ANALYSIS OF RANGE OF MOTION IN FEMALE RECREATIONAL TENNIS PLAYERS WITH AND WITHOUT LATERAL ELBOW TENDINOPATHY

Abstract

Background:

Intrinsic factors including altered joint motion in the upper extremity may lead to altered biomechanics in tennis players and could result in symptoms of lateral elbow tendinopathy.

Purpose:

To compare upper extremity passive motion and elbow carrying angle between three groups of women: recreational tennis players with LET, non-symptomatic recreational tennis players, and a control group of non-tennis players.

Study Design:

Cross-sectional.

Methods:

A convenience sample of 63 women was recruited and placed into one of the three groups: non-symptomatic tennis players (NSTP), symptomatic tennis players (STP), and a control group. Elbow carrying angle, passive range of motion of the shoulder, elbow, forearm, and wrist were measured during a single session.

Results:

A significant difference was found between the groups for wrist flexion (p < 0.00), forearm pronation (p = 0.002), elbow flexion (p = 0.020) and extension (p = 0.460), as well as shoulder internal rotation (p < 0.00). No significant differences were found in other motions or carrying angle between the three groups (p =0.059). Post-hoc comparisons indicated that shoulder internal rotation and wrist flexion was less in both STP and NSTP groups compared with the control group. Elbow flexion and forearm pronation were greater in STP than the other two groups.

Conclusion:

Impairments including loss of shoulder internal rotation and wrist flexion and greater motion at the elbow and forearm were found in the UE of symptomatic tennis players. Evaluation of passive motion and muscle length should be performed prior to establishing a rehabilitation plan for symptomatic tennis players.

Levels of Evidence:

3

INTRODUCTION

The role of rehabilitation in the conservative management of lateral elbow tendinopathy (LET) remains elusive due to questionable long-term efficacy of improvements in pain, strength, and function.^1,2 A variety of conservative interventions are used clinically; however, no one treatment regimen has been shown to effectively treat LET. Multimodal interventions that include therapeutic exercise and joint mobilizations, local to the elbow or regionally, have been shown to have promising short- and mid-term success in the management of symptoms associated with LET.^3-6 Evidence related to the effectiveness of other therapeutic interventions, such as dry needling,⁷ taping,⁸ and other electrotherapeutic modalities¹ is growing, however, the long-term benefits of these interventions remains unknown.

Conservative management of LET is further confounded by high recurrence rates, with a recent study reporting a recurrence rate of up to 38% within one year of receiving treatment.⁹ Nilsson and colleagues reported that after two-years of being discharged from physical therapy, greater than 50% of patients report pain and functional loss secondary to a relapse in LET.¹⁰

High recurrence rates of LET and the uncertainty of whether conservative management has a positive effect on long-term outcomes, warrants a closer examination of factors contributing to the pathology itself. Many factors, both extrinsic and intrinsic, have been implicated in the etiology of LET. Extrinsic factors include training or technique errors,¹¹ environmental conditions, and the long-term use of equipment that may alter external forces applied to the upper extremity (UE).¹² Intrinsic factors include altered joint osteo- or arthrokinematics as well as muscular imbalances or weakness^13,14 in the UE, that may lead to altered biomechanics and result in microtrauma to the involved tissues.^15-17

Tennis players frequently present with alterations in joint mobility of the UE due to the extreme ranges of motion required in the sport.¹⁸ Because muscles acting on the upper extremity cross multiple joints, their length and tension are affected by joint position. Passive range of motion (PROM) alterations of the UE may lead to improper form with various tennis strokes¹⁹ or may result in changes in the muscular requirements necessary to provide UE dynamic stability or power, each of which could contribute to the development of LET.

Laban et al,¹⁹ in a retrospective study of 19 participants with LET, found that each participant had decreased passive internal rotation of the shoulder. The authors suggested that these participants used increased wrist flexion to compensate for the loss of the passive arc of motion at the shoulder resulting in forceful eccentric contractions on the wrist extensor muscles.²⁰ Abbott et al²⁰ found significant differences in pre-intervention passive shoulder external rotation range of motion (ROM) between the unaffected and affected shoulders of participants with LET. After an intervention of mobilization to the elbow was applied, no significant difference remained in shoulder external rotation ROM.²⁰ These studies seem to suggest that it is possible that alterations in normal UE joint ROM may result in force overloads or stretch-induced trauma to the wrist extensors in tennis players. Furthermore, as the aforementioned studies suggest, more evidence on joint ROM of the elbow, forearm, and wrist in tennis players compared to non-athletes is needed.

In addition to joint motion, the carrying angle of the elbow may be implicated in the development of LET. The carrying angle is the angle between the upper arm and the supinated forearm when the elbow is held in extension.²¹ Normally, a certain degree of valgus is expected between the upper arm and forearm. If the carrying angle of the elbow is atypical, abnormal stresses may further impact the soft tissues at the joint. Researchers have discerned that a long standing varus deformity of the elbow carrying angle has been associated with excessive forces on the lateral collateral ligament²² as well as the osteotendinous interface.²³

The high demands on the extensor musculature from repeated muscular contractions in extreme positions of the UE, abnormal carrying angle at the elbow with or without subtle instability, and extrinsic factors such as alterations in the biomechanics in an individual's tennis swing causing stretch-induced trauma may each contribute to pathophysiology contributing to symptoms of LET. There are no studies that have examined an association between carrying angle and lateral elbow tendinopathy. A better understanding of the intrinsic factors related to joint position and motion that may result in abnormal stresses to the elbow would allow clinicians to focus treatment interventions toward reducing these stresses in individuals with symptomatic LET and provide preventative strategies for the at-risk population. The objective of the study was to compare UE passive motion and elbow carrying angle between three groups of women: recreational tennis players with LET, asymptomatic recreational tennis players, and a control group of non-tennis players.

METHODS

Design: This was a cross-sectional, descriptive analysis of UE joint PROM and carrying angle of the dominant extremity between three groups of subjects.

Participants: A convenience sample of women was recruited from local tennis clubs and neighborhoods. Sixty-three participants satisfied the eligibility criteria for inclusion in one of the three groups for a one-time testing session. A group consisting of female recreational tennis players with symptoms of LET in the dominant extremity (STP) and two samples of active adult females with no elbow pain: one a control group and the other a sample of female tennis players without symptoms of LET (NSTP), were recruited. An a priori power analysis indicated that at an alpha level of 0.05, and a conventional large effect size of 0.40 for a power of 0.80, a minimum sample of 21 per group was required.²⁴ This study was approved by the Institutional Review Board of Mercer University (H1906153_01) and written informed consent was obtained from all participants.

Inclusion Criteria

Females between 18-65 years of age were eligible to participate. Tennis players were required to be actively involved in recreational tennis play at least twice a week for 10 weeks immediately preceding data collection.

To qualify for inclusion in the symptomatic LET group of recreational tennis players, three out of four diagnostic criteria^25,26 must have been met for inclusion. All diagnostic criteria were required to be negative for a participant to be included in one of the asymptomatic groups, including pain local to the lateral epicondyle, replication of pain with palpation, pain with Mill's long extensor stretch maneuver, and pain with resisted wrist extension (Figure 1).

Figure 1.

Diagnostic Criteria.

Exclusion Criteria

Participants were excluded by phone interview if they had undergone previous surgery to the elbow or shoulder, had a history of rheumatoid disease or neurologic impairment or had recent (less than one year) surgery to the upper quarter. They were excluded if the participant participated in professional tennis activities or if they participated in sports activities regularly (on a twice weekly basis or more) that required extremes of motion of the dominant upper extremity including other racket sports, pitching, swimming, golf, or weight-training. Subjects were excluded if they did not demonstrate sufficient fluency in spoken or written English to communicate with the research examiner. Those participants who qualified after phone interview were invited for further examination. Those participants whose differential diagnosis tests were negative, ruling out possible cervical radiculopathy, radial tunnel syndrome, and signs of intra-articular elbow dysfunction (including posterior lateral rotatory instability, joint crepitus, popping, or mechanical joint block to motion) were invited to participate and were subsequently tested for group assignment (Figure 2).

Figure 2.

Differential diagnosis tests.

Procedure

A questionnaire was administered to all participants to collect data on demographics, activity levels, and tennis specific information, if applicable. Dependent variables including elbow carrying angle and PROM (shoulder, elbow, forearm and wrist) of the dominant UE were collected by the same examiner during a single session for each participant. The PROM and stabilization procedures followed guidelines as outlined by the American Society of Hand Therapists in a seated position for the wrist and in supine for the elbow.²¹ Intra-rater reliability of UE passive motion measurement using a goniometer has been previously established.^27-30 Intraclass correlation coefficients (ICC) range from 0.86 to 0.99, ^27-30 except for forearm pronation (ICC=0.79)²⁷ and wrist extension (ICC = 0.66 to 0.94).²⁸ The carrying angle of the elbow was measured in standing with the elbow in zero degrees of extension and the forearm in supination (Figure 3). A single examiner recorded the resting measurement with no application of pressure. Prior to each PROM measurement, the participant was passively moved by the investigator for one repetition to the point of a firm end-feel to demonstrate the action.

Figure 3.

Measurement of elbow carrying angle.

DATA ANALYSIS

Statistical Procedures

Statistical analysis included measures of central tendency and variability for the descriptive data. Dependent variables were compared between the three groups using one-way analysis of variance (ANOVA). Post hoc analysis was conducted using the Bonferroni multiple comparison procedure using SPSS. The significance level was set at p < .05 level.

PARTICIPANTS

Results

Sixty-seven participants underwent physical examination, but four were excluded from the study with suspected cervical spine pathology or for otherwise not meeting diagnostic criteria. Sixty-three participants, with a mean age of 44.9 ( + 8.1) years satisfied the eligibility criteria for inclusion in one of the three groups. Descriptive characteristics for the groups are presented in Table 1. Comparison of means using an ANOVA revealed no significant differences between the STP, the NSTP and the control groups for the variables of age (p = .33) or body mass index (BMI) (p = .72). Comparison of means using independent t-tests revealed no significant differences between the STP and the NSTP groups in years of tennis play (p = .23), days played per week (p = .83) or hours of daily tennis play (p = .49).

Table 1.

Participant Characteristics. Values are mean ± SD (range) unless otherwise indicated.

Variable	STP (n=21)	NSTP(n=21)	Controls (n=21)	p-values
Age(yrs)	44.9 ± 5.2	46.8 ± 9.9	43.0 ± 8.4	.329
BMI (kg/m2)	23.7 ± 3.0	23.9 ± 2.9	23.2 ± 3.6	.536
Years of tennis play	9.48 ± 9.0	13.95 ± 14.0	n/a	.226
Days of tennis play per week	2.48 ± .068	2.43 ± 0.75	n/a	.830
Hours of tennis play per day	1.90 ± 0.54	2.00 ± .32	n/a	.489

Abbreviations: BMI = body mass index; NSTP = non-symptomatic tennis players; STP = symptomatic tennis players. No statistically significant differences were found among groups (p>0.05).

No participant was currently receiving treatment for a neck condition or experiencing neck pain at the time of data collection. Those participants in the NSTP and control groups who reported elbow pain in the past 90 days indicated on the diagram within the questionnaire that the pain was not located at the lateral epicondylar region. Participants in the STP group reported duration of symptoms for a mean duration of 26.4 weeks ( + 16).

Passive Range of Motion

A significant difference was found between the groups for wrist flexion (p<0.00), forearm pronation (p = 0.002), elbow flexion (p = 0.020) and extension (p=.0460), as well as shoulder internal rotation (p < 0.00). (Table 2). No significant differences were found among the three groups for carrying angle (p = 0.246) or PROM of wrist extension (p = 0.972), radial (p = 0.201) and ulnar deviation (p = 0.256), forearm supination (p = 0.059), shoulder flexion (p = 0.835), abduction (p=.0625), and external rotation (p = 0.333).

Table 2.

Passive range of motion and elbow carrying angle results (all are reported in degrees).

$$$		Mean	95% CI
			Lower	Upper	p-value
Shoulder Flexion	STP	179.52	175.52	183.53	.835
	NSTP	179.86	176.00	183.72
	Control	178.38	174.87	181.89
Shoulder Abduction	STP	182.48	179.88	185.07	.625
	NSTP	180.90	177.62	184.19
	Control	180.62	177.45	183.79
Shoulder IR	STP	60.00	56.80	63.20	<.001*
	NSTP	60.57	57.40	63.74
	Control	68.86	65.55	72.16
Shoulder ER	STP	98.62	96.09	101.14	.333
	NSTP	96.19	92.82	99.56
	Control	95.52	91.89	99.16
Elbow Flexion	STP	156.67	154.63	158.70	.020*
	NSTP	152.57	149.81	155.33
	Control	156.38	154.25	158.51
Elbow Hyper-Ext	STP	8.38	6.71	10.05	.046*
	NSTP	5.19	3.09	7.29
	Control	5.95	3.97	7.93
Pronation	STP	87.43	84.48	90.37	.002*
	NSTP	80.14	76.93	83.36
	Control	82.29	79.69	84.88
Supination	STP	96.48	93.37	99.58	.059
	NSTP	92.10	88.84	95.35
	Control	92.43	89.99	94.87
Wrist Flexion	STP	83.33	79.94	86.73	<.001*
	NSTP	80.48	75.90	85.05
	Control	92.10	90.19	94.00
Wrist Extension	STP	80.24	77.60	82.87	.972
	NSTP	79.90	76.10	83.71
	Control	80.43	77.06	83.80
Wrist Ulnar Deviation	STP	41.43	39.00	43.86	.256
	NSTP	40.48	37.58	43.37
	Control	43.43	40.79	46.07
Wrist Radial Deviation	STP	22.76	20.84	24.69	.201
	NSTP	20.52	18.34	22.71
	Control	22.43	20.67	24.18
Elbow Carrying Angle	STP	9.62	7.86	11.38	.246
	NSTP	10.52	9.35	11.70
	Control	8.90	7.68	10.13

STP=symptomatic tennis players; NSTP=non-symptomatic tennis players; 95%CI = 95% confidence interval; IR = internal rotation; ER = external rotation

* indicates a significant difference at p<0.05

Post-hoc comparisons using the Bonferroni correction indicated that passive forearm pronation was significantly greater in the STP when compared with the NSTP and control groups. Passive elbow flexion was significantly greater in the STP and control groups when compared to the NSTP group. Passive wrist flexion and shoulder internal rotation were significantly greater in the control group compared with both groups of tennis players. (Table 3).

Table 3.

Pair-wise comparisons for PROM using Bonferroni test Mean Difference (all are reported in degrees).

Pair-wise comparison	Wrist flexion	Forearm pronation	Elbow hyperextension	Elbow flexion	Shoulder IR
STP and NSTP	2.86	7.29*	3.19	4.10*	0.57
NSTP and Control	11.62*	2.14	0.76	3.81*	8.86*
STP and Control	8.76*	5.14*	2.43	0.29	8.29*

STP=symptomatic tennis players; NSTP=non-symptomatic tennis players; hyper-ext = hyperextension; IR = internal rotation; reported in absolute values

* indicates a significant difference at p<0.05

The total arc of passive motion was calculated for shoulder internal/external rotation, forearm rotation, wrist ulnar and radial deviation, as well as for elbow and wrist flexion and extension. No significant differences were found among the three groups in total passive motion for wrist ulnar/radial deviation. However, significant differences among the three groups in the total arc of motion were detected in all other joints (p ≤ .015) (Table 4). Pair-wise comparisons using the Bonferroni test for total arc of passive motion indicated that there were differences between groups that were not evident with isolated measurements (Table 5). Specifically, sagittal plane arc of motion comparisons at the wrist indicated differences with the STP group being less than control, albeit greater than NSTP group. With regard to forearm rotation, the STP group had greater total ROM than both the NSTP and control groups. The total arc of elbow ROM in the sagittal plane was greater in the STP when compared to NSTP. Differences were also present for shoulder rotation with the control group having a trend for greater ROM than the NSTP and STP groups.

Table 4.

Total arc of passive range of motion (all are reported in degrees).

$$$		Mean	95%CI
			Lower	Upper	p-value
Wrist sagittal plane motion	STP	163.57	158.43	168.71	.011*
	NSTP	160.38	152.72	168.04
	Control	172.52	167.99	177.06
Wrist coronal plane motion	STP	64.19	61.45	66.93	.075
	NSTP	61.00	57.30	64.70
	Control	65.86	63.00	68.71
Forearm rotation	STP	183.90	179.40	188.41	.001*
	NSTP	172.24	166.82	177.66
	Control	174.71	171.99	177.44
Elbow sagittal plane motion	STP	165.05	162.47	167.63	.002*
	NSTP	157.76	154.22	161.31
	Control	162.33	159.94	164.73
Shoulder rotation	STP	158.62	155.19	162.06	.015*
	NSTP	156.76	152.64	160.89
	Control	164.38	160.28	168.48

STP=symptomatic tennis players; NSTP=non-symptomatic tennis players; n = number in the sample; SD=standard deviation; 95%CI = 95% confidence interval

* indicates significant difference at p<0.05

Table 5.

Pair-wise comparisons for total arc of PROM using Bonferroni test.

Mean Difference (all are reported in degrees)
Pair-wise comparison	Shoulder rotation	Elbow sagittal plane motion	Forearm rotation	Wrist sagittal plane motion
STP and NSTP	1.86	7.29*	11.67*	3.19
NSTP and Control	7.62*	4.57	2.48	12.14*
STP and Control	5.76	2.71	9.19*	8.95

STP=symptomatic tennis players; NSTP=non-symptomatic tennis players; hypertext = hyperextension; IR = internal rotation; absolute values reported

* indicates significant difference at p<0.05

DISCUSSION

This study compared UE passive motion and elbow carrying angle between STP, NSTP, and a control group of non-tennis players. An important finding from this study was that passive forearm pronation was significantly greater in the affected arm of the STP group when compared with the forearms of the NSTP and control groups. The total arc of forearm pronation and supination motion was also greater than the other two groups. Total arc of elbow flexion and extension was significantly greater in the STP group as well, suggesting a pattern of excessive elbow and forearm passive motion among STP.

When the elbow is in full extension with forearm pronation, as in the follow through of a tennis serve, the extensor carpi radialis brevis (ECRB) muscle fibers are in a stretched position which may make them more vulnerable to irritation compared to when the elbow and forearm are in midposition.³¹ The shearing forces on the undersurface of the ECRB may be made worse when the forearm is pronated due to the head of the radius rotating anteriorly against the undersurface of the ECRB.³² This effect has been established in a study by Bunata et al³³ who assessed the elbows of 60 cadavers (85 examinations on 30 males and 30 females with mean age of 73 years) and found that with the elbow extended, the ECRB undersurface made contact with the lateral edge of the capitellum. The authors of the aforementioned study also noted that the extensor carpi radialis longus (ECRL) may act to compress the ECRB against the underlying bone due to its more superficial position related to the ECRB.³³ Interestingly tennis players have considerable forearm muscle hypertrophy compared to controls potentially enhancing compression along the underlying skeletal structures.³⁴

Several authors advocate stretching of the forearm musculature in the treatment of LET with the elbow extended, forearm pronated and wrist flexed.³⁰,^35-39 However, because hypermobility of joints of the upper or lower extremities in other athletes has been associated with increased injury rates,³²,^40-45 one should be cautious of over-stretching flexible musculature and joints (Figures 4 and 5). This is especially true for women and children since general hypermobility is more common in these individuals.^43,46 Of further consideration and caution is the possibility that the ECRB may have irritation occurring on its underside from contact with radial head and/ or capitellum, and stretching the structures would essentially replicate the mechanism of injury. Overstretching the elbow into hyperextension and the forearm into excessive pronation should be avoided in tennis players with symptoms of LET who demonstrate adequate flexibility at the elbow and forearm, and which is supported by Kwak and colleagues who found that subtle instability is present in elbows with lateral epicondylalgia.⁴⁷

Figure 4.

Excessive Elbow Extension.

Figure 5.

Excessive Forearm Pronation.

Ligamentous hyperlaxity and over-lengthened muscles in the forearm may lead to osteophyte formation and valgus extension overload.^48,49 Ligamentous hyperlaxity may also lead to deficits in proprioceptive feedback within the sensorimotor system due to diminished mechanoreceptor functioning in the periarticular tissues including ligaments, joint capsule, tendon, and muscle around the joint. Although there are no known studies that directly document the effect of ligamentous hyperlaxity on joint proprioception at the elbow, the effect of ligamentous laxity on the knee and ankle proprioception are well documented.^50-52 It is possible that hyperlaxity may be related to the altered motor responses, such as decreased fine motor control,⁵³ abnormal EMG findings,^54,55 and changes in force production⁵⁶ seen in patients with LET.

The results of the current study also indicate that both the symptomatic and asymptomatic tennis player groups had limitations in passive shoulder internal rotation and in passive wrist flexion compared with the control group. Because the limitations in wrist flexion and shoulder internal rotation motion are equally present in the symptomatic and NSTP groups, one would question whether these deficits in PROM are directly related to symptoms at the elbow. However, the results of this study cannot discern a cause or effect. Several authors who have studied tennis players have reported similar results in the shoulder with significantly lower internal rotation ROM in the dominant arm when compared to the non-dominant arm.^57-60 This adaptation is considered to be a factor that may increase the risk of UE injury in overhead athletes.^60,61 Kibler et al⁶² have documented that the losses in internal rotation are progressive over time in competitive tennis players. These adaptations may be too readily accepted by the athlete as merely part of the sport and may not appear to adversely affect functional activity.⁵⁹ However, many authors assert that these changes may be indicative of overuse and injury of the musculature and/or shoulder capsule and may predispose the athlete to otherz injuries.^20,57,58,60,^62-64

Laban and colleagues¹⁹ propose a technique error that results in compensatory muscle action by the wrist extensors when attempting to compensate for an “elbow leading” backhand. The wrist extensors are overused in a lengthened position in attempts to drive the ball by “snapping” the wrist into extension for power during the backhand drive.¹⁹ This may lead to excessive stress on the extensor expansion at its attachment to the lateral epicondyle during the backhand stroke and may result in connective tissue changes that might effectively shorten the wrist extensors thus limiting wrist flexion. This hypothesis is supported by Morris et al⁶⁵ who found high activity in the wrist extensors in each of the tennis swings as demonstrated with analysis via electromyography.

The current evidence of increased passive motion of the forearm and elbow coupled with the loss of glenohumeral internal rotation range of motion and wrist flexion should be considered when establishing a treatment plan for symptomatic tennis players and when establishing a preventative exercise regimen for non-symptomatic tennis players. Muscle length and joint motion impairments identified in the evaluation should be addressed with stretching in attempts to restore normal arm function and minimize risk of injury.^58,60,62 For example, because forearm pronation is a component motion of upper limb internal rotation, excessive forearm pronation during the tennis swing may be a compensatory pattern for loss of shoulder motion.⁶⁶ Therefore, the loss of shoulder internal rotation should be considered in the therapeutic management of LET by addressing soft tissue restrictions. The posterior capsule and shoulder external rotator trigger points have been specifically implicated in the loss of glenohumeral internal rotation range of motion.^67,68 It is prudent to also consider that PROM limitations in tennis players may be normal adaptations serving to protect the player from injury or that may serve to improve performance.⁶⁰ Nevertheless, the results from this study suggest that a full evaluation of PROM and muscle length is needed to establish an appropriate treatment program for tennis players.

LIMITATIONS

This study was cross-sectional; therefore, greater motion at the elbow and forearm cannot be assumed to be a risk factor for developing LET. Additionally, no variables related to sensorimotor function were measured. This study included a small sample of female participants who, except the control group, played recreational tennis; therefore, the results cannot be generalized to males or other levels of tennis players. Future research is needed examining potential alterations in range of motion, joint mobility, and sensorimotor functioning, including joint proprioception, of the upper extremity in other populations with LET.

CONCLUSION

The results of this study demonstrate that differences in UE joint motion exist in tennis players with lateral elbow tendinopathy compared with non-tennis players and non-symptomatic tennis players. Impairments including loss of shoulder internal rotation and wrist flexion coupled with greater motion at the elbow and forearm may contribute to abnormal stresses in the UE symptomatic tennis players. The results implicate the need for clinicians to focus treatment interventions toward motion impairments at the shoulder in individuals with symptomatic lateral elbow tendinopathy while considering other more flexible joints at the forearm and elbow. Evaluation of passive motion and muscle length should be performed prior to establishing a rehabilitation plan for symptomatic tennis players.