The Power Of The Earth's Natural Energy

1. A plant begins its life as a seed.

2. The soil gives the seed the warmth to start growing.

3. A sprouting seed needs water to help it grow into a healthy plant. 

4. A plant also needs energy from the sun to grow big and strong. This is heat and light energy.

5. The power of the Earth’s natural energy has helped the plant to grow.

6. Wind energy helps to spread a plant’s seeds. This starts the life cycle of a plant all over again.



Earth's energy budget accounts for the energy Earth receives from the Sun. Much of this energy is lost when the earth re-radiates it back into outer space, and the rest of the energy is distributed throughout the five components of Earth's climate system. This system is made up of earth's water, ice, atmosphere, rocky crust, and all living things.

Quantifying changes in these amounts is required to accurately model the Earth's climate.

Incoming, top-of-atmosphere (TOA) shortwave flux radiation, shows energy received from the sun (Jan 26–27, 2012).

Outgoing, longwave flux radiation at the top-of-atmosphere (Jan 26–27, 2012). Heat energy radiated from Earth (in watts per square metre) is shown in shades of yellow, red, blue and white. The brightest-yellow areas are the hottest and are emitting the most energy out to space, while the dark blue areas and the bright white clouds are much colder, emitting the least energy.

Received radiation is unevenly distributed over the planet, because the Sun heats equatorial regions more than polar regions. Energy is absorbed by the atmosphere, hydrosphere, and lithosphere, and, in a process informally described as Earth's heat engine, the solar heating is redistributed through evaporation of surface water, convection, rainfall, winds, and ocean circulation. When the incoming solar energy is balanced by an equal flow of heat to space, the Earth is said to be in radiative equilibrium and under that condition, global temperatures will be stable.


Disturbances of Earth's radiative equilibrium, such as an increase of greenhouse gases, will change global temperatures in response. However, Earth's energy balance and heat fluxes depend on many factors, such as atmospheric composition (mainly aerosols and greenhouse gases), the albedo (reflectivity) of surface properties, cloud cover and vegetation and land use patterns. Changes in surface temperature due to Earth's energy budget do not occur instantaneously, due to the inertia of the oceans and the cryosphere. The net heat flux is buffered primarily by becoming part of the ocean's heat content, until a new equilibrium state is established between radiative forcings and the climate response.

Energy budget


A Sankey diagram illustrating the Earth's energy budget described in this section — line thickness is linearly proportional to relative amount of energy.

In spite of the enormous transfers of energy into and from the Earth, it maintains a constant temperature because, as a whole, there is no net gain or loss: Earth receives the same amount of energy via insolation (all forms of electromagnetic radiation) as it emits via atmospheric and terrestrial radiation (shifted to longer electromagnetic wavelengths) to space.

To quantify Earth's heat budget or heat balance, let the insolation received at the top of the atmosphere be 100 units, as shown in the accompanying illustration. Called the albedo of Earth, around 35 units are reflected back to space: 27 from the top of clouds, 2 from snow and ice-covered areas, and 6 by other parts of the atmosphere. The 65 remaining units are absorbed: 14 within the atmosphere and 51 by the Earth’s surface. These 51 units are radiated to space in the form of terrestrial radiation: 17 directly radiated to space and 34 absorbed by the atmosphere (19 through latent heat of condensation, 9 via convection and turbulence, and 6 directly absorbed). The 48 units absorbed by the atmosphere (34 units from terrestrial radiation and 14 from insolation) are finally radiated back to space. These 65 units (17 from the ground and 48 from the atmosphere) balance the 65 units absorbed from the sun; thereby demonstrating no net gain of energy by the Earth.

Incoming radiant energy (shortwave)

The total amount of energy received per second at the top of Earth's atmosphere (TOA) is measured in watts and is given by the solar constant times the cross-sectional area of the Earth. Because the surface area of a sphere is four times the cross-sectional surface area of a sphere (i.e. the area of a circle), the average TOA flux is one quarter of the solar constant and so is approximately 340 W/m². Since the absorption varies with location as well as with diurnal, seasonal and annual variations, the numbers quoted are long-term averages, typically averaged from multiple satellite measurements.

Of the ~340 W/m² of solar radiation received by the Earth, an average of ~77 W/m² is reflected back to space by clouds and the atmosphere and ~23 W/m² is reflected by the surface albedo, leaving ~240 W/m² of solar energy input to the Earth's energy budget. This gives the earth a mean net albedo of 0.29.

Earth's internal heat and other small effects

The geothermal heat flux from the Earth's interior is estimated to be 47 terawatts.[9] This comes to 0.087 watt/square metre, which represents only 0.027% of Earth's total energy budget at the surface, which is dominated by 173,000 terawatts of incoming solar radiation.

Other minor sources of energy are usually ignored in these calculations, including accretion of interplanetary dust and solar wind, light from stars other than the Sun and the thermal radiation from space. Earlier, Joseph Fourier had claimed that deep space radiation was significant in a paper often cited as the first on the greenhouse effect.

Longwave radiation

Longwave radiation is usually defined as outgoing infrared energy leaving the planet. However, the atmosphere absorbs parts initially, or cloud cover can reflect radiation. Generally, heat energy is transported between the planet's surface layers (land and ocean) to the atmosphere, transported via evapotranspiration and latent heat fluxes or conduction/convection processes. Ultimately, energy is radiated in the form of longwave infrared radiation back into space. Evapotranspiration is the process by which water is transferred from the land to the atmosphere by evaporation from the soil and other surfaces and by transpiration from plants.

Recent satellite observations indicate additional precipitation, which is sustained by increased energy leaving the surface through evaporation (the latent heat flux), offsetting increases in longwave flux to the surface.

Earth's energy imbalance

If the incoming energy flux is not equal to the outgoing energy flux, the result is an energy imbalance, that amounts to net heat added to or lost by the planet (if the incoming flux is larger or smaller than the outgoing respectively). Earth's energy imbalance measurements provided by Argo floats have detected an accumulation of ocean heat content (OHC). The estimated imbalance was measured during a deep solar minimum of 2005-2010 to be 0.58 ± 0.15 W/m². Later research estimated the surface energy imbalance to be 0.60 ± 0.17 W/m².

Measurement
Several satellites indirectly measure the energy absorbed and radiated by Earth and by inference the energy imbalance. The NASA Earth Radiation Budget Experiment (ERBE) project involves three such satellites: the Earth Radiation Budget Satellite (ERBS), launched October 1984; NOAA-9, launched December 1984; and NOAA-10, launched September 1986.

Today NASA's satellite instruments, provided by CERES, part of the NASA's Earth Observing System (EOS), are designed to measure both solar-reflected and Earth-emitted radiation.


Natural greenhouse effect

The major atmospheric gases (oxygen and nitrogen) are transparent to incoming sunlight but are also transparent to outgoing thermal (infrared) radiation. However, water vapor, carbon dioxide, methane and other trace gases are opaque to many wavelengths of thermal radiation. The Earth's surface radiates the net equivalent of 17 percent of the incoming solar energy in the form of thermal infrared. However, the amount that directly escapes to space is only about 12 percent of incoming solar energy. The remaining fraction, 5 to 6 percent, is absorbed by the atmosphere by greenhouse gas molecules.







Atmospheric gases only absorb some wavelengths of energy but are transparent to others. The absorption patterns of water vapor (blue peaks) and carbon dioxide (pink peaks) overlap in some wavelengths. Carbon dioxide is not as strong a greenhouse gas as water vapor, but it absorbs energy in wavelengths (12–15 micrometres) that water vapor does not, partially closing the "window" through which heat radiated by the surface would normally escape to space. (Illustration NASA, Robert Rohde)

When greenhouse gas molecules absorb thermal infrared energy, their temperature rises. Those gases then radiate an increased amount of thermal infrared energy in all directions. Heat radiated upward continues to encounter greenhouse gas molecules; those molecules also absorb the heat, and their temperature rises and the amount of heat they radiate increases. The atmosphere thins with altitude, and at roughly 5–6 kilometres, the concentration of greenhouse gases in the overlying atmosphere is so thin that heat can escape to space.

Because greenhouse gas molecules radiate infrared energy in all directions, some of it spreads downward and ultimately returns to the Earth's surface, where it is absorbed. The Earth's surface temperature is thus higher than it would be if it were heated only by direct solar heating. This supplemental heating is the natural greenhouse effect. It is as if the Earth is covered by a blanket that allows high frequency radiation (sunlight) to enter, but slows the rate at which the low frequency infrared radiant energy emitted by the Earth leaves.

Climate sensitivity

A change in the incident radiated portion of the energy budget is referred to as a radiative forcing.

Climate sensitivity is the steady state change in the equilibrium temperature as a result of changes in the energy budget.


Climate forcings and global warming

Climate forcings are changes that cause temperatures to rise or fall, disrupting the energy balance. Natural climate forcings include changes in the Sun's brightness, Milankovitch cycles (small variations in the shape of Earth's orbit and its axis of rotation that occur over thousands of years) and volcanic eruptions that inject light-reflecting particles as high as the stratosphere. Man-made forcings include particle pollution (aerosols) that absorb and reflect incoming sunlight; deforestation, which changes how the surface reflects and absorbs sunlight; and the rising concentration of atmospheric carbon dioxide and other greenhouse gases, which decreases the rate at which heat is radiated to space.

A forcing can trigger feedbacks that intensify (positive feedback) or weaken (negative feedback) the original forcing. For example, loss of ice at the poles, which makes them less reflective, causes greater absorption of energy and so increases the rate at which the ice melts, is an example of a positive feedback.

The observed planetary energy imbalance during the recent solar minimum shows that solar forcing of climate, although natural and significant, is overwhelmed by anthropogenic climate forcing.


In 2012, NASA scientists reported that to stop global warming atmospheric CO2 content would have to be reduced to 350 ppm or less, assuming all other climate forcings were fixed. The impact of anthropogenic aerosols has not been quantified, but individual aerosol types are thought to have substantial heating and cooling effects.

Rapid IV versus Oral Rehydration: Responses to Subsequent Exercise Heat Stress

ABSTRACT
KENEFICK, R. W., K. M. O`MOORE, N. V. MAHOOD, and J. W. CASTELLANI. Rapid IV versus Oral Rehydration: Responses to
Subsequent Exercise Heat Stress. Med. Sci. Sports Exerc., Vol. 38, No. 12, pp. 2125–2131, 2006. Purpose: This study sought to
determine the effect of rapid intravenous (IV) versus oral (ORAL) rehydration immediately after dehydration, on cardiovascular,
thermoregulatory, and perceptual responses during subsequent exercise in the heat. Methods: Eight males (21.4 +/- 0.7 yr; 176.2 +/-1.6 cm; 75.2 +/- 3.7 kg; 63.7 +/- 3.6 mLIkgj1
Iminj1 V˙ O2max, 9.0 +/- 1.7% fat) participated in three randomized trials. Each trial consisted
of a 75-min dehydration phase (36-C; 42.5% rh, 47 +/- 0.9% V˙ O2max) where subjects lost 1.7 L (IV and no-fluid (NF) trials) to 1.8 L of
fluid (ORAL trial). In the heat, fluid lost was matched with 0.45% saline in 20 min by either IV or ORAL rehydration; no fluid was
given in the NF trial. Subjects then performed a heat-tolerance test (HTT; 37.0-C, 45% rh, treadmill speed of 2.4 mIs
j1
, 2.3% grade)
for 75 min or until exhaustion (Tre of 39.5-C). During the HTT, thermal and thirst sensations, RPE, rectal temperature (Tre), heart rate
(HR), and mean weighted skin temperature (Tsk) were measured. Results: Plasma volume in the IV treatment was greater (P G 0.05)
after rehydration compared with ORAL and NF. However, during the HTT there were no overall differences (P > 0.05) in HR, Tre,
Tsk, RPE, thermal sensations, or HTT time (ORAL, 71 +/- 8 min; IV, 73 +/- 5 min; NF, 39 +/- 29 min) between the ORAL and IV
treatments. Sensations of thirst were lower (P G 0.05) in ORAL compared with IV and NF, likely because of oropharyngeal stimuli.
Conclusions: Despite a more rapid restoration of plasma volume, IV rehydration was not advantageous over ORAL rehydration in
regards to physiological strain, heat tolerance, RPE, or thermal sensations. Key Words: THERMOREGULATION, HYDRATION,
EXERCISE-INDUCED DEHYDRATION, FLUID REPLACEMENT

Dehydration resulting from physical exercise in the
heat, followed by a brief period of rehydration and
the continuation of activity or competition, is a
common scenario for athletes, laborers, and military
personnel. Restoration of body fluids through the use of
rapid intravenous (IV) rehydration is typical in clinical
settings to restore body fluid losses. More recently, the use
of rapid IV rehydration has been used in these work–
rehydration–work scenarios to quickly restore body fluid
loss from thermoregulatory sweating. In the latter scenario,
it is assumed IV rehydration provides a more rapid
restoration of body fluid by circumventing factors such as
gastric emptying and intestinal absorption associated with
oral rehydration. However, to our knowledge, no investigation
has studied rapid IV rehydration in a work–

rehydration–subsequent work scenario comparable with those commonly employed in athletic or occupational
situations.

Studies specifically comparing IV with oral rehydration
have reported similar attenuation of cardiovascular and
thermoregulatory strain and RPE during subsequent exercise
in the heat, with a similar effect on exercise performance
(2,3,12,17). However, these studies have either
employed exercise in the heat to induce hypohydration on
the day before experimental testing (2,12), have used
rehydration protocols lasting more than 100 min (3,12,17),
have not matched oral and IV fluid temperatures (2), or
have not matched volume restoration with sweat losses
incurred during exercise (2,3,11,12,17). To date, no study
has employed a protocol that would represent a true event
scenario where an individual would work, exercise or
compete in the heat and become hypohydrated, rehydrate
over a short period of time, and again exercise in a hot
environment.

The purpose of this study was to determine the effects of
rapid (G 30 min) IV versus oral rehydration immediately
after dehydration, on cardiovascular, thermoregulatory, and
perceptual responses during subsequent exercise in the
heat. We hypothesized that IV rehydration would result in
a more rapid restoration of plasma volume and body fluid
compartments than would oral rehydration, thus allowing
for greater heat tolerance and reduced physiological and
perceptual strain (Table 1). 


METHODS

Subjects
Eight non–heat-acclimated men volunteered to participate
in this investigation. Physical characteristics (mean +/-
SEM) were age, 21.4 +/- 0.7 yr; height, 176.2 +/- 1.6 cm;
weight, 75.2 +/- 3.7 kg; VO2max, 63.7 +/- 3.6 mL.kg-1
.min-1
;
% body fat, 9.0 +/- 1.7%; and BMI, 24.3 +/- 0.9 kgImj2
.
Subjects completed a written informed consent document
and a medical history questionnaire after being informed of
the purpose of the experiment and possible risks. The
committee on the use of human subjects in research at the
university approved all procedures.
Preliminary Testing
Height was measured using a stadiometer (Detecto,
Webb City, MO), and body mass was determined using
an electronic scale (General GE510, Cape Coral, FL). A
modified Costill–Fox (5) treadmill test was used to
determine V˙ O2max (mLIkg–1.min–1). Body density was
estimated using skinfold calipers (Harpenden, Ann Arbor,
MI) and procedures and equations as described by Jackson
et al. (9). Percent body fat was then calculated using the
Siri equation (21).

Experimental Testing

Experimental design. The subjects performed three
experimental trials in a randomized order, separated by at
least 1 wk. Experimental testing involved two experimental
treatments and a control trial, each consisting of three
stages: a dehydration phase (Dh), a rehydration phase (Rh),
and a heat-tolerance test (HTT). Only the rehydration
phase differed among trials. Rh treatments were randomly
assigned and consisted of intravenous rehydration (IV;
0.45% saline), oral rehydration (ORAL; 0.45% saline), and
no fluid (NF). We chose 0.45% saline because it can safely
be administered as an IV fluid and is commonly used as an
IV fluid in clinical, athletic, and occupational settings.
Subjects were given detailed instructions on the recording
of food and fluid intake and were then asked to maintain a
3-d dietary record during the 3 d before each experimental
trial. These food diaries were then analyzed for energy,
carbohydrate, fat, protein, sodium, and potassium content
(Food Processor II, ESHA Research, Salem, OR). There
were no differences (P > 0.05) among the experimental
treatments in total kilocalories, carbohydrate, protein, fat,
sodium, and potassium intake. Subjects were asked to

refrain from any recreational or exercise training for 24 h
before experimental testing. They were also instructed to
drink 450 mL of water the night before testing, to drink
450 mL of water the morning of testing, and to abstain
from eating for 12 h before each experimental treatment.
On arrival at the laboratory (0700–0800 h), subjects
provided a urine sample for determination of urine specific
gravity (USG; Spartan Refractometer, model A 300 CL,
Japan). A USG of 1.023 T 0.006 (1) was used to verify that
the subject was adequately hydrated prior to each trial.
Subjects were then fitted with a monitor (UNIQ heartwatch,
Computer Instrument Corp., Hempstead, NY) to
measure heart rate (HR), and a flexible thermistor (Yellow
Springs Instruments, series 401, Yellow Springs, OH) was
inserted 10 cm beyond the external anal sphincter to monitor
rectal temperature (Tre). A Teflon catheter was then inserted
into a superficial forearm vein, and a male luer adapter
(model 5877, Abbott Hospital, Inc., Chicago, IL) was
inserted into the catheter port for acquisition of subsequent
blood samples. The catheter port and male luer adapter were
kept patent with heparin lock flush solution. In the IV trials
only, a second cannula was placed in the opposite arm to
administer the IV fluid during the Rh phase. The subject
then entered the environmental chamber (Harris Environmental
Systems, Andover, MA), which was set at 36.9 T
0.1-C and 42.2 T 1.5% rh, and stood quietly for a 20-min
equilibration period. A 10-mL blood sample (baseline) was
taken, and subjects then consumed a standard breakfast of
one bagel, one banana, and 240–350 mL (depending on
body weight) of fruit juice. This meal was served approximately
45–60 min before the start of the dehydration phase
of the experiment and contained a total of 426 kcal, 1.7 g of
fat, 98.5 g of carbohydrate, 9.7 g of protein, 395 mg of
sodium, and 1180 mg of potassium.

Dehydration
Subjects were weighed immediately before the start of
exercise in the Dh phase. During the Dh phase, the subjects
walked or ran for 75 min at 50% V˙ O2max (mean treadmill
speed of 2.4 mIs
j1
, 2.3% grade) in the environmental
chamber. Airflow (6.1 mIs
j1
), generated by two fans, was
directed at the subject to enhance evaporative sweat loss.
Oxygen consumption (V˙ O2) was measured every 8 min via
a pnuemotach (Hans Rudolph, Kansas City, MO) attached
to a metabolic cart (SensorMedics, Inc., Yorba Linda, CA)
to ensure the proper exercise intensity. The mean %V˙ O2max
for the three dehydration trials ranged from 47.0 to 49.1%.
In addition, every 8 min, Tre and HR were monitored for
safety. HR that exceeded 180 bpm for 5 min resulted in
termination of testing, as did a rectal temperature of more
than 39.5-C. Body weight was measured every 25 min. At
the end of the Dh period, a 10-mL blood sample was drawn
and analyzed.

Rehydration
After the Dh phase, subjects remained in the environmental

chamber standing for the 30-min rehydration period at 37-C. The first 5 min of the rehydration period consisted
of taking a 10-mL blood sample and measuring body
weight. This body weight was subtracted from the body
weight measured immediately before starting exercise in the
Dh phase, to determine the amount of fluid lost. Because
subjects did not urinate during the Dh phase of the experiment,
there was no need to correct weight loss for urine
volume. During the next 20 min of rehydration, the entire
amount of fluid lost during dehydration was matched with
0.45% saline (15-C) either by IV Rh (1710.0 T 0.1 mL) or by
ORAL Rh (1790.0 T 0.2 mL), or, alternately, no fluid was
given (NF). For the ORAL trial, the saline solution was
mixed with a nonnutritive sweetener (1 gI225 mLj1 of
0.45% saline; Kool Aid) to improve palatability. Servings
were administered in equal amounts every 4 min during
the 20-min period. The composition of ORAL was 79.0 T
1.0 mEq Na+
ILj1
, 1.00 T 0.01 mEq K+
ILj1
, 2.5 T 0.1 mEq
Ca++ILj1
, and 146.0 T 1.0 mOsmIkgj1 of water. During
IV, Rh constant pressure was maintained on the saline bag
to ensure a rapid flow rate (~85.5 mLIminj1
). During the
last 5 min of the rehydration period, body weight was again
measured, and after rehydration (pre-HTT), 10-mL blood
samples were drawn, skin thermistors were placed on each
subject, and subjects urinated if needed. Skin thermistors
(Yellow Springs Instruments, series 401, Yellow Springs,
OH) were placed on the upper arm, chest, upper thigh, and
calf of each subject`s left side for measurement of mean
weighted skin temperatures (Tsk) (16).

HTT

Immediately after the 30-min rehydration period, the
subjects performed a 75-min HTT at the same workload
(50% V˙ O2max) of the Dh phase of the trial. Environmental
conditions in the chamber were 37.0 T 0.1-C, 42.2 T 1.5%
rh. Measures of Tsk, thirst (thirst) (7), and thermal
(thermal) (8) sensations, ratings of perceived exertion
(RPE), V˙ O2, hemoglobin (Hb), hematocrit (Hct), and Posm
were measured at pre-HTT, minute 25, and post-HTT. As
in the Dh phase, HR and Tre were monitored every 8 min
for safety. HR exceeding 180 bpm for 5 min, Tre of more
than 39.5-C, signs or symptoms of heat intolerance, or
volitional exhaustion resulted in termination of the HTT.

Analysis of blood samples. Ten-milliliter blood
measures were analyzed at five time points: pre-Dh, postDh,
pre-HTT, 25 min, and post-HTT. Blood was
transferred to tubes containing lithium heparin, and
samples of whole blood were taken for analysis of Hb
and Hct. Hct was determined in triplicate by the microcapillary
technique after centrifugation for 4 min. Values
were not corrected for trapped plasma. Hb was determined
in triplicate by the cyanomethemoglobin method (Kit 525,
Sigma Chemical, Inc. St. Louis, MO). Percent change in
plasma volume (%APV) was calculated using the equation
of Dill and Costill (6) from appropriate Hct and Hb values.
All %APV values were calculated using postdehydration
as the initial time point. Plasma volume was calculated
using pre-Dh body mass (18), and changes in plasma volume were calculated using %$PV values. After
centrifugation, plasma was separated and analyzed for
Posm. Posm (mOsmIkgj1 H2O) was measured in triplicate,
via freezing-point depression (MicroOsmometer model
3MO, Advanced Instruments, Needham Heights, MA).

Statistical analysis. An analysis of variance (time
condition) with repeated measures was used to compare
differences among the trials. A Newman–Keuls post hoc
analysis was used to determine significant differences
within and between conditions. A power analysis selecting
conventional alpha (P G 0.05) and beta (0.20) values
determined that eight subjects would be sufficient to detect
a 10% improvement in physical performance during the
HTT. All data are presented as means T SE.

RESULTS

Dehydration
Pre-Dh USG were not different (P > 0.05) among
treatments and the NF trial, averaging 1.010 T 0.002.
During IV treatment, pre-Dh Posm was greater (P G 0.05)
than during the ORAL treatment. However, by post-Dh
(pre-HTT), Posm values were elevated (P G 0.05) above
pre-Dh values but were not different (P > 0.05) among the
treatments and the NF trial. There were no differences (P >
0.05) in exercise intensity (%V˙ O2max) during the Dh phase
among the treatments and the NF trial. The percent of preDh
body weight lost in the Dh protocol was similar (P >
0.05) among the treatments and the NF trial.

Rehydration
There were no differences (P > 0.05) in the Rh time,
total time post-Dh to pre-HTT, or volume of fluid given in
the IV and ORAL trials. Urine volume was greater (P G
0.05) post-Rh in the IV treatment (505 T 36 mL) compared
with the NF (385 T 35 mL) and ORAL (312 T 48 mL)
treatments. Post-Rh percent weight loss (compared with the
pre-Dh body weight) was similar between the ORAL (0.4 T
0.3%) and IV (0.26 T 0.2%) treatments but was lower (P G
0.05) than NF (2.8 T 0.5%).

HTT

Exercise time and intensity. The mean exercise time
for the HTT was greater (P G 0.05) in the ORAL (70.6 T
8.2 min) and IV (72.6 T 4.7 min) treatments compared with
NF (38.7 T 28.9 min). Exercise intensity (relative or
%V˙ O2max) throughout the HTT was not different (P >
0.05) among the three treatments. The average oxygen
uptake and average %V˙ O2max during the HTT for all three
treatments was 31.5 T 6.0 mLIkgj1
Iminj1 and 49.2 T 4.3%,
respectively. Percent body weight lost during the HTT was
2.28 T 0.4% in the ORAL trial, 2.55 T 0.6% in the IV trial,
and 1.3 T 0.7% in the NF trial. During the NF trial, one
subject was unable to start the HTT because of syncope
and symptoms of heat exhaustion. This subject`s data are
included in the analysis of the Dh and Rh phases of the 
experiment; however, in the analysis of the HTT, N = 7 for
the NF trial, compared with N = 8 for the ORAL and IV
treatments. During the NF trial, three subjects were able to
complete the 75-min HTT, and four completed 50 min of
the HTT. Of the four subjects who stopped at 50 min of the
HTT during the NF trial, one was stopped because of a
core temperature of 39.5-C, and the other three stopped
because of volitional exhaustion. Only one subject stopped
at 50 min of the HTT in the ORAL and IV treatments
because of volitional exhaustion.
Osmolality and hemodynamic responses. Pre-HTT
(post-Dh) Posm values were significantly (P G 0.05)
elevated from pre-Dh values but were not different (P >
0.05) among treatments and the NF trial, averaging 302.7 T
2.3 mOsmIkgj1 H2O. In addition, at 25 min and post-HTT,
Posm were not different (P > 0.05) among the treatments
and the NF trial. The mean of the NF trial and treatments
at 25 min was 302.0 T 1.7 mOsmIkgj1 H2O and 306.7 T
1.7 mOsmIkgj1 H2O post-HTT. Pre-HTT plasma volume
in the IV treatment was greater (P G 0.05) compared with
the corresponding plasma-volume value in the ORAL
treatment and the NF trial. At 25 min of the HTT and
post-HTT, plasma volume was not different (P > 0.05)
among the NF trial and the treatments (Fig. 1).

[FIGURE 1:VPlasma volume as a function of time after rehydration
and during the HTT. Values are means T SE; ORAL and IV, N = 8;
NF, N = 7. Pre-Dh is considered the reference point. # Significant
difference (P G 0.05) from corresponding ORAL and NF values. Mean
exercise time for the HTT was 38.7 T 28.9 min in the NF, 70.6 T
8.2 min in the ORAL, and 72.6 T 4.7 min in the IV trials.]

Cardiovascular and thermoregulatory responses.
In the NF trial, measures of HR at the pre-HTT and 25-min
time points were greater (P G 0.05) than corresponding
ORAL and IV values. HR was not different (P > 0.05)
among the treatments and the NF trial at the post-HTT time
point (Fig. 2A). Tre was lower (P G 0.05) pre-HTT in the
IV treatment compared with the ORAL and NF trials.
However, Tre was not different (P > 0.05) among the
treatments or in the NF trial at the 25-min and post-HTT
time points (Fig. 2B). Tsk was not different (P > 0.05)
among the treatments or in the NF trial at the pre-HTT and
25-min time points. However, Tsk in the NF trial was greater
(P G 0.05) post-HTT compared with the ORAL and IV

treatments (Fig. 2C).
[FIGURE 2VHeart rate (A), Tre (B), and Tsk (C) as functions of time
after rehydration and during the HTT. Values are means T SE; ORAL
and IV, N = 8; NF, N = 7. * Significant difference (P G 0.05) from
corresponding ORAL and IV values; # significant difference (P G 0.05)
from corresponding ORAL and NF values. Mean exercise time for the
HTT was 38.7 T 28.9 min in the NF, 70.6 T 8.2 min in the ORAL, and
72.6 T 4.7 min in the IV trials.]

Perceptual responses. The NF trial pre-HTT and
25-min thermal sensations were greater (P G 0.05)
compared with ORAL and IV. However, thermal sensations
were not different (P > 0.05) among the treatments
and the NF trial at the 25-min and post-HTT time points
(Fig. 3A). RPE was not different (P > 0.05) among the
treatments and the NF trial at the pre-HTT, 25-min, and
post-HTT time points (Fig. 3B). Sensations of thirst were
different (P G 0.05) among the treatments and in the NF

trial at the pre-HTT and 25-min time points. However, both 
the IV and NF post-HTT sensations of thirst were greater
(P G 0.05) compared with ORAL (Fig. 3C).

[FIGURE 3--Thermal sensations (A), RPE (B), and sensations of thirst
(C) as functions of time after rehydration and during the HTT. Values
are means T SE; ORAL and IV, N = 8; NF, N = 7. * Significant
difference (P G 0.05) from corresponding ORAL and IV values; # significant difference (P G 0.05) from corresponding ORAL and NF
values; a significant difference (P G 0.05) from corresponding IV and
NF values; a significant difference (P G 0.05) from corresponding
ORAL values. Mean exercise time for the HTT was 38.7 T 28.9 min in
the NF, 70.6 +/- 8.2 min in the ORAL, and 72.6 +/- 4.7 min in the IV
trials.]

DISCUSSION
The purpose of this study was to determine the effects of
rapid IV versus oral rehydration immediately after a
dehydration-exercise bout on heat tolerance and cardiovascular,
thermoregulatory, and perceptual responses during
subsequent exercise in the heat. This is the first study we
are aware of that has attempted to match fluid loss with
fluid restoration and fluid temperature within a limited

period of time (~20 min) for rehydration. Theoretically, IV 
rehydration should cause a more rapid plasma-volume
restoration compared with oral rehydration. Thus, we
hypothesized that the more readily available fluid after IV
rehydration would allow for better thermoregulation, less
cardiovascular and perceptual strain, and greater heat
tolerance. The findings of the present study demonstrate
that plasma volume was restored more rapidly and that Tre
was significantly reduced immediately after IV rehydration.
Despite this response, there were no significant
improvements in exercise duration or reductions in cardiovascular
and thermoregulatory strain, thermal sensations,
and ratings of perceived exertion between oral and
IV rehydration during subsequent exercise in the heat.
Sensations of thirst, however, were significantly lower in
the ORAL treatment compared with the IV and NF
treatments.
The dehydration protocol used in the present study
induced a modest (2.8%) decrease in body mass and
resulted in a significant decrease in plasma volume. We
chose this work–rehydration–work scenario because it
would represent an exercise duration and intensity similar
to a variety of actual sporting events or work settings.
Despite the modest fluid losses seen here, we believe that
the results of this study would be similar if a larger fluid
loss occurred from any combination of greater exercise
duration, intensity, or environmental heat stress, provided
that the fluid loss was matched with fluid intake during
rehydration.

Although rehydration duration and fluid volume were not
different between the IV and ORAL treatments, plasma
volume in the IV treatment was restored above pre-Dh
values and was higher at the beginning of subsequent
exercise. Studies that have used IV versus oral saline
rehydration after a dehydration protocol have reported
varied changes in plasma volume. Castellani et al. (3)
reported no difference in the percent change in plasma
volume between oral and IV rehydration with 0.45% saline
after a 75-min rest period and during exercise in the
heat. Differences between the present study and that of
Castellani et al. (3) are likely attributable to their measurement
of the percent change in plasma volume after 75 min
of rest. We previously (11) reported a more rapid plasmavolume
restoration with 0.9 and 0.45% IV rehydration
compared with 0.45% oral rehydration. In that study, by
35 min of rest after rehydration, there were no differences
in plasma-volume restoration between the IV and oral
treatments. Maresh et al. (12) and Casa et al. (2), using
0.45% IV rehydration, reported plasma-volume restoration
rates similar to those seen the present study, despite using
a protocol that induced dehydration on the day before
experimental testing and rehydration back to j2% of
initial body weight. By 5 min of exercise in the heat in
those studies (2,12), and by 25 min of exercise in the
present study, there were no differences in the changes in
plasma volume between the IV or oral treatments.
It is likely that the fluid that directly enters the
vasculature with IV rehydration is distributed to all body

fluid compartments and does not stay in the vasculature 
specifically. Hypohydration induced by exercise heat stress
has been shown to cause a loss of fluid not only from
plasma but also from interstitial and intracellular fluid
volumes (4,20). General calculations predict that the
administration of 1.8 L of 0.45% saline, as in the present
study, could be expected to increase plasma volume after
equilibration by approximately 144 mL, extracellular fluid
by 1056 mL, and intracellular fluid by 600 mL (13). Based
on previous findings (2,11) and those of the present study,
equilibration of IV fluid occurs by 35 min of rest and
within 5–25 min of exercise. Thus, rapidly infusing
intravenous saline for 20 min is no more advantageous in
plasma-volume restoration than drinking the same solution
by 25 min of exercise.
Both IV and ORAL rehydration occurred in a 37-C
environment; however, immediately after rehydration, Tre
was 1.0-C lower in the IV treatment compared with ORAL
and NF. This difference in Tre after IV rehydration may be
attributed to a number of possible causes. First, it is possible
that the large volume of 15-C fluid rapidly entering the
vasculature may have contributed to the lower Tre observed.
Using predictive equations by Kay and Marino (10), the
addition of 1.7 L of fluid at 15-C would theoretically lower
body core temperature by 0.7-C. It is also possible that
during the rehydration period, the more rapid restoration of
plasma volume may have reestablished skin blood flow and
sweating responses, permitting greater thermoregulation.
Either of these factors individually, or in combination, may
account for the 1-C decrease in Tre immediately after IV
rehydration. However, it is important to note that by 25 min
of exercise during the HTT, Tre levels were not different
among any of the treatments.
During the HTT, skin temperatures were not different
between the two rehydration treatments, and they were
significantly lower than for NF at the end of the HTT
(Fig. 2C). In addition, the percent body-weight loss between
the ORAL and IV treatments was not different, indicating
that during exercise, total sweat losses were not different.
Castellani et al. (3) also did not observe differences in sweat
rate, Tre, or Tsk between oral and IV rehydration during
exercise in a hot environment. However, Casa et al. (2) observed
lower Tre and Tsk during exercise in the heat after oral
rehydration compared with IV rehydration. Differences in Tre
and Tsk between our study and that of Casa et al. (2) may be
attributable to the different temperatures of the oral and IV
fluids administered. In their study, the oral fluid and IV fluid
were 10-C and 22-, respectively. Accumulation of approximately
1.35 L at 10-C in the stomach could create a heat sink
where a large volume of cooler fluid would pull heat from the
body. Theoretical calculations using their mean data at time
point zero predict a 0.6-C change in core temperature, which
is the approximate difference between actual control and
drink rectal temperatures at that time point (10).
One especially unique finding in the present study is
that regarding sensations of thirst. A strong relationship
between Posm and thirst sensation has been well defined
(15,22). However, gargling with tap water has been shown

to reduce sensations of thirst despite elevated Posm (19).
In the present study, Posm was significantly elevated after
dehydration and was not different among the rehydration
and NF treatments throughout the HTT. Despite this lack of
difference in Posm, sensations of thirst remained lower in
the ORAL trial compared with the IV and NF treatments
throughout the HTT. Maresh et al. (12) also did not observe
differences in Posm with oral and IV rehydration using halfnormal
saline, reporting lower sensations of thirst with oral
rehydration. Riebe et al. (17) reported greater Posm with no
rehydration compared with IV and oral rehydration with
0.45% saline. They also reported significantly lower
sensations of thirst with oral rehydration compared with
IV, and they attributed this finding to stimulating oropharyngeal
receptors. The findings of these previous studies
(12,17,19) and those of the present study suggest that thirst
sensation might be influenced to a greater extent by reflexive
oropharyngeal mechanisms than Posm.
There is the possibility that a learned response regarding
thirst sensation could exist, such as feeling thirsty after
exercising in a hot environment, which could have altered the
reports of thirst perception. However, in order not to
influence reports of thirst sensation, subjects in the present
study were only informed of the general purpose of study, and
not of the specific research question regarding thirst
perception. Further, while a learned response might have
contributed to subjects` reports of thirst sensation, within
each experimental treatment and the NF trial, subjects`
reports were consistent (Fig. 3C). In the present study,
neither thermal sensations nor RPE were different between
the rehydration treatments throughout the HTT (Fig. 3A
and B). Maresh et al. (12) suggest that thermal sensations
are an important cue to perception of exertion during
exercise in the heat. They reported lower thermal sensations
and ratings of perceived exertion at 15 min of exercise in the
heat with oral rehydration. In addition, they reported a
strong correlation (r = 0.83) between Tsk and thermal
sensations with oral rehydration. In particular, Tsk has been
reported to account for much of the variance in RPE in a hot
environment (14). However, in the present study there was a
weak correlation (r = 0.33) between Tsk and thermal
sensations for all of the treatments. Differences between
the findings of Maresh et al. (12) and those of the present
study may be attributable to the different temperatures of
fluids used in oral (10-C) and IV (22-C) rehydration.
Because we did not observe any overall differences in Tre
and Tsk between the rehydration treatments, it stands to
reason that IV and oral rehydration equally attenuated
thermal sensations and perceived exertion compared with
NF. Our findings are in agreement with Riebe et al. (17),
who, despite reporting strong correlations between Tsk and
overall RPE, did not observe significant differences in Tsk or
RPE between oral and IV rehydration treatments.
We had hypothesized that the greater plasma-volume
restoration associated with IV rehydration would allow for
a greater ability to thermoregulate, less cardiovascular and
perceptual strain, and a greater ability to perform exercise
in the heat. Similar to core and skin temperature, there

were no differences in cardiovascular strain between the 
ORAL and IV rehydration treatments, as HR during the
HTT were not different (Fig. 2A). Casa et al. (2) also did
not report differences in HR with rehydration back to j2%
body weight using either 0.45% oral and IV rehydration
during exercise at 74% V˙ O2peak, in 37-C. Given that we
did not observe differences in thermoregulatory, cardiovascular,
or perceptual strain between the two rehydration
treatments, it is not surprising that exercise time in the heat
was not different. Studies that have examined the effect of
IV versus oral rehydration on exercise time (2,3,11,12)
have also not reported any significant differences. Thus,
the initial increase in plasma volume after IV rehydration
does not seem to offer any cardiovascular, thermoregulatory,
or perceptual benefit that would ultimately contribute
to a greater ability to exercise in a hot environment.
These data suggest that preexercise plasma-volume values
are not important, as long as fluid is resorted and available
during subsequent exercise.

CONCLUSION
The findings of the present study demonstrate that

although plasma volume was restored more rapidly by IV
rehydration, there were no overall differences in heat
tolerance, cardiovascular and thermoregulatory responses,
thermal sensations, or ratings of perceived exertion between
oral and IV rehydration. IV rehydration was responsible
for a 1-C lower core temperature immediately after
rehydration. However, by 25 min of exercise, there was no
difference in core temperature among any of the treatments.
Compared with IV and NF, sensations of thirst were
significantly lower during oral rehydration, likely because
of oropharyngeal stimuli. Despite a more rapid restoration
ofplasma volume, IV rehydration did not offer any performance
advantage over drinking or in relieving cardiovascular,
thermoregulatory, or perceptual strain during
moderate exercise in the heat.
The authors thank the subjects who donated their time and effort
to participate in this study. The authors also thank Melissa Hazzard
and Sandra Zurcher for their technical support. Lastly, the authors
thank Michael N. Sawka for his editorial assistance.
The views, opinions, and/or findings in this report are those of
the authors and should not be construed as official Department of
the Army position, policy, or decision unless so designated by other
official designation. All experiments were carried out in accordance

to state and federal guidelines.


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Impermeable Facts of Human Skin Penetration and Absorption

“Nanu-Nanu!”

Who would have guessed that Mork from Ork would have inspired such an interpretation of the scientific study of skin absorption?  While researching the topic, it is easy for the reader to be convinced that skin absorbs whatever it touches—just like the Mork & Mindy character and his habit of drinking liquids by sticking his finger in a glass.  While this would certainly make wine tasting parties fascinating to observe, the suggestion that skin absorbs whatever is applied to it is an irresponsible exaggeration of the facts.

Skin is a fascinatingly complicated system, designed to protect against external harms (bacteria, UV radiation, etc,) regulate body heat, and manage nutrient levels and water loss.  Many a chemical is frustrated at the inability to penetrate this protective barrier—but some substances can penetrate the skin and absorb into our bodies.  Whether these chemicals cause harm depends on the amounts that penetrates and are absorbed, and how the chemical acts once it is inside the body.  Does it throw a party and set up shop, or do the bouncers of your body show the chemical the door?

Is That a Horny Layer, or are you Just Happy to See Me?

Skin is comprised of three primary regions, the outer epidermis and middle dermis and the lowest area, the hypodermis.  The epidermis consists of multiple strata (i.e. layers,) with its superficial the most crucial in prevention of skin penetration.  This outermost layer of the epidermis, the stratum corneum (flattened cells, also known as the horny layer,) serves as your body’s primary defense—and it’s dang good at its job.

The stratum corneum, thick with dead skin cells (mostly keratin) and various waxy substances, acts as a wall of protection from external moisture, chemicals, UV radiation and is your foremost guard against the bacterial world.  As these dead bits fall of, or exfoliated from the body, the lower layers of skin replenish the surface with additional keratin.

Meet the lower layers!  The stratum lucidum is the translucent, second layer of the epidermis in thicker areas, which sits atop the stratum granulosum.  The granulosum is responsible for keratin protein production.  The stratum spinosum and the lowest layer, the stratum basale, new cells are produced and pushed upwards.  Collectively, these layers form the flexible shield against your environment…and that’s the way they all became the Brady Bunch!

Let’s take a closer look (A microscopic glance!) at what substances penetrate skin, and which actually absorb into our bodies!

Penetrating and Absorbing the Facts

Not everything we touch or put on our skin is fully absorbed into our bodies.  Otherwise, we’d quite literally be drinking our own bathwater (or swell up like sponges during a swim!)  Wait, you say!  Doesn’t some water get into our skin to cause it to wrinkle?  Remember that dead skin cells fill the stratum corneum—these cells are Jiffy Popped as they soak up the water, which is what causes the “wrinkled” look.

Now, if water were to penetrate the surface layer of skin, we could end up with unpleasant fluid blisters, or as mentioned above never swim in a public pool again.  Luckily, this isn’t a risk, and after a short while, the water evaporates and our stratum corneum returns to normal.

The distinction between penetration and absorption is a crucial one where measurement of chemical risk is concerned.

>Skin Penetration represents the amount of a topically chemical that exists between the top layer (stratum corneum) and the bottom layer (stratum basale.)  During penetration, the body does not yet absorb the chemical, and it cannot affect the body systems.

>Skin Absorption occurs when the topically applied chemical breaks the skin barrier to reach the bloodstream.  Whether this chemical becomes a risk is determined by what occurs after absorption.  You body can filter (The bouncers!) out the chemical via bodily fluids, or bio-accumulation (build up) occurs.
Many variables affect the speed (or probability) of penetration and absorption.  First, the composition of the chemical to which skin is exposed.  The area of skin that is exposed (thinner-skinned areas are more susceptible to penetration and thicker skin is less) and the condition of the skin are all significant factors.
There are a number of scare statistics running about on the internet that state our bodies absorb a tremendous amount of topically applied chemicals.  A few interesting ones that I’ve come across:

>Our skin absorbs ____ number of pounds of cosmetics each year

>Our skin absorbs a high percentage of everything we apply to it each day/year/etc.

>A chemical was found in human urine, therefore we are absorbing and slowly marching towards oblivion by said chemical

>If skin didn’t absorb everything we apply to it, then why does a medication patch delivery work so well?

Such statements are exaggerations, distortions, or a little of both where skin penetration and absorption are concerned.  The composition of the chemical exposed to skin determines its possibility of entering the skin—primarily the molecule size and solubility of the chemical.

For the purpose of this paper, we’ll limit our scope to chemicals in skin care and cosmetics (you’re welcome!)

The design of cosmetic and skin care formulas is to benefit the outer layer of skin— absorption into the body would waste the effects of these products.  Antioxidants in skin care won’t do their job if they don’t stay in the layers of skin—it is challenging enough to develop a formula that enables an ingredient to penetrate the surface layer!  The majority of cosmetics are not soluble in skin (i.e. lipid, or fat-soluble) and are too large in molecule to fit through the stratum corneum.  Precisely because of these qualities, some skin care formulas require specially developed “penetration enhancers” to deliver ingredients like vitamin C or retinol.

This includes transdermal medication patches!  These types of medicine require formulation specifically for this purpose, requiring chemical engineering to create a molecule that is soluble in skin, and small enough to penetrate and absorb into the body.

Much controversy has arisen over the ingredients in skin care products that inadvertently absorb into our body and the possible risk to our health.  Does absorption equal harm?

Everything is a Risk, but Not Necessarily a Harm

Absorption into the body doesn’t equate to bodily harm.  What happens after a chemical is absorbed makes the distinction!  Our bodies design will filter out molecules and water, disposing of what doesn’t belong by excretion via bodily fluids.  Safety testing for the effect of ingredients that absorb into our bodies:

>Evaluates how (and how long) we are exposed (topical or oral application, etc)

>Composition of the ingredient, (molecule size, solubility, etc)

>How the ingredient behaves after absorption

These are crucial points for research, as a study of how an ingredient reacted when fed to a test subject is somewhat relevant in understanding what happens when you drink your body lotion—but not as relevant in studies that demonstrate topical application.  This is a very, very important point to consider when reading the latest scare report on cosmetics and skin care.  Often, such reports cite research that fed large quantities of a pure substance to arrive at their conclusions—hardly honest use of a reference!

Determining the safety of a chemical in skin absorption is about risk assessment.  The toxicity of an ingredient is in the amount absorbed and accumulated, or “the dose makes the poison.”  The nutrients and substances we depend on for our health can kill us in a large enough amount.  When a chemical penetrates our skin and is absorbed into our bodies, is may be converted into another chemical form, metabolized or accumulate.

At the dose in which a chemical becomes harmful (toxic) is the threshold, less than this amount is safe, and more becomes a danger.  Our body is designed to break down chemicals into other forms that are easily excreted via fluids.  The threshold is the over/under amount of our bodies ability to process a chemical and still keep the body healthy.

Considering this, when you read about the latest scare over a chemical detected in urine, remember what we’ve just discussed!  A chemical eliminated from the system isn’t an indicator of threat to health, but your body working as intended and filtering the substance out.  The faster this process occurs, the less (if any) impact on your health.

Flushing out the Truth

It’s far too easy to present a frightening statistic in a believable manner, which is why it’s important to question the motives of a flashy headline that proclaims death by lipstick/body lotion/etc.  It’s also easy to present distorted research on skin penetration and absorption—as it can be complicated to research to find the truth.  The facts are that very little is capable of penetrating skin, and even less is absorbed into our body.  So the next time you read a headline, judge for yourself what’s true by asking questions and consider the source!