Chronic diseases are the leading cause of death worldwide with increasing prevalence in all age groups, genders, and ethnicities. Most chronic disease deaths occur in middle-to low-income countries but are also a significant health problem in developed nations. Multiple chronic diseases now affect children and adolescents as well as adults. Being physically inactive is associated with increased chronic disease risk. Global societies are being negatively impacted by the increasing prevalence of chronic disease which is directly related to rising healthcare expenditures, workforce complications regarding attendance and productivity, military personnel recruitment, and academic success. However, increased physical activity (PA) and exercise are associated with reduced chronic disease risk. Most physiologic systems in the body benefit positively from PA and exercise by primary disease prevention and secondary disease prevention/treatment. The purpose of this brief review is to describe the significant global problem of chronic diseases for adults and children, and how PA and exercise can provide a non-invasive means for added prevention and treatment.
Mitochondria are vital organelles that provide energy for muscle function. When these organelles become dysfunctional, they produce less energy as well as excessive levels of reactive oxygen species which can trigger muscle atrophy, weakness and loss of endurance. In this review, molecular evidence is provided to show that exercise serves as a useful therapeutic countermeasure to overcome mitochondrial dysfunction, even when key regulators of organelle biogenesis are absent. These findings illustrate the complexity and compensatory nature of exercise-induced molecular signaling to transcription, as well as to post-transcriptional events within the mitochondrial synthesis and degradation (i.e. turnover) pathways. Beginning with the first bout of contractile activity, exercise exerts a medicinal effect to improve mitochondrial health and whole muscle function.
It is well-established that regular contraction maintains morphological and functional integrity of skeletal muscle, whereas rigorous exercise training can upregulate muscle metabolic and contractile function. However, when muscles stop contraction, such as during immobilization (IM) and denervation, withdrawal of IGF/Akt/mTOR signaling allows FoxO-controlled protein degradation pathways to dominate. Mitochondria play an important role in regulating both protein synthesis and degradation via several redox sensitive signaling pathways such as mitochondrial biogenesis, fusion and fission dynamics, ubiquitin-proteolysis, autophagy/mitophagy, and apoptosis. During prolonged IM, downregulation of PGC-1α and increased mitochondrial oxidative damage facilitate fission protein and inflammatory cytokine production and activate mitophagic process, leading to a vicious cycle of protein degradation. This “mitostasis theory of muscle atrophy” is the opposite pathway of hormesis, which defines enhanced muscle function with contractile overload. The demonstration that PGC-1α overexpression via transgene or in vivo DNA transfection can successfully restore mitochondrial homeostasis and reverse myocyte atrophy supports such a proposition. Understanding the mechanism governing mitostasis can be instrumental to the treatment of muscle atrophy associated with bedrest, cancer cachexia and sarcopenia.
Increased cardiovascular fitness, V˙O2max, is associated with enhanced endurance capacity and a decreased rate of mortality. High intensity interval training (HIIT) is one of the best methods to increase V˙O2max and endurance capacity for top athletes and for the general public as well. Because of the high intensity of this type of training, the adaptive response is not restricted to Type I fibers, as found for moderate intensity exercise of long duration. Even with a short exercise duration, HIIT can induce activation of AMPK, PGC-1α, SIRT1 and ROS pathway as well as by the modulation of Ca2+ homeostasis, leading to enhanced mitochondrial biogenesis, and angiogenesis. The present review summarizes the current knowledge of the adaptive response of HIIT.
Demographic aging is one of the most serious challenges facing our society. Although we live longer, we do not live better because it is considered that approximately 16-20% of our life is spent in late-life morbidity. Older people have the greatest risk of developing frailty increasing the risk of presenting various adverse health events such as low quality of life, disability, hospitalization and even death. Frail men and women over 65 years old have lower muscle quality and muscle mass and higher percentage of body fat than non-frail people of the same age. In this review we will address the main physiological changes in the muscular and nervous system associated to aging. More specifically we will review the changes in muscle mass, quality, and strength relating them with the decrease in capillarization and muscular oxidative capacity as well as with the alterations in protein synthesis in the muscle with aging. The last section of the manuscript will be devoted to the animal models of frailty and the indexes developed to measure frailty in these models. We will finally address the importance of exercise training as an intervention to delay or even reverse frailty.
Physical activity data in primary school-aged children are limited in Vietnam. Although tools to measure social ecological influences on physical activity are validated in English, they are not available in Vietnamese. Due to cultural and contextual differences, their psychometric properties need to be tested. Five scales were translated into Vietnamese and evaluated for internal consistency and test re-test reliability, including self-efficacy, perceived social influences, and beliefs self-administered by students, and parental support for physical activity and parental perceived safety of the neighbourhood, self-administered by parents. Compared to the original scales, two items from the parental perceived neighbourhood safety were removed due to the cultural context. Another item of the self-efficacy scale was also removed as it correlated poorly with the other items in the scale at both administrations. The adjusted scales were found to be reliable and appropriate for use among students and parents to measure social ecological influences on physical activity in the Vietnamese context.
Objective
Conclusion
High vibration transfer from a tennis racquet to the player may cause discomfort, and is hypothesized to influence performance and the onset of muscle fatigue. This study examined a racquet with a novel vibration damping technology (VDT) designed to mitigate frame vibration. Racquet vibration, post-impact vibration transfer to the player, arm electromyographic activity and tennis performance were compared to a non-VDT racquet. Nineteen young adult, competitive tennis players hit forehands and serves until near exhaustion on two days; using one of the two racquets each day. Tri-axial accelerometers mounted to racquet shaft, hand and forearm recorded vibration behaviour. Surface electromyography recorded activity of five arm muscles. In comparison to the non-VDT racquet, the VDT design showed: 1) A significantly lower mean normalised acceleration signal energy at the racquet during unfatigued play (−40%) and at near exhaustion (−34%), which corresponded to a 20-25% lower signal energy at the hand. 2) Reduced signs of arm muscle fatigue at near exhaustion, which was most pronounced in biceps and wrist extensors. 3) Players hit 11% more forehands and placed 40% more hits in the target area at near exhaustion.
VDT effectively reduces racquet vibration. Initial evidence indicates that it may delay muscle fatigue, which was associated with increased ball placement accuracy.
Human lifespan and life expectancy have increased worldwide, but the number of years that we spend free of chronic or debilitating disorders, known as healthspan, has not shifted along with increased lifespan. This unfavourable trend presents a tremendous global social-economical problem. We propose a model of promoting optimal human health with proactive, holistic interventions across the lifespan, which require multi-disciplinary, innovative approaches to research and care. We contend that this is the only hope that we have to face the challenges of population growth and aging, as well as the upward trend in non-communicable disease prevalence.