We have known for some time that the epidemiology of human stroke is sexually dimorphic until late in life, well beyond the years of reproductive senescence and menopause. Now, a new concept is emerging: the mechanisms and outcome of cerebral ischemic injury are influenced strongly by biological sex as well as the availability of sex steroids to the brain. The principal mammalian estrogen (17 β estradiol or E2) is neuroprotective in many types of brain injury and has been the major focus of investigation over the past several decades. However, it is becoming increasingly clear that although hormones are a major contributor to sex-specific outcomes, they do not fully account for sex-specific responses to cerebral ischemia. The purpose of this review is to highlight recent studies in cell culture and animal models that suggest that genetic sex determines experimental stroke outcome and that divergent cell death pathways are activated after an ischemic insult. These sex differences need to be identified if we are to develop efficacious neuroprotective agents for use in stroke patients.

Background and Purpose-Emerging data suggest that the molecular cell death pathways triggered by ischemic insults differ in the male and female brain. Cell death in males is initiated by poly(ADP-ribose) polymerase-1 (PARP-1) activation; however, manipulation of this pathway paradoxically increases ischemic damage in females. In contrast, females are exquisitely sensitive to caspase-mediated cell death. The effect of caspase inhibition in PARP-1 knockout mice was evaluated to determine if the detrimental effects of PARP deletion in females were secondary to increased caspase activation. Methods--Focal stroke was induced by transient or permanent middle cerebral artery occlusion (MCAO) in wild-type (WT) and PARP-1 Ϫ/Ϫ mice of both sexes. The pan-caspase inhibitor, quinoline-Val-Asp(Ome)-CH2-O-phenoxy (Q-VD-OPh), was administered 90 minutes after middle cerebral artery occlusion. Infarct size and neurological sores were assessed. Separate cohorts were used for protein analysis for PAR, Apoptosis inducing factor (AIF), caspase-9, and caspase-3. Results-WT mice of both sexes had increased nuclear AIF after stroke compared to PARP-1 Ϫ/Ϫ mice. PARP-1

Wave reflection is lower in competitive endurance athletes who have higher fitness levels and who exercise at a higher intensity, for a longer duration, and more frequently as compared with recreationally active individuals. These differences may be due to functional changes that occur as a result of training.

Effects of moderate-velocity strength training on peak muscle power and movement velocity: do women respond differently than men? J Appl Physiol 99: [1712][1713][1714][1715][1716][1717][1718] 2005. First published July 7, 2005; doi:10.1152/japplphysiol.01204.2004.-The effects of a 10-wk unilateral knee extension strength training (ST) program on peak power (PP) and peak movement velocity (PV), at given absolute (force load) and relative (same % of 1 repetition maximum) resistances (loads), were examined in 30 older men [64 yr (7 SD)] and 32 older women [62 yr (6 SD)]. PP increased significantly in both men and women at the same absolute (P Ͻ 0.001) and relative loads (P Ͻ 0.01) with ST. Men had a significantly greater increase in relative PP than women with ST at 60% (P Ͻ 0.01) and 70% (P Ͻ 0.001) of 1 repetition maximum when covarying for baseline differences and age. However, when each subject was tested at the same absolute load and when PP was normalized for the muscle volume of the trained knee extensors (i.e., absolute muscle power quality), women increased by 9% (P Ͻ 0.05), whereas men did not change. Both men and women increased their absolute PV (P Ͻ 0.001) but decreased their relative PV significantly with ST (P Ͻ 0.05). However, when baseline values and age were covaried, women had significantly less of a decrease in relative PV quality with ST than men (P Ͻ 0.01), although the difference was small. These normalized data suggest that ST-induced increases in PP depend on muscular hypertrophy in men, but not in women, providing further support for the hypothesis developed from our previous report (Ivey FM, Tracy BL, Lemmer JT, NessAiver M, Metter EJ, Fozard JL and Hurley BF. J Gerontol A Biol Sci Med Sci 55: B152-B157, 2000) that improvements in muscle function with ST result from nonmuscle mass adaptations to a greater extent in women than men. resistance training; aging SARCOPENIA IS THE LOSS of muscle mass with advanced age and is associated with dysfunction, poor health status, and the loss of muscle strength and power in older adults (17, 18). Muscle power accounts for a greater amount of the variance in physical performance than strength in older adults (3, 9) and deteriorates at a faster rate than strength with advanced age (2,16,21). Previous cross-sectional data suggest that this decline in peak muscle power with age is associated with muscle structure and function, tendon characteristics, and sarcopenia in specific muscle groups (20).Previous reports on the effects of strength training (ST) on muscle power did not report how the training affected power per unit of the muscle involvement [muscle power quality (MPQ)], or peak velocity (PV) (5,8,12,13,15), the latter possibly being an important component of power and possibly functional abilities in the elderly. The expression of peak power (PP) and movement velocity normalized for muscle volume (MV) allows better understanding of potential mechanisms (e.g., hypertrophy and neuromuscular adaptations) for training-induced adaptations. It is also ...