Expired Study
This study is not currently recruiting Study Participants on ClinicalConnection.com. If you would like to find active studies please search for clinical trials.

Salt Lake City, Utah 84108


Parkinson disease is a degenerative neurologic condition characterized by slowness of movement, tremor, and loss of balance control. It results in significant degrees of disability for affected individuals. Exercise and medication management are two treatments frequently used to treat Parkinson disease, and although some individuals benefit from these treatments, by what effect exercise works is presently not known. We will examine muscle structure and movement control responses to strengthening exercises and compare them to the therapeutic response observed as a result of medication intake. This process will allow us to better understand the mechanisms underlying the therapeutic effects of strengthening exercise for persons with Parkinson disease.

Study summary:

Idiopathic Parkinson disease (IPD) is the model movement disorder to explore the motor function of the basal ganglia. (Morris ME, 2005) Alterations in the output of the basal ganglia lead to reductions in muscle force output and movement amplitude while inactivity and impaired mobility contribute to the loss of muscle size and strength. Collectively these factors lead to reductions in the size and speed (hypokinesia) of functional movements such as gait. Hypokinesia during gait initiation and gait are biomechanical events that can precipitates movement deficits such as bradykinesia and falls. Previous studies have suggested that resistance training is beneficial in the management of persons with PD. Although anatomic, behavioral, and mobility related improvements have been demonstrated with resistance training intervention, it is unclear if the observed changes are derived solely from peripheral musculoskeletal changes or from central nervous system mediated alterations in force output and movement amplitude. The responsiveness of muscle force, movement amplitude, and hypokinesia to the CNS mediated effects of dopamine replacement provide a model system to which the effects of resistance training can be compared. In order to examine this question, we plan to conduct a controlled trial to rigorously examine the effects of high force resistance training on muscle structure, muscle force output, and hypokinesia in persons with moderate IPD and in the process, characterize the potentially differential effects of resistance training effects and dopamine replacement. This study assembles a team of investigators with experience in high force resistance training, measurement of the biomechanical and clinical balance function in persons with PD, and the statistical analysis expertise. Persons with IPD will be recruited, examined, and if they meet the inclusion criteria will be randomly assigned to one of two groups (experimental or standard care control). A battery of tests including muscle structure, muscle force production, and measures of hypokinesia and will be assessed on and off dopamine replacement medication both prior to and after a 12 week resistance training intervention. The first specific aim of the study is to determine if high force resistance training results in improvements in muscle structure, muscle force output, and hypokinesia in persons with moderate IPD. The second specific aim is to characterize and compare any differential effects of high force resistance training and dopamine replacement on muscle force output and hypokinesia in persons with moderate IPD. We hypothesize that dopamine replacement and resistance training will interact to improve muscle force output and reduce hypokinesia. In addition, we hypothesize that examination of kinematic patterns during gait initiation will reveal differential effects on lower extremity hypokinesia. The results of this study will help to better understand the differential contributions of resistance training and dopamine replacement on hypokinesia in persons with PD.


Inclusion Criteria: male or a female at least 40 years of age or older neurologist diagnosed idiopathic PD (using UK Brain Bank Criteria) ambulatory and medically cleared by their physician to participate in an exercise regimen clinical signs of hypokinesia (reduced movement amplitude during ADL tasks) or postural instability have a Folstein Mini-Mental State Examination score > 23 currently taking dopamine replacement medication Exclusion Criteria: previous surgical management of PD (pallidotomy, DBS) motor fluctuations and or dyskinesias uncontrolled by medications. central nervous system disorder (e.g., other than Parkinson's disease) myopathic disease (e.g., focal myopathy) that affects skeletal muscle structure/function rheumatological disease that has an effect on muscle and/or mobility unstable cardiovascular disease that limits exercise abilities impaired knee flexion, <90 degrees, extreme claustrophobia (secondary to the inability to perform the MRI scans) regular (2-3x/week) aerobic or resistance exercise performed over the past 6 months



Primary Contact:

Principal Investigator
Lee Dibble, PhD, PT
University of Utah Department of Physical Therapy

Backup Contact:


Location Contact:

Salt Lake City, Utah 84108
United States

There is no listed contact information for this specific location.

Site Status: N/A

Data Source: ClinicalTrials.gov

Date Processed: October 09, 2019

Modifications to this listing: Only selected fields are shown, please use the link below to view all information about this clinical trial.

Click to view Full Listing

This study is not currently recruiting Study Participants on ClinicalConnection.com. The form below is not enabled.