Stretch sensitive reflexes as an adaptive mechanism for maintaining limb stability

Abstract

The often studied stretch reflex is fundamental to the involuntary control of posture and movement. Nevertheless, there remains controversy regarding its functional role. Many studies have demonstrated that stretch reflexes can be modulated in a task appropriate manner. This review focuses on modulation of the long-latency stretch reflex, thought to be mediated, at least in part, by supraspinal pathways. For example, this component of the stretch reflex increases in magnitude during interactions with compliant environments, relative to its sensitivity during interactions with rigid environments. This suggests that reflex sensitivity increases to augment limb stability when that stability is not provided by the environment. However, not all results support the stabilizing role of stretch reflexes. Some studies have demonstrated that involuntary responses within the time period corresponding to the long-latency reflex can destabilize limb posture. We propose that this debate stems from the fact that multiple perturbation-sensitive pathways can contribute to the long-latency stretch reflex and that these pathways have separate functional roles. The presented studies suggest that neural activity occurring within the period normally ascribed to the long-latency stretch reflex is highly adaptable to current task demands and possibly should be considered more intelligent than “reflexive”.

Introduction

Observations of stretch reflexes, rapid excitatory responses of a muscle following stretch, were reported as early as 1751 by Robert Whytt (Pearce, 1997). Since that time it has been revealed that the stretch reflex is a complex muscle reaction, with multiple excitatory responses occurring at different latencies following a muscle stretch (Hammond, 1955). In the human upper limb for example, stretching the biceps brachii produces a ‘short latency’ response in the same muscle beginning approximately 20 ms after the onset of stretch, and a ‘longer latency’ response beginning around 50 ms after stretch onset (Hammond, 1955, Marsden et al., 1972). Both short and longer latency responses are generally regarded as involuntary actions since they occur prior to the fastest voluntary reaction, which in the biceps brachii has been shown to begin 90–100 ms following an auditory or proprioceptive ‘go’ signal (Hammond, 1956).

Though usually considered to be involuntary, the behavior of both short and long-latency stretch reflexes can be modulated in a task dependent manner. This modulation has led to much debate regarding the functional role of these fundamental responses. There is strong evidence from decerebrate animal preparations that the shortest latency stretch reflexes, mediated by the spinal cord, serve to compensate for muscle nonlinearities and regulate muscle stiffness over a wide range of operating conditions (Nichols and Houk, 1976, Hoffer and Andreassen, 1981). In these studies, stretch reflexes generally augment the intrinsic properties of a muscle to oppose external perturbations of muscle length, thereby increasing stability of the musculoskeletal system. While there also are ample data supporting contributions of the short latency stretch reflex to stiffness regulation in humans, the role of longer latency stretch reflexes is less clear. Longer latency reflexes also have been reported to contribute to limb stiffness and stability, but counter examples have been provided in which these involuntary actions appear to destabilize limb posture (see review by Hasan, 2005). We propose that these apparently contradictory results arise largely from the fact that multiple pathways can contribute to perturbation-evoked muscle activity occurring in the period corresponding to the long-latency stretch reflex, and the attempt to ascribe a single functional role to these multiple pathways. This review summarizes literature supporting this proposal, and describes conditions under which the role of the long-latency stretch reflex is consistent with the regulation of limb stiffness and stability.