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Letters and Responses |
In response to the article, "Passive Versus Active Stretching of Hip Flexor Muscles in Subjects With Limited Hip Extension: A Randomized Clinical Trial" by Winters et al (September 2004), I would like to point out some issues that bring into question the validity of the basic premise of this trial. I believe that both stretching techniques contained an active stretching component; therefore, the results do not meet the stated purpose of the trial.
The authors explained their intent: "The purpose of our study was to determine if there is a difference between active and passive stretching for increasing hip extension [range of motion]...." In the "Design" section, one of the independent variables was "group (passive and active)." It is quite obvious that a purely passive stretch is required to compare and contrast with a stretch that would be considered active.
In the "Intervention" section, the authors described the 2 techniques used as examples of "passive stretching." The first technique was described as follows: "The subject was told to keep the trunk erect and the pelvis in a posterior tilt and to lean forward by flexing the contralateral hip and knee in order to maximize the stretching sensation in the groin of the ipsilateral limb." The commands "keep the trunk erect" and "keep... the pelvis in a posterior tilt" both require active muscle participation to complete the tasks. The inclusion of an active component to the experimental design would seem to automatically render the claim of "passive stretching" moot.
The instruction to "keep a posterior tilt" requires activation of muscles that are antagonists to the hip flexors. Risking oversimplification, both the abdominal muscles and the hip flexors attach to the pelvis and lie anterior to the axis of rotation of the hip joint. The abdominal muscles run proximally, and the hip flexors run distally to attach to the femur. The abdominal muscles can create a posterior tilt by producing a cranially directed force on the pelvis; this motion would actively stretch the hip flexors by pulling cranially on the proximal attachments of the hip flexors. In essence, posterior tilting can produce hip extension.
Posterior tilt also can be accomplished via another muscular force couple, this time involving the hip extensors pulling caudally on the pelvis, posterior to the axis of rotation of the hip joint. Actively tightening the hip extensors was the fundamental requirement for the "active stretching" group, to which the "passive stretching" group was to be compared. Whether the participants maintained posterior tilt via an abdominal strategy or a hip extensor strategy (or both) is not important in this instance because both active strategies invalidate the required "passive" technique. Both posterior tilting muscular strategies would activate muscles that are antagonistic to the hip flexors and would actively stretch the hip flexors at their proximal attachments. The authors further muddy the water by stating, "No subjects were excluded from the study...due to an inability to correctly perform the stretching procedures used in this study."
I appreciate the efforts of any clinician to find better ways of producing therapeutic effects. In this instance, I would argue that what is being compared is not what the authors intended, and any inference of the effectiveness of these techniques should recognize this.
BVANHATTEN{at}WYOMING.COM
The stated purpose of our study was to determine whether there is a difference between active and passive stretching for increasing hip extension range of motion (ROM) in people who have a lower-extremity injury or low back pain and who presumably have hip-flexor muscle tightness.
Van Hatten's main point of disagreement and concern relates to the validity of data for the passive stretching intervention used in our study. In our study, subjects were instructed to keep their trunk erect and maintain a static posterior pelvic tilt. It is his contention that, because a pelvic tilt can produce hip extension, subjects performed an active, not passive, stretch intervention. This would mean, in essence, that 2 different active stretching programs were compared and that no inference could be made from the results of the study as to whether a passive or active stretching intervention is more effective for increasing hip extensor ROM.
Active stretching, as described by proponents of the method,1,2 involves repeated contractions of the primary muscle agonist of the restricted target motion or primary muscle antagonist of the muscle group suspected of being tight and limiting motion. This concept of active stretching also has been reported in the peer-reviewed literature.3 Therefore, in our clinical trial, we chose to use an active stretching intervention that involved the primary hip extensors (gluteus maximus and hamstring muscles) and was consistent with the concept of active stretching.1–3
The purpose of a clinical trial typically is to determine whether there is a difference between the interventions compared. The active and passive techniques compared in our study were operationally defined, are used by clinicians, and are depicted clearly in the figures for the reader. Van Hatten makes the argument that our passive stretching intervention should be considered active because it included a stabilizing contraction. Indeed, a basic premise of any stretching exercise to increase joint ROM is that one segment of the joint needs to be stabilized while the other segment moves in the opposite direction in order for effective stretching to occur. An example would be a stretch of the gastrocnemius muscle. The quadriceps femoris muscle must contract to maintain knee extension; otherwise, dorsiflexion of the ankle will not impart a stretching force to the gastrocnemius muscle. Would anyone argue that the stabilizing force imparted by the quadriceps femoris muscle is considered an active stretching intervention? We do not believe so.
Does the fact that subjects in our study maintained a posterior pelvic tilt constitute an active stretching component? In our opinion, the answer is "no." Contrary to Van Hatten's statement at the end of his letter, the interventions compared in our study were precisely what we intended to compare.
Staff Physical Therapist
Musculoskeletal Care Clinic
Kimbrough Ambulatory Care Center
Fort Meade, Md
Officer in Charge of Physical Therapy
LaPointe Health Clinic
Fort Campbell, Ky
Executive Officer to Air Force Surgeon General
Bolling AFB
Washington, DC
Staff Physical Therapist
Womack Army Medical Center
Fort Bragg, NC
Staff Physical Therapist
Department of Physical Therapy
Walter Reed Army Medical Center
Washington, DC
Executive Fellow
Army Medical Specialist Corps
Fort Sam Houston, Tex
Associate Professor
US Army-Baylor University Graduate
Program in Physical Therapy
MCCS/HMT
3151 Scott Rd, Room 1303
Fort Sam Houston, TX 78234-6138
Robert.Wainner{at}CEN.AMEDD.ARMY.MIL
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