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INFLUENCE OF HORMONES ON KNEE JOINT LAXITY AND JOINT MECHANICS IN HEALTHY FEMALES
Presentation 0755, Joint Mechanics. 14:15, Room 201ABC
S142
INFLUENCE OF HORMONES ON KNEE JOINT LAXITY AND JOINT MECHANICS IN HEALTHY FEMALES S.K. Park¹, D.J. Stefanyshyn¹, D.A. Hart², B. Loitz-Ramage², J.R. Ronsky³ ¹Human Performance Laboratory, Faculty of Kinesiology, ²McCaig Centre for Joint Injury & Arthritis Research, Faculty of Medicine, ³Department of Mechanical Engineering, University of Calgary, Canada email: [email protected], web: www.kin.ucalgary.ca/hpl INTRODUCTION Increased female participation in sports activities has resulted in an increased incidence of joint injuries such as Anterior Cruciate Ligament (ACL) tears. It has been reported that females tear their ACL two to eight times more frequently than their male counterparts [1] but factors contributing to this gender difference remain unclear. Recently, hormonal influences on joint laxity and the ACL have been suggested as a strong potential factor for the higher ACL injury incidence among female athletes [2]. Thus, this study investigated the effects of hormones on knee joint laxity and lower extremity biomechanics which may increase female athletes’ injury risk.
There were also significant decreases in peak knee rotational moments during the ovulatory phase (Figure 1). *
Moment (Nm)
Follicular
*
Ovulation
*
Luteal
20
15
*
10
5
METHODS Healthy females (n=18), who have a normal menstrual cycle (29.22 ± 3.1 days) and do not take oral contraceptive agents, were recruited for the study. Serum estradiol, and progesterone levels, right knee joint laxity (KT-2000 arthrometer), lower extremity kinematics/kinetics, and electromyographic (EMG) measurements were recorded at three times during the subjects’ menstrual cycles. The first measurements (follicuar phase) were taken between day 3 and 7 when both hormonal levels are expected to be low. The second data collection (ovulation) occurred within 24 to 48 hours after estrogen surge based on the ovulation predictor kit (Clearblue, Beford, UK) results. The third data collection (luteal phase) occurred approximately 7 days later following the peak estrogen surge. Hormone levels & phases were compared against knee joint laxity measurements. Joint kinematics, kinetics, and EMG data using motion analysis were analyized during various tasks: walking, running, cutting, jumping, and landing. All the measurements were performed by one experimenter to eliminate interater differences. RESULTS AND DISCUSSION Estradiol and progesterone levels differed significantly across the three testing sessions. The highest estradiol and progesterone levels were found on the luteal test day. Knee laxity increased during the ovulation phase (Table 1). Based on a multiple regression analysis, estradiol and progesterone levels explains 80.1 % of the maximum knee laxity: maximum knee laxity (mm) = 11.075 + coefficients + 0.002*(estradiol) + 0.01*(progesterone) (R² = 0.801). The coefficients in the multiple regression analysis are subject specific.
0
run
cut
land
Figure 1 Knee rotational moment (Nm) during movement testing at three phases (run: external rotation, cut: internal rotation, land: external rotation moment) (* P <0.05). CONCLUSIONS Significant changes were found in knee laxity from the follicular to the luteal phases of the menstrual cycle with increased knee joint laxity during the ovulatory phase. This indicates that the effect of hormones on increased knee laxity may be greater during the ovulation phase. Since there is an antagonistic relationship between two hormones in the ACL tissue [3], the effect of estrogen on knee laxity may be decreased during the luteal phase because of the high level of progesterone. Interestingly, there was a tendency towards decreased peak knee rotational moment during ovulatory phase when knee laxity increased. This decreased joint loading may be a protective joint mechanism in healthy subjects. However, it is not known to what degree this decreased joint loading may compensate for increased joint laxity in order to prevent injury. Further investigation of EMG patterns may help to understand the relationship between knee laxity, muscle activity and joint biomechanics. REFERENCES 1. Arendt E., Dick R. Am J Sports Med 23, 694-701, 1995 2. Shultz SJ., et al. MSSE 36, 1165-1174, 2004 3. Romani W., et al. J Women’s Health 12 287-298, 2003 ACKNOWLEDGEMENTS: CIHR Gender and Health
Table 1 Hormone levels (estradiol & progesterone) and knee joint laxity at three test intervals (mean ± SD). Variables Follicular phase Ovulation phase Luteal phase ( 6.33 ± 1.50 days) (16.06 ± 3.54 days) (23.39 ± 3.62 days) 162.64 ± 85.23 305.61 ± 167.04 478.28 ± 296.30 Estradiol (pmol/L) 3.46 ± 1.55 9.94 ± 7.64 36.05 ± 19.97 Progesterone (nmol/L) 13.45 ± 2.38 14.90 ± 2.70* 14.85 ± 2.60* Manual max knee laxity (mm) 4.84 ± 1.77 5.29 ± 1.74* 4.91 ± 1.53 89N knee laxity (mm) * Indicate > follicular phase (P<0.05) Journal of Biomechanics 40(S2)
XXI ISB Congress, Podium Sessions, Monday 2 July 2007
S142
INFLUENCE OF HORMONES ON KNEE JOINT LAXITY AND JOINT MECHANICS IN HEALTHY FEMALES S.K. Park¹, D.J. Stefanyshyn¹, D.A. Hart², B. Loitz-Ramage², J.R. Ronsky³ ¹Human Performance Laboratory, Faculty of Kinesiology, ²McCaig Centre for Joint Injury & Arthritis Research, Faculty of Medicine, ³Department of Mechanical Engineering, University of Calgary, Canada email: [email protected], web: www.kin.ucalgary.ca/hpl INTRODUCTION Increased female participation in sports activities has resulted in an increased incidence of joint injuries such as Anterior Cruciate Ligament (ACL) tears. It has been reported that females tear their ACL two to eight times more frequently than their male counterparts [1] but factors contributing to this gender difference remain unclear. Recently, hormonal influences on joint laxity and the ACL have been suggested as a strong potential factor for the higher ACL injury incidence among female athletes [2]. Thus, this study investigated the effects of hormones on knee joint laxity and lower extremity biomechanics which may increase female athletes’ injury risk.
There were also significant decreases in peak knee rotational moments during the ovulatory phase (Figure 1). *
Moment (Nm)
Follicular
*
Ovulation
*
Luteal
20
15
*
10
5
METHODS Healthy females (n=18), who have a normal menstrual cycle (29.22 ± 3.1 days) and do not take oral contraceptive agents, were recruited for the study. Serum estradiol, and progesterone levels, right knee joint laxity (KT-2000 arthrometer), lower extremity kinematics/kinetics, and electromyographic (EMG) measurements were recorded at three times during the subjects’ menstrual cycles. The first measurements (follicuar phase) were taken between day 3 and 7 when both hormonal levels are expected to be low. The second data collection (ovulation) occurred within 24 to 48 hours after estrogen surge based on the ovulation predictor kit (Clearblue, Beford, UK) results. The third data collection (luteal phase) occurred approximately 7 days later following the peak estrogen surge. Hormone levels & phases were compared against knee joint laxity measurements. Joint kinematics, kinetics, and EMG data using motion analysis were analyized during various tasks: walking, running, cutting, jumping, and landing. All the measurements were performed by one experimenter to eliminate interater differences. RESULTS AND DISCUSSION Estradiol and progesterone levels differed significantly across the three testing sessions. The highest estradiol and progesterone levels were found on the luteal test day. Knee laxity increased during the ovulation phase (Table 1). Based on a multiple regression analysis, estradiol and progesterone levels explains 80.1 % of the maximum knee laxity: maximum knee laxity (mm) = 11.075 + coefficients + 0.002*(estradiol) + 0.01*(progesterone) (R² = 0.801). The coefficients in the multiple regression analysis are subject specific.
0
run
cut
land
Figure 1 Knee rotational moment (Nm) during movement testing at three phases (run: external rotation, cut: internal rotation, land: external rotation moment) (* P <0.05). CONCLUSIONS Significant changes were found in knee laxity from the follicular to the luteal phases of the menstrual cycle with increased knee joint laxity during the ovulatory phase. This indicates that the effect of hormones on increased knee laxity may be greater during the ovulation phase. Since there is an antagonistic relationship between two hormones in the ACL tissue [3], the effect of estrogen on knee laxity may be decreased during the luteal phase because of the high level of progesterone. Interestingly, there was a tendency towards decreased peak knee rotational moment during ovulatory phase when knee laxity increased. This decreased joint loading may be a protective joint mechanism in healthy subjects. However, it is not known to what degree this decreased joint loading may compensate for increased joint laxity in order to prevent injury. Further investigation of EMG patterns may help to understand the relationship between knee laxity, muscle activity and joint biomechanics. REFERENCES 1. Arendt E., Dick R. Am J Sports Med 23, 694-701, 1995 2. Shultz SJ., et al. MSSE 36, 1165-1174, 2004 3. Romani W., et al. J Women’s Health 12 287-298, 2003 ACKNOWLEDGEMENTS: CIHR Gender and Health
Table 1 Hormone levels (estradiol & progesterone) and knee joint laxity at three test intervals (mean ± SD). Variables Follicular phase Ovulation phase Luteal phase ( 6.33 ± 1.50 days) (16.06 ± 3.54 days) (23.39 ± 3.62 days) 162.64 ± 85.23 305.61 ± 167.04 478.28 ± 296.30 Estradiol (pmol/L) 3.46 ± 1.55 9.94 ± 7.64 36.05 ± 19.97 Progesterone (nmol/L) 13.45 ± 2.38 14.90 ± 2.70* 14.85 ± 2.60* Manual max knee laxity (mm) 4.84 ± 1.77 5.29 ± 1.74* 4.91 ± 1.53 89N knee laxity (mm) * Indicate > follicular phase (P<0.05) Journal of Biomechanics 40(S2)
XXI ISB Congress, Podium Sessions, Monday 2 July 2007