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J Appl Physiol 82: 278-283, 1997;
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Journal of Applied Physiology
Vol. 82, No. 1, pp. 278-283, January 1997
EXERCISE AND MUSCLE

Pliometric contraction-induced injury of mouse skeletal muscle: effect of initial length

Kam D. Hunter and John A. Faulkner

Department of Physiology and Institute of Gerontology, University of Michigan, Ann Arbor, Michigan 48109-2007

ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES

ABSTRACT

Hunter, Kam D., and John A. Faulkner. Pliometric contraction-induced injury of mouse skeletal muscle: effect of initial length. J. Appl. Physiol. 82(1): 278-283, 1997.---For single pliometric (lengthening) contractions initiated from optimal fiber length (Lf), the most important factor determining the subsequent force deficit is the work input during the stretch. We tested the hypothesis that regardless of the initial length, the force deficit is primarily a function of the work input. Extensor digitorum longus muscles of mice were maximally activated in situ and lengthened at 2 Lf /s from one of three initial fiber lengths (90, 100, or 120% of Lf) to one of three final fiber lengths (150, 160, or 170% of Lf). Maximal isometric force production was assessed before and after the pliometric contraction. No single mechanical factor, including the work input (r2 = 0.34), was sufficient to explain the differences in force deficits observed among groups. Therefore, the force deficit appears to arise from a complex interaction of mechanical events. With the data grouped by initial fiber length, the correlation between the average work and the average force deficit was high (r2 = 0.97-0.99). Consequently, differences in force deficits among groups were best explained on the basis of the initial fiber length and the work input during the stretch.

fiber length; force deficit; muscle damage; muscle strain; pliometric contractions

INTRODUCTION

PLIOMETRIC (lengthening) contractions are more likely than isometric or miometric (shortening) contractions to produce damage to muscle fibers in muscle groups of humans (16) or single muscles of mice (13). The damage observed immediately after a pliometric contraction protocol occurs to individual sarcomeres singly or in small groups scattered throughout individual muscle fibers (3). The magnitude of the ultrastructural injury is difficult to assess directly with light or electron microscopy because of the focal nature of the damage produced. The decrease in maximum isometric force production that results from the ultrastructural damage may be expressed as a "force deficit" (3). The force deficit is calculated as the difference in maximum force production before and after a pliometric contraction protocol, expressed as a percentage of the initial value. The force deficit is the best indicator of the totality of the contraction-induced injury (9).

With protocols of repeated pliometric contractions, the force deficit may result from fatigue as well as from injury (14). A single pliometric contraction does not produce fatigue and consequently allows the resulting force deficit to be attributed entirely to damage inflicted on skeletal muscle fibers (3). Furthermore, the ultrastructural damage observed after a single pliometric contraction is not different from that seen after protocols of repeated pliometric contractions (3). Because mechanical variables such as force production and work input may be measured precisely during a single stretch, the single stretch protocol permits definitive investigations of the process of the immediate mechanical injury to skeletal muscle fibers.

Although the exact sequence of events by which pliometric contractions produce muscle fiber injury remains undetermined, mechanical factors that are important in determining the magnitude of the injury include the peak force (14), average force (3), and the stretch of muscle fibers beyond optimal length (Lo) (11). Single pliometric contractions initiated from Lo produce damage in both whole muscles (3) and single fibers (12). Under these circumstances, the magnitude of the damage, represented by the force deficit, is best predicted by the work input on the muscle during the stretch, calculated as the product of the displacement imposed and the average force produced. After a single stretch, the work input is a strong predictor of the force deficit (r2 = 0.7-0.8), but these studies have utilized only stretches initiated at the optimal length for force production (3, 12).

The role of initial fiber length in the generation of the force deficit is controversial. After repeated maximal voluntary pliometric contractions of the biceps muscle by human volunteers, a greater force deficit occurred after protocols that began at long lengths compared with those that began at short lengths (15). With voluntary pliometric exercise, precise information on muscle fiber recruitment patterns, initial lengths, or final lengths cannot be obtained. For soleus muscles of rats studied in vitro, Warren et al. (17) observed no difference in the force deficit after repeated pliometric contractions with a change in initial length from 85% of Lo to 90% of Lo. The lack of any initial lengths on the descending limb of the length-force curve and the small range of initial lengths employed limited the interpretation of these data. For six sartorius muscles tested in vitro from three frogs, Wood et al. (18) reported a greater force deficit after 60 pliometric contractions performed on the descending limb of the length-force curve compared with contractions carried out on the ascending limb. The specific fiber lengths and displacements utilized were not reported, and the use of repeated-contraction protocols with concomitant induction of fatigue complicated the interpretation of the data. No previous studies have examined the force deficit after pliometric contractions initiated from a comprehensive range of fiber lengths under conditions in which mechanical contractile variables can be measured precisely and their relationship to the force deficit determined.

During daily activities, muscles are activated with fibers at a wide range of initial lengths (6). Our purpose was to clarify the association of the force deficit after pliometric contractions with specific mechanical events by using a range of initial fiber lengths to provide a more comprehensive simulation of in vivo conditions. For stretches from a single initial length, the final fiber length and strain cannot be varied independently because both are determined by the displacement imposed. In an in situ single-muscle preparation (7), we employed a systematic interaction of initial fiber lengths, imposed displacements, and final fiber lengths, such that the independent effects of these variables could be resolved. We tested the specific hypothesis that regardless of the initial fiber length, final fiber length, or displacement, the force deficit after a single stretch of a maximally activated muscle is determined by the work input on the muscle.

METHODS

Animals. Adult male CD-1 mice (30 ± 1 g) were obtained from the Charles River Breeding Colony. Before experimentation, the mice were housed in a pathogen-free barrier facility in the Unit for Laboratory Animal Medicine at the University of Michigan.

Operative procedure. An in situ muscle preparation was used in this study (2, 13, 19). The in situ muscle preparation with stimulation through the peroneal nerve and with blood flow to the muscle intact provides a model of contraction-induced injury more comparable with the in vivo model than does the noninnervated and ischemic in vitro model (8). Mice were anesthetized with pentobarbital sodium (75 mg/kg ip). Supplemental doses were administered as required to prevent response to tactile stimuli. An incision was made at the ankle, and the distal tendon and extreme distal portion of the extensor digitorum longus (EDL) muscle were exposed. A 5-0 silk suture was tied to the tendon, and the tendon was cut distal to the suture. The mouse was then placed on a Plexiglas platform maintained at 37°C through the use of a circulating water bath. The exposed muscle and tendon were moistened periodically with warm saline. The hindlimb was stabilized by pinning the knee and securing the foot to the platform with cloth tape. The distal tendon of the EDL muscle was tied to the lever arm of a servomotor (model 305, Cambridge Technology, Watertown, MA), which monitored both the position of the muscle and the force production by the muscle. A microcomputer directed the servomotor to move the lever arm through a specified displacement at constant velocity. The displacement and force data were displayed on a storage oscilloscope and sampled by the microcomputer.

Measurement of contractile properties. Two electrodes were inserted percutaneously adjacent to the peroneal nerve for stimulation of the EDL muscle. The nerve was stimulated with pulses of 200-µs duration at supramaximal voltage (1-5 V). The length of the muscle was adjusted during repeated twitches until the twitch force (Pt) was maximum. This length was defined as Lo. Lf was defined as the length of the muscle fibers when the muscle length was Lo and was determined by multiplying Lo by a previously determined Lf /Lo ratio of 0.44 (1). Because previous work in our laboratory has shown that isometric force production for EDL muscles of mice in situ is invariably maximum at a stimulation frequency of 300 Hz (13), maximum isometric tetanic force (Po) before the single pliometric contraction was produced by stimulating the muscle for 200 ms at this frequency.

Pliometric contraction protocol. A series of protocols were used in which initial fiber length and final fiber length were varied, with concomitant changes in both the relative fiber displacement and the strain imposed. During normal everyday activities, muscle fibers may be stretched by 40% or more (6). Single stretches of 40% produce muscle damage in situ (3), suggesting that muscle damage can result from single pliometric contractions during everyday activity. Some protocols employed utilized single stretches beyond this range to extend the variation in force deficits produced. Each EDL muscle underwent a single pliometric contraction starting from a muscle length calculated to correspond to one of three different fiber lengths: a short initial length of 90% Lf, optimal initial length of 100% Lf, or a long initial length of 120% Lf. A maximum isometric tetanic contraction was initiated, and after 100 ms of stimulation at 300 Hz the muscle was stretched at a velocity of 2 Lf /s. The stimulation was halted on attainment of the final length, and after a 5-ms hold time the muscle was returned to its initial length at the same velocity used for the stretch. A velocity of 2 Lf /s has been utilized effectively in a previous study of muscle damage from single pliometric contractions and corresponds to ~10% of the maximal velocity of shortening of the EDL muscle of the mouse at 37°C (3).

Of twenty-four muscles studied at each initial length, eight were stretched to a muscle length calculated to correspond to a "short" final fiber length of 150% Lf, eight to a "medium" final fiber length of 160% Lf, and eight to a "long" final fiber length of 170% Lf. The relative displacement of the stretch was defined as the magnitude of the stretch, expressed as a percentage of Lf. The strain imposed was calculated as the magnitude of the stretch divided by the initial fiber length. The integrated area under the force curve during the muscle lengthening was used to determine the average force. The work input to stretch the muscle was calculated by multiplying the average force by the magnitude of the stretch. The work input was divided by the duration of lengthening in seconds to give the power absorbed by the muscle. Po production at Lo was reassessed 2 min after the performance of the pliometric contraction. The muscle was then removed from the mouse, and the tendons were trimmed. Excess fluid was blotted from the muscle, and the muscle was weighed. The mouse was killed with an overdose of pentobarbital sodium, and a pneumothorax was created to ensure death.

Total fiber cross-sectional area (CSA) was calculated by dividing the muscle mass by the product of Lf and 1.06 g/cm3, the density of mammalian skeletal muscle. To minimize variability due to differences in the mass of individual muscles, Po was normalized to specific Po (kN/m2) by dividing by the CSA. The peak force and average force were also normalized by CSA, and the power absorbed and work input during the stretch were normalized by muscle mass. Values of Po for injured muscles were obtained, and the force deficit was then calculated.

Statistical analysis. Data are expressed as means ± SE. Data were analyzed by a two-way analysis of variance with randomized block design using the SAS statistical program (SAS Institute). On attainment of a significant F-statistic (P < 0.05), group means were compared by utilizing an alpha  = 0.05 significance level and with the Bonferroni correction for multiple comparisons.

RESULTS

The body mass of the 44 mice was 30.3 ± 0.5 g (n = 44). For the EDL muscles, the mass was 8.9 ± 0.2 mg, the fiber length was 5.5 ± 0.03 mm, the CSA was 1.5 ± 0.02 cm2, and the preinjury specific Po was 240 ± 4 kN/m2 (n = 72). These values agree well with previous reports of the morphological and contractile properties for EDL muscles of young mice in situ (1, 13). Among the nine experimental groups, no differences were observed in the control values for morphological or contractile properties measured before the pliometric contraction protocol.

For stretches from any given initial fiber length, increasing the imposed relative displacement and, therefore, the final fiber length produced an increased force deficit (Fig. 1). In general, although an increase in the final fiber length did not affect the average force produced, the work input increased due to the greater magnitude of the stretch (Table 1). For variables examined singly, the final fiber length provided the best correlation with force deficit, but the coefficient of determination was only r2 = 0.48 (Table 2).

Fig. 1. Force deficit after single stretch of maximally activated muscle is plotted as function of initial and final muscle fiber lengths and is expressed as percentage of optimal fiber length (Lf). Values are the means ± SE. Small bars directly below x-axis indicate 3 initial fiber lengths utilized in this study. Lines extending from small bars to each of 3 final lengths utilized illustrate relative displacements of stretches involved, and arrowheads point to bar representing force deficit resulting from that particular stretch. * Significantly different from stretch of same final fiber length initiated from Lf, alpha  < 0.05.
[View Larger Version of this Image (27K GIF file)]

Table 1. Initial fiber length, final fiber length, displacement, and strain for each single pliometric contraction protocol, along with contractile parameters measured during stretch and subsequent force deficit

Protocol Initial Length, %Lf Final Length, %Lf Relative Displacement, %Lf Strain, %  Peak Force, kN/m2 Average Force, kN/m2 Work, J/kg Power, W/kg Force Deficit, % 
SI-SF 90 150 60 67 660 ± 80  500 ± 20  281 ± 11* 940 ± 40  11 ± 2 
SI-MF 90 160 70 78 780 ± 120  540 ± 40  354 ± 26* 1,010 ± 70  21 ± 2dagger
SI-LF 90 170 80 89 750 ± 50  510 ± 10  383 ± 8  960 ± 20  29 ± 2*
OI-SF 100 150 50 50 590 ± 50  470 ± 20  223 ± 12  890 ± 50  10 ± 2dagger
OI-MF 100 160 60 60 620 ± 30  500 ± 20  281 ± 9  940 ± 30  20 ± 4 
OI-LF 100 170 70 70 880 ± 80  540 ± 20  358 ± 14  1,020 ± 40  42 ± 4dagger
LI-SF 120 150 30 25 590 ± 80  410 ± 30  115 ± 9* 770 ± 60  0 ± 1*
LI-MF 120 160 40 33 630 ± 60  420 ± 20* 159 ± 7* 800 ± 40* 8 ± 1*
LI-LF 120 170 50 42 600 ± 30* 440 ± 20* 206 ± 8* 830 ± 30* 24 ± 8*dagger
Values are means ± SE; n = 7-8 muscles per group. Lf, optimal fiber length; SI, short initial length (90% Lf ); OI, optimal initial length (100% Lf ); LI, long initial length (120% Lf ); SF, short final length (150% Lf ); MF, medium final length (160% Lf ); LF, long final length (170% Lf ). * Significantly different from protocol of same final length beginning at Lf, P < 0.05.  dagger Significantly different from protocol of same relative displacement, P < 0.05.

Table 2. Coefficients of determination of mechanical variables for one-variable and stepwise multipleregression models of force deficit

Variable One-Variable Model (Coefficient of Determination) Stepwise MultipleRegression Model (Partial Coefficient of Determination)
Final length 0.48 0.48
Relative displacement 0.39 NS
Work 0.34 NS
Strain 0.29 0.05
Average force 0.11 NS
Power 0.11 NS
Initial length 0.09 0.07
Peak force 0.09 NS
Model r2 0.60
NS, contribution of variable to variance in force deficit did not reach level of significance necessary for inclusion in stepwise regression analysis; model r2, coefficient of determination of multiple- regression model, including final length, initial length, and strain.

Although the final fiber length was an important determinant of the magnitude of contraction-induced injury, the force deficit was also dependent on the initial fiber length (Fig. 1). For any given final fiber length, muscles that performed a pliometric contraction starting from the longest initial fiber length (120% Lf) exhibited a smaller force deficit than did muscles that performed a pliometric contraction initiated from Lf (Fig. 1). For any given final fiber length, increasing the initial fiber length generally decreased the work input during the stretch because of the decreased displacement of the stretch, and in some cases a decreased average force developed during the stretch (Table 1). On the basis of a stepwise multiple-regression analysis of the individual data points to include multiple variables, the regression equation that contained initial fiber length, strain, and final fiber length provided the best prediction of the force deficit with a total r2 = 0.60 (Table 2).

For all data points, the coefficient of determination obtained between work input and force deficit was r2 = 0.34 (Table 2). Three pairs of protocols imposed stretches of identical relative displacement on muscles starting from different initial fiber lengths (Table 1). Despite no difference in the work input in each pair, in two of these three cases the muscles stretched from the longer initial fiber length demonstrated a greater force deficit than did muscles stretched from the shorter initial fiber length (Fig. 2). Therefore, the specific hypothesis that the force deficit after a single stretch of a maximally activated muscle is determined solely by the work input during the stretch was not supported.

Fig. 2. Force deficit (ascending bars) and work input (descending bars) for 3 pairs of protocols in which stretches of identical relative displacement were imposed on muscles starting from different fiber lengths. x-Axis indicates magnitude of relative displacement for protocols in each pair, and labels above each bar indicate initial and final lengths for individual protocols. SI, short initial length (90% Lf); OI, optimal initial length (100% Lf); LI, long initial length (120% Lf); SF, short final length (150% Lf); MF, medium final length (160% Lf); LF, long final length (170% Lf). Values are means ± SE. * Force deficit different from that for other protocol of identical displacement, alpha  < 0.05.
[View Larger Version of this Image (54K GIF file)]

To separate out the effects of the initial and final muscle fiber length and the work input, a regression analysis of the average values for force deficit and work input was carried out with the protocols categorized by final fiber length (Fig. 3A) and initial fiber length (Fig. 3B). When the protocols were grouped by initial fiber length, the correlations between the average work input during the stretch and the average force deficit exhibited after the stretch were high (r2 = 0.97-0.99), whereas the correlations were lower with the protocols grouped by the final fiber length (r2 = 0.39-0.94). Consequently, despite our finding that the final fiber length was the single best predictor of the magnitude of the force deficit, the differences in force deficits among groups can best be explained on the basis of differences in initial fiber length and work input, rather than differences in work input and final fiber length.

Fig. 3. Relationship between average force deficit after single stretch of maximally activated muscle and average work input during stretch for all protocols. Values are means ± SE for both work and force deficit. A: data grouped by final muscle fiber length reached during stretch. B: data grouped by initial muscle fiber length of stretch. Lines for each series in B are best-fit lines obtained by using linear regression model.
[View Larger Version of this Image (20K GIF file)]

DISCUSSION

Previous investigations of pliometric contraction-induced injury have identified strain (11) and work input (3, 12) as critical mechanical components of the injury process. On the basis of a protocol of 900 repeated pliometric contractions initiated from Lf, Lieber and Friden (11) concluded that the imposed strain is the sole variable determining the magnitude of contraction-induced injury. In contrast, after a single stretch from optimal length of a maximally activated whole muscle (3) or single permeabilized fiber (12), 70-80% of the variation in force deficit was explained by the work input during the stretch. In each of these three studies, the restriction of the pliometric contraction protocols to a single initial length limits the significance of the close relationship observed between the strain or work input and the force deficit. We now report that for single stretches of maximally activated whole muscles initiated from a range of fiber lengths, none of the individual variables examined explained >50% of the variation in force deficit, and even the best stepwise regression model, including multiple variables, explained only 60% of the variation. For each of the eight mechanical variables examined, including imposed strain and work input, differences in the force deficits among protocols were found even when no difference existed in the mechanical variable. We conclude that given the range of contractile conditions experienced in vivo, no single mechanical variable is solely responsible for the totality of contraction-induced injury. These results illustrate the complexity of the mechanical events that initiate damage during pliometric contractions. The strong prediction reported previously (3, 12) of the force deficit after a single stretch from the work input was only supported when the data were grouped by initial fiber length. As in previous studies, for a given initial fiber length the relationship between average work input and average force deficit remained linear (3, 12), but an increase in the initial fiber length appeared to decrease the threshold for a force deficit and increase the slope of the relationship between force deficit and work input.

Our observation of an increased force deficit for muscles activated at longer lengths even when the work input was the same could be explained by an increased heterogeneity in sarcomere lengths. During isometric activation of single fibers, the heterogeneity in sarcomere lengths increases with increasing initial fiber length (5). The working hypothesis that has emerged (3, 12) is that injury occurs during pliometric contractions because of the exacerbation of the sarcomere length heterogeneity developed during isometric activation as the sarcomeres at longer lengths after the isometric activation are lengthened further during the stretch and lose overlap of thick and thin filaments. Brown and Hill (4) demonstrated that the stretch of individual sarcomeres beyond overlap can occur during pliometric contractions of intact single frog fibers. In passive fibers, the thick and thin filaments in sarcomeres stretched beyond overlap failed to interdigitate properly on return to resting length and became damaged (10). Such a phenomenon may explain one type of ultrastructural damage that can occur after stretches of activated muscle fibers. Brooks et al. (3) reported severe ultrastructural damage and force deficit after stretches of passive whole muscles from Lf through strains of 60% or greater, when all the sarcomeres were calculated to be stretched beyond the length at which loss of thick and thin filament overlap occurred. These observations along with those of the present study are consistent with the hypothesis that the stretch of individual sarcomeres beyond overlap during pliometric contractions induces fiber injury.

For single pliometric contractions beginning from Lf, our force deficits were ~50% less than those reported by Brooks et al. (3) for the same strains. Our hold time at the final stretched length after the conclusion of stimulation was 5 ms, compared with a hold time of 100 ms in the study of Brooks et al. To test the hypothesis that the force deficit is a function of the hold time, five EDL muscles of mice performed single pliometric contractions of 60% displacement from Lf with a 100-ms hold time. The resulting force deficits were approximately twice as large as those after pliometric contractions of the same displacement by using a 5-ms hold time. These data support the hypothesis, and we conclude that the smaller force deficits in this study compared with those reported by Brooks et al. result from the shorter hold time. After the cessation of activation, the decline in force production is not immediate. Consequently, it is possible that an increased hold time may result in a greater force deficit through an increase in the number of sarcomeres stretched beyond myofilament overlap or an increase in the ultrastructural damage to sarcomeres already stretched beyond myofilament overlap.

In conclusion, when maximally activated muscles perform single pliometric contractions with variations in both initial and final fiber lengths, no single contractile parameter completely explains the differences observed in the subsequent force deficit. Although the final length to which the muscle fibers are stretched is the best single predictor of the force deficit, differences in force deficit among the groups are best explained on the basis of the initial length of the stretch and the work input during the stretch. The results are consistent with a working model in which muscle fibers are injured by pliometric contractions because of the development of sarcomere length heterogeneity such that some sarcomeres are stretched beyond thick and thin filament overlap.

ACKNOWLEDGEMENTS

This research was supported by National Institute on Aging Grant AG-06157.

FOOTNOTES

Address for reprint requests: J. A. Faulkner, Institute of Gerontology, Univ. of Michigan, Rm. 972-974, 300 N. Ingalls Bldg., Ann Arbor, MI 48109-2007.

Received 11 January 1996; accepted in final form 27 August 1996.

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0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society


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