Spring-loaded body mass equivalent horizontal reactive countermovement jump ground contact and flight times, but not peak forces, are comparable to vertical jumping.

Horizontal (cylinder-based) sledge jumping has been shown to ameliorate multi-system deconditioning induced by long-term bed-rest. However, biomechanics differ from 1 g vertical jumping, in particular prolongation of ground contact times (GCT), reduction of peak force, rate of force development (RFD) (and presumably stretch shortening cycle [SSC] efficacy) and stiffness, whilst also requiring relatively complex equipment. Thus, we sought to determine if horizontal spring-loaded countermovement jumps were more analogous to vertical jumping. 9 healthy (5 female) subjects (27 ± 7yrs; 169.0 ± 5.3 cm; 63.6 ± 2.6 kg) performed 10 reactive countermovement jumps vertically, and horizontally (randomized) when lay on a spring-loaded carriage performed against loading (at lift-off) equivalent (±6%) to their body weight. Jump kinetics, kinematics and lower limb/trunk electromyographic activity were compared between conditions (paired t-tests). Mean flight and GCTs did not differ, however, peak jump height (p = 0.003; d = -0.961) was greater when jumping horizontally. In contrast, ground reaction forces (zGRF) during take-off (p < 0.001; d = 1.645) and landing (p = 0.002; d = 1.309), peak acceleration (p = 0.001; d = 1.988), leg stiffness (p = 0.001; d = 2.371) and RFD (p = 0.023; d = 1.255) were lower horizontally. Mean rectus femoris activity was lower during landing (p = 0.033; d = 0.691) when horizontal, but did not differ during either take-off or land-lift. Mean medial gastrocnemius activity was significantly (p = 0.018; d = 0.317) lower during horizontal take-off. Spring-loading (1 g at take-off) maintained short GCTs and flight times presumably maintaining muscle SSC efficacy in a manner that appears intuitive (in young active subjects), simple, robust and potentially compatible with spaceflight. Whether appropriate jump characteristics can be achieved in older subjects and in µg/hypogravity needs to be determined. However, greater jump height, lower peak zGRF, RFD and leg stiffness along with reduced lower limb and trunk muscle activity suggests that 1 g at take-off is insufficient to replicate vertical jump biomechanics. Thus, further investigation is warranted to optimize, and evaluate spring-loaded jumping as a gravity-independent multi-systems countermeasure on Earth, and in Space.

Oxytocin: an emerging regulator of prolactin secretion in the female rat.

In the female rat, a complex interplay of both stimulatory and inhibitory hypothalamic factors controls the secretion of prolactin. Prolactin regulates a large number of physiological processes from immunity to stress. Here, we have chosen to focus on the control of prolactin secretion in the female rat in response to suckling, mating and ovarian steroids. In all three of these states, dopamine, released from neurones in the mediobasal hypothalamus, is a potent inhibitory signal regulating prolactin secretion. Early research has determined that the relief of dopaminergic tone is not sufficent to account for the full surge of prolactin secretion observed in response to the suckling stimulus, launching a search for possible prolactin-releasing factors. This research has subsequently broadened to include searching for prolactin-releasing factors controlling prolactin secretion after mating or ovarian steroids. A great deal of literature has suggested that this prolactin-releasing factor may include oxytocin. Oxytocin receptors are present on lactotrophs. These oxytocin receptors respond to exogenous oxytocin and antagonism of endogenous oxytocin inhibits lactotroph activity. In addition, the pattern of oxytocin neuronal activity and oxytocin release correlate with the release of prolactin. Here, we suggest not only that oxytocin is stimulating prolactin secretion, but also that prolactin secretion is controlled by a complex network of positive (oxytocin) and negative (dopamine) feedback loops. We discuss the available literature and attempt to describe the circuitry we believe may be responsible for controlling prolactin secretion.