The primary aim of the current study was to determine the effect of two doses of chronic high-intensity interval training (HIT) on changes in maximal fat oxidation (MFO) and body composition. Sedentary women (N = 23, age and V˙O2max = 24.2 ± 6.2 yr and 30.3 ± 5.2 mL·kg-1·min-1, respectively) completed either high (HI) (80%-90% maximal workload) or moderate (MOD) intensity (60%-80% maximal workload) HIT on a cycle ergometer 3 d·wk-1 for 12 wk consisting of 6-10 sixty-second bouts interspersed with active recovery. Seven women of similar age and fitness level served as controls. Every 3 wk, substrate oxidation was assessed during progressive exercise via indirect calorimetry to determine MFO and minimum fat oxidation, and body composition was assessed every 6 wk. Repeated-measures ANOVA was used to examine changes in substrate oxidation in response to training, with training group used as a between-subjects variable. Results revealed improved MFO (P = 0.04, 19%-25%) and minimum fat oxidation (P = 0.001, 22-24 W) in response to HIT, yet the magnitude of improvement was similar (P > 0.05) between training paradigms. No change (P > 0.05) in body weight, percent body fat, or waist-hip circumference was revealed with training. These data suggest that 12 wk of either moderate or more strenuous interval training similarly enhance fat oxidation in sedentary women but do not alter body weight or body composition.
1 June 2017 in Topics in Spinal Cord Injury Rehabilitation
A sedentary lifestyle occurring soon after spinal cord injury (SCI) may be in contrast to a preinjury history of active physical engagement and is thereafter associated with profound physical deconditioning sustained throughout the lifespan. This physical deconditioning contributes in varying degrees to lifelong medical complications, including accelerated cardiovascular disease, insulin resistance, osteopenia, and visceral obesity. Unlike persons without disability for whom exercise is readily available and easily accomplished, exercise options for persons with SCI are more limited. Depending on the level of injury, the metabolic responses to acute exercise may also be less robust than those accompanying exercise in persons without disability, the training benefits more difficult to achieve, and the risks of ill-considered exercise both greater and potentially irreversible. For exercise to ultimately promote benefit and not impose additional impairment, an understanding of exercise opportunities and risk...
Individuals with spinal cord injuries (SCI) commonly present with component risk factors for cardiometabolic risk and combined risk factors for cardiometabolic syndrome (CMS). These primary risk factors include obesity, dyslipidemia, dysglycemia/insulin resistance, and hypertension. Commonly referred to as “silent killers”, cardiometabolic risk and CMS increase the threat of cardiovascular disease, a leading cause of death after SCI. This narrative review will examine current data and the etiopathogenesis of cardiometabolic risk, CMS, and cardiovascular disease associated with SCI, focusing on pivotal research on cardiometabolic sequelae from the last five years. The review will also provide current diagnosis and surveillance criteria for cardiometabolic disorders after SCI, a novel obesity classification system based on percent total body fat, and lifestyle management strategies to improve cardiometabolic health.
11 June 2013 in European Journal of Applied Physiology
Spinal cord injury (SCI) results in an array of cardiometabolic complications, with obesity being the most common component risk of cardiometabolic disease (CMD) in this population. Recent Consortium for Spinal Cord Medicine Clinical Practice Guidelines for CMD in SCI recommend physical exercise as a primary treatment strategy for the management of CMD in SCI. However, the high prevalence of obesity in SCI and the pleiotropic nature of this body habitus warrant strategies for tailoring exercise to specifically target obesity. In general, exercise for obesity management should aim primarily to induce a negative energy balance and secondarily to increase the use of fat as a fuel source. In persons with SCI, reductions in the muscle mass that can be recruited during activity limit the capacity for exercise to induce a calorie deficit. Furthermore, the available musculature exhibits a decreased oxidative capacity, limiting the utilization of fat during exercise. These constraints must be considered when designing exercise interventions for obesity management in SCI. Certain forms of exercise have a greater therapeutic potential in this population partly due to impacts on metabolism during recovery from exercise and at rest. In this article, we propose that exercise for obesity in SCI should target large muscle groups and aim to induce hypertrophy to increase total energy expenditure response to training. Furthermore, although carbohydrate reliance will be high during activity, certain forms of exercise might induce meaningful postexercise shifts in the use of fat as a fuel. General activity in this population is important for many components of health, but low energy cost of daily activities and limitations in upper body volitional exercise mean that exercise interventions targeting utilization and hypertrophy of large muscle groups will likely be required for obesity management.