Fall arrest strategy training improves upper body response time compared to standard fall prevention exercise in older women: A randomized trial

Introduction: Exercise can decrease fall risk in older adults but less is known about training to reduce injury risk in the event a fall is unavoidable. The purpose of this study was to compare standard fall prevention exercises to novel Fall Arrest Strategy Training (FAST); exercises designed to improve upper body capacity to reduce fall-injury risk in older women. Method: Forty women (mean age 74.5 years) participated in either Standard (n=19) or FAST (n=21) twice per week for 12 weeks. Both interventions included lower body strength, balance, walking practice, agility and education. FAST added exercises designed to enhance forward landing and descent control such as upper body strengthening, speed and practice of landing and descent on outstretched hands. Results: Both FAST and Standard significantly improved strength, mobility, balance, and fall risk factors from pre to post-intervention. There was a significant time by group interaction effect for upper body response time where FAST improved but Standard did not (p = .038). Discussion: FAST resulted in similar gains in factors that reduce fall risk as a standard fall prevention program; with the additional benefit of improving speed of arm protective responses; a factor that may help enhance landing position and reduce injury risks such as head impact during a forward fall

Neutrophil-derived catecholamines mediate negative stress effects on bone

Abstract Mental traumatization is associated with long-bone growth retardation, osteoporosis and increased fracture risk. We revealed earlier that mental trauma disturbs cartilage-to-bone transition during bone growth and repair in mice. Trauma increased tyrosine hydroxylase-expressing neutrophils in bone marrow and fracture callus. Here we show that tyrosine hydroxylase expression in the fracture hematoma of patients correlates positively with acknowledged stress, depression, and pain scores as well as individual ratings of healing-impairment and pain-perception post-fracture. Moreover, mice lacking tyrosine hydroxylase in myeloid cells are protected from chronic psychosocial stress-induced disturbance of bone growth and healing. Chondrocyte-specific β2-adrenoceptor-deficient mice are also protected from stress-induced bone growth retardation. In summary, our preclinical data identify locally secreted catecholamines in concert with β2-adrenoceptor signalling in chondrocytes as mediators of negative stress effects on bone growth and repair. Given our clinical data, these mechanistic insights seem to be of strong translational relevance