How to get athletes to eat their vegetables: nitrate and performance (part 1)

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For 9 years of my life I was a competitive cross country runner.  For 9 years of my life I heard the same types of nutritional recommendations: high carbohydrate, low fat, lots of water, eat within 30 minutes of a workout.  I know now that total calories seems to matter most (to which increasing dietary fat definitely helps), carbohydrate loading isn’t relevant to most events, and I don’t need to carry around a gallon of water everywhere I go to keep my urine clear.  Future posts will dissect each of these in detail for endurance and strength athletes.  Fruits and vegetables were mentioned casually, but never was it suggested that certain vegetables may in fact increase endurance performance.

Now the evidence is mounting that some vegetables can indeed increase certain performance measures.  Specifically, it is the dietary nitrate that does so.

In 2007, Larsen et al. (1) published a seminal paper on dietary nitrate and oxygen cost during exercise.  Using 9 well trained male cyclists or triathletes in a double-blind placebo-controlled cross-over design, subjects avoided foods with moderate or high nitrate content (vegetables, cured meats, strawberries, grapes, tea) during the 2 3-day test periods.  One group consumed 0.1 mmol sodium nitrate per kg bodyweight/day (for a 150# person ~ 420 mg) and the other the same amount of sodium chloride three times per day for 3 days, separated by a 10 day washout period, then the groups were reversed.  This nitrate dose can be achieved with about 150-250 grams of a nitrate-rich vegetable like spinach, lettuce or beetroot (see table below).

Testing was done on a cycle ergometer, and pulmonary ventilation, oxygen uptake (VO2), CO2 output (VCO2), respiratory exchange ratio, and heart rate were analyzed during the tests.  Blood was taken to obtain lactate, haemoglobin, and haematocrit concentrations, and blood pressure was taken at rest.  Measurements were taken at 5 workrates: 45, 60, 70, 80, and 85% VO2peak.

Resting systolic blood pressure was lower after nitrate supplementation (112 +/- 8 mmHg) compared to placebo (120 +/- 5.9 mmHg).  Resting diastolic blood pressure was also lower after nitrate supplementation (68 +/- 5.5 mmHg) compared to placebo (74 +/- 6.8 mmHg).  Plasma nitrate increased at rest to 182 +/- 55 uM in the nitrate supplemented group, while in the placebo group were 27 +/- 6.9 uM.  Nitrate at rest was 226 +/- 87 nM in the nitrate group and 124 +/- 28 nM in the placebo.  Nitrite concentrations decreased more in the nitrate group during exercise.

During submaximal exercise, VO2 was lower in the tests in the nitrate group, and no difference in heart rates were noticed.   Lactate concentration, pulmonary ventilation, pulmonary ventilation/VO2 ratio, and resting energy expenditure were unchanged.  Average gross efficiency (work rate/energy expenditure) and delta efficiency (increase in work rate/increase in energy expenditure) were increased in the nitrate group.

During maximal work capacity, no differences were found in VO2peak,  maximal pulmonary ventilation, maximal heart rate, or maximal work rate.

Perceived exertion at both submaximal and maximal exercise was not different between the groups.

So that is nice and great, but sodium nitrate is not easy to get.

Bailey et al. (2) just recently published a paper utilizing a dietary source of nitrate, beetroot juice.

They measured plasma nitrite concentration, blood pressure, muscle oxygenation, and VO2 response to exercise transitions.

Eight recreationally active males consumed 5.5 mmol/day nitrate (~340 mg) as 0.5 L organic beetroot juice (Beet It) or a placebo for 6 days, sipping regularly through the day.  In a cross-over fashion, a 10 day washout period followed and subjects switched groups.  As in the previous study, the subjects were asked to avoid nitrate rich foods.

They found that plasma nitrite was increased in the beetroot juice (BRJ) group compared with the placebo, on average by 96%.  Elevations did change change significantly across the days when measured (days 4,5,6), suggestive that less than 6 days of consumption will maximize nitrite concentration.

BRJ had a significantly reduced systolic blood pressure overall (6 mmHg), and did not change significantly across days when measured (days 4,5,6).  Diastolic blood pressure and mean arterial pressure were not significantly different between the groups.

Deoxygenated haemoglobin (reflects balance between local O2 delivery and utilization), oxygenated haemoglobin, and total haemoglobin (index of vascular red blood cell content) were measured at moderate and severe exercise.

During moderate exercise, deoxygenated haemoglobin amplitude was decreased by 13% in BRJ (reduction in fractional O2 extraction), oxygenated haemoglobin was increased at baseline and at 2 minutes into exercise but not at the end in BRJ, and total haemoglobin was increased at baseline but not during exercise.

During severe exercise, the above measures were unaltered in both groups, suggesting no change in muscle oxygenation.

With regard to oxygen uptake at a moderate exercise, BRJ had a 19% decrease in pulmonary VO2 response amplitude compared to placebo, and the ratio of the increase in O2 consumed per minute to the increase of external power output was reduced in BRJ.  Absolute VO2 over the last 30 seconds of exercise was lower in BRJ.

CO2 output (VCO2), pulmonary ventilation, respiratory exchange ratio, heart rate, and lactate concentration were not significantly different between the groups.

During severe exercise, primary VO2 amplitude was significantly elevated in BRJ, while the VO2 slow component amplitude was significantly less compared to placebo.  At failure, VO2 was not different.

The BRJ had an increased time to task failure (BRJ: 675 +/- 203 seconds vs Placebo: 583 +/- 145 seconds), the measure of exercise tolerance.

CO2 output (VCO2), pulmonary ventilation, respiratory exchange ratio, heart rate, and lactate concentration were not significantly different between the groups.

*The beetroot juice caused beeturia (red urine) and red stools in the subjects, an important thing to note should you or clients try this method.

The biggest findings were the reduction in oxygen cost at a given submaximal work rate of 19%, and a 16% increase in time to failure during severe exercise.  The authors note that the latter improvement would likely be much smaller during time-trials in which the subjects aims to complete the distance in the shortest time possible (sprint), an emphasis that was lost in media summaries of this research.  They do suggest it may still result in a performance enhancement.  Further research is necessary, of course.

The most convincing results are from the submaximal testing, suggesting that dietary nitrate may increase time to failure in long distance exercise, though this also must be rigorously tested.  Until then, nitrate intake through vegetables can be safely increased with our understanding of their importance for general health and any ergogenic benefits are a bonus.

Mechanisms

Basic metabolism: dietary nitrate is absorbed through the stomach/intestine and is concentrated into the salivary glands and secreted into the oral cavity.  There, some of it is converted to nitrite by commensal nitrate-reducing bacteria.  When swallowed, it enters systemic circulation where it is bioactive as nitrite or is further reduced to nitric oxide (NO).  This is a pathway independent of the well known NOS mediated arginine->nitric oxide.  Previous research has shown that certain conditions favor conversion to nitric oxide, like hypoxia and acidosis (NO synthases operate poorly).  Exercise may promote these conditions thus favoring conversion.

There are multiple theoretical mechanisms described by authors based on these and previous research that require further research before we know how nitrate exerts its exercise related effects.  Nitric oxide production during exercise seems to be one factor in the regulation of local blood flow; when a muscle is receiving less or using more O2, more NO is generated shifting flow distribution (via vasodilation).  This however does not explain the reduction in O2 cost as seen in the results.  Instead, nitrite and NO may act more directly as NO is able to inhibit cytochrome oxidase activity, slowing conversion of O2 to H2O.  Also, NO may reduce ‘slippage’ of mitochondrial proton pumps, thus increasing oxidative phosphorylation efficiency.  Additionally, nitrite can accept electrons itself, possibly functioning in place of O2 in the process.  There is also the possibility that NO could reduce the ATP cost of exercise by lowering SR Ca2+ release by protecting channels from ROS induced release, since Ca2+ is energetically expensive to resequester.  NO also promotes mitochondrial biogenesis, possibly enhancing adaptation to subsequent exercise.

Significance

As noted in the texts, previous research has shown that during submaximal exercise, oxygen uptake and workload is tightly coupled.  That is, oxygen consumption at any given submaximal workload is basically independent of such factors as different individuals, on different occasions in the save individual, general health, or fitness level.  This research showing otherwise suggests a novel method to increase muscular efficiency.  Hyperoxic gas also reduces the O2 cost of heavy and severe exercise by reducing amplitude of the VO2 slow component, while steady-state VO2 during moderate exercise does not change.  To find a reduction with nitrate consumption without any increase in estimated non-oxidative energy production (lactate did not differ between the groups) is novel.  The only other dietary change effecting oxygen uptake kinetics I am aware of not mentioned by the authors of either of these papers is creatine supplementation, however because of other mechanisms through which creatine works it is not ideal for endurance purposes.

Most importantly, this gives us a powerful tool when educating active populations about the importance of plant foods.  Instead of repeating vague recommendations about the importance of fruits and vegetables on health (everyone “knows” this after all), we can show them how a smartly designed high vegetable diet may improve performance.  If a population is able to personally relate to the information, it may better resonate with them.

It may be difficult to consume the amount of vegetables required to reach these nitrate levels, so future research should also focus on practicality (as the selection of beet root juice for the latest study did).  Please send me feedback on how you or your clients may incorporate this information into their diet of high energy requirement.

Bailey et al. (2) note a significance for non athletic populations as well; elderly or certain diseased subjects may benefit from a reduction in VO2 as their energy requirements represent a high fraction of the Vo2 max.  Physical activity and quality of life could potentially be improved.

It should be noted that on a typical Western diet, ~60-80% of nitrate comes from the diet, and the average American intake of nitrate is only 40–100 mg per day (3). Recall the study doses that were well over 300 mg.  The Dietary Approaches to Stop Hypertension (DASH) diet, recommends 8-10 servings of vegetables per day and is used clinically to lower blood pressure, can vary significantly depending on selected vegetables.  Hord et al. (3) analyzed 2 example DASH diets based on a database of measured nitrate contents in select foods and found a dramatic difference in potential total nitrate (1222 mg vs 174 mg).

nitrateDASH

(Hord et al. 2009)

It should be noted that nitrate content of vegetables can vary dramatically dependent on a number of environmental factors, making it impossible to calculate with much accuracy.  A variety of vegetables is most desirable, however choosing from specific groups (e.g. leafy greens) may result in a higher nitrate intake:

nitratecontent

(Hord et al. 2009)

Unanswered Questions

Future research will need to explore effects such as gender, age, fitness, activity level, nitrate dose, and disease on outcomes.  As summarized previously, detailed mechanisms are still elusive and must be elucidated.

It also remains to be tested if dietary nitrate can enhance exercise time to failure during long distance endurance exercise, which will be important for real world application.

There is some lingering concern that nitrate/nitrite is harmful to health.  Part 2 will review evidence suggesting this is not the case and in fact they are essential to health, along with more detailed metabolism and biochemistry.

References

1.  Larsen FJ, Weitzberg E, Lundberg JO, & Ekblom B (2007). Effects of dietary nitrate on oxygen cost during exercise.Acta physiologica (Oxford, England), 191 (1), 59-66 PMID: 17635415

2.  Bailey SJ, Winyard P, Vanhatalo A, Blackwell JR, Dimenna FJ, Wilkerson DP, Tarr J, Benjamin N, & Jones AM (2009). Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans. Journal of applied physiology (Bethesda, Md. : 1985) PMID: 19661447

3.  Hord NG, Tang Y, & Bryan NS (2009). Food sources of nitrates and nitrites: the physiologic context for potential health benefits. The American journal of clinical nutrition, 90 (1), 1-10 PMID: 19439460