ABSTRACT
Sports participation confers many health benefits yet greatly increases injury risk. Long-term health outcomes in former athletes and transition to life after competitive sports are understudied. Ending a sport may pose physical and psychosocial challenges. The purpose was to determine the lived experiences of former competitive athletes and how their sports participation impacted their long-term health and well-being. Former college varsity athletes participated in semistructured interviews focusing on their experiences, including past and current health, the impact of injuries, activity, exercise, diet and transition to life after competitive sport. Thematic analysis was completed using a collaborative, iterative process. Thirty-one (16 female, 15 male) former college athletes aged 51.3±7.4 years were interviewed. Six themes emerged: (1) lifelong athlete identity; (2) structure, support and challenges of the college athlete experience; (3) a big transition to life beyond competitive sport; (4) impact of competitive sport on long-term health; (5) facilitators and barriers to long-term health after sport and (6) transferable life skills. Continuing sports eased the transition for many but often delayed their postathlete void. Challenges included managing pain and prior injury (eg, If I didn't have my knee injury, I would definitely be more active), reducing energy needs and intake (eg, When I was an athlete, I could eat anything; and unfortunately, that's carried into my regular life), lack of accountability, changed identity and lost resources and social support. Participants suggested a programme, toolkit, mentoring or exit course to facilitate the transition. While former athletes benefit from transferrable life skills and often continue sports and exercise, they face unique challenges such as managing pain and prior injury, staying active, reducing energy intake and changing identity. Future research should develop and evaluate a toolkit, programme and other resources to facilitate life after ending competitive sports under 'normal' conditions (eg, retirement) and after a career-ending injury.
ABSTRACT
While sports medicine has traditionally focused on recovering from injury and returning athletes to sport safely after injury, there is a growing interest in the long-term health of athletes. The purpose of this scoping review was to (1) summarise the literature (methodologies and findings) on physical function, body composition and cardiometabolic health in midlife (age 40-65 years) former competitive athletes compared with non-athlete controls, (2) identify areas for future study in long-term health in athletes and (3) determine outcomes that could be evaluated in a future systematic review(s). We searched PubMed, CINAHL, Web of Science and SPORTDiscus for studies published between 2000 and 2022 evaluating former athletes and controls on physical function, body composition and/or cardiometabolic measures using MeSH terms. We identified 20 articles that met our criteria. Outcomes varied considerably across studies, most of which were cross-sectional and evaluated only males. Limited data suggest that former endurance athletes have leaner body compositions, higher aerobic capacity and better cardiometabolic indicators than controls; former athletes who maintain higher physical activity (ie, self-reported exercise) are healthier than those who do not; and former team sport athletes, who have higher injury prevalence, may have poorer functional performance than controls who were recreationally active in college. Studies rarely evaluated functional performance, did not control for prior injury or diet and seldom assessed current physical activity levels. Future research should include females and evaluate sex differences, control for prior sports-related injury(ies), quantify physical activity, use standardised outcome measures including performance-based functional assessments and incorporate longitudinal designs.
ABSTRACT
KEY POINTS: The mechanisms responsible for the loss in muscle power and increased fatigability with ageing are unresolved. We show that the contractile mechanics of fibres from the vastus lateralis of old men were well-preserved compared to those of young men, but the selective loss of fast myosin heavy chain II muscle was strongly associated with age-related decrements in whole-muscle strength and power. We reveal that the combination of acidosis (H+ ) and inorganic phosphate (Pi ) is an important mediator of muscle fatigue in humans by inhibiting the low- to high-force state of the cross-bridge cycle and peak power, but the depressive effects of these ions on cross-bridge function were similar in fibres from young and old men. These findings suggest that the age-related loss in muscle power is primarily determined by the atrophy of fast fibres, but the age-related increased fatigability cannot be explained by an increased sensitivity of the cross-bridge to H+ and Pi . ABSTRACT: The present study aimed to identify the mechanisms responsible for the loss in muscle power and increased fatigability with ageing by integrating measures of whole-muscle function with single fibre contractile mechanics. After adjusting for the 22% smaller muscle mass in old (73-89 years, n = 6) compared to young men (20-29 years, n = 6), isometric torque and power output of the knee extensors were, respectively, 38% and 53% lower with age. Fatigability was â¼2.7-fold greater with age and strongly associated with reductions in the electrically-evoked contractile properties. To test whether cross-bridge mechanisms could explain age-related decrements in knee extensor function, we exposed myofibres (n = 254) from the vastus lateralis to conditions mimicking quiescent muscle and fatiguing levels of acidosis (H+ ) (pH 6.2) and inorganic phosphate (Pi ) (30 mm). The fatigue-mimicking condition caused marked reductions in force, shortening velocity and power and inhibited the low- to high-force state of the cross-bridge cycle, confirming findings from non-human studies that these ions act synergistically to impair cross-bridge function. Other than severe age-related atrophy of fast fibres (-55%), contractile function and the depressive effects of the fatigue-mimicking condition did not differ in fibres from young and old men. The selective loss of fast myosin heavy chain II muscle was strongly associated with the age-related decrease in isometric torque (r = 0.785) and power (r = 0.861). These data suggest that the age-related loss in muscle strength and power are primarily determined by the atrophy of fast fibres, but the age-related increased fatigability cannot be explained by an increased sensitivity of the cross-bridge to H+ and Pi .