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Exercise improves all aspects of health, including immunity. It is well known that exercise at a level consistent with most national physical activity guidelines can improve immune responses to vaccination, lower the incidence of infection and latent viral reactivation, lower chronic low-grade inflammation, and is associated with a reduction in many hallmark features of an aging immune system, especially in older adults [1]. The lymphoid compartment is particularly susceptible to agerelated changes and also appears to be most responsive to exercise. For instance, the blood T-cell compartment in physically active compared to sedentary older adults express fewer markers of differentiation and exhaustion and have higher numbers and proportions of naïve Tcells. Moreover, T-cells (particularly CD8+ T-cells) from those who are physically active have an enhanced ability to secrete IL-2 and proliferate in response to antigenic stimulation, while NK-cells in those who are physically active have an increased ability to secrete effector cytokines and perform anti-tumor cytotoxic functions [1]. While the beneficial effects of exercise on immunity are apparent, details of the mechanisms responsible have remained opaque. We do know that exercise evokes the release of several cytokines from contracting skeletal muscle (i.e. ‘myokines’) that can have a direct impact on the peripheral lymphoid compartment. For instance, IL7 is released from muscle during exercise which can, in turn, help preserve thymic mass and T-cell production to potentially help sustain the naïve T-cell compartment with advancing age. Similarly, IL-15 released by muscle can maintain peripheral T-cell and NK-cell numbers and enhance NK-cell cytotoxicity and cytokine secretion. While these links between exercise-released myokines and immune maintenance are intuitive and have been demonstrated in cross-sectional studies, they have yet to be tested mechanistically [1]. Furthermore, the optimal exercise prescription/dose as a function of the FITT (frequency, intensity, time and type) criteria and principles of exercise training (e.g. overload, progression) required to evoke positive changes in immunity remain elusive. A recent study in mice by Shen et al. indicates that the positive effects of exercise on immunity could be due to an enhanced production of common lymphoid progenitors (CLPs) facilitated by mechanical loading [2]. The authors showed that bone marrow stromal cells expressing the leptin receptor and osteolectin (an osteogenic growth factor) also express PIEZO1, a mechanoreceptor triggering stem cell factor production by osteogenic progenitors, which in turn helps maintain CLPs. Deleting PIEZO1 from osteolectin+ cells depleted osteolectin+ cells and CLPs. The authors further showed that deleting stem cell factor (SCF) a critical growth factor for the maintenance of hematopoietic stem cells and early restricted progenitors from osteolectin+ cells did not affect hematopoietic stem cells or most restricted progenitors, but did deplete CLPs and impaired lymphopoiesis, bacterial clearance and survival following acute bacterial infection. Leptin receptor+ osteolectin+ cells are osteogenic progenitors that are short lived and divide rapidly, decreasing in number with age and increasing in number after fracture. With this in mind, Shen et al. found that voluntary wheel running increased the frequencies of peri-arteriolar osteolectin+ cells and CLPs, whereas hindlimb suspension (a common rodent model of mechanical unloading) decreased the numbers of these cells. Collectively, their results show that a periarteriolar bone marrow niche for osteogenesis and lymphopoieses is depleted during aging, essential for

Is mechanical loading essential for exercise to preserve the aging immune system?