ReviewThe how and why of arm swing during human walking
Highlights
► The mechanisms and functions of arm swing in human gait are discussed. ► Arm swing is largely passive but active control is required as well. ► This active component may be generated by Central Pattern Generators (CPGs). ► To explain function, some examples from pathological arm swing are given. ► Ways in which arm swing may be used as a therapeutic aid are presented.
Introduction
Humans walk bipedally, and thus, it is unclear why we normally swing our arms during gait, as this has no direct function for propulsion. As a consequence, most (clinical) studies on gait tend to ignore arm swing altogether, and modeling studies often lump head (H), arms (A) and trunk (T) into a HAT unit assuming that this unit moves as one mass.
Still, some of the earliest studies on gait also included analysis of the arm movements during gait. These studies suggested that the arms swing purely passively,2 as a consequence of the movements of the thorax, gravity, and inertia [1], [2]. In addition, the first full gait analysis, performed by Braune and Fischer also included detailed descriptions of arm movements during gait [3], although these movements are merely reported, not interpreted. More than 40 years after the study by Braune and Fischer, Elftman [4] used their data to analyze arm swing during walking in detail, and concluded that since net moments in the shoulder joints were present, arm swing during gait is not passive, and driven by muscle activity. Only several years later, these ideas were confirmed by electromyographic findings by Fernandez Ballesteros [5] and Hogue [6]. Later studies however, reasoned that such active shoulder torques are only small, and suggested that arm swinging may be largely passive [7], [8]. To date, the debate of how arm swing comes about (i.e. whether it is caused by accelerations of the shoulder girdle or muscular activity) seems to be still going on [8], [9], [10], [11].
Apart from the question whether arm swing is actively controlled or merely passive, there seems to be no consensus on why humans swing their arms during gait (i.e. what the purpose of arm swing is, if it has a purpose at all). Suggested reasons include minimizing energy consumption, optimizing stability, and optimizing neural performance.
In the present review, we aim at giving an overview of why and how humans swing their arms during gait. First, we will discuss the potential (dis) advantages of having swinging arms. Second, we will go into detail on the debate whether arm swing is arising actively or passively. Third, we will describe the possible function of the active muscular contribution to arm swinging in normal gait, and discuss the possibility that a Central Pattern Generator (CPG) generates this activity. Fourth, we will discuss examples from pathological cases, in which arm swinging is affected. Lastly, using the ideas presented in earlier parts of this paper, we will suggest ways in which arm swing may be used as a therapeutic aid.
Section snippets
Arm swing: why?
Regardless of whether arm swing is passive or active, or partly passive and partly active (which seems most likely), one of the important questions is why humans walk with their arms swinging out of phase with the legs. Over the years, multiple reasons have been suggested, including optimizing stability, optimizing energy consumption, and maximum use of the neuronal heritage of quadrupedal gait. Below, we will outline findings of the former two ideas (i.e. arm swing to optimize stability, and
Arm swing: how?
As outlined in the introduction, the question whether arm swing is passive or active was one of the first questions asked when arm swing was studied. An obvious first step is to calculate net joint moments in the shoulder during gait. Elftman [4] was the first to do so, and reported shoulder moments up to 7.5 Nm. These findings have later been confirmed by several authors [10], [29], [30], although reported shoulder moment peaks vary as much as 6 fold (e.g. 2.2 Nm reported by Collins et al. [10],
Neural control of arm swing
If we assume that the arms swing is partly passive, the question arises as to why there is arm muscle activity during gait (persisting even when the arms are constrained; see [5], [9]). Arm muscle activation may come about by the way the nervous system (more particularly the spinal cord) is built, with interconnected Central Pattern Generators (CPG) generating locomotion patterns [34]. In a leading review, Dietz [35] has argued that bipedal and quadrupedal locomotion share common spinal
Arm swing and pathology
As outlined in Section 1, arm swing during gait has an important role in decreasing energetic cost of locomotion. Several pathologies may lead to various abnormalities in arm movements during walking. It may therefore be expected that pathological gait is energetically more demanding, not only because of the pathology, but also because of affected arm movements. Indeed, it has been reported that preventing arm swing during gait does change the gait pattern in healthy adults, in particular with
Discussion and conclusion
We set out to review the how and why of arm swing during normal and pathological gait. In reviewing the literature, it becomes apparent that the question of “how” cannot be easily answered at the time, as there is as of yet no study showing in how far muscles actively generate arm swing, and what part of it is passive (i.e. generated by accelerations at the shoulder girdle, inertia, and gravity). The question of “why” however, seems to have converged on two answers. Firstly, as described in
Conflict of interest
None of the authors has a conflict of interest.
Acknowledgements
The authors wish to thank Firas Massaad for his contribution with respect to the critical inspection of the classic papers (see footnote 1). We thank Dr. Johann P. Kuhtz-Buschbeck for allowing us to use a modified version of his figure. SMB was funded by a FWO Visiting Fellowship (GP.030.10N) and by an FWO grant (G.0901.11). JD and PM were supported by grant from ‘Bijzonder Onderzoeksfonds’ KU Leuven (OT/08/034 and PDMK/12/180) and one from the “Hercules stichting”.
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Both authors contributed equally to this work.