About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Home Print this page Email this page Users Online: 554

 Table of Contents  
Year : 2019  |  Volume : 19  |  Issue : 2  |  Page : 43-50

Acute potassium phosphate intake after exercise has no effect on subsequent exercise-induced performance time, substrate oxidation, and food intake in men

1 Department of Sport Health Sciences, Faculty of Physical Education, Helwan University, Cairo, Egypt
2 Department of Nutrition and Food Sciences, American University of Beirut, Beirut, Lebanon
3 Lifestyle and Health Research Center, Health Sciences Research Center, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia
4 Department of Exercise Physiology, College of Sport Sciences and Physical Activity, King Saud University, Riyadh, Saudi Arabia

Date of Submission15-Nov-2018
Date of Decision18-Apr-2020
Date of Acceptance12-May-2020
Date of Web Publication07-Jul-2020

Correspondence Address:
Dr. Shaea A. Alkahtani
Department of Exercise Physiology, College of Sport Sciences and Physical Activity, King Saud University, Riyadh
Saudi Arabia
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/sjsm.sjsm_28_18

Rights and Permissions

Background: Phosphorus availability during exercise is believed to positively affect adenosine triphosphate availability, increase glycogen synthesis, and enhance exercise performance.
Aim: The aim of the present study was to examine the effect of potassium phosphate intake after exercise on physiological responses during subsequent running at anaerobic threshold and on appetite and food intake postexercise in men.
Settings and Design: Nine moderately active young men (age, 22 ± 3 years; body mass index, 22.3 ± 3.0 kg/m2; and peak oxygen uptake (VO2peak) 48.5 ± 6.3 ml/kg/min) underwent two experimental conditions. Each condition consisted of two time-to-exhaustion treadmill running tests (time to exhaustion [TTE]) (bout 1 and 2), separated by 3 h recovery. During the recovery, either 500 mg phosphorus in the form of potassium phosphate or placebo was consumed with a glucose solution (1.2 g glucose/10 ml water × body weight) over 3 h.
Methods: Expired gas was collected during the running. Appetite using visual analog scale and food intake from access to an ad libitum meal were measured after the second TTE run. Exercise intensity, VO2,and running speed were 67 ± 3% VO2peak, 32.3 ± 4.5 ml/kg/min, and at 10.1 ± 1.1 km/h, respectively.
Statistical Analysis Used: Data were checked for normality, and Kolmogorov–Smirnov test was performed. Physiological variables, duration of exercise tests, and postexercise food intake and appetite sensations were analyzed using univariate ANOVA with interaction of exercise order and conditions.
Results: There was no group effect in running time of the 2nd TTE although running time was reduced by ~ 5% in the placebo condition and by ~ 37% in the potassium phosphate condition in comparison to running time of the 1st TTE. A group × time interaction was present for the 1st exercise bout (P = 0.03). There were no interactions of condition (placebo and potassium phosphate) and running bouts (1st and 2nd) on respiratory exchange ratio, whole-body fat oxidation, and carbohydrate oxidation, but the interaction effect on VO2trended toward significance (F = 3.97, P = 0.06). There were no differences between conditions for appetite sensations and food intake.
Conclusions: An acute dose of potassium phosphate after exercise did not affect subsequent exercise performance, exercise-induced substrate oxidation, and food intake. Potassium phosphate did not seem to affect metabolic responses and appetite in an ecological setting with repeated exercise and access to food during recovery.

Keywords: Exercise capacity, food intake, phosphorus, physical exercise

How to cite this article:
Daoud HA, Obeid O, Alghannam AF, Alkahtani SA. Acute potassium phosphate intake after exercise has no effect on subsequent exercise-induced performance time, substrate oxidation, and food intake in men. Saudi J Sports Med 2019;19:43-50

How to cite this URL:
Daoud HA, Obeid O, Alghannam AF, Alkahtani SA. Acute potassium phosphate intake after exercise has no effect on subsequent exercise-induced performance time, substrate oxidation, and food intake in men. Saudi J Sports Med [serial online] 2019 [cited 2023 Dec 8];19:43-50. Available from: https://www.sjosm.org/text.asp?2019/19/2/43/289159

  Introduction Top

An excess of phosphorus availability may increase hexokinase activity and thus further stimulate glycogen synthesis. The process of glycogen synthesis is phosphorus dependent since many steps are controlled by phosphorylation–dephosphorylation reactions. Through the process of glycogenesis, hexokinase converts glucose into glucose-6-phosphate by subtracting a phosphorus molecule from adenosine triphosphate (ATP). The same concept applies for glucokinase activity and hepatic glycogenesis. In an animal model, increased phosphorus content of the meal was reported to increase the level of glycogen in liver and this may improve exercise performance.[1] The concentration of phosphoenolpyruvate was increased and fructose 2, 6-bisphosphate concentration was decreased in phosphorus-deficient rats that had lower glycogen concentration when compared to rats with normal phosphorus intake.[2]

Phosphorus supplementation was reported to have several ergogenic effects when consumed on a chronic basis. Phosphorus is believed to increase endurance of aerobic exercise through increased levels of erythrocytes 2,3-diphosphoglycerate (2,3-DPG).[3] High levels of 2,3-DPG reduce the affinity of hemoglobin to oxygen and consequently increase the availability of oxygen during exercise. However, it needs to be noted that a causal link between phosphorus intake and increased levels of 2,3-DPG remains somewhat controversial. Increased levels of 2,3-DPG were also associated with increases in maximal oxygen consumption (VO2 max)[4],[5],[6],[7] In addition, phosphorus salts are also known to buffer lactate which is produced with the anaerobic breakdown of carbohydrates (CHOs). It is appreciated that fasting serum phosphorus is minimally affected by phosphorus intake, but postprandial serum is highly affected by phosphorus ingestion.[8] Phosphorus supplementation is known to increase postprandial intracellular glucose uptake and liver glycogen synthesis[1] may suggest that it can postpone exercise-induced fatigue.[8]

Human endurance performance is a key measure to assess human health and exercise performance.[9],[10] The efficacy of nutritional interventions on exercise performance and fatigue are commonly assessed through two laboratory-based tests: time to exhaustion (TTE) and time trial (TT).[11],[12] TT tests focus on examining performance of a given exercise task, usually by completing set amount of work or distance as quickly as possible; TTE tests focus on the capacity for exercise, requiring individuals to exercise until the point of volitional exhaustion.[13] The latter is arguably more generalizable to different populations, such as recreational exercises, athletes, and military personnel where the capacity for the working muscles to sustain external forces over long periods is of importance.[14] Some studies examined the effect of phosphorus supplementation on TT exercise and high-intensity interval exercise to simulate elite cycling competition. For example, phosphate supplementation did not affect TT among athletes,[15] but there were mixed results when the phosphorus loading period was 6 days. This raises the question whether phosphorus supplement is a preparatory chronic supplement or effective as an acute supplement.[16]

There was an improvement in high-intensity interval exercise and TT in day 1 and 4 after a loading period of 6 days.[15] In a study with elite cyclists, sodium phosphate in a dose of 50 mg/kg of fat-free mass per day for 6 days was ingested, and control group received 4 g of glucose in same doses. The experimental group increased maximal oxygen uptake, maximal minute ventilation, as well as oxygen pulse, and had a decrease in resting heart rate.[5] In another study, 1 g of sodium phosphate, compared with lactose placebo and control trials, was provided to trained male cyclists four times a day for 6 days prior to performing a 16.1 km (10 mile) cycling TT. Power output was greater after sodium phosphate loading than the control and placebo trials, and time to complete the 16.1 km was shorter than placebo, but not the control trial. Heart rate, minute ventilation, respiratory exchange ratio (RER), and blood lactate concentration were not affected by sodium phosphate loading, but there was a tendency of increased VO2.[3] Thus, it has not been confirmed yet whether phosphorus has to be ingested in a chronic or an acute manner.

A phosphorus-induced meal was able to improve insulin sensitivity. This is associated with increased uptake of phosphorus by peripheral tissues (e.g., liver and muscle). The increased peripheral uptake of phosphorus is likely to be used for the phosphorylation of metabolites as well as supporting glycogen and protein synthesis.[8] Therefore, the failure of phosphorus to support performance may relate in part for possible utilization for anabolic processes (protein synthesis) rather than energy production to support performance. Our hypothesis is that the ergogenic effect of phosphorus is related to its postprandial or acute effect.

The role of phosphorus on nutritional responses such as nutrient preferences, appetite sensation, and food intake might be different between rest and exercise conditions. Phosphorus supplementation increases diet-induced thermogenesis and decreases food intake. Obeid et al. found that the addition of 500 mg phosphorus to different preloads caused a substantial reduction in subsequent energy intake (27%–33%), including a significant decrease in sucrose intake.[17] Bassil and Obeid observed that phosphorus has an additional effect on energy metabolism through the enhancement of energy expenditure and/or diet-induced thermogenesis.[18] Obeid et al. conducted several studies on the effects of phosphorus preloads on ad libitum glucose tolerance and energy intake at subsequent meals, which would have applications in weight loss and diabetes treatment.[8],[19] However, it is not clear whether phosphorus intake would affect postprandial exercise-induced energy expenditure of active and athletic young adults, which is important in nutrition monitoring in different sports. Effects of 6 days of sodium phosphate (50 mg/kg of fat-free mass per day) on appetite, energy intake, and aerobic capacity were investigated in trained individuals. There was no difference between phosphate and placebo-ingested meal in appetite and energy intake, but unexpectedly, there was no difference in peak oxygen uptake (VO2peak) between conditions which may have affected the outcomes.[15] There is a lack of studies investigating nutritional intake after exercise and phosphorus intake.

The effect of phosphorus supplementation on exercise capacity is far from clear and this may be partially due to the time of phosphorus intake. In most studies, phosphorus was given for few days, but was not ingested on the day of testing. The fact that a phosphorus-induced meal may improve postprandial ATP and glycogen synthesis, it cannot be excluded that pre-event phosphorus intake would affect performance. The aim of this study was to examine the acute effect of phosphorus intake in the form of potassium phosphate supplement after exercise on subsequent exercise responses and food intake.

  Methods Top

Participant characteristics

Nine moderately active men who engaged in regular aerobic training between 2 and 5 h a week participated in the study (mean ± standard deviation, age 22 ± 3 years, body mass index 22.3 ± 3.0 kg/m2, HRrest69 ± 7 beats/min, and VO2peak48.5 ± 6.3 ml/kg/min). The criterion of selection was to be engaged in aerobic exercise of more than 120 min/week. Exclusion criteria included metabolic disorders such as diabetes, renal, and endocrinological diseases. Procedures were explained both verbally and in writing. Participants provided written informed consent before commencing the experiment, which included a lay language of the benefits and risk of participation, and the content of consent form was institutionally approved by the Internal Review Board, King Saud University.

Study procedure

The study used a placebo-controlled, blinded, randomized, cross-over experimental design. Participants were advised to maintain their normal diet and to avoid intense exercise on the day before each experimental visit with placebo and potassium phosphate testing. The study included three visits to the laboratory of the Department of Exercise Physiology, King Saud University, after an overnight fast of at least 8 h. The study protocol was approved by the Institute of Review Board, College of Medicine at King Saud University (IRB No. E-16-1935).

Visit 1: Exercise intensity determination

Height and weight were measured, and a graded treadmill exercise test was performed. Participants started the graded exercise test at 6 km/h for 3 min, and speed was increased by 1 km/h in each 3-min incremental stage until participants reached 85% of age-predicted HRmax. After a 10-min rest, participants resumed running at the speed of the last stage at an inclination of 3.5° for 3 min, and inclination was increased by 2.5° in each subsequent 3-min stage until volitional exhaustion.[20] Hans-Rudolph mask and a Polar heart rate chest strap were worn. Expired air was automatically collected and analyzed every 30 s throughout the test using Parvo Medics Analyzer (TrueOne® 2400, Metabolic Measurement System, Parvo Medics Inc., USA), to determine VO2 max at the point of VO2 plateau or 3 secondary markers including ± 10 beats of maximal heart rate, RER ≥1.12, and RPE ≥18. Anaerobic threshold (AT) was determined at the point of excess CO2 production, using the scatterplots of O2 and CO2.

Visit 2 and 3: Repeated time to exhaustion exercise trials

Participants were tested with potassium phosphate or placebo in random order within 2 weeks and performed in each visit two TTE tests (session 1 and 2) interspersed by 3 h recovery. The TTE has previously been examined and the protocol used a speed equivalent to 70% VO2 max until the point of volitional exhaustion, which was reduced to 4.4 km/hr for 2 min intervals. The procedure was repeated for a second time and only on the third occasion when participants did not reach volitional exhaustion. Fatigue accepted and TTE recorded when participants indicated they could no longer sustain the prescribed exercise intensity.[13] In our study, participants started the exercise test with standard walking at a speed of 5 km/h, for 5 min, followed by running at the speed that elicited AT. When participants could not sustain the running speed at AT, the speed was reduced to 4.4 km/h for 2 min after which they resumed the running speed at AT until voluntary exhaustion. The time of total running at AT was recorded. Expired air was collected and analyzed throughout the exercise tests. CHO and fat oxidation were estimated for 10-min intervals.[21]

A total of 5 placebo or potassium phosphate (Potassium Phosphate Tabs/Potassium Phosphate Placebo Tabs, Nutra Science TCC Company, NY, USA) tablets were labeled by green and red color known by a colleague who are not of the authorships and assistants and were administered after the first time-to-exhaustion exercise on each day. One tablet (containing 100 mg of phosphorus in the form of potassium phosphate or placebo) was ingested every 30 min during the 3-h recovery, which was stemmed from our previous publication.[17] This was ingested with a soluble glucose drink (1.2 g of glucose in 10 ml of water × body weight), and flavor (28 g), and was provided every 30 min during the 3-h recovery.[13]

Subjective appetite sensations including hunger, satisfaction, desire to eat, and fullness were measured using a paper-based 100-mm anchored visual analog scale pre and post each time-to-exhaustion run. Delta scoring data of each exercise test were calculated to indicate participants' responses.[22]

Immediately after the completion of the second time-to-exhaustion run, participants had access to two pizzas with preferred selection of three options, cheese, vegetarian, and pepperoni. All pizzas had the same weight of paste, which was 170 g and 540 kcal/100 g. All pizzas had the same basal ingredients, and the additional amount of cheese and peperoni was manipulated. Participants could consume as they preferred and food intake was recorded.[23]

Statistical analysis

The data were checked for normality, and Kolmogorov–Smirnov test was insignificant, and also skewness and kurtosis value <1. Levene's test was also performed to check for the homogeneity between variables and its P values were not significant (P > 0.05). Physiological variables, duration of exercise tests, and postexercise food intake and appetite sensations were analyzed using univariate ANOVA with interaction of exercise order and conditions. The same was performed for physiological variables with the inclusion of the duration of session (time) in the model as a covariate. The level of significance was ≤0.05.

  Results Top

Time-to-exhaustion running was performed at the intensity of AT, which was determined at 67 ± 3% VO2peak, VO2 at 32.3 ± 4.5 ml/kg/min, and speed at 10.1 ± 1.1 km/h. Following 3-h recovery, the time-to-exhaustion was reduced by ~ 5% in the placebo condition and ~ 37% in the potassium phosphate condition compared to the time-to-exhaustion of the first run that day [Table 1]. However, there was a 27% difference in the duration of the first time-to-exhaustion run between the two conditions (P < 0.01). Coefficient of variation was 48% in the first exercise bout in both conditions and was 32% and 15% in placebo and potassium phosphate condition, respectively. The overall responses of HR (169 ± 1 and 173 ± 2 beats/min) and RPE (17 ± 1 and 17 ± 1) were not different for the second time-to-exhaustion run in placebo and potassium phosphate conditions, respectively [Table 1]. Further, there were no interactions of conditions (placebo and potassium phosphate) and time-to-exhaustion runs (1st and 2nd) on RER, whole-body fat oxidation, and CHO oxidation rates, and the interaction effect on VO2 tended to be significant (F = 3.97, P = 0.06).
Table 1: Physiological observations, rate of perceived exertion and performance time for placebo and potassium phosphate conditions during repeated bouts of running to exhaustion at anaerobic threshold

Click here to view

As shown in [Table 2], including time to the model (session order (1st and 2nd) × exercise condition (placebo and potassium phosphate) × time (serial data)) did not explain changes in VO2. The interactions of session order × exercise condition on RER and fat oxidation were significant (P = 0.02 and 0.03), which was not influenced by the inclusion of time. On the other hand, the interactions of session order × exercise condition on CHO oxidation were significant (P < 0.01), but the inclusion of time to the interaction factors revealed a significant effect on CHO oxidation (P = 0.03).
Table 2: Interactions of study factors (session order, exercise session, time) on substrate oxidation

Click here to view

[Figure 1] shows fat oxidation during the 1st and 2nd time-to-exhaustion running in placebo and potassium phosphate conditions, and data present the first 40 min only. [Figure 2] shows the comparison between placebo and potassium phosphate in delta values for post- and preappetite sensations, including hunger, satisfactory, fullness, and desire to eat, and there were no significant differences in all appetite variables. In addition, the differences in sweet and salt preferences between placebo and potassium phosphate conditions (△sweet = −0.3 ± 6.0 mm and 18.0 ± 9.5 mm, P > 0.05) and (△salt = 9.6 ± 11.5 mm and −14.1 ± 10.6 mm, P > 0.05) were not significant. Moreover, there was no difference in energy intake between potassium phosphate and placebo conditions for ad libitum food intake (t = 0.22, P = 0.83).
Figure 1: Rate of fat oxidation during placebo (dotted) and potassium phosphate (solid) at 1st (triangle) and 2nd (square) exercise bout. Data are shown as mean ± standard error of mean

Click here to view
Figure 2: Comparison between delta appetite sensations at placebo (lined) and potassium phosphate (solid black) exercise session. Data are shown as mean ± standard error of mean

Click here to view

  Discussion Top

Phosphate increases buffering capacity and 2,3-DPG which increases O2 dissociation into muscles and increases phosphate availability for ATP synthesis.[3] Thus, phosphate may be considered an ergogenic aid although it does not have the accumulated evidence such as caffeine, nitrate, beta-alanine, and bicarbonate.[16] Potassium phosphate dosing in the present study involved an acute intake of 500 mg after exhaustive exercise in preparation for subsequent exhaustive exercise, but no effects on exercise time and substrate oxidation were observed. Burke suggested that there are some supplements which are appropriate for acute loading on the same day of competition, whereas other supplements require several days to weeks for chronic loading to be effective such as creatine and beta-alanine.[16] The most robust dosing protocol for phosphate is a loading period for 3–6 days of 3–5 g/fat-free body weight a day as sodium phosphate, which was effective in repeated high-intensity bouts of cycling, and may be effective in endurance events and team sports that include intermittent high-intensity activities.[24] From our observations, it seems that the acute preexercise intake of 500 mg of potassium phosphate did not affect time-to-exhaustion exercise. However, it cannot be excluded that phosphate needs to be taken for several days to be effective.[5],[15],[24]

While several studies examined the effect of phosphate during repeated high-intensity exercise, the present study used TTE, which was designed to examine the ability of phosphate to resynthesize glycogen after glycogen lowering. TTE tends to be used to examine exercise capacity, and TT is preferable to examine exercise performance.[12] The intensity of TTE is not consistent among studies, and the present study used the individual AT, which is an appropriate method to increase the sensitivity of the test considering individual variations. Whereas Jeukendrup et al.[25] observed large variations in TTE compared with TT, some recent studies observed better sensitivity of TTE than what older studies reported,[11] and a recent study concluded that TTE is a reliable test to examine exercise capacity and the coefficient of variance was 5.4%.[13] Although the present study implemented a cross-over design with similar testing procedures (e.g., encouragement), variations in the time-to-exhaustion in the first bout occurred, which likely is due to insufficient familiarization rather than reliability of TTE, particularly among 3 outliers out of 9 participants. Repeated practice of TT before supplement intake is common to reach <1% variation in order to increase the reliability of the test.[26] Inadequate familiarization of TTE before commencing the exercise sessions with placebo and potassium phosphate was an issue in the present study and is highly recommended for future work.

As shown in [Table 2], the variations in time-to-exhaustion of the first bout did not affect the time-to-exhaustion of the second bout 3 h later, neither did it affect VO2 and fat oxidation, but it significantly affected exercise-induced CHO oxidation. The time-to-exhaustion of the 2nd bout in the placebo condition was longer than in the potassium phosphate condition, and exercise-induced CHO oxidation was greater in the potassium phosphate condition. Thus, the participants in the potassium phosphate condition likely experienced further glycogen lowering than in placebo condition, which might increase the reliance on CHO. Hinckson and Hopkins suggested a shift from aerobic to anaerobic energy pathways with increased fatigue at the end of TTE.[27] Therefore, the effect of phosphorus intake on the rate of CHO oxidation cannot be excluded because phosphorus is known to increase postprandial intracellular glucose uptake.[8] However, the increase of CHO oxidation with potassium phosphate intake did not seem to be associated with delaying fatigue in the second bout of exhaustive exercise. In the second bout, fat oxidation during placebo and potassium phosphate conditions were similar and both greater than bout 1. It should be noted that the exercise intensity in the present study was set at individual AT and appropriate to examine fat oxidation, but potassium phosphate intake was ineffective.[28]

Appetite sensations revealed a slightly higher fullness and satisfactory and less hunger with potassium phosphate intake, but were not statistically significant, and food intake was not influenced by potassium phosphate intake. On the other hand, there is evidence of the effect of phosphorus on diet induced thermogenesis and decreased energy intake including sucrose intake.[8],[17],[18],[19] Thus, the present study suggested that the effect of potassium phosphate on appetite and energy intake in rest is not present after exhaustive exercise, either because of the different energy demands or due to decreased synergistic effect of acute potassium phosphate intake during exercise. For example, the preference for sweet increased after exercise with potassium phosphate intake in the present study, which might be a taste response to the increase in exercise-induced CHO oxidation. It was reported that the digestion of CHO modulates rat's preference of CHO tastes and appetite.[29] There is evidence that CHO mouth rinsing can activate the contralateral primary sensorimotor cortex to a greater extent than matched taste placebo, suggesting that CHO activate the reward regions in the limbic system.[30] Another study also suggested that CHO activates brain regions that is related to reward and motor control can improve exercise performance, and there may be unidentified oral receptors of CHO independent of those for sweetness.[31] This is important because specific conditions including timing, doses, exercise modality, and the combination with other organic aids are expected to play a role in the effectiveness of supplements.[32] For example, a dose of 50 mg/kg of fat-free mass of sodium phosphate per day for 6 days did not affect appetite and energy intake in trained individuals.[15] This dose of phosphate intake led to faster sprint time compared with beetroot juice and placebo, and combination of phosphate and beetroot juice tended to be faster than all other trials.[33] However, the same protocol did not improve sprint time compared with and in combination with caffeine.[34] The acute dose of 500 mg of potassium phosphate did not affect exercise-induced appetite sensations and food intake, which might be diminished due to the greater impact of exercise demands.

The present study was unique in that it used a recent robust study design of repeated TTE to examine the effect of potassium phosphate intake, whereas previous studies examined TT and intermittent exercise.[13] We examined an acute dose that is known to affect diet-induced thermogenesis and food intake in rest.[8] A limitation of the present study was the absence of a familiarization session for the time-to-exhaustion running and the level of fitness of the study participants. Future studies are recommended to increase the dose up to 1000 mg. We also do not know whether capsulated intake of potassium phosphate as was done in the present study would differ from intake of a powder in solution. In conclusion, an acute potassium phosphate intake after exhaustive exercise did not affect subsequent performance of exhaustive exercise, substrate oxidation, or food intake. Future studies are suggested to reexamine acute effect of potassium phosphate, with increasing the dose and including sufficient familiarization sessions.


The authors thank Mr. Maad Dafterdar, the general coordinator, and all research assistants and participants. The authors also thank the Deanship of Scientific Research and RSSU at King Saud University for their technical support and American University of Beirut for their collaboration.

Financial support and sponsorship

This study received a grant from the Research Centre of College of Sport Science and Physical Activity, Deanship of Scientific Research at King Saud University.

Conflicts of interest

There are no conflicts of interest.

  References Top

Mattar LE, Mattar MA, Batal M, Mouneimne Y, Obeid OA. Stimulation of postprandialin vivo glycogenesis and lipogenesis of rats fed high fructose diet with varied phosphate content. Nutr Res 2010;30:151-5.  Back to cited text no. 1
Wensheng X, Tran TL, Finegood DT, Van De Werve G. Dietary Pi deprivation in rats affects liver CAMP, glycogen, key steps of gluconeogenesis and glucose production. Biochem J 2000;352:227-32.  Back to cited text no. 2
Folland JP, Stern R, Brickley G. Sodium phosphate loading improves laboratory cycling time-trial performance in trained cyclists. J Sci Med Sport 2008;11:464-8.  Back to cited text no. 3
Cade R, Conte M, Zauner C, Mars D, Peterson J, Lunne D, et al. Effects of phosphate loading on 2,3-diphosphoglycerate and maximal oxygen uptake. Med Sci Sports Exerc 1984;16:263-8.  Back to cited text no. 4
Czuba M, Zajac A, Poprzecki S, Cholewa J, Woska S. Effects of sodium phosphate loading on aerobic power and capacity in off road cyclists. J Sports Sci Med 2009;8:591.  Back to cited text no. 5
Kreider R, Miller G, Williams M, Somma C, Nasser T. Effects of phosphate loading on oxygen uptake, ventilatory anaerobic threshold, and run performance. Med Sci Sports Exerc 1990;22:250-6.  Back to cited text no. 6
Stewart I, McNaughton L, Davies P, Tristram S. Phosphate loading and the effects on VO2 max in trained cyclists. Res Q Exerc Sport 1990;61:80-4.  Back to cited text no. 7
Khattab M, Abi-Rashed C, Ghattas H, Hlais S, Obeid O. Phosphorus ingestion improves oral glucose tolerance of healthy male subjects: A crossover experiment. Nutr J 2015;14:112.  Back to cited text no. 8
Basset FA, Boulay MR. Specificity of treadmill and cycle ergometer tests in triathletes, runners and cyclists. Eur J Appl Physiol 2000;81:214-21.  Back to cited text no. 9
Imboden MT, Kaminsky LA, Peterman JE, Hutzler HL, Whaley MH, Fleenor BS, et al. Cardiorespiratory fitness normalized to fat-free mass and mortality risk. Med Sci Sports Exerc 2020. [Ahead of Print].  Back to cited text no. 10
Currell K, Jeukendrup AE. Validity, reliability and sensitivity of measures of sporting performance. Sports Med 2008;38:297-316.  Back to cited text no. 11
Laursen PB, Francis GT, Abbiss CR, Newton MJ, Nosaka K. Reliability of time-to-exhaustion versus time-trial running tests in runners. Med Sci Sports Exerc 2007;39:1374-9.  Back to cited text no. 12
Alghannam AF, Jedrzejewski D, Tweddle M, Gribble H, Bilzon J, Betts JA. Reliability of time to exhaustion treadmill running as a measure of human endurance capacity. Int J Sports Med 2016;37:219-23.  Back to cited text no. 13
Alghannam AF, Tsintzas K, Thompson D, Bilzon J, Betts JA. Exploring mechanisms of fatigue during repeated exercise and the dose dependent effects of carbohydrate and protein ingestion: Study protocol for a randomised controlled trial. Trials 2014;15:95.  Back to cited text no. 14
West JS, Ayton T, Wallman KE, Guelfi KJ. The effect of 6 days of sodium phosphate supplementation on appetite, energy intake, and aerobic capacity in trained men and women. Int J Sport Nutr Exerc Metab 2012;22:422-9.  Back to cited text no. 15
Burke LM. Practical issues in evidence-based use of performance supplements: Supplement interactions, repeated use and individual responses. Sports Med 2017;47:79-100.  Back to cited text no. 16
Obeid O, Dimachkie S, Hlais S. Increased phosphorus content of preload suppresses ad libitum energy intake at subsequent meal. Int J Obesity 2010;34:1446-8.  Back to cited text no. 17
Bassil M, Obeid O. Phosphorus supplementation recovers the blunted diet induced thermogenesis in overweight and obese subjects. FASEB J 2015;29:LB372.  Back to cited text no. 18
Obeid OA. Low phosphorus status might contribute to the onset of obesity. Obes Rev 2013;14:659-64.  Back to cited text no. 19
Taylor H, Buskirk E, Henschel A. Maximal oxygen intake as an objective measure of cardio-respiratory performance. J Applied Physiol 1955;8:73-80.  Back to cited text no. 20
Frayn KN. Calculation of substrate oxidation ratesin vivo from gaseous exchange. J Appl Physiol Respir Environ Exerc Physiol 1983;55:628-34.  Back to cited text no. 21
Stubbs R, Hughes D, Johnstone A, Rowley E, Reid C, Elia M, et al. The use of visual analogue scales to assess motivation to eat in human subjects: A review of their reliability and validity with an evaluation of new hand-held computerized systems for temporal tracking of appetite ratings. Br J Nutr 2000;84:405-15.  Back to cited text no. 22
Alkahtani S, Eisa A, Kannas J, Shamlan G. Effect of acute high-intensity interval cycling while viewing a virtual natural scene on mood and eating behavior in men: A randomized pilot trial. Clin Nutr Exp 2019;28:92-101.  Back to cited text no. 23
Buck CL, Wallman KE, Dawson B, Guelfi KJ. Sodium phosphate as an ergogenic aid. Sports Med 2013;43:425-35.  Back to cited text no. 24
Jeukendrup A, Saris WH, Brouns F, Kester AD. A new validated endurance performance test. Med Sci Sports Exerc 1996;28:266-70.  Back to cited text no. 25
Lansley KE, Winyard PG, Bailey SJ, Vanhatalo A, Wilkerson DP, Blackwell JR, et al. Acute dietary nitrate supplementation improves cycling time trial performance. Med Sci Sports Exerc 2011;43:1125-31.  Back to cited text no. 26
Hinckson EA, Hopkins WG. Reliability of time to exhaustion analyzed with critical-power and log-log modeling. Med Sci Sports Exerc 2005;37:696-701.  Back to cited text no. 27
Jeukendrup AE, Wallis GA. Measurement of substrate oxidation during exercise by means of gas exchange measurements. Int J Sports Med 2005;26 Suppl 1:S28-37.  Back to cited text no. 28
Sclafani A. Carbohydrate taste, appetite, and obesity: An overview. Neurosci Biobehav Rev 1987;11:131-53.  Back to cited text no. 29
Turner CE, Byblow WD, Stinear CM, Gant N. Carbohydrate in the mouth enhances activation of brain circuitry involved in motor performance and sensory perception. Appetite 2014;80:212-9.  Back to cited text no. 30
Chambers E, Bridge M, Jones D. Carbohydrate sensing in the human mouth: Effects on exercise performance and brain activity. J Physiol 2009;587:1779-94.  Back to cited text no. 31
Jeukendrup AE. Nutrition for endurance sports: Marathon, triathlon, and road cycling. J Sports Sci 2011;29 Suppl 1:S91-9.  Back to cited text no. 32
Buck CL, Henry T, Guelfi K, Dawson B, McNaughton LR, Wallman K. Effects of sodium phosphate and beetroot juice supplementation on repeated-sprint ability in females. Eur J Applied Physiol 2015;115:2205-13.  Back to cited text no. 33
Kopec BJ, Dawson BT, Buck C, Wallman KE. Effects of sodium phosphate and caffeine ingestion on repeated-sprint ability in male athletes. J Sci Med Sport 2016;19:272-6.  Back to cited text no. 34


  [Figure 1], [Figure 2]

  [Table 1], [Table 2]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded63    
    Comments [Add]    

Recommend this journal