research findings are inconclusive, several wellcontrolled studies support
the theory that phosphate salt supplementation may enhance functional
capacity of the aerobic energy system. The results of these studies indicate
that the improvement in aerobic metabolism is caused by an increase in
erythrocyte 2,3-DPG, which decreases the affinity of hemoglobin for oxygen,
what facilitates the release of oxygen to muscle tissue during exercise
(Cade et al., 1979;
Farber et al., 1984;
Gibby et al., 1978).
Other authors that conducted similar research did not show any changes
in this metabolite after phosphate salt intake (Bredle et al., 1988;
Kreider et al., 1990).
Most of the current research evaluating the ergogenic effects of phosphate
salts refers to the early experiments of Cade et al., 1984.
They reported a significant (p < 0.05) increase in the concentration
of erythrocyte 2,3-DPG (13. 00 vs. 13.92 mg·g Hb-1) in a group
supplemented with phosphate salts. Additionally, a 6 to12% increase in
VO2max was observed for subjects given phosphate salts. Similar
results were reported by Stewart et al., 1990,
who evaluated the effects of sodium phosphate
intake on VO2max, time to volitional exhaustion, the concentration
of 2,3-DPG, and serum inorganic phosphate concentration in 8 well-trained
cyclists. The experimental procedure in this study included sodium phosphate
intake of 3.6 g·day-1 or a placebo over a 3-day period. After
the supplementation protocol, the exercise tests were repeated, and a
7-day rest period was incorporated. Following the 7-day rest period, the
entire procedure was performed once again.
The obtained results showed insignificant changes in resting 2,3-DPG concentration,
yet the post- exercise 2,3-DPG values were significantly (p < 0.05)
higher in the group supplemented with sodium phosphate. Additionally,
a significant (p < 0.01) increase in VO2max was registered
in the subjects that were given phosphate salts.
A similar experiment was conducted by Kreider et al. (1990),
where the effects of phosphate salt intake on VO2max, VO2
at the ventilation threshold, and the 5-mile run time were evaluated.
The results of this experiment showed a 9% increase in VO2max
(73.9 ± 5.0 vs. 80.3 ± 4.0 ml·kg-1·min-1) and a
12 % improvement in VO2VAT (58.0 ± 4.0 vs. 64. 8 ± 2.0 ml·kg-1·min-1)
in subjects supplemented with sodium phosphate. The concentration of 2,3-DPG
was not considered in this research.
On the contrary, research conducted by Bredle et al., 1988
showed no changes in 2, 3-DPG and VO2max in a group of athletes
supplemented with phosphate salts for 4 days, with a dose of 5.7 g·day-1.
Brennan et al. (2001)
documented similar findings to the Bredle study in a group of well-trained
cyclists (VO2max = 60.6 ± 4.4 ml·kg-1·min-1),
who were supplemented with sodium diphosphate (4 g·day-1).
The results of our study are in accordance to those obtained by Cade et
Stewart et al., 1990
and Kreider et al. (1990).
The experiment showed a significant (p < 0.05) increase in VO2max
following sodium triphosphate intake for 6 days, with a dose of 50mg·kgFFM-1·d-1.
Significant (p < 0.05) changes in VO2max were registered
for both absolute and relative values. Further supplementation with phosphate
salts, with a dose of 25mg·kgFFM-1·d-1, over a period
of 21 days, did not increase the level of aerobic power, yet in comparison
to baseline level, the changes in absolute and relative values of VO2max
were significant, respectively.
Our research confirms that changes in VO2max obtained in a
short- term supplementation procedure can be maintained for a longer period
of time by continued intake of phosphate salts in smaller doses. This
protocol also increased the ventilation threshold. VO2max decreased
in the 3rd phase of the research by 1.4%, in comparison to
the second phase of the experiment, yet these values were significantly
higher in relation to baseline values.
A significant improvement in VO2VAT in the group supplemented
with phosphate salts caused a shift in VAT towards much higher loads.
In the 2nd and 3rd phases of the experiment, a 5.4%
increase in PVAT, in comparison to baseline values was registered (280.4
vs. 295W). The intake of sodium triphosphate caused a delay in the drastic
increase of carbon dioxide concentration in the blood (pCO2),
stimulating respiration. The delay in hyperventilation, aimed at the removal
of excess CO2 from the body, indicates a better supply of oxygen
to muscle tissues in the supplemented group.
One of the indexes of tissue oxygen saturation includes oxygen pressure
(pO2) in capilarized blood. According to Dempsey et al., 1971,
an increase in erythrocyte 2,3-DPG is accompanied by a simultaneous rise
in capillary pO2. The changes in rest and post-exercise values
of capillary pO2 were insignificant in the group that was given
sodium phosphate, yet a tendency for an increase in this variable, due
to supplementation, was observed. A similar tendency was registered in
the resting concentration of 2,3-DPG in group S.
The statistical analysis showed a significant relationship between the
resting concentration of 2,3-DPG (2,3-DPGrest) and VO2max.
There were no significant changes in post-exercise concentration of 2,3-DPG
(2,3-DPGmax) and values of delta (∆) 2,3-DPG in group
S, yet a slight decrease in these variables occurred in the second and
third phases of the experiment. The decrease in these variables could
have been caused by a significant (p < 0.05) increase in peak power
output (Pmax) in group S. After 6 days of supplementation (50mg·kgFFM-1·d-1),
a insignificant rise in Pmax occurred, yet the continued intake
of sodium phosphate for 3 weeks (25mg·kgFFM-1·d-1)
caused a significant (p < 0.05) increase in this variable. An increase
in Pmax caused a drop in post-exercise pH, which may have influenced
the concentration of 2,3-DPG (2,3-DPGpost). According to Bard
and Teasdale, 1979,
a decrease in blood pH by 0.010 units causes a simultaneous (4%) drop
in 2,3-DPG concentration.
Additionally, the level of erythrocyte 2,3-DPG can be modified by the
serum concentration of inorganic phosphates (P). This is confirmed in
our research by the significant relationship between the concentration
of inorganic phosphates (P) in blood serum and the level of 2,3-DPGrest
(r = 0.49; p = 0.01). In case of hypophosphatemia, a drop in the concentration
of 2,3-DPG occurs, while under conditions of hyperphosphatemia, the opposite
takes place (Lichtman et al. 1971;
Card and Brain, 1973).
Not all research conducted with phosphate loading confirm this relationship.
Cade et al., 1984,
after 3 days of supplementation with phosphate salts, observed a significant
( p< 0.05) increase in the resting level of serum phosphates, as well
as a rise in the concentration of 2,3-DPG. In a similar experiment, Kreider
et al. (1990)
also registered a significant increase (17%) in resting concentration
of blood serum inorganic phosphates after supplementation, yet changes
in 2,3-DPG were not analyzed. Bredle et al., 1988
also showed a significant increase (35%) in the concentration of blood
serum phosphates after 4 days of supplementation with calcium phosphate,
however, they did not show significant changes in 2,3-DPG, P50,
pH and VO2max. In a research project conducted by Mannix et
with a single intake of calcium phosphate, a significant increase in the
concentration of serum phosphates (13%) and 2,3-DPG (11%) occurred, yet
no changes in VO2max or heart muscle work capacity were registered.
In a more recent experiment, Bremner et al., 2002
showed significant relationships between the concentration of inorganic
phosphates in the blood and erythrocyte phosphate level, as well as the
erythrocyte concentration of phosphates and the level of 2,3-DPG. No relationship
was observed between the concentration of blood serum phosphates and erythrocyte
The applied 6-day supplementation protocol in our research caused a significant
(30%) increase in the concentration of phosphates in blood serum, as well
as a 25% rise in erythrocyte 2,3-DPG. The authors suggest that the increase
in 2,3-DPG is most likely the effect of increased concentration of erythrocyte
In our research project a continuous rise in serum inorganic phosphate
(P) concentration was observed in the group supplemented with sodium phosphate.
During the second phase of research, a significant blood serum (p <
0.05) increase in inorganic phosphates (P) occurred (0.8 ± 0.16 vs. 1.0
± 0.22 mmol·l-1). Continued intake of sodium phosphate in the
third phase of the experiment caused a further increase in this variable,
yet it was insignificant in comparison to the previous phase, however
it was significant (p < 0.05) in relation to initial values. It must
be indicated that the initial concentration of serum inorganic phosphates
(P) in group S equaled 0.8 ± 0.16 mmol·l-1, which indicates
a state of hypophosphatemia, which occurs when serum P concentration falls
below 0.9 mmol·l-1. In athletes, such a state is most often
caused by incomplete recovery from training and competition, or dietary
phosphate deficiency. In the control group, the concentration of P was
in the lower range of daily allowance and equaled (0.95 ± 0.09 mmol·l-1).
On the other hand, a significant relationship detected between the serum
concentration of inorganic phosphates and VO2max, as well as
P and VO2VAT, indicates that the effectiveness of phosphate
loading depends on the initial concentration of P in the blood.
The available data regarding ergogenic benefits of phosphate salts are
predominantly related to short-term supplementation, lasting from 3 to
6 days. The majority of these projects were based on the assumption presented
by Cade et al., 1984,
who suggested that longer supplementation protocols are not justified,
since continued intake of phosphate salts does not further increase the
level of 2,3-DPG, nor does it change VO2max. This phenomenon
could be explained by the hormonal regulation of blood serum concentration
of inorganic phosphates. A key role is played here by the parathyroid
hormone (PTH), which increases the elimination of phosphates through the
kidneys. Long-term intake of phosphate salts causes an increased secretion
of parathyroid hormone, which increases the elimination of phosphates
through urine (Chase and Aurback, 1968).
Our research suggests that the time of phosphate supplementation should
consider the initial concentration of blood serum inorganic phosphates
and changes in this variable throughout the supplementation protocol.
conducted an experiment in which he analyzed the influence of a 1g dose
of phosphate salts on the concentration of blood inorganic phosphate and
calcium, as well as PTH concentration. The results indicated a significant
(p < 0.05) increase in the concentration of phosphates, and no changes
in the level of calcium and PTH.
Silverberg et al., 1986
also showed a significant increase in the concentration of blood inorganic
phosphates, and a lack of change in the level of serum calcium and PTH,
1 hour after a single intake of 1g of sodium phosphate. Continued intake
of phosphate salts for 5 days, in a dose of 2g/d, caused a significant
increase in the concentration of PTH.
Most research (Silverberg et al., 1986;
thus, confirm that a transition state of increased blood concentration
of P does not cause hypocalcaemia, and does not increase the concentration
of PTH. On the other hand, prolonged hyperphosphatemia significantly affects
the blood concentration of these variables. In our research, group S showed
significant changes (p < 0.05) in serum concentration of Ca following
long-term sodium phosphate intake (Table
1). A lack of significant changes in the concentration of Ca following
the first 6 days of supplementation was most likely the effect of a low
blood serum P concentration.
After the 6-day supplementation protocol with tri-sodium phosphate, a
significant increase in VEmax was registered (p < 0.05).
This variable continued to increase during the next 3 weeks of supplementation,
yet the changes were statistically insignificant. When compared to baseline
values, the changes in VEmax, after the long-term phosphate
salt intake were statistically significant (p < 0.05). The increase
in VEmax in group S may be explained by improved function of
the diaphragm. This assumption can be partially confirmed by the research
of Aubier et al., 1985,
where the effects of hypophosphatemia on the function of the diaphragm
in patients (n = 8) with severe respiratory inefficiency were analyzed.
A high relationship (r = 0.73) between blood concentration of phosphates
and transdiaphragmatic pressure was observed. These results indicate that
hypophosphatemia impairs the function of the diaphram.
Several authors indicate an ergogenic effect of phosphate salt intake
on heart efficiency at rest, as well as during exercise. This hypothesis
is based on the fact that hypophosphatemia decreases stroke volume (Fuller
et al., 1978;
O'Connor et al., 1977; Rubin and Naris, 1990).
O'Connor et al., 1977
suggest that the increased contractibility of the heart muscle is caused
by increased concentration of cell ATP, which is low during hypophosphatemia.
Animal research confirmed the data on improved heart work capacity following
phosphate salt intake (Darsee et al., 1978;
Several other research projects, which used sodium or calcium phosphate
intake, showed a significant decrease of cardiac output and stroke volume
during exercise of moderate intensity (Farber et al., 1984;
Lunne et al. 1990;
Moore et al. 1981), and significant improvements in these variables during
endurance exercise with maximal intensity (Kreider, 1992).
Bredle et al., 1988
indicated a significant (p < 0.05) increase in serum inorganic phosphate
concentration and heart function, following 4 days of supplementation
with 176 mmol·day-1 of calcium phosphate. A significant (p
< 0.05) decrease in cardiac output was registered during an endurance
exercise protocol, conducted at 70% of VO2max. There were no
changes in 2,3-DPG and VO2max values, yet a significant (p
< 0.05) increase was observed in arteriovenous oxygen difference, which
suggests a better supply of oxygen to the tissues. This data indicates
that phosphate salt intake may improve the function of the cardio-respiratory
The analysis of heart rate (HR) in our research indicated significant
changes in resting and exercising heart rates in the group of cyclists
supplemented with sodium phosphate. The changes in exercise heart rate
may be explained by increased stroke volume and improved contractibility
of the heart muscle. These assumptions can be confirmed by Kreider et
who showed that sodium phosphate intake significantly improves the functioning
of the heart muscle. Echocardiographic evaluations in a group of cyclists
supplemented with phosphate salts, indicated a significant (4%) increase
in stroke volume during this period of time.
The analysis of results in group S also showed an improvement in oxygen
pulse (O2/HR), which is a non-invasive index of evaluating
work capacity of the cardio-respiratory system; and simultaneously, a
good indicator of physical fitness in endurance sport disciplines.
Other than improving the supply of oxygen to the tissues, phosphate salt
intake may improve the acid-base balance during intensive exercise. Phosphates
are very active in buffering processes and participate in the acid-base
balance of blood plasma, as well as inside the muscle cells. The buffering
capacity of phosphates is rather low in the extracellular fluids, yet
they play a significant role in the intracellular fluids, where the concentration
of phosphates is much higher (Avioli, 1988).
Some authors suggest that the intake of sodium phosphate may increase
the buffering capacity of muscle cells, and may increase work capacity
during exercise of high intensity (Cade et al., 1984;
Kreider, 1992; Miller et al., 1991).
For example, Cade et al., 1984
showed that phosphate salt intake lowered lactate concentration during
exercise of submaximal intensity.
Other research projects indicated a shift of lactate threshold towards
higher loads (Kreider et al. 1990;
1992; Miller et al. 1991).
Similar results were presented by Stewart et al., 1990,
who showed a minor but significant decrease in (p < 0.05) post-exercise
lactate concentration after an endurance exercise protocol, following
3 days of sodium phosphate intake.
The supplementation protocol applied in our research did not confirm the
buffering properties of phosphate salts. The analysis of resting and post-exercise
lactate concentrations, and the level of LT, showed no significant changes
in these variables due to supplementation. There were also no significant
changes in the acid-base variables in the S group. The only significant
(p < 0.05) changes occurred in the resting values of base excess (BErest)
and in the extracellular fluids (BEecfrest) during the third
phase of the experiment.