Effect of Exercise on Arterial Stiffness in Healthy Young, Middle-Aged and Older Women: A Systematic Review.

Arterial stiffness, an age-dependent phenomenon, is improved with exercise, which in turn may prevent cardiovascular diseases in women. However, there is a lack of consolidated information on the impact of exercise on arterial stiffness among healthy women. The aim of this review was to (i) analyse the effect of exercise on arterial stiffness in healthy young, middle-aged, and older women, and (ii) recommend types, intensity, and frequency for each age group. Database searches on PubMed, ScienceDirect, Web of Science, and Scopus were conducted using PRISMA guidelines until September 2022. The keywords were: exercise, women/female, and arterial stiffness. The inclusion criteria were: healthy women, supervised exercise, and arterial stiffness measures. Study quality and bias were assessed using the PEDro scale. Fifty-one papers were classified into young (n = 15), middle-aged (n = 14), and older (n = 22) women. Improvements in arterial stiffness were observed among: young women (Pulse Wave Velocity, PWV: 4.9-6.6 m/s), following an 8-week high-intensity aerobic (3 days/week) or hypoxic high-intensity interval training; middle-aged women (PWV: 5.1-7.9 m/s), aerobic exercise with moderate intensity or stretching exercise at "moderate to heavy" (Borg Scale), 20-30 s per site, 10 s of rest interval for 30 min; and for older women (PWV: 7.9-15.6 m/s), resistance training at light intensity, aerobic exercise at any intensity, or a combination of the two exercises. This review shows that arterial stiffness increases with age in healthy women and has an inverse relationship with exercise intensity. Therefore, when prescribing exercise to improve arterial stiffness, age and arterial stiffness measures should be accounted for.

The volume of brisk walking is the key determinant of BMD improvement in premenopausal women.

SUMMARY: Osteoporosis is an increasing health problem in postmenopausal women. Our findings indicated that long-term brisk walking with a volume greater than 16 per week is effective for improving BMD in premenopausal women. PURPOSE: To examine the effects of brisk walking on bone mineral density (BMD) in premenopausal women, and further determine the effective frequency, intensity, time and volume (frequency x duration) of brisk walking for training strategy prescription. METHODS: 222 healthy premenopausal women were recruited for BMD measurement. According to the survey of their physical activity level, 84 subjects (age: 46±1.8) whose physical activity index ≥40 were categorized into the brisk walking group, and 138 subjects (age: 47±2.2) whose physical activity index <40 were assigned to the sedentary group. The BMD of these two groups were statistically compared with an independent t test. Next, 35 subjects from the original sedentary group were recruited for BMD measurement after 2-year moderate brisk walking. According to the volume of physical activity per week, they were divided into the control group (n = 10, aged 49±0.9), volume 8 group (n = 4, aged 48±1.2), volume 12 group (n = 7, aged 49±1.4), volume 16 group (n = 8, aged 49±1.3), and volume 20 group (n = 6, aged 49±1.5). ANOVA was used to analyze BMD before and after brisk walking among the five groups. RESULTS: The BMD in the brisk walking group (1.00±0.008 g/cm2) was significantly higher than that in the sedentary group (0.89±0.008 g/cm2) (P<0.001). Stepwise regression analysis revealed that the volume of brisk walking was significantly correlated with BMD (P<0.001). In particular, brisk walking with a volume greater than 16 (a score of duration up to 4 and a score of frequency up to 4 or 5) per week is effective for improving BMD in premenopausal women (P = 0.03, P = 0.002, respectively). CONCLUSIONS: Long-term brisk walking is an efficient way to improve BMD. Taking brisk walks for 30 minutes per day 3 or more times per week (volume>16) is recommended to prevent bone loss in premenopausal women.

Myosin X Interaction with KIF13B, a Crucial Pathway for Netrin-1-Induced Axonal Development.

Myosin X (Myo X) transports cargos to the tips of filopodia for cell adhesion, migration, and neuronal axon guidance. Deleted in Colorectal Cancer (DCC) is one of the Myo X cargos that is essential for Netrin-1-regulated axon pathfinding. The function of Myo X in axon development in vivo and the underlying mechanisms remain elusive. Here, we provide evidence for the role of Myo X in Netrin-1-DCC-regulated axon development in developing mouse neocortex. The knockout (KO) or knockdown (KD) of Myo X in cortical neurons of embryonic mouse brain impairs axon initiation and contralateral branching/targeting. Similar axon deficits are detected in Netrin-1-KO or DCC-KD cortical neurons. Further proteomic analysis of Myo X binding proteins identifies KIF13B (a kinesin family motor protein). The Myo X interaction with KIF13B is induced by Netrin-1. Netrin-1 promotes anterograde transportation of Myo X into axons in a KIF13B-dependent manner. KIF13B-KD cortical neurons exhibit similar axon deficits. Together, these results reveal Myo X-KIF13B as a critical pathway for Netrin-1-promoted axon initiation and branching/targeting.SIGNIFICANCE STATEMENT Netrin-1 increases Myosin X (Myo X) interaction with KIF13B, and thus promotes axonal delivery of Myo X and axon initiation and contralateral branching in developing cerebral neurons, revealing unrecognized functions and mechanisms underlying Netrin-1 regulation of axon development.