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a Institute of Gerontology and Department of Physiology, University of Michigan, Ann Arbor
Susan V. Brooks, Institute of Gerontology, 300 N. Ingalls, Room 961, University of Michigan, Ann Arbor, MI 48109-2007 E-mail: svbrooks{at}umich.edu.
Decision Editor: Edward J. Masoro, PhD
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MOST activities involve complex body movements that require muscles to perform combinations of contractions wherein the muscles remain at fixed length, shorten, or are stretched. Of the three types of contractions, those in which activated muscles are stretched (lengthening contractions) are most likely to cause significant injury to skeletal muscle fibers (1). Initially, the injury is mechanical and highly focal within single sarcomeres or small groups of sarcomeres (2)(3). The mechanical injury initiates a cascade of events leading to a more severe secondary injury throughout a segment of the injured fiber that peaks approximately 3 days after the initial mechanical injury (1). Athletes condition their muscles gradually to withstand the high forces and strains of lengthening contractions for the prevention of contraction-induced injury in specific sporting activities. In contrast, much of the general population is not conditioned for even minimally demanding stretches of activated muscles that may occur unexpectedly in the activities of daily living.
The greater susceptibility of muscles in old animals, including human beings, to injury (4)(5)(6) suggests that in older individuals, conditioning may be required to withstand even the mechanical requirements of lengthening contractions encountered in daily life (7). Despite this potential requirement for conditioning in the elderly population, the impaired ability of muscles in old animals to recover from injury (8) may make the achievement of a conditioned state difficult. Furthermore, following severe injury, muscles in old animals can sustain permanent deficits in force development, mass, and number of fibers present in the cross section (8). Consequently, a conditioning program that is too demanding for muscles in elderly individuals could produce prolonged and potentially irreversible structural and functional deficits.
The demonstration of a muscle "conditioned" for pro-tection from injury requires both the demonstration of morphological damage and a significant force deficit in unconditioned muscles (9)(10) and the attainment after a conditioning program of no evidence of morphological damage to muscle fibers or a force deficit. Previous investigations of single and repeated exposure to a wide variety of exercise protocols administered to both humans (11)(12)(13)(14)(15)(16) and rodents (17) concluded that conditioned muscles were produced. Despite the conclusions of these studies that muscles were conditioned, clear demonstrations of damage to muscles following protocols described as "injury-producing protocols" were not presented. As a consequence, the degree of protection could not be assessed in terms of the extent and magnitude of damage to muscle fibers following the injury-producing protocols in conditioned compared with unconditioned muscles. The purpose of this study was to design and implement a conditioning program that would protect skeletal muscles of adult and old mice from contraction-induced injury. The hypotheses were tested that (i) skeletal muscles of both adult and old mice condition to repeated weekly protocols of lengthening contractions such that they are not injured by a contraction protocol that previously caused injury, but (ii) conditioning occurs more slowly for muscles of old than adult mice.
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90% of their final body mass (18), decreasing the contribution of significant growth during the conditioning program that would occur in younger mice. The median life span of female B6D2F1 mice housed under SPF conditions is 28 months, and the 10th percentile survival point is 34 months (18). An age range of 22–24 months, which corresponds to the 70th to 80th percentile survival point, was chosen in the present study to represent an age range prior to that at which significant deficits in skeletal muscle mass and force are observed in mice (19)(20). We reasoned further that the likelihood for mice to survive the repeated exposure to anesthesia required for completion to the conditioning program would decrease for mice beyond the median life span. The 7- to 9-month-old and 22- to 24-month-old age groups will be termed "adult" and "old," respectively. Prior to experimentation, all mice were housed in an SPF facility in the Core Facility for Aged Rodents at the University of Michigan. Following the first day of conditioning, mice were housed in microisolator cages in an SPF return room located adjacent to the experimentation site and supervised by the University of Michigan Unit for Laboratory Animal Medicine. All experimental procedures and housing conditions were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.
Measurement of Contractile Properties in vivo
All contraction protocols were administered by using an apparatus designed for the evaluation in vivo of the biomechanical behavior of the muscles of the mouse ankle (21). The apparatus permits repeated administration of contraction protocols. For each contraction protocol, mice were anesthetized with an intraperitoneal injection of pentobarbital sodium, 40 mg/kg, with supplemental injections given as needed to achieve and maintain a state with no response to tactile stimuli. The total dose of anesthesia fluctuated greatly, depending on the individual mouse and the week of conditioning.
The anesthetized mouse was placed in the experimental apparatus upon a Plexiglas platform that was maintained at 37°C. The foot was aligned and stabilized within a plastic "shoe" fixture, using wires surrounded by Silastic tubing (Dow Corning, Midland, MI). The knee was stabilized with a blunt screw pin at the femoral condyle; care was used so that blood flow to the hind limb was not compromised. The shoe fixture was attached to a torque transducer (model QWFK-8M, Sensotec, Columbus, OH) such that the center of rotation of the ankle joint was collinear with the axis of the torque transducer. As a way to impose rotation of the ankle joint, the torque transducer was mounted on the shaft of a custom-built servomotor. Control of the motor and collection of data from the torque transducer were accomplished with LabVIEW software (Version 2.2.1, National Instruments, Austin, TX) on a Macintosh computer (model Quadra 700, Apple Computer, Cupertino, CA).
The muscle moment arm is the perpendicular distance from the line of action of a muscle to the joint center of rotation and transforms the linear movement of muscle into rotation about a joint. In a separate group of mice of the same strain, moment arms were calculated directly by dividing the measured torque by known forces at different ankle angles throughout the range of motion (22). The resultant moment arms were used for the determination from ankle torque measurements of the isometric forces and the peak forces developed during stretches of the dorsiflexor muscle group.
Initial evaluations of isometric contractions were made with the ankle positioned and maintained at 10° of plantarflexion, demonstrated in preliminary experiments to be the optimum angle for force production. Fine needle electrodes penetrated the skin and were placed parallel and adjacent to the peroneal nerve for stimulation of the dorsiflexor muscle group. The maximum isometric twitch force was determined by increasing the voltage of individual 0.2-millisecond pulses until force no longer increased. A frequency–force curve was generated for each muscle group from records of the force exerted during periods of stimulation with trains of pulses at increasing frequencies. The plateau in the frequency–force curve was defined as the maximum isometric tetanic force (Po); Po was typically elicited by a stimulation frequency of 150 Hz to 200 Hz, consistent with previous reports (21).
Conditioning Program
The conditioning program consisted of a once-a-week protocol of repeated forced stretches of maximally activated muscles (lengthening contractions). Each week, the Po of the dorsiflexor muscle group was determined in vivo prior to initiation of the lengthening contraction protocol. Values for Po measured each week along with control Po values, defined as the maximum value for Po measured during the conditioning program, are shown in Fig. 1. The decision to report isometric forces relative to the highest Po attained during the conditioning program was based on the wide variation for when the maximum value was achieved for individual animals. For individual adult mice, maximum values occurred during every week except for week 2, and for old mice during every week except weeks 2 and 3. Stimulus pulses of 0.2-millisecond duration and the frequency that resulted in Po were used for all lengthening contractions. During each lengthening contraction, the ankle was held stationary for the first 200 milliseconds to allow full activation of the dorsiflexor muscles prior to being stretched. During the final 500 milliseconds of the contraction, the ankle was rotated from the starting position of 10° plantarflexion to a final position of 50° plantarflexion.
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For each bout, a lengthening contraction occurred every 5.0 seconds and continued for 60 contractions, or until isometric force stabilized to within 50 mN of the prior 10th contraction. Our rationale for termination of a bout upon stabilization of isometric force was that the stabilization indicated that the maximum extent of injury had been achieved, a level of muscle fatigue was present that would prevent further injury, or some combination of the two. As a result of this design, bout 3 typically consisted of 20% fewer contractions than bout 1. Furthermore, the average number of contractions during week 6 was 20% lower than during week 1, and individual mice differed with respect to the total number of contractions during the conditioning program. Despite the individual differences and changes in contraction numbers throughout the conditioning program, the conditioning programs administered to the adult and old groups were not different.
Each week, following the lengthening contraction protocol, the mouse was removed from the apparatus and returned to its cage for recovery. After all mice had been administered the lengthening contraction protocol each week, the mean group Po was calculated for both adult and old mice and the control Po was recalculated. All mice continued the conditioning program until muscles in mice from both age groups met the criterion of conditioned muscles. Our working definition for conditioned dorsiflexor muscles in adult and old mice was the point at which the mean group Po was not different from the control Po for 2 weeks in succession. A working definition for conditioned muscles was necessary because a strict definition in terms of the elimination of damage to muscle fibers could not be applied during the course of the conditioning program. Three groups of muscles were evaluated and compared. For all mice, the dorsiflexor muscles of the left leg were the experimental muscles. Consequently, muscles from the left leg of the mice that completed the conditioning program were designated conditioned muscles. In an additional group of mice, the muscles in the left leg were subjected to only a single protocol of lengthening contractions in vivo, and these muscles were designated unconditioned muscles. The muscles of the right legs from both groups of mice served as unconditioned and unexercised control muscles.
Final Evaluation of Conditioned and Unconditioned Muscles
Final evaluations for evidence of injury to conditioned muscles were conducted 3 days after administration of the lengthening contraction protocol in the sixth week, and evaluations of unconditioned muscles were made 3 days after administration of the single lengthening contraction protocol. A time period of 3 days was chosen because at this time the decrease in force development and the morphological evidence of the damage are most severe in EDL and TBA muscles of mice (1)(24). As a way to assess the magnitude of injury at the final evaluation, the following actions were taken: (i) Po of the dorsiflexor muscle group was measured in vivo; (ii) Po of EDL muscles was measured in vitro; and (iii) the percentages of damaged muscle fibers in single cross sections of TBA and EDL muscles were determined.
Measurements of force as an assessment of injury..-- Final evaluations of Po of the dorsiflexor muscles were made as described above and were used to determine the force deficit induced in conditioned and unconditioned muscles by the lengthening contraction protocol. The force deficit, which provided a measure of the magnitude of injury, was calculated as the difference in Po measured prior to and 3 days following the lengthening contraction protocol expressed as a percentage of Po prior to the lengthening contractions. Clearly, the presence of multiple muscles in the dorsiflexor group complicates the interpretation of measurements made in vivo. Because of the dominance of the TBA muscles in the dorsiflexor group, immediately following the collection of final data in vivo, conditioned, unconditioned, and contralateral control EDL muscles were analyzed for force production in vitro.
EDL muscles were isolated and 5-0 silk suture was tied securely to the proximal and distal tendons. The muscles were removed from the limb and immersed in a bath containing buffered physiological salt solution (composition: NaCl, 137 mM; NaHCO3, 24 mM; glucose, 11 mM; KCL, 5 mM; CaCl2, 2 mM; MgSO4, 1 mM; NaH2PO4, 1 mM; and tubocurarine chloride, 0.025 mM) maintained at 25°C (1). The pH was maintained at approximately 7.4 by bubbling with a gas mixture of 95% O2 and 5% CO2. The distal tendon was attached to a fixed post and the proximal tendon was tied to the lever arm of a servomotor (Model 300H, Aurora Scientific Inc., Richmond Hill, Ontario, Canada). Muscles were stimulated directly by an electrical field generated between two platinum plate electrodes with 0.2 millisecond pulses of supramaximal intensity. Stimulation voltage and muscle length were adjusted until a single stimulus pulse elicited maximum twitch force. Force was measured during periods of stimulation at increasing frequencies until a plateau was reached at Po. For EDL muscles, force deficits resulting from the lengthening contraction protocol administered in vivo were calculated as the difference in Po of conditioned or unconditioned EDL muscles and Po of their respective contralateral control EDL muscles expressed as a percentage of the Po developed by the control muscle.
Optimal length (Lo) was measured with the EDL muscle attached and in the bath. For the Lo of TBA muscles to be obtained, the ankle of each leg was positioned with 10° of plantarflexion, and muscle lengths were measured in situ. Subsequently, TBA muscles were removed and the mice were euthanized with an overdose of anesthetic. The Lf for each muscle was calculated as the product of Lo and Lf /Lo ratios (23).
Morphology as an assessment of injury..-- For all EDL and TBA muscles, tendons were trimmed; muscles were blotted, weighed, and cut transversely in half. The proximal end of each muscle was weighed, dehydrated at 80°C for a minimum of 1 week, and then weighed again for calculation of dry mass/wet mass ratios. The distal end of each muscle was mounted in tissue-freezing medium (Triangle Biomedical Sciences, Durham, NC) and frozen in isopentane cooled with dry ice. Muscles were sectioned, stained with hematoxylin and eosin (H&E), and analyzed for mean single fiber cross-sectional area (CSA) and percentage of the fibers in a cross section that were damaged. Criterion for a damaged fiber was either that the fiber was infiltrated with macrophages or was in the process of degeneration.
Statistics
All data were reported as the mean ± 1 standard error of the mean (SEM). A two-way analysis of variance (ANOVA) was used to analyze data for effects of muscle group (conditioned, unconditioned, control) and age (adult, old), and for interactions between these two groups. A two-way repeated measures (one factor repetition) ANOVA was used to test for effects of the conditioning program and of age on isometric forces and peak forces developed during the stretch during the initial and final lengthening contraction protocols. In all cases, Tukey post hoc analyses were used to determine individual differences between groups. For all statistical tests, the accepted level of significance was set a priori at p 
.05.
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Conditioning Program
At the beginning of the experiment, the Po of dorsiflexor muscles in adult and old mice were not different (Fig. 1). During weeks 2 and 3, the Po of muscles in adult mice decreased to 75–80% of the control value, whereas that of the old mice remained decreased to a similar level from week 2 through week 4. As a result, the Po for muscles of adult mice recovered and stabilized at control values by week 4 and that of old mice by week 5. Consequently, by the sixth week, dorsiflexor muscles in both age groups met our working criterion for conditioned muscles of developing Po not different from the control Po for 2 weeks in succession, and the final lengthening contraction protocol was administered during week 6.
First Exposure to Lengthening Contraction Protocol
In addition to the similarity of both initial and control Po between dorsiflexor muscles of adult and old mice, a high degree of consistency was observed between the age groups for the forces developed throughout the entire lengthening contraction protocol in week 1. Essentially no differences between the age groups were observed for either the isometric force or the peak force during the stretch during administration of the first 180 lengthening contraction protocol (Fig. 2 and Fig. 3). For muscles in both adult and old mice, force decreased continuously in each bout such that by the end of the protocol in week 1, the isometric force and peak force during the stretch were 35% and 55%, respectively, of the initial values (Fig. 2 and Fig. 3). In addition, the recovery in force during the rest periods between bouts was not different for muscles in adult and old mice. Furthermore, 10 minutes after completion of the protocol, the recovery of isometric force to 81 ± 6% and 76 ± 5% of the initial values for muscles in adult and old mice, respectively, was not different between the two age groups.
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In contrast to the lack of an effect of the 6-week conditioning program on Po, for muscles in both adult and old mice, the peak force developed during the stretch was significantly increased in week 6 compared with week 1 (Fig. 3). The effect of conditioning to increase peak force was not different for muscles in adult and old mice. The contribution of passive force to the total force measured during stretches was considerable and variable, with passive extension properties of the muscles, tendons, and ankle joint being negligible at 15° of plantarflexion but contributing 15% of the force at 25° and 45% at 50°. Despite the magnitude of the contribution, no consistent effect of the conditioning program on the passive tension was observed. Consequently, we conclude that the increase in peak stretch force was not due to changes in the passive force characteristics.
Final Evaluations of Conditioned and Unconditioned Muscles
The force deficits measured for conditioned and unconditioned muscles 3 days following the lengthening contraction protocol are shown in Fig. 4. No effect of age was observed on the force deficits of either the whole dorsiflexor muscle groups evaluated in vivo or the EDL muscles evaluated in vitro. Consequently, the data from both age groups were pooled. For dorsiflexor muscles, the force deficit of 11.2 ± 4.6% for conditioned muscles was less than half of that for unconditioned muscles, 27.4 ± 5.4%. Compared with measurements made on the whole dorsiflexor muscle groups, the effectiveness of conditioning to decrease the force deficit was even greater based on evaluations of EDL muscles. The pooled force deficit for conditioned EDL muscles from adult and old mice of 7.8 ± 2.9% was less than one third of the force deficit of 25.4 ± 2.9% measured for unconditioned EDL muscles (Fig. 4).
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Conditioned muscles..-- In both adult and old mice, the protection from contraction-induced injury provided by the conditioning program was not accompanied by changes in muscle mass, Lf, single fiber CSA, or dry mass/wet mass (Table 1 and Table 2 ). Muscle mass, Lf, and single fiber CSA were not different for conditioned compared with control EDL muscles (Table 1 ). In addition, no differences were observed for dry mass/wet mass among any of the groups of EDL muscles in adult mice (Table 1 ). In old mice, dry mass/wet mass of conditioned EDL muscles was 7% lower than that of control EDL muscles, but was not different from that of unconditioned muscles. Similarly, no differences were observed between conditioned and control TBA muscles for mass, single fiber CSA, or dry mass/wet mass in either adult or old mice (Table 2 ). In old mice, the mean Lf of conditioned TBA muscles was 4% lower than that of control TBA muscles but not different from the Lf of unconditioned TBA muscles. Finally, the similarity of the effects of the conditioning program on the properties of muscles in adult and old mice was supported by values for Po of conditioned EDL muscles, 243 ± 10 kN/m2 and 244 ± 12 kN/m2, that were not different.
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9% was not consistent in the strictest sense with our hypothesis that conditioned muscles would not be injured. Devor and Faulkner (9) also concluded that, following degeneration induced by treatment with the myotoxic agent, bupivacaine, newly regenerated fibers in muscles of old rats were protected from contraction-induced injury although injury was not completely eliminated in their bupivacaine-treated muscles. Most certainly a lengthening contraction protocol could be designed that would produce no evidence of contraction-induced injury to conditioned muscles, but these results emphasize the rigor that must be used when conclusions are drawn regarding the degree of protection provided by a conditioning program or treatment. The secondary hypothesis, that the achievement of a conditioned muscle requires a longer period of conditioning for muscles in old compared with adult mice, was also supported. Although not tested rigorously, the hypothesis was supported on the basis of our working definition of conditioned muscles that dorsiflexor muscles in adult mice generated Po not different from control values by week 4, whereas muscles in old mice did not achieve control values for Po until week 5. Although 6 weeks of once-a-week lengthening contraction protocols clearly conditioned muscles in both adult and old mice to be more resistant to contraction-induced injury, the lack of precision in the weekly evaluations with the shoe apparatus prevented determination of exactly when any given individual within a group was conditioned. A distinct possibility is that within groups of both adult and old mice, some muscles conditioned more slowly and others more rapidly than the remainder of the group.
The rate and magnitude of the decline in force during a lengthening contraction protocol are functions of both fatigue and injury (1)(6)(8). Muscles of old mice were less able to sustain force and power over time than muscles of young mice (19). Consequently, the lack of any difference between muscles in adult and old mice for either the isometric force or the peak force developed during the stretch throughout the first lengthening contraction protocol was surprising. The metabolic requirements of exercise involving predominantly lengthening contractions is only 25% of that required for comparable exercise composed largely of shortening contractions (25). Under these circumstances, the metabolic cost of the lengthening contraction protocol may have been such that fatigability was not a factor for muscles in either adult or old mice. In addition, muscles of old mice are more susceptible to injury during protocols of stretches of maximally activated muscles (4)(6). Despite greater susceptibility to injury reported previously for muscles in old compared with younger animals (4)(6), Gosselin (26) recently reported that a moderate protocol of 20 lengthening contractions resulted in a force deficit of 25% that was similar for muscles from adult and old rats. In the present study, the nature of the contraction protocol was apparently mild enough as to produce equivalent force deficits of 25% at 3 days for muscles of adult and old animals.
Contraction-induced injury is initiated by a mechanical event, which involves focal damage to single sarcomeres (27). During isometric contractions, the development of heterogeneity in sarcomere lengths (27)(28) increases the likelihood of large strains and injury of specific sarcomeres, even during relatively small stretches (27)(29)(30)(31). The damage that occurs during the contractions can produce a delayed secondary injury characterized by an inflammatory response, free radical damage, phagocytosis, and ultimately the degeneration of segments of severely damaged fibers (1)(6)(32). The secondary injury, which is typically more severe than the initial injury, peaks between 1 and 5 days later (1)(24). The adaptations responsible for protection from injury provided by conditioning are not known (33). The importance of the magnitude of strain and the degree of sarcomere heterogeneity as predictors of the magnitude of the damage suggests that the adaptation may involve changes that prevent excessive stretch of small groups of sarcomeres greater than the stretch imposed on the muscle (9)(27)(31). Alternatively, numerous cellular adaptations could blunt the free radical damage associated with the secondary injury (6)(32).
The present experiments were not designed to distinguish between effects on the initial and secondary injury, but the significant increase between weeks 1 and 6 in the ability to maintain isometric force during the contraction protocol suggests a mechanism of the conditioning process on the initiation of injury. The decrease in force attributable to fatigue remained in the conditioned muscles, but the conditioned muscles were able to maintain higher forces during the stretches as a result of a decrease in the force deficit from injury. Furthermore, precise experiments have been directed to the specific roles of average and peak force, strain, and work done to stretch a muscle fiber or muscle in the initiation of injury (4)(29)(30)(34)(35). When muscle fibers are maximally activated and the stretch is initiated from a given initial fiber length, the relationship of the work done during the stretch and the resultant force deficit has a coefficient of determination of greater than 80% (29). As a consequence of the higher isometric and peak stretch forces maintained during week 6 compared with week 1, the average forces developed and therefore the work inputs were greater during the lengthening contraction protocol for conditioned compared with unconditioned muscles. The observation of greater work input's resulting in a dramatically reduced amount of damage during the contractions for conditioned compared with unconditioned muscles also supports an effect of conditioning on the initial mechanical injury (4).
In the present study, the conditioning program resulted in significant protection from contraction-induced injury for muscles in both adult and old female mice, despite no substantial changes in muscle morphological properties. Taken together, the data on muscle mass, single fiber CSA, fiber length, and dry mass/wet mass from conditioned, unconditioned, and control muscles suggest that the conditioning program did not cause hypertrophy or significant changes in overall protein or water content. The elevated forces maintained throughout the contraction protocol by conditioned muscles in the absence of any structural change is consistent with the working hypothesis that conditioning affected the intrinsic sarcomere strength within myofibrils. The process of injury to weak sarcomeres and regeneration of stronger sarcomeres is a potential mechanism by which conditioning results in protection from injury. Newly regenerated fibers in muscles of young and old animals are clearly more resistant to contraction-induced injury (9). In contrast to the present finding of conditioning in muscles of adult and old female mice without any structural change, a similar 6-week conditioning program resulted in hypertrophy of 20% in dorsiflexor muscles of young male mice (36). Whether the mechanisms underlying the adaptations that allow muscles to withstand lengthening contractions without injury are different in males and females is not known.
Similar abilities of adult and old subjects to adapt to moderate protocols of exercise have been reported based on serum creatine kinase (CK) activity and subjective accounts of pain (37). Although Clarkson and Dedrick (37) showed comparable reductions in serum CK activity in adult and old subjects following a second compared with the first bout of exercise with lengthening contractions (37), CK activity is often a poor marker of actual muscle damage. In rats treated with vitamin E in an attempt to protect skeletal muscles from contraction-induced injury, serum CK activity 3 hours and 3 days following a protocol of repeated lengthening contractions administered to EDL muscles in situ was not different from that of nonexercised control animals (38). Despite the lack of evidence of muscle damage based on CK activity in the treated animals, force deficits of greater than 50% and damage to more than 30% of the fibers in a cross section were observed at 3 days in the muscles exposed to the lengthening contractions (38). Similarly, marked discrepancies have been reported between serum CK activity and the magnitude of damage assessed through a direct morphological examination of muscles in adult and old subjects following a bout of exercise with lengthening contractions (5). Consequently, the use of CK activity as an indicator of protection from damage should be viewed with caution, particularly in the elderly population (5).
Our previous reports of a greater susceptibility to contraction-induced injury and a slower and impaired recovery (6)(8) were consistent with subjective, anecdotal, and experimental (5) observations of muscle injuries to the elderly. The observation that during the lengthening contraction protocols used in the present study there was no difference in either the fatigability or induction of injury to fibers in muscles of adult and old mice has major implications for the design of conditioning programs for the elderly population. Furthermore, despite the intensity of the contraction protocols, in terms of the level of activation, the number of contractions and the amount of damage induced relative to typical exercise programs for human beings, protective effects were achieved in both adult and old mice. The successful conditioning response with no evidence of permanent damage in muscles of old female mice provides strong support for the use of conditioning with lengthening contractions to maintain and enhance the muscle strength of elderly men and women.
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We thank Robert Dennis and Stephanie Miller for their assistance with the modifications to the in vivo apparatus and the technical support and Cheryl Hassett and Krystyna Pasyk for their contributions to the morphological assessments.
The current address of J. Opiteck is Duke Clinical Research Institute, Duke University Medical Center, Durham, NC 27713.
Received July 19, 2000
Accepted October 31, 2000
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