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A Microstructural Model for Primary Creep

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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

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.

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.

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

THE DEVELOPMENT OF CREEP SUBSTRUCTURE

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

1349

1350 DERBY and ASHBY: A MODEL FOR PRIMARY CREEP

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

sources.

for bulk (0,) and boundary (6D,) (that is, cell-wall)

diffusion, approximately

where G is the shear modulus and a < 1. The second

7CCSD,

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-

(3)

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

of

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,

C2S2QD

R=--.-..-

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.

DERBY and ASHBY: A MODEL FOR PRIMARY CREEP 1351

take the mobile dislocation density to be given by

(14)

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)

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

dislocation.

EVALUATION OF THE MODEL

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

1352 DERBY and ASHBY: A MODEL FOR PRIMARY CREEP

0.25 0.25

1.0

r

1.0

t

1

I I I I

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.

DERBY and ASHBY: A MODEL FOR PRIMARY CREEP 1353

0.25

0.25

OV I I

0.25 -

0

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.

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

(1976).

REFERENCES A. M. Brown and M. F. Ashbv. ., Scriota

. metall. 14. 1297

(1980).

1. J. C. Ion, A Barbosa, M. F. Ashby, B. F. Dyson and P. J. Henderson and M. McLean, Creep and Fracture of

M. McLeann, NPL Report DMA A115, (1986). Engineering Materials and Structures (edited bv B.

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).

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