November 2013

Energetics of landing: Effects of ankle instability

cloudy-skyA diminished capability for energy dissipation at the knee after ground impact during landing in patients with chronic ankle instability may result in greater demands on the ankle joint. Modifying landing strategies could potentially reduce the risk of musculoskeletal injury.

By Masafumi Terada, MS, ATC, and Phillip A. Gribble, PhD, ATC, FNATA  

Participation in physical activity has an important role in a healthy lifestyle, but it is associated with an inherent risk of injury. Chronic ankle instability (CAI) is common after an initial acute lateral ankle sprain in physically active populations,1-3 preventing patients from returning to their occupations1,4 and leading to decreased health-related quality of life.2,5 CAI is a condition characterized by self-reported disability, perceived instability (repeated episodes of “giving way”), recurrent ankle sprains, or all of these.6,7

Potentially, CAI also may predispose an individual to the early onset of osteoarthritis,8-10 which imposes a severe economic burden on the healthcare system worldwide.11,12 Therefore, CAI is a significant public health concern in the physically active population. While research has examined various factors that may contribute to CAI, with the aim of minimizing the complications of CAI and maximizing the potential health benefits of a physically active lifestyle,13-21 the mechanisms underlying the alterations associated with CAI are not fully understood.

Energy dissipation and CAI

Joint energetics have been suggested as biomechanical factors that contribute to lower extremity injury during a functional task.22 External forces and moments of force resulting from the foot’s impact with the ground during landing and the stance phase of gait can create a kinetic energy event. This can increase velocity at the hip, knee, and ankle joints in the sagittal plane, possibly leading to excessive unintended lower extremity joint motion. An internal force produced by eccentric extensor muscle actions contributes to the dissipation of the impact energy at each lower extremity joint.23,24 It has been proposed that a greater ability to dissipate energy during functional tasks would be beneficial, as the lower extremity joints can provide adequate shock absorption while reducing stresses on the surrounding static joint stabilizers through their wide anatomical range of motion.23,25,26 Thus, investigation of energy dissipation patterns during landing as part of a sports-related functional task may provide insight into the factors contributing to CAI.

In our recent work,27 we observed altered energy dissipation patterns at the knee and ankle during a stop jump task in a CAI population. In participants with CAI the contribution to total energy dissipation was significantly greater at the ankle and less at the knee during the 100-ms interval following initial contact compared with healthy control participants (Figure 1). Therefore, our findings suggest the presence of CAI may alter the kinetic chain relationship throughout the lower extremity.

Individual joints of the lower extremity work together and influence each other during functional activities to provide dynamic joint stabilization throughout the kinetic chain. The demonstrated energy dissipation pattern at the ankle in our study may be an effort to increase landing stiffness and reduce stress on the static stabilizers in the unstable ankle by maximizing the contribution of the plantar flexors.

Suppressed gamma and alpha motoneuron activations and decreased corticospinal excitability in the muscles surrounding the ankle have been observed in individuals with CAI.16,19,28 These inhibitions may make the muscle spindles less sensitive and lead to a decrease in muscle-tendon stiffness through lack of activation or tone in these muscles, resulting in an increase in electromechanical delay (EMD).29 EMD is a measure of the time necessary for activation of a muscle to provide protective tension on its bony attachments and is an indirect indication of muscle stiffness and tone.16,29

It has been reported that EMD of the fibularis longus muscle in individuals with CAI (23.6-33.7 ms) is longer than in those without CAI (19.5-19.8 ms).16,30 The longer EMD associated with CAI may influence the energy dis­sipation pattern during functional tasks. An increase in EMD of the fibularis longus muscle may slow development of the muscle-tendon stiffness necessary for ankle joint protection.29 To compensate for increased EMD and decreased muscle-tendon stiffness following ground impact, individuals with CAI may perform stiff landings at the ankle through a centrally mediated feed-forward compensatory mechanism. As landing stiffness increases, the relative contribution of the ankle plantar flexors increases while those of the knee and hip extensors decrease.23,31

Investigators have described CAI as creating interplay between peripheral afferent nerves and a centrally mediated alteration in sensorimotor control, which is manifested in altered lower extremity movement patterns.32,33 Therefore, it is possible the energy dissipation pattern de­m­on­strated by participants with CAI in our recent investigation may result from alterations in feedback and feed-forward neuromuscular control processes, which likely increases landing stiffness to compensate for an increase in EMD and a decrease in muscle-tendon stiffness and to protect the affected ankle joint.27

Placing greater demands on the ankle joint to dissipate energy with limited ability to transfer force up the kinetic chain, however, could induce rapid fatigability during repetitive movements that may be related to development of CAI.

Potential knee injury implications

There is limited information to suggest a potential link between a history of ankle sprain and risk of knee injury.34,35 Our recent data27 on altered capability of kinetic energy dissipation at the knee joint, combined with previous findings of less knee flexion during a jump-landing task,14,32,36 may provide insight regarding future knee joint injury mechanisms in individuals with CAI.

A more extended knee position, as well as decreased contributions from the knee to total energy dissipation, may contribute to an increase in knee injury risk. Previous authors have suggested that a decreased knee flexion angle during landing can lead to inadequate energy attenuation capability at the knee,22,37 such that the knee joint experiences large compressive impact forces,25 which in turn can lead to cartilage lesions and osteoarthritis38 and increase the risk of anterior cruciate ligament (ACL) injury.22 Further, previous studies  have shown that restricted ankle dorsiflexion range of motion (DF-ROM) increases risk for patellar tendinopathy in young basketball athletes.34,39 Backman et al34 found a lower ankle DF-ROM in limbs with a history of  two or more ankle sprains compared with those with zero or one sprain as well as a trend of a higher incidence of patellar tendinopathy of limbs with two or more ankle sprains compared with those with zero or one ankle sprain.

These findings indicated that a history of ankle sprains may predispose for restricted ankle DF-ROM, potentially increasing risk for developing patellar tendinopathy. It has been observed that participants with restricted ankle DF-ROM have significantly decreased energy dissipation at the knee and increased energy dissipation at the ankle joint compared with those without restricted ankle DF-ROM.40 Altered lower extremity landing biomechanics due to restricted ankle DF-ROM following an ankle sprain may increase load on the patellar tendon and risk for developing patellar tendinopathy.

In addition to diminished relative knee energy dissipation, increasing the demand on the plantar flexors to dissipate kinetic energy may be associated with an increased risk of future knee injury.22,41 An energy dissipation strategy with greater contribution from the ankle plantar flexors may minimize the contribution of the proximal extensor muscles, putting the knee in a potentially injurious position.22,41 Fleming et al42 have observed that greater gastrocnemius contraction results in significant increases in ACL strain when the knee is in a more extended position. Further, soleus muscle inhibition was previously documented in individuals with CAI.28,43 This suggests the gastrocnemius muscle may be responsible for dissipating kinetic energy at the ankle in individuals with CAI. Research has also suggested22 that a landing pattern with greater ankle energy dissipation during the first 100 ms of landing may increase risk of ACL injury by resulting in greater gastrocnemius muscular force, which could contribute to increased ACL load. In our recent investigation27 participants with CAI demonstrated a greater amount of energy dissipated at the ankle during the first 100 ms of landing compared with those without CAI, implying this energy dissipation pattern may have the potential for knee injury risk.

Modifying energy dissipation pattern

It has been accepted that the magnitude of energy dissipation can be controlled by adjusting the orientation of body segments relative to the ground reaction force (GRF) throughout a functional task.23,24,26,44 Sagittal plane lower extremity joint motions during a dynamic task, specifically ankle dorsiflexion and knee flexion, play a significant role in attenuating the forces at impact.23,45 The plantar flexors and knee extensors, which eccentrically control ankle dorsiflexion and knee flexion during landing, dissipate the majority of the kinetic energy.23 Limited availability of ankle dorsiflexion reduces the ability of the knee extensors to decelerate the body’s center of mass (COM) and dissipate landing impact, which increases the demand on the ankle plantar flexors to dissipate energy, resulting in limited ability to transfer force up the kinetic chain.46,47

Norcross et al22 reported a strong association between energy dissipation capability and sagittal plane kinematics at the knee and ankle joints. Decreased availability of ankle dorsiflexion has been observed in the CAI population.48 Additionally, DeVita and Skelly23 observed that landing with smaller knee flexion angles reduced dissipation of the kinetic energy by the knee musculature. It has been reported that participants with CAI demonstrated less knee flexion after initial contact during a jump-landing task than those without CAI.14,36

With an extended knee at landing, the knee extensor muscles are in a less advantageous position to dissipate the experienced external loading after ground impact and store elastic energy.

The strength capability of the knee extensors is one of the critical elements of controlling energetic behaviors.49 Deficits in force production by the knee extensors have been shown in individuals with CAI.13 Decreased force production by the knee extensors also leads to earlier activation of the ankle plantar flexors to provide compensatory dynamic knee stabilization by increasing joint stiffness.50

Therefore, improving the availability of ankle dorsiflexion, increasing knee flexion during a jump-landing task, and improving knee extensor strength may be beneficial for maximizing the capacity for energy dissipation and should be considered as potential clinical interventions in patients with CAI.

However, sagittal plane kinematics at the knee and ankle are simply not enough to explain these relationships. Trunk flexion and stabilization of the body’s COM are also important contributors to energy attenuation capability.24,32,51 Decreased trunk flexion may be a compensatory response to the reduced ability of the knee extensors to decelerate the body and attenuate landing impact.52-54

Several authors have suggested the presence of CAI may influence the location of COM.14,32,43 Improving jump-landing strategies, such as increasing trunk flexion and controlling the location of the COM before and during landing, may also be addressed in clinical interventions for patients with CAI. It will be beneficial for future investigations to determine whether such modifications in those with CAI could reduce both the CAI itself and the risk of future musculoskeletal injuries at the proximal joints.


Figure 1. Energy dissipa- tion strategies demon- strated by participants with CAI (A) and healthy controls (B).

Figure 1. Energy dissipation strategies demonstrated by participants with CAI (A) and healthy controls (B).

The reorganization of the central nervous system with altered feedback responses following an ankle sprain may globally influence movement and muscle activation patterns during functional activities. Our recent work indicates the presence of CAI likely results in a landing strategy that shifts a greater demand for dissipating the kinetic energy of the landing impact to the ankle by increasing knee extension and use of the ankle plantar flexors.

Decreased knee extensor strength, coupled with altered knee kinematics and reduced ankle dorsiflexion availability, may lead to diminished capability for energy dissipation at the knee after ground impact during jump-landing tasks in CAI populations, which may result in greater demands on the ankle joint to attenuate external loading after ground impact. It will be important for clinicians and researchers to understand how the presence of CAI influences energy dissipation patterns in the entire lower extremity.

In the future, it also will be important to consider energetic behaviors associated with CAI that may be used to develop more effective interventions to target these potentially modifiable energy dissipation patterns. Continued work in this area is needed to determine whether the suggested modifications could reduce CAI, improve the level of function related to CAI, and minimize the risk for future knee injury.

Masafumi Terada, MS, AT, ATC, is a doctoral candidate in the Musculoskeletal Health and Movement Science Laboratory, Department of Kinesiology, at the University of Toledo in Ohio. Phillip A Gribble, PhD, ATC, FNATA, is professor of kinesiology, director of the Graduate Athletic Training Education Program, and codirector of the Musculoskeletal Health and Movement Science Laboratory at University of Toledo.

Disclosure: We certify that no party having a direct interest in the results of the research supporting this article has conferred or will confer a benefit on us or on any organization with which we are associated. No conflicts of interest are directly relevant to the content of this study.


1. Hiller CE, Nightingale EJ, Raymond J, et al. Prevalence and impact of chronic musculoskeletal ankle disorders in the community. Arch Phys Med Rehabil 2012;93(10):1801-1807.

2. Anandacoomarasamy A, Barnsley L. Long term outcomes of inversion ankle injuries. Br J Sports Med 2005;39(3):e14.

3. Konradsen L, Bech L, Ehrenbjerg M, Nickelsen T. Seven years follow-up after ankle inversion trauma. Scand J Med Sci Sports 2002;12(3):129-135.

4. Verhagen RA, de Keizer G, van Dijk CN. Long-term follow-up of inversion trauma of the ankle. Arch Orthop Trauma Surg 1995;114(2):92-96.

5. Arnold BL, Wright CJ, Ross SE. Functional ankle instability and health-related quality of life. J Athl Train 2011;46(6):634-641.

6. Gribble PA, Delahunt E, Bleakley C, et al. Selection criteria for patients with chronic ankle instability in controlled research: a position statement of the International Ankle Consortium. J Orthop Sport Phys Ther 2013;43(8):585-591.

7. Hiller CE, Kilbreath SL, Refshauge KM. Chronic ankle instability: evolution of the model. J Athl Train 2011;46(2):133-141.

8. Hirose K, Murakami G, Minowa T, et al. Lateral ligament injury of the ankle and associated articular cartilage degeneration in the talocrural joint: anatomic study using elderly cadavers. J Orthop Sci 2004;9(1):37-43.

9. Valderrabano V, Hintermann B, Horisberger M, Fung TS. Ligamentous posttraumatic ankle osteoarthritis. Am J Sports Med 2006;34(4):612-620.

10. Valderrabano V, Horisberger M, Russell I, et al. Etiology of ankle osteoarthritis. Clin Orthop Relat Res 2009;467(7):1800-1806.

11. Brown TD, Johnston RC, Saltzman CL, et al. Posttraumatic osteoarthritis: a first estimate of incidence, prevalence, and burden of disease. J Orthop Trauma 2006;20(10):739-744.

12. Dibonaventura M, Gupta S, McDonald M, Sadosky A. Evaluating the health and economic impact of osteoarthritis pain in the workforce: results from the National Health and Wellness Survey. BMC Musculoskelet Disord 2011;12:83.

13. Gribble PA, Robinson RH. An examination of ankle, knee, and hip torque production in individuals with chronic ankle instability. J Strength Cond Res 2009;23(2):395-400.

14. Gribble PA, Robinson RH. Alterations in knee kinematics and dynamic stability associated with chronic ankle instability. J Athl Train 2009;44(4):350-355.

15. Hiller CE, Nightingale EJ, Lin CW, et al. Characteristics of people with recurrent ankle sprains: a systematic review with meta-analysis. Br J Sports Med 2011;45(8):660-762.

16. Hopkins JT, Brown TN, Christensen L, Palmieri-Smith RM. Deficits in peroneal latency and electromechanical delay in patients with functional ankle instability. J Orthop Res 2009;27(12):1541-1546.

17. Kaminski TW, Buckley BD, Powers ME, et al. Effect of strength and proprioception training on eversion to inversion strength ratios in subjects with unilateral functional ankle instability. Br J Sports Med 2003;37(5):410-415.

18. McKeon PO, Hertel J. Spatiotemporal postural control deficits are present in those with chronic ankle instability. BMC Musculoskelet Disord 2008;9:76.

19. Pietrosimone BG, Gribble PA. Chronic ankle instability and corticomotor excitability of the fibularis longus muscle. J Athl Train 2012;47(6):621-626.

20. Ross SE, Guskiewicz KM, Yu B. Single-leg jump-landing stabilization times in subjects with functionally unstable ankles. J Athl Train 2005;40(4):298-304.

21. Wikstrom EA, Bishop MD, Inamdar AD, Hass CJ. Gait termination control strategies are altered in chronic ankle instability subjects. Med Sci Sports Exerc 2010;42(1):197-205.

22. Norcross MF, Blackburn JT, Goerger BM, Padua DA. The association between lower extremity energy absorption and biomechanical factors related to anterior cruciate ligament injury. Clin Biomech 2010;25(10):1031-1036.

23. Devita P, Skelly WA. Effect of landing stiffness on joint kinetics and energetics in the lower extremity. Med Sci Sports Exerc 1992;24(1):108-115.

24. McNitt-Gray JL. Kinetics of the lower extremities during drop landings from three heights. J Biomech 1993;26(9):1037-1046.

25. Lafortune MA, Lake MJ, Hennig EM. Differential shock transmission response of the human body to impact severity and lower limb posture. J Biomech 1996;29(12):1531-1537.

26. Zhang SN, Bates BT, Dufek JS. Contributions of lower extremity joints to energy dissipation during landings. Med Sci Sports Exerc 2000;32(4):812-819.

27. Terada M, Pfile KR, Pietrosimone BG, Gribble PA. Effects of chronic ankle instability on energy dissipation in the lower extremity. Med Sci Sports Exerc 2013;45(11):2120-2128.

28. McVey ED, Palmieri RM, Docherty CL, et al. Arthrogenic muscle inhibition in the leg muscles of subjects exhibiting functional ankle instability. Foot Ankle Int 2005;26(12):1055-1061.

29. Mora I, Quinteiro-Blondin S, Perot C. Electromechanical assessment of ankle stability. Eur J Appl Physiol 2003;88(6):558-564.

30. Eechaute C, Vaes P, Duquet W, Van Gheluwe B. Reliability and discriminative validity of sudden ankle inversion measurements in patients with chronic ankle instability. Gait Posture 2009;30(1):82-86.

31. Schmitz RJ, Shultz SJ. Contribution of knee flexor and extensor strength on sex-specific energy absorption and torsional joint stiffness during drop jumping. J Athl Train 2010;45(5):445-452.

32. Gribble P, Robinson R. Differences in spatiotemporal landing variables during a dynamic stability task in subjects with CAI. Scand J Med Sci Sports 2010;20(1):e63-e71.

33. Gutierrez GM, Knight CA, Swanik CB, et al. Examining neuromuscular control during landings on a supinating platform in persons with and without ankle instability. Am J Sports Med 2012;40(1):193-201.

34. Backman LJ, Danielson P. Low range of ankle dorsiflexion predisposes for patellar tendinopathy in junior elite basketball players: a 1-year prospective study. Am J Sports Med 2011;39(12):2626-2633.

35. Kramer LC, Denegar CR, Buckley WE, Hertel J. Factors associated with anterior cruciate ligament injury: history in female athletes. J Sports Med Phys Fitness 2007;47(4):446-454.

36. Terada M, Pietrosimone BG, Gribble PA. Alterations in neuromuscular control at the knee in individuals with chronic ankle instability. J Athl Train (In Press.)

37. Yeow CH, Lee PV, Goh JC. Sagittal knee joint kinematics and energetics in response to different landing heights and techniques. Knee 2010;17(2):127-131.

38. Childs JD, Sparto PJ, Fitzgerald GK, et al. Alterations in lower extremity movement and muscle activation patterns in individuals with knee osteoarthritis. Clin Biomech 2004;19(1):44-49.

39. Malliaras P, Cook JL, Kent P. Reduced ankle dorsiflexion range may increase the risk of patellar tendon injury among volleyball players. J Sci Med Sport 2006;9(4):304-309.

40. You JY, Lee HM, Luo HJ, et al. Gastrocnemius tightness on joint angle and work of lower extremity during gait. Clin Biomech 2009;24(9):744-750.

41. Schmitz RJ, Kulas AS, Perrin DH, et al. Sex differences in lower extremity biomechanics during single leg landings. Clin Biomech 2007;22(6):681-688.

42. Fleming BC, Renstrom PA, Ohlen G, et al. The gastrocnemius muscle is an antagonist of the anterior cruciate ligament. J Orthop Res 2001;19(6):1178-1184.

43. Brown C, Ross S, Mynark R, Guskiewicz K. Assessing functional ankle instability with joint position sense, time to stabilization, and electromyography. J Sport Rehabil 2004;13(2):122-134.

44. McNitt-Gray JL, Hester DM, Mathiyakom W, Munkasy BA. Mechanical demand and multijoint control during landing depend on orientation of the body segments relative to the reaction force. J Biomech 2001;34(11):1471-1482.

45. Gross TS, Nelson RC. The shock attenuation role of the ankle during landing from a vertical jump. Med Sci Sports Exerc 1988;20(5):506-514.

46. Tabrizi P, McIntyre WM, Quesnel MB, Howard AW. Limited dorsiflexion predisposes to injuries of the ankle in children. J Bone Joint Surg Br 2000;82(8):1103-1106.

47. Weinhandl JT, Smith JD, Dugan EL. The effects of repetitive drop jumps on impact phase joint kinematics and kinetics. J Appl Biomech 2011;27(2):108-115.

48. Hoch MC, Staton GS, Medina McKeon JM, et al. Dorsiflexion and dynamic postural control deficits are present in those with chronic ankle instability. J Sci Med Sport 2012;15(6):574-579.

49. Montgomery MM, Shultz SJ, Schmitz RJ, et al. Influence of lean body mass and strength on landing energetics. Med Sci Sports Exerc 2012;44(12):2376-2383.

50. Nyland JA, Caborn DN, Shapiro R, Johnson DL. Fatigue after eccentric quadriceps femoris work produces earlier gastrocnemius and delayed quadriceps femoris activation during crossover cutting among normal athletic women. Knee Surg Sports Traumatol Arthrosc 1997;5(3):162-167.

51. Blackburn JT, Padua DA. Sagittal-plane trunk position, landing forces, and quadriceps electromyographic activity. J Athl Train 2009;44(2):174-179.

52. Blackburn JT, Padua DA. Influence of trunk flexion on hip and knee joint kinematics during a controlled drop landing. Clin Biomech 2008;23(3):313-319.

53. Kulas AS, Hortobagyi T, Devita P. The interaction of trunk-load and trunk-position adaptations on knee anterior shear and hamstrings muscle forces during landing. J Athl Train 2010;45(1):5-15.

54. Kulas AS, Windley TC, Schmitz RJ. Effects of abdominal postures on lower extremity energetics during single-leg landings. J Sport Rehabil 2005;14(1):58-71.

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