Age-Related Declines in Lower Limb Muscle Function are Similar in Power and Endurance Athletes of Both Sexes: A Longitudinal Study of Master Athletes

The age-related decline in muscle function, particularly muscle power, is associated with increased risk of important clinical outcomes. Physical activity is an important determinant of muscle function, and different types of physical activity e.g. power-based versus endurance-based exercise appear to have differential effects on muscle power. Cross-sectional studies suggest that participation in power-based exercise is associated with greater muscle power across adulthood but this has not been investigated longitudinally. We recruited eighty-nine male and female power and endurance master athletes (sprint and distance runners respectively, baseline age 35–90y). Using jumping mechanography, we measured lower limb muscle function during a vertical jump including at least two testing sessions longitudinally over 4.5 ± 2.4y. We examined effects of time, discipline (power/endurance) and sex in addition to two- and three-way interactions using linear mixed-effects models. Peak relative power, relative force and jump height, but not Esslingen Fitness Index (indicating peak power relative to sex and age-matched reference data) declined with time. Peak power, force, height and EFI were greater in power than endurance athletes. There were no sex, discipline or sex*discipline interactions with time for any variable, suggesting that changes were similar over time for athletes of both sexes and disciplines. Advantages in lower limb muscle function in power athletes were maintained with time, in line with previous cross-sectional studies. These results suggest that improvements in lower limb function in less active older individuals following power-based training persist with continued adherence, although this requires further investigation in interventional studies

Greater maintenance of bone mineral content in male than female athletes, and in sprinting and jumping than endurance athletes: a longitudinal study of bone strength in elite masters athletes

Summary: We investigated longitudinal changes in tibia bone strength in master power (jumping and sprinting) and endurance (distance) athletes of both sexes. Bone mass but not cross‐sectional moment of inertia was better maintained in power than endurance athletes over time, particularly in men and independent of changes in performance. Objective: Assessment of effects of sex and athletic discipline (lower limb power events e.g. sprint running and jumping versus endurance running events) on longitudinal changes in bone strength in masters athletes. Methods: We examined tibia and fibula bone properties at distal (4% distal‐proximal tibia length) and proximal (66% length) sites using peripheral quantitative computed tomography (pQCT) in seventy‐one track and field masters athletes (30 male, 41 female, age at baseline 57.0±12.2y) in a longitudinal cohort study that included at least two testing sessions over a mean period of 4.2±3.1y. Effects of time, as well as time*sex and time*discipline interactions on bone parameters and calf muscle cross‐sectional area (CSA) were examined. Results: Effects of time were sex and discipline‐dependent, even following adjustment for enrolment age, sex, and changes in muscle CSA and athletic performance. Male sex and participation in power events was associated with better maintenance of tibia bone mineral content (BMC, an indicator of bone compressive strength) at 4% and 66% sites. In contrast, there was no strong evidence of sex or discipline effects on cross‐sectional moment of inertia (CSMI, an indicator of bone bending and torsional strength – P > 0.3 for interactions). Similar sex and discipline‐specific changes were also observed in the fibula. Conclusions: Results suggest that male athletes and those participating in lower limb power‐based rather than endurance‐based disciplines have better maintenance of bone compressive but not bending and torsional strength

A BAX/BAK and Cyclophilin D-Independent Intrinsic Apoptosis Pathway

Most intrinsic death signals converge into the activation of pro-apoptotic BCL-2 family members BAX and BAK at the mitochondria, resulting in the release of cytochrome c and apoptosome activation. Chronic endoplasmic reticulum (ER) stress leads to apoptosis through the upregulation of a subset of pro-apoptotic BH3-only proteins, activating BAX and BAK at the mitochondria. Here we provide evidence indicating that the full resistance of BAX and BAK double deficient (DKO) cells to ER stress is reverted by stimulation in combination with mild serum withdrawal. Cell death under these conditions was characterized by the appearance of classical apoptosis markers, caspase-9 activation, release of cytochrome c, and was inhibited by knocking down caspase-9, but insensitive to BCL-XL overexpression. Similarly, the resistance of BIM and PUMA double deficient cells to ER stress was reverted by mild serum withdrawal. Surprisingly, BAX/BAK-independent cell death did not require Cyclophilin D (CypD) expression, an important regulator of the mitochondrial permeability transition pore. Our results suggest the existence of an alternative intrinsic apoptosis pathway emerging from a cross talk between the ER and the mitochondria