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Acfa mefoll. Vol. 35, No. 6, pp. 1349-1353, 1987 OOOl-6160/87 $3.00 + 0.

Printed in Great Britain. All rights reserved Copyright 0 1987Pergamon Journals Ltd


B. DERBY’ and M. F. ASHBY’
‘Department of Metallurgy and Science of Materials, University of Oxford, Parks Road,
Oxford OX1 3PH and 2Engineering Department, University of Cambridge,
Trumpington Street, Cambridge CB2 lPZ, England

(Received 10 October 1986)

Abstract-The evolution of primary creep is modelled by the formation of sub-cells in which a pattern
of internal stresses exists. The internal stresses have two components, one a general isotropic impediment
to dislocation movement, the other an elastic back stress leading to kinematic hardening. The stresses are
built up by the polarised accumulation of dislocations and they recover by diffusional relaxation within
the sub-cells. The model differs from others in focussing on the sub-cell size and misorientation as the
important state variables.

Resume-Nous modelisons l’evolution du fluage primaire a partir de la formation de sous-cellules dam

lesquelles existe une repartition don&e de contraintes internes. Les contraintes internes ont deux
composantes: la premiere est un obstacle isotrope au mouvement des dislocations, la seconde est une
contrainte en retour provoquant un durcissement cinematique. Les contraintes proviennent d’une
accumulation rirferentielle des dislocations, et elles se restaurent par relaxation de diffusion a l’interieur
des sous-cellules. Ce modtle differe des autres parce qu’il insiste sur le fait que la taille et la d&orientation
des sous-cellules sont les variables d’ttat importantes.

Zusammenfaasung-Die Entwicklung des prim&en Kriechens wird mit der Bildung von Subzellen
modelliert, in denen ein strukturiertes inneres Spannungsfeld besteht. Die inneren Spannungen haben zwei
Komponenten, eine davon bewirkt eine allgemeine Behinderung der Versetzungsbewegung, die andere
besteht aus einer elastischen Riickspannung, die zu kinematischer Verfestigung fiihrt. Diese Spannungen
werden durch die polarisierte Ansammlung von Versetzungen erzeugt und erholen sich durch Relaxation
tiber Diffusion innerhalb der Subzellen. Das Model1 unterscheidet sich von anderen darin, da13es sich auf
GriiBe und Fehlorientierung der Subzelle als die wichtigen Zustandsvariablen beschrlnkt.

INTRODUCTION of the problem. It leads to a set of differential

equations for creep which resemble those of Ion et al.
Most constitutive equations for primary creep are [1] and provides some additional physical basis for
empirical fits (usually a power-law or an exponential) their treatment.
to the creep curve at constant load and temperature.
They are not based on physical models for the
evolution of the structure and stresses within the
creeping material; and because of this, they cannot Consider a creeping solid with a current cell-size of
describe the development of the creep strain when w and a cell boundary misorientation of 8 (Fig. 1).
stress or temperature vary during the test, or when The cell boundary area per unit volume is then
large changes of either stress or temperature cause a
change of creep mechanism. A, = C,/w (1)
Here we outline a model for dislocation creep in where C, is a geometrical constant (about 3). Creep
which we link the deformation behaviour of the strain results from the motion of a mobile population
microstructure of the dislocation sub-cells and the of dislocations, driven by the applied shear stress u.
stresses in them. The creep rate is determined by the But this motion is impeded by an internal stress,
action of the applied stress on mobile dislocations which we consider to have two components. One, S, ,
which are impeded by internal stresses. We consider is a short range internal stress which must be over-
the internal stress as having two components: one, a come to allow any dislocation motion. We consider
general impediment to all dislocation motion from this to be derived from the microstructure via a
interactions with the microstructure; the other, an characteristic pinning length proportional to the cell
elastic back stress, related to the applied stress, size w, because any motion in a given cell wall is likely
created by the inhomogeneous deformation of the to be unrelated to that in neighbouring cells. This will
sub-ceils. The stresses are built up by the polarised give an upper bound to the internal stress equal to the
accumulation of dislocations, and they recover by Orowan bowing stress, i.e.
diffusional relaxation within sub-cells. The model
differs from others in focussing on the sub-cell size s, =ctGb (2)
and misorientation as the important state-variables W


Fig. 2. A hard cell cannot deform plasticity. To ensure

compatability it shears elastically setting up the back stress
Fig. 1. Dislocations glide across cells, enter walls where they
S,. This shear (and thus S,) can be recovered by diffusion
can climb slowly. 2. A short range internal stress S, = b/w
of matter across the cell which restores it to its original
must be overcome for any movement. 3. A long range back
shape. The mechanism, stress driven diffusion, is analagous
stress S, must also be overcome. This derives from cells
to Coble or NabarreHerring creep.
which suffer less plastic shear than average and thus
contribute an elastic stress opposed to deformation. The
resistance to deformation may come from small size (hence volume, k is Boltzmanns constant, T is the absolute
large S,), higher work-hardening or (perhaps) lack of
temperature and D is a composite diffusion coefficient
for bulk (0,) and boundary (6D,) (that is, cell-wall)
diffusion, approximately
where G is the shear modulus and a < 1. The second
component S, is a long range internal stress which D = D,+w.
derives from the non-uniform deformation of the
inhomogeneous sub-structure. It is an elastic back The evolution of the cell size is calculated as
stress which is created by the necessary deformation follows. When the deformation rate is greater than
of hard regions of the material which suffer less that for which w is the steady-state cell size, the
plastic shear for one of a number of reasons (e.g. internal stress S2 quickly builds up (because R is too
smaller cell size, higher work hardening or lack of small). Then dislocations which break free from one
sources). The increment of strain hardening will cell wall do not cross a cell and join the wall on the
always be in the opposite sense to the applied stress other side because S, (which opposes a) prevents
and hence allows a Bauschinger effect. This is given them. Dislocations halt before reaching the boundary
in differential form by and rearrange to form a new cell wall (Fig. 3). If the
dS, = G (H d& - R dt). mean slip distance is I the increase in stored dis-
location density per increment of strain is
In the simplest case, H is a hardening coefficient
related to the volume fraction of the material which, dp = dclbl. (7)
at any one time, cannot undergo plastic deformation: The increase in cell wall area per unit volume is then
and R is a recovery term.
The terms H and R are calculated as follows. A dA, = b dp/6 = de/l31 (8)
“harder-than-average” cell, embedded in a matrix of
“average-hardness” cells behaves like a non-
deforming inclusion. An increment of plastic shear
strain dc in the matrix produces an increase in
internal stress in the hard cell of
da, x G dc
and the average increase in the long range back stress
dS, o fG dc (4)
wherefis the volume fraction of non-deforming cells;
thus H =J
This internal stress is removed again if diffusion
takes place across the cell (Fig. 2). The diffusion
problem closely parallels that for diffusional (or
Nabarro-Herring-Cable) creep, leading immediately
to Fig. 3. The formation of a new cell wall. The back stress S,
is suRiciently large to cause gliding dislocations to come to
2kTw’ rest part-way across a cell where they rearrange to form a
new cell wall, subdividing the old cell and thus reducing the
where C, is a constant (about 40), R is the atomic cell size.

possibilities of the model. Following Argon [2] we

take the mobile dislocation density to be given by


These dislocations glide at a velocity which depends

on the difference between the applied stress and the
internal stresses. If the dislocation velocity is a linear
function of effective stress (as it is if a viscous drag
acts on them)

Fig. 4. Cell wall dissolution occurs by the shrinkage and

and if the viscous drag is caused by a diffusion
anihilation of some cells. Consider a cell on wall as a sample
tilt boundary of angle 8. If the wall dislocations migrate 6x controlled process (like climb)
into the smaller cell then they must undergo a climb Bdx to
preserve their relative positions. For a cell of size w a volume (16)
wf?Sx~ must diffuse to accommodate the climb of each
and from equation (7), if the mean slip length is set On rearrangement of equation (2), (3), (13) and (15),
to the cell size w, the change in cell size is the model-based equations become
-= -_. (9)
dc G@ (174
The cell shrinkage must be balanced by a recovery S, ab
process eliminating cell wall area and hence allowing __=- (17b)
G w
growth. During creep, cell walls are observed to
migrate. If the migration is such that the external !&f&-C 2
R’-Stfr*& (17c)
stress does work then the stress exerts a pressure atI G G 0w
per unit area on the boundary. In addition the cell
wall energy y acts with a further shrinkage pressure
of approximately 4y/w. This driving force causes
some cells to shrink and annihilate thus increasing the (17d)
mean cell size. The total pressure exerted is then

pxre+~* UO)
R’ = g (taking B x b3). (174
Now C, and C3 are geometrical constants for each of
(The first term can the thought of as the driving force
the recovery processes. The diffusion controlled parts
for dynamic recovery, the second for static recovery.)
of the equations governing creep rate, back stress and
The work done in moving the wall 6x is ph. In cell size are very similar (i.e. they all have R’dt in
advancing Sx the wall dislocations (here considered
common). This is to be expected as they all describe
as a simple tilt boundary) must climb a distance 86x
climb of dislocations in ceil walls.
to preserve the boundary structure (Fig. 4) and thus
After an initial transient, dislocation creep reaches
a volume
steady state when no further change in mean values
6V = wbtJSx. 7 =w*tF 6x (11) of cell size and internal stress will occur. Rearranging
equation (17) for the steady state gives the following
must be transported across the cell. This gives the relations
work done per atom moved as pQ/@. The coarsening
rate of a cell can then be calculated; it is

[ =HCR'(~)'("-:-")] (18a)
Assembling these results, and using the fact that
y z Gbe and that, near steady state, I x w, gives [~(~~(1+~)=~~]

. (13)
[ =gR’(;y(d -2-“).I (18b)
Finally, we need an equation for the strain rate. We
adopt the simplest form that allows us to explore the Experimental measurements show that the mean

0.25 0.25



0 200 400 600 600 1000
0 6000 16,000
Time (8)
Time (s)
Fig. 6. Creep curve for f.c.c. material at 0.8 Thl for a stress
Fig. 5. Creep curve for f.c.c. material at 0.8 Tr,, for a stress of 3 x 1O-4 G and an initial grain size of 100 pm. Steady
of 1 x 10m4G and an initial grain size of 1OOpm. Steady state strain rate 5.8 x 10e5 s-’ and subgrain size (d) stress
state strain rate of 1.2 x 10e6 s-’ and subgrain size (d) stress function of ud = 10 Gb. Transient strain is 6.4%.
function of od = 14 Gb. Transient strain is 2.5%.

steady-state cell size (w*) is related to the applied Once steady state is reached S, and S, are propor-
stress during creep by w* = constant (of order 10 Gb) tional to 0 the applied stress, and hence a stress
[4]. It has been found from stress drop experiments exponent of 3 is often referred to as normal law creep
that the mean steady-state internal stress is linearly and is expected, together with a creep constant [C in
related to the applied stress by a factor of about 0.7 equation (17a)] in the range l-10 [6]. Inserting the
[5]. Inserting these values into equation (18) gives above values into the model [equation (17)] and using
an iterative solution on a computer produces the
C, C, H Sj’
-=; x0.7 (assuming S,>>S,) (19a) following creep curves using diffusion data typical of
c2 an f.c.c. metal (Figs 5 and 6). The expected mono-
tonic primary curve of pure metal is shown. If the
stress is increased during a test a new primary curve
starts and on stress drop there is an incubation period
before the resumption of strain (Fig. 7). Both these
where S! is the steady-state value of S,. phenomenon are in accordance with observation.


0.25 -

0.20 -

0 20,000 40,000

Time (s)
Fig. 7. The influence of changes in stress during creep, all
curves are for conditions of Fig. 5. Above: creep stress
increased by 20% after 25,OOOs,note new transient creep
curve before new higher stable creep rate. Below: creep
stress reduced by 20% after 25,000 s, note slight negative
creep and “incubation period” before creep restarts at a s2
lower strain rate.

The quantitites CJH and C,C, are the time con-

stants for the microstructure during creep and are
expected to be of the same order. However, consider
a material with a high concentration of undeformable
phase (e.g. hard precipitates). The bowing stress will
be fixed by the particle spacing and the hardening
coefficient (H) will be large. If the recovery of this
stress still requires dislocation sources and sinks (e.g.
a coherent precipitate) there will now be an imbal-
ance in the time constants and a longer time will
occur before recovery is effective. This produces an
increase in creep rate with time or a transition from
primary to pseudotertiary creep (Fig. S), a prediction I I I I 1
0 400 600 1200 1600 2000
consistent with observations of an increase in creep Time k.)
rate with dislocation density observed in some super- Fig. 8. Primary to pseudotertiary creep from imbalance in
alloys [7]. The final form of the equations has much recovery time constants. Material and conditions as in
in common with those of other, more empirical Fig. 6.
models for primary creep, notably that of LeGac and
Duval [8]. S. Takeuchi and A. S. Argon, J. Mater. Sci. 11, 1542
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2. A. S. Argon, Scripta metall. 14, 1001 (1970). Wilshire and D. R. J. Owen, p. 319. Pinehdge, Swansea
3. J. P. Hirth and J. Lothe, Theory of Dislocations. (1984).
McGraw-Hill, New York (1968). H. LeGac and P. Duval, IUTAM Symp. on Physics and
4. 0. D. Sherby and P. M. Burke, Prog. Mater. Sci. 13, Mechanics of Ice (Edited by P. Tryde), p. 5 1. Springer,
325 (1967). Berlin (1980).