Self-massage and Autonomic Response: Future Direction

Abstract

Self-massage (SM) is an active technique where participants use various instruments to apply pressure to soft tissue with an attempt to mimic manual therapy techniques. Within the literature, there are many techniques associating positive responses to the phenomena controlled by the central nervous system (i.e. stretching and manual therapies). The purpose of this short communication is to present the literature regarding similar techniques to SM and their effects on the central nervous system. Furthermore, there is no research investigating the safety of performing SM techniques prior to performance. Considering SM is non-invasive and practical , findings of such research would be applicable in clinical and performance settings. Thus, the authors encourage further research that satisfies the needs of these gaps. 2 Keywords Foam rolling; heart rate variability; rolling massage; self-manual therapy; self-myofascial release 3 Short Communication Self-massage (SM) is an active technique [1], where participants use foam rollers, lacrosse balls or rolling sticks to apply pressure to soft tissue with the goal of breaking up adhesions between skeletal muscle and the surrounding connective tissue.Foam rollers are a nonuniform cylinder consisting of a hollow hard inner core enclosed in a layer of ethylene vinyl acetate foam [2] and roller massagers are devices involving dense foam wrapped around a solid plastic cylinder [3], but differ from foam rollers as they have a central axle that is grasped by the hands and rolled over the tissue of interest[3]. It is common for SM to be prescribed at low loads for long durations [4].Usually, SM can be performed via foam rolling or rolling massage and is used to acutely facilitate joint range-of-motion [2,5,6] without decreasing performance [7,8] or not [9,10] and reduce delayed onset muscle soreness [11,12]. While it is believed that SM techniques can provide structural changes to connective tissue such as fascia, there is no evidence to support this mechanism[3]. There is literature suggesting neural mechanisms explain performance alterations post static stretching, which may explain the benefits from SM. For example, Drew et al. [13] observed that spontaneous baroreflex sensitivity decreased with increasing contraction intensity with subsequent local circulatory occlusion. After 15-seconds of stretching, heart rate increased 6±1, 6±1, 8±1, and 6±2 for 0, 30, 50, and 70%, respectively. The authors suggest that passive calf muscle stretching decreases cardiac va-gal outflow irrespective of the levels of blood pressure increase caused by muscle metaboreflex activation, and implies that central modulation of baroreceptor input, mediated by the actions of stretch-activated mechanoreceptive muscle afferent fibers. Results of Farinatti et al. [14,15]found that sympathetic activity increased during stretching, while parasympathetic activity increased post-stretching. Costa e Silva et al. [16] found hypoten-sive effects after stretching exercises with low volumes. It is suggested that static stretching results in activation of type III fibers and metaboreceptors in skeletal muscle, resulting in an inhibition of the vagal and baroreflex stimulation, thus contributing to cardiovascular alterations. These results demonstrate an isolated