Abstract

Muscle weakness is a secondary motor symptom of Parkinson’s disease (PD), especially in the subtype characterized by postural instability and gait difficulty (PIGD). Since the PIGD subtype also presents worse bradykinesia, we hypothesized that it also shows a decreased rate of force development, which is linked to an increased risk of falling in PD. Therefore, we investigated the effects of PD and PD subtypes on a force production profile and correlated the force production outcomes with clinical symptoms for each PD subtype. We assessed three groups of participants: 14 healthy older adults (OA), 10 people with PD composing the PIGD group, and 14 people with PD composing the tremor-dominant group. Three knee extension maximum voluntary isometric contractions were performed in a leg extension machine equipped with a load cell to assess the force production. The outcome measures were: peak force and rate of force development (RFD) at 50 ms (RFD50), 100 ms (RFD100), and 200 ms (RFD200). We observed lower peak force, RFD50, RFD100, and RFD200 in people with PD, regardless of subtypes, compared with the OA group (p < 0.05 for all comparisons). Together, our results indicated that PD affects the capacity to produce maximal and rapid force. Therefore, future interventions should consider rehabilitation programs for people with PD based on muscle power and fast-force production, and consequently reduce the likelihood of people with PD falling from balance-related events, such as from an unsuccessful attempt to avoid a tripping hazard or a poor and slower stepping response.

Highlights

  • No statistical difference was observed between Parkinson’s disease (PD) subtypes (TD and postural instability and gait difficulty (PIGD))

  • Lower peak force and RDF50, RDF100, and RDF200 controlling for covariates, such as age, sex, BMI, and only), these results were observed in people with PD, regardless of the subtype, compared to older adults (OA)

  • People with PD exhibited lower rate of force development (RFD) than OA, which might be due to bradykinesia and might be associated with basal ganglia deficits, which contribute to lower agonist activation, which impairs force production in a different extension

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Summary

Introduction

Parkinson’s disease (PD) is characterized by the presence of non-motor and motor symptoms, and reduced muscle function (strength and neuromuscular control) is one of the motor symptoms presented by people with PD [1]. Physiopathological aspects of PD may reflect motor control impairments and can lead to deficits in force modulation and production [2]. The underlying mechanism of the deficiencies in force modulation and force control is not agreed upon, central aspects of these deficits are likely related to impairments in muscle function in PD [3]. Impairments in basal ganglia structures reflect abnormalities in force recruitment [4], for example, by reducing the antagonist muscles’ activation followed by an augmented activation of antagonists muscles

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