This study used animal models to examine potential similarities between dependence on physical activity (i.e., exercise) and dependence on morphine. Using C57BL/6 mice, the study also tested the hypothesis that physical exercise (e.g., long-term wheel running) may enhance vulnerability to the development of morphine dependence. The existence of an endorphin-related dependence induced by physical activity was also assessed. Naloxone was used to precipitate morphine withdrawal in mice accustomed to morphine. Specifically, the study sought to assess the intensity of addiction provoked by injection of morphine in mice that engaged in wheel-running activity as opposed to inactive mice. After 25 days of free access to activity wheel, mice that engaged in wheel-running demonstrated increased vulnerability to naloxone-induced withdrawal symptoms, which may be linked to activation of peripheral, as opposed to central, opioid receptors. These results indicate a behavioral interaction in which engaging in wheel running appears to potentiate the effects of morphine addiction. Implications of these findings for understanding human behavior and exercise addiction are also discussed.
Anthony Ferreira, Fabien Cornilleau, Fernando Perez-Diaz and Charles Cohen-Salmon
Mark R. Forwood
Experiments to design physical activity programs that optimize their osteogenic potential are difficult to accomplish in humans. The aim of this article is to review the contributions that animal studies have made to knowledge of the loading conditions that are osteogenic to the skeleton during growth, as well as to consider to what extent animal studies fail to provide valid models of physical activity and skeletal maturation. Controlled loading studies demonstrate that static loads are ineffective, and that bone formation is threshold driven and dependent on strain rate, amplitude, and duration of loading. Only a few loading cycles per session are required, and distributed bouts are more osteogenic than sessions of long duration. Finally, animal models fail to inform us of the most appropriate ways to account for the variations in biological maturation that occur in our studies of children and adolescents, requiring the use of techniques for studying human growth and development.
Yanmei Niu, Hong Yuan and Li Fu
Insulin resistance (IR) is a common pathophysiological feature of Type 2 diabetes. Although the mechanisms leading to IR are still elusive, evidence has shown that aerobic exercise can reverse this process. To investigate the effects of aerobic exercise on IR, the authors created an IR animal model by feeding C57BL/6 mice a high-fat diet for 8 wk. They then compared the effect of 6 wk of treadmill training (60 min/d) at 75% VO2max on mice in normal-diet (NE) and high-fat-diet (HE) groups with their sedentary control groups. Levels of skeletal-muscle AMPKα (AMP-activated protein kinase α), ACC (acetyl-CoA carboxylases), and CPT1 (carnitine palmitoyltransferase 1) mRNA and AMPKα, pAMPK-Thr172, ACC, pACC-Ser79, and CPT1 protein expressions were analyzed. In addition, fasting serum levels of insulin, triglyceride, and cholesterol were measured. The results demonstrate that 6 wk of exercise increased AMPKα mRNA expression by 11% and 25 % (p < .01) in the NE and HE groups, respectively, and AMPKα protein expression by 37.9% and 20.1% (p < .01) in NE and HE compared with their sedentary control. In addition, ACC mRNA and protein expressions declined, whereas CPT1 mRNA and protein expressions were elevated in both exercise groups compared with sedentary control groups. In addition, pAMPK-Thr172 and pACC-Ser79 expression increased significantly in the NE and HE groups compared with sedentary control groups. In conclusion, our results demonstrate that 6 wk of aerobic exercise can effectively ameliorate IR by increasing the expression of AMPKα and pAMPK-Thr172, thereby activating the key enzymes that facilitate lipid metabolism.
Christopher Tack, Faye Shorthouse and Lindsy Kass
and animal models of tendon and muscle injury. Although it has been reported that randomization and blinding in animal studies are often not stringently adhered to ( Hess, 2011 ), the choice was made to include these trials but be explicit in critique of these processes. Despite continuing debate
Ryan P. Durk, Esperanza Castillo, Leticia Márquez-Magaña, Gregory J. Grosicki, Nicole D. Bolter, C. Matthew Lee and James R. Bagley
consumed per day) and homogenous macronutrient intake by our participants, as fat intake has been proposed to contribute to microbial dysbiosis in animal models ( Martinez et al., 2017 ; Murphy et al., 2015 ). Thus, the association between macronutrient intake and F/B observed in previous reports may be a
Stephen P. Sayers
Duchenne muscular dystrophy (DMD) is a disease affecting muscle fiber integrity in boys that leads to progressive weakness in skeletal muscle and premature death. Currently, there is no known cure for the disease. Different interventions have been explored to delay the progression of the disease and improve the quality of life for the DMD patient. Physical activity is one treatment that has generated controversy due to the increased mechanical stress placed on the muscle during contraction. This review explores the literature in animal models and human DMD patients and evaluates the known theoretical risks and benefits of increased physical activity in DMD patients.
Turner A. “Tab” Blackburn Jr.
Rehabilitation procedures for anterior instabilities of the knee were compiled in 1984. Since then these procedures have changed drastically. Immediate weight-bearing, immediate range of motion into full extension, and post-op Day 1 quadricep exercise are only three of the changes that streamline this rehabilitation process. Many of the biomechanical and healing restraints are still the same. But it appears that the human body heals much faster than the animal models used to predict successful treatment of anterior instabilities of the knee. As always, the pendulum swings and puts different emphasis on rehab ideas and techniques that were not used a few years ago. The present paper reflects the latest in this rehabilitation process.
George T. Baker III and George R. Martin
Aging is characterized by numerous physical, physiological, biochemical, and molecular changes. The rates at which aging processes occur are highly variable among individuals and are thought to be governed by both environmental and genetic factors. Lifestyle factors such as exercise, dietary, and smoking habits have been demonstrated to alter many of the changes usually associated with human aging. However, at present caloric restriction is the only experimental paradigm that has consistently been demonstrated in animal models to extend not only physiological vigor but also life span. The positive effects of exercise on physiological fitness and the reduction in the risks of certain diseases have been well documented. However, its effects on life span are not as clear. This article explores some of the basic mechanisms thought to be involved causally in the processes of aging, and outlines current and potential interventive strategies to retard or ameliorate the rates of decline in physiological function with advancing age.
Alison B. Pritchard Orr, Kathy Keiver, Chris P. Bertram and Sterling Clarren
Physical activity (PA) has been demonstrated to have positive effects on cognitive function, particularly executive function (EF) skills. Animal models suggest PA may be effective in ameliorating some of the neuropsychological effects of fetal alcohol spectrum disorder (FASD), but this approach has not been extended to humans. The purpose of this study was to develop a PA program, FAST Club, for children with FASD and to evaluate its effect on a measure of EF. Using a wait-list control design, 30 children age 7–14 yr participated in FAST Club for 2 × 1.5-hr sessions/week for 8 weeks. EF was assessed using the Children’s Color Trails Test. Significant improvements in T scores on the Children’s Color Trails Test were seen immediately postprogram, and this improvement was sustained at 3 months postprogram. These findings provide evidence to support the use of PA as a means to improve EF in children with FASD.
Cecilia Persson, Jon Summers and Richard M. Hall
A spinal cord injury may lead to loss of motor and sensory function and even death. The biomechanics of the injury process have been found to be important to the neurological damage pattern, and some studies have found a protective effect of the cerebrospinal fluid (CSF). However, the effect of the CSF thickness on the cord deformation and, hence, the resulting injury has not been previously investigated. In this study, the effects of natural variability (in bovine) as well as the difference between bovine and human spinal canal dimensions on spinal cord deformation were studied using a previously validated computational model. Owing to the pronounced effect that the CSF thickness was found to have on the biomechanics of the cord deformation, it can be concluded that results from animal models may be affected by the disparities in the CSF layer thickness as well as by any difference in the biological responses they may have compared with those of humans.