandins 1994; 48: 43-51
[99.] Jeremy JY, Mikhailidis DP, Dandona P. Adrenergic modulation of vascular prostacyclin (PGI2) secretion. Eur J Pharmacol 1985; 114: 33-40
[100.] Wilson JR, Kapoor SC. Contribution of prostaglandins to exercise-induced vasodilation in humans. Am J Physiol 1993; 265: H171-5
[101.] Staessen J, Cattaert A, Fagard R, et al. Hemodynamic and humoral effects of prostaglandin inhibition in exercising humans. J Appl Physiol 1984; 56 (1): 39-45
[102.] Carney JA, Slinger SJ, Walker BL. The phospholipid composition of pig lung surfactant. Lipids 1971; 6: 624-9
[103.] Karim SMM, Rao B. General introduction and comments. In: Karim SMM, editor. Prostaglandins and reproduction. Baltimore (MD): University Park Press, 1975: 8-9
[104.] Ferreira SH, Vane JR. Prostaglandins: their disappearance from and release into the circulation. Nature (Lond) 1967; 216: 868-73
[105.] Horton EW. Biological significance of the prostaglandins. In: Gross F, Labhart A, Mann T, et al., editors. Prostaglandins. Heidelberg: Springer-Verlag, 1972: 179-90
[106.] Lemon P. Do athletes need more dietary protein and amino acids? Int J Sport Nutr 1995; 5 Suppl.: S39-61
Correspondence and reprints: Samuel N. Cheuvront, 436 Sandels Building, Department of Nutrition, Food, and Exercise Sciences, Florida State University, Tallahassee, FL 32306-1493, USA.
The Zone Diet and Athletic Performance: Correspondence ContentsReferences Section: CORRESPONDENCE I am writing regarding the recently published article entitled The Zone Diet and Athletic Performance[ 1] by Samuel Cheuvront. I believe Mr Cheuvront has made many erroneous statements.
For example, in the abstract of his review Mr Cheuvront mistakenly refers to the Zone Diet used for elite athletes as a '40/30/30' diet. However, I recommended a much higher fat content for athletic performance.[ 2] Furthermore, his statement that a mixed diet will have no effect on pancreatic hormone release is incorrect. Work by Westphal et al.[ 3] and more recently by Ludwig et al.[ 4] have shown that changing the protein-to-carbohydrate ratio in a single meal will have a significant impact on the release of insulin and glucagon during the postprandial period. Also in Mr Cheuvront's abstract, he mistakenly states that glucagon has lipolytic actions. It is well known that at physiological concentrations, glucagon has no lipolytic action. Nowhere in any of my writings have I ever stated that glucagon has any lipolytic action.
I have made it clear in both my first book, The Zone, and in a subsequent book, Mastering the Zone,[ 5] that elite athletes must add significant amounts of extra fat (and primarily monounsaturated fat) to their diet. This is to maintain their percentage body fat in an appropriate range suitable for the needs of their particular sport. Therefore the Zone Diet for elite athletes is not a calorie-restricted programme as Mr. Cheuvront implies, nor are his calculations for the calories required for a typical male marathon runner close to those that I would recommend for an elite athlete.
Many of Mr Cheuvront's arguments are based on the importance of muscle glycogen levels. He ignores the results of one of the very few long term (greater than 7 days) dietary studies done at Ohio State University, which indicated that a higher carbohydrate diet produces a 33% increase in muscle glycogen compared to a lower carbohydrate diet for the same individual. Yet even with significant increase in muscle glycogen levels, there was no improvement in endurance.[ 6] If muscle glycogen levels were overwhelmingly important in athletic performance, I would expect that a 33% increase in their levels should manifest itself in some type of performance increases. Earlier studies showed that swimmers following a higher carbohydrate diet had statistically significant increases in their lactic acid formation under performance conditions when compared with swimmers following a lower carbohydrate diet.[ 7] One might assume that this increase in lactic acid formation on a higher carbohydrate diet comes from less efficient oxygen transfer. Since the dietary protocols were the same in both studies, one can assume that the swimmers on the high carbohydrate diet also had significantly increased muscle glycogen compared to swimmers following a lower carbohydrate diet. Thus, it would appear that research at Ohio State University indicates that a higher carbohydrate diet will produce more muscle glycogen, decrease oxygen transfer and provide no improvement in performance. Perhaps there is some magical threshold above which increased muscle glycogen has no role in athletic performance.
This paradoxical relationship between muscle glycogen levels and performance is also indicated in a study conducted with the Navy SEALS, who one might assume maintain high levels of fitness.[ 8] This study indicates that the amount of carbohydrate consumed by these highly trained athletes ranged from 42 to 51% of their total calories with an average of 230g per day. It should be noted that this is more than 50% lower in absolute amount in grams of carbohydrate than was used in the 'moderate' carbohydrate diet employed by the Ohio State researchers with their swimmers and runners. Using the dietary guidelines of the Zone Diet for an 80kg SEAL (assuming 10% body fat), such an individual would require 210g of carbohydrates per day. That amount is similar to the self-selected intake by these highly trained individuals. Furthermore, dietary records indicate that they were consuming approximately 1730 calories per day. If these individuals were following the formulas described in The Zone for elite athletes, their caloric intake would be more than 2700 calories. I find it interesting that such trained individuals are not demonstrating a drop-off in performance even though their diet contains approximately the same amount of carbohydrate as recommended by the Zone Diet, but with 1000 calories less energy than recommended by the Zone Diet.
Mr Cheuvront further calls the study done by Munio et al as 'scant evidence' that high fat (and thus a lower carbohydrate) diet improves performance, even though both endurance and maximal oxygen uptake (V•O2max) were improved with a high degree of statistical significance.[ 9] A 10% improvement of V•O2max in highly trained distance runners should be cause for further exercise physiology research as opposed to a simple dismissal by Mr Cheuvront.
Mr Cheuvront also seems to be unaware of subsequent work by Leddy et al. that shows a high carbohydrate diet has adverse effects on the cardiovascular risk profile of elite athletes when compared to a lower carbohydrate, higher fat diet.[ 10] Exactly the same conclusions are reached in patients with type 2 diabetes mellitus.[ 11]
Mr Cheuvront goes on to state: '...the bottom line message of the Zone diet, which is clearly to avoid insulin production.' That statement is an outright falsehood. Other statements that he makes, such as 'the Zone generally regards insulin as the enemy', are equally outrageous. Nowhere are such statements or even the implication of such statements ever made in any of my works. In fact, it is an absurd statement. The goal of the Zone Diet is to maintain an appropriate zone of insulin. That means maintaining adequate insulin levels, but not excessive insulin levels (hyperinsulinaemia), as hyperinsulinaemia is clearly detrimental to physiological performance.
In the discussion of eicosanoids, contradictory statements are made relative to his premise that the Zone Diet cannot affect performance. For example, he makes statements such as 'it appears then that an undefined critical balance rather than an absolute quantity of exogenous eicosanoid precursors may determine the degree of potential prostaglandin synthesis'. That is a rather obtuse description of the goal of the Zone Diet. Statements Mr Cheuvront makes that seem to support the Zone Diet include:
• 'It is therefore a reasonable postulation that vasoactive prostaglandins could act as one class of metabolites responsible for regulating muscle blood flow.'
• 'Changes in the production of vasoactive prostaglandins from series 2 to series 1 prostaglandins could theoretically improve performance.'
• 'The lipid biochemistry related to the Zone diet is factual.'
Mr Cheuvront overlooks the points that blood flow and therefore oxygen transfer can be reduced by excess production of both thromboxane A2 and prostaglandin E2 (PGE2) because of their adverse effects on platelet aggregation. The conflicting effects of PGE2 (i.e. acting as vasodilator in certain tissues, but increasing platelet aggregation) are due to the differential effects of various eicosanoid receptors.[ 12, 13] For example, there are 4 discrete receptors for prostaglandins of the E series, each of them using a different set of second messengers. A molecular definition of a 'bad' eicosanoid is one that operates through the IP3/DAG pathway, whereas the definition of a 'good' eicosanoid is one that operates through the cyclic AMP pathway. PGE1 appears to bind only to the EP2 receptor that mediates its message by increasing cyclic AMP levels. On the other hand, PGE2 binds to all 4 EP receptors, including the EP3 receptor that decreases cyclic AMP levels. Thus, depending on the concentration of EP receptors and types in a specific tissue, PGE2 can have diametrically opposite physiological effects. This has been demonstrated in a recent study with various rat liver fractions.[ 14] It should also be noted that thromboxane A2 operates through the IP3/DAG second messenger pathway via its TP receptor, and that insulin also acts via the same second messenger. Hyperinsulinaemia and overproduction of 'bad' eicosanoids are synergistic in producing adverse physiological responses because of the positive feedback loops of increased insulin on increasing arachidonic acid production and the effect of leukotrienes derived from arachidonic acid causing an increase in insulin production.[ 15]
Finally, Mr Cheuvront quotes Lemon[ 16] in stating that endurance athletes require 1.2 to 1.4g of protein per kg of total bodyweight and neglects to report that strength athletes would require 1.4 to 1.8g per kg of total body weight. The protein requirements for the Zone Diet are based on lean body mass, not total bodyweight. Assuming an athlete has 10% body fat, then his or her lean body mass will be 90% of total body weight. Therefore, for a strength athlete, my upper limit for protein recommendations for the Zone Diet would be 2.2g of protein per kg of lean body mass. If I use Lemon's upper estimate of 1.8g of protein per kg of total body weight, then I would have to divide his estimate by 0.9 to compare the 2 numbers directly. This would correspond to 2.0g of protein per kg of lean body mass, which is pretty close to my stated upper limit. An endurance athlete who does no strength training would only require a maximum of 1.8g of protein per kg of lean body mass according to the calculations I put forward in The Zone. Again converting Lemon's estimates (assuming 10% body fat), then the upper limit would be approximately 1.6g of protein per kg of lean body mass. For both endurance and strength athletes, my estimates of protein requirements are within 10% of Lemon's estimates: a surprisingly good convergence from 2 different sources.
References [1.] Cheuvront SN. The zone diet and athletic performance. Sports Med 1999; 27 (4): 213-28
[2.] Sears B. The zone. New York (NY): Regan Books, 1995
[3.] Westphal SA, Gannon MC, Nutrall FQ. Metabolic response to glucose ingested with various amounts of protein. Am J Clin Nutr 1990; 62: 267-72
[4.] Ludwig DS, Majzoub JA, Al-Zahrani A, et al. High glycemic index foods, overeating, and obesity. Pediatrics 1999; 103: E26
[5.] Sears B. Mastering the zone. New York (NY): Regan Books, 1997
[6.] Sherman WM, Doyle JA, Lamb DR, et al. Dietary carbohydrate, muscle glycogen, and exercise performance during 7 d of training. Am J Clin Nutr 1993; 57: 27-31
[7.] Lamb DR, Finehardt KF, Bartels RL, et al. Dietary carbohydrate and intensity of interval swim training. Am J Clin Nutr 1990; 52: 1058-63
[8.] Jacobs I, Prusaczyk WK, Goforth HW. Muscle glycogen, fiber type, aerobic fitness, and anaerobic capacity of west coast U.S. Navy Sea-Air-Land Personnel (SEALS). Report 92-10, Naval Medical Research and Development Command. Bethesda (MD): Naval Medical Research and Development Command, 1992
[9.] Munio DH, Leddy JJ, Horvath PJ, et al. Effect of dietary fat on metabolic adjustments to maximal V•O2 and endurance in runners. Med Sci Sports Exerc 1994; 26: 81-8
[10.] Leddy J, Horvath P, Rowland J, et al. Effect of a high or a low fat diet on cardiovascular risk factors in male and female runners. Med Sci Sports Exerc 1997; 29: 17-25
[11.] Garg A, Bonanome A, Grundy SM, et al. Comparison of a high carbohydrate diet with a high-monounsaturated fat diet in patients with non-insulin-dependent diabetes mellitus. N Engl J Med 1988; 319: 829-34
[12.] Coleman RA, Eglen RM, Jones RL, et al. Prostanoid and leukotriene receptors: a progress report from the IUPHAR working parties on classification and nomenclature. Adv Prostaglandin Thromboxane Leukot Res 1995; 23: 283-5
[13.] Colman RA, Smith WL, Narumiya S. International union of pharmacology classification of prostanoid receptors: properties, distribution, and structure of the receptors and their subtypes. Pharmacol Rev 1994; 46: 205-29
[14.] Fennekohl A, Schieferdecker HL, Jungermann K, et al. Differential expression of prostanoid receptors in hepatocytes, Kupffer cells, sinusoidal endothelial cells and stellate cells of rat liver. J Hepatalogy 1999; 30: 38-47
[15.] Pek SB, Nathan MH. Role of eicosanoids in biosynthesis and secretion of insulin. Diabetes Metab 1994; 20: 146-9
[16.] Lemon P. Do athletes need more dietary protein and amino acids? Int J Sports Nutr 1995; 5: S39-61
The Zone Diet and Athletic Performance: Author's Reply ContentsReferences Section: CORRESPONDENCE The author's reply:
I appreciate the opportunity to respond to Dr Sears' letter. After careful evaluation of the criticisms offered of my review, I find little more than the selectively reported information already offered in The Zone. When examined more fully, this 'evidence' fails to substantiate any part of the Zone theory, much less refute my recently published opposition. For the purpose of clarity, the same male marathon runner previously described[ 1] will be used as the elite athlete in this discussion.
The Zone diet is by definition a 40/30/30 diet (40% carbohydrate, 30% protein, 30% fat). Carbohydrate, protein and fat are consumed as 'blocks' (1 carbohydrate block = 9g of carbohydrates, 1 protein block = 7g protein, 1 fat block = 1.5g fat) in a 1 : 1 : 1 ratio. One sentence in The Zone suggests that elite athletes consume a ratio of 1 : 1 : 2, or 3g of fat for every 7g of protein. This then is the 'much higher' fat that Dr Sears implies will support energy needs and maintain optimal body fat levels. The overall prescription is the same as previously outlined[ 1] for a 64kg, 7.5% body fat marathon runner (e.g. 130g protein, 58g fat, 173g carbohydrate and 1735 total kcal). If this recommendation actually implies doubling the originally prescribed fat intake (based on SEAL calculations given in Dr Sears' letter), then the diet becomes 116g fat (46%), 31% carbohydrate, 23% protein and 2257 total calories. However, total energy needs under this plan would still be only half of the previously calculated needs for living, training and competing for said athlete.[ 1]
Dr Sears suggests that Navy SEALS maintain performance on <> 65% run fewer than 26 miles weekly.[ 5] The athlete in question (above) can run 26.2 miles in roughly 130 to 150 minutes! Therefore, although Navy SEALS are skilled soldiers, they do not appear to be endurance athletes. This flawed comparison should be disregarded.
Misrepresented research findings abound in The Zone and persist in Dr Sears' opposing letter. The study by Sherman et al.[ 6] is one of very few to demonstrate that <> 600 g/day) carbohydrate intakes. These findings are the minority, but still represent carbohydrate intakes twice those suggested by the Zone (173g). Total energy intakes were also significantly higher (3500 kcal) than our Zone estimate. It is equally important to realise that inadequate total energy intake in the presence of moderate carbohydrate consumption (approximately 370g) has been shown[ 7] to impair endurance performance despite smaller reductions in muscle glycogen (20%) relative to the study by Sherman et al. (33%). In this experiment,[ 7] the mean energy expenditures for training alone (2293 kcal) exceeded even the 'generous' Zone prescription above. Therefore, a Zone diet prescription remains inadequate in both total calories and total carbohydrate and could not possibly support the training and competition efforts of elite endurance athletes.
Another example given by Dr Sears focuses on a paper discussed in my review.[ 8] An 80% and a 40% carbohydrate diet (both providing > 500 g/day) were compared. Performances were no different between the 2 groups. This can be explained by both groups receiving an adequate absolute quantity of carbohydrate. Dr Sears points to the higher lactate values in the 80% carbohydrate group as evidence that 'a higher carbohydrate diet will... decrease oxygen transfer...'. To the best of my knowledge, this is the first time that any yet-to-be-discovered relationship between carbohydrate intake and exercise anoxia has been put forth. Even the author of this study himself explains this phenomenon simply as the result of greater carbohydrate availability and, subsequently, greater carbohydrate oxidation mass action effect. This is a concept well understood by exercise physiologists. Similarly, the 'high fat' diet reported to improve V•O2max above values achieved on a 'high carbohydrate' diet were 438 g/day (50% carbohydrate, 38% fat, 12% protein) and 638 g/day (73% carbohydrate, 15% fat, 12% protein), respectively.[ 9] Both diets contained 3500 kcal. This is simply not a low carbohydrate diet. More importantly, it is not a Zone diet.
Other obtuse interpretations are brought in to support the Zone as well. It is quite clear that fat intake is tied to hyperlipidemia and cardiovascular disease. The report by Leddy et al.[ 10] of a high fat diet (42% of kcal) improving high density lipoprotein (HDL)-cholesterol and a diet low in fat (16% of kcal) and high in carbohydrate reducing HDL-cholesterol is a finding which stands in relative isolation. The majority of carbohydrate feeding studies show no effect of high carbohydrate diets on HDL-cholesterol.[ 11] Additionally, statements supporting the capacity of a Zone diet to alter insulin production appear to be overstated. A closer look at one referenced paper[ 12] shows that at the 0.6 to 1.0 ratio of protein to carbohydrate suggested in the Zone (30g protein + 50g carbohydrate vs 50g carbohydrate or 50g protein + 50g carbohydrate vs 50g carbohydrate), the area under the insulin curve was not statistically different (0.6) or was actually greater (1.0) than when compared to the response of carbohydrate alone.[ 12] Although the insulin to glucagon ratios were altered, the magnitude of change may be inconsequential given the absolute rise observed in insulin. More importantly, no scientific support is ever offered to substantiate the proposed physiological consequences of these changes. With regard to athletes, the hyperinsulinaemic effect of a high glycaemic index meal given 3 hours prior to exhaustive treadmill exercise has recently been shown to be of no consequence to performance anyway, despite higher insulin levels relative to the low glycaemic index trial.[ 13]
Although some controversy exists, the lipolytic action of glucagon has in fact been demonstrated in humans at physiological concentrations.[ 14] In addition, Dr Sears himself includes a reference in his book[ 15] which determined that glucagon concentrations were the single best predictor of free fatty acid appearance during prolonged exercise. The association made between the Zone and 'fat burning' relies on an unfounded connection between glucagon, good eicosanoid production and growth hormone release. The logical interpretation of higher glucagon levels stimulating a 'Zone' of fat burning was surmised given the pure 'leap of faith' required for the alternative explanation. Furthermore, insulin is consistently blamed throughout The Zone for impaired performance, heart disease, cancer and diabetes, to name a few. In fact, hyperinsulinaemia (to which no value, acute or chronic, is offered) is said to put people in 'carbohydrate hell'.[ 16] The statements offered in my review represent the general tone conveyed by The Zone and should not be interpreted as quotes.
Dr Sears has offered little to advance the debate over control of eicosanoid production by dietary intervention. Table I of my review clearly points out the obvious contradictions outlined in The Zone, but this has not been contested. Dr Sears suggests that I have overlooked the potential for a normal diet (55 to 60% carbohydrate, 25 to 30% fat, 10 to 15% protein) to invoke a measurable elevation in PGE2 and thromboxane A2 (TXA2), thus elevating blood viscosity to the point of reducing convective blood oxygen transfer to active tissues. This statement is physiologically unfounded. When indomethacin was administered to volunteers for 3 days to block PGE2 and TXA2 production,[ 17] no differences were observed between indomethacin and placebo trials for V•O2max, cardiac output or any measure of systemic hemodynamics. What's more, athletes are generally observed to have lower whole blood viscosity when compared to non-athletes,[ 18] even though the macronutrient distribution of their calorie intakes are similar to the general population (49% carbohydrate, 35% fat, 16% protein).[ 4]
Finally, the fact that Zone protein intakes are based on a g/kg fat-free mass scale is readily acknowledged in my review. However, since 1965 the Food and Agricultural Organization and World Health Organization have conventionally determined nitrogen (N) intake needs in mg N/kg of total bodyweight. This was later extrapolated to mg of protein per kg of total body weight based upon protein's average 16% N composition. This remains the current basis for National Research Council protein intake recommendations. It is therefore more correct to compare Dr Lemon's 1.8 g/kg of protein to Dr Sears' 2.2 g/kg fat-free mass by dividing Dr Sears' value by 0.9, not Dr Lemon's. The result is a Zone protein intake of 2.4 g/kg total body weight: more than 30% greater than the highest scientific estimates.
In conclusion, Dr Sears' rebuttal has not successfully rejected any aspect of the earlier review of The Zone Diet and Athletic Performance.[ 1] The details underlying the many persistent fragments of research offered by The Zone, when clearly disseminated, do not support the intricate theories being proposed. Any future debate of the Zone will likely remain an exercise in futility unless empirical, peer reviewed, scientific support for existing theories can corroborate what is at present only anecdotal evidence.
References [1.] Cheuvront SN. The zone diet and athletic performance. Sports Med 1999; 27 (4): 213-28
[2.] DeBolt JE, Singh A, Day BA, et al. Nutritional survey of the US Navy SEAL trainees. Am J Clin Nutr 1988; 48: 1316-23
[3.] Deuster PA, Kyle SB, Moser PB, et al. Nutritional survey of highly trained women runners. Am J Clin Nutr 1986; 45: 954-62
[4.] Grandjean AC. Macronutrient intake of US athletes compared with the general population and recommendations made for athletes. Am J Clin Nutr 1989; 49: 1070-6
[5.] Shwayhat AF, Linenger JM, Hofherr LK, et al. Profiles of exercise history and overuse injuries among United States Navy Sea, Air, and Land (SEAL) recruits. Am J Sports Med 1994; 22 (6): 835-40
[6.] Sherman WM, Doyle JA, Lamb DR, et al. Dietary carbohydrate, muscle glycogen, and exercise performance during 7 d of training. Am J Clin Nutr 1993; 57: 27-31
[7.] Costill DL, Flynn MG, Kirwan JP, et al. Effects of repeated days of intensified training on muscle glycogen and swimming performance. Med Sci Sports Exerc 1988; 20 (3): 249-54
[8.] Lamb DR, Rinehardt KF, Bartels RL, et al. Dietary carbohydrate and intensity of interval swim training. Am J Clin Nutr 1990; 52: 1058-63
[9.] Muoio DM, Leddy JJ, Horvath AB, et al. Effect of dietary fat on metabolic adjustments to maximal V•O2 and endurance in runners. Med Sci Sports Exerc 1994; 26 (1): 81-8
[10.] Leddy J, Horvath P, Rowland J, et al. Effect of a high or a low fat diet on cardiovascular risk factors in male and female runners. Med Sci Sports Exerc 1997; 29 (1): 17-25
[11.] Frayn KN, Kingman SM. Dietary sugars and lipid metabolism in humans. Am J Clin Nutr 1995; 62 Suppl.: 250-63S
[12.] Westphal SA, Gannon MC, Nuttall FQ. Metabolic response to glucose ingested with various amounts of protein. Am J Clin Nutr 1990; 52: 267-72
[13.] Wee S, Williams C, Gray S, et al. Influence of high and low glycemic index meals on endurance running capacity. Med Sci Sports Exerc 1999; 31 (3): 393-9
[14.] Carlson MG, Snead WL, Campbell PJ. Regulation of free fatty acid metabolism by glucagon. J Clin Endocr Metab 1993; 77: 11-5
[15.] Galbo H, Holst JJ, Christensen NJ. Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol 1975; 38 (1): 70-6
[16.] Sears B. The zone. New York (NY): Regan Books, 1995
[17.] Staessen J, Cattaert A, Fagard R, et al. Hemodynamic and humoral effects of prostaglandin inhibition in exercising humans. J Appl Physiol 1984; 56 (1): 39-45
[18.] Eichner ER. Antithrombotic effects of exercise. Am Fam Phys 1987; 36 (5): 207-11
By Samuel N. Cheuvront, Department of Nutrition, Food, and Exercise Sciences Florida State University Tallahassee, Florida USA