The Routledge Handbook on Biochemistry of Exercise

Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse

• Editorial: Routledge
• Año: 2020
• ISBN:
  9781000284492
• Edición: 1
• Categoría: Medicina
• Categoría: Biochimica in medicina

From its early beginnings in the 1960s, the academic field of biochemistry of exercise has expanded beyond examining and describing metabolic responses to exercise and adaptations to training to include a wide understanding of molecular biology, cell signalling, interorgan communication, stem cell physiology, and a host of other cellular and biochemical mechanisms regulating acute responses and chronic adaptations related to exercise performance, human health/disease, nutrition, and cellular functioning.

The Routledge Handbook on Biochemistry of Exercise is the first book to pull together the full depth and breadth of this subject and to update a rapidly expanding field of study with current issues and controversies and a look forward to future research directions. Bringing together many experts and leading scientists, the book emphasizes the current understanding of the underlying metabolic, cellular, genetic, and cell signalling mechanisms associated with physical activity, exercise, training, and athletic performance as they relate to, interact with, and regulate cellular and muscular adaptations and consequent effects on human health/disease, nutrition and weight control, and human performance.

With more emphasis than ever on the need to be physically active and the role that being active plays in our overall health from a whole-body level down to the cell, this book makes an important contribution for scholars, medical practitioners, nutritionists, and coaches/trainers working in research and with a wide range of clients. This text is important reading for all students, scholars, and others with an interest in health, nutrition, and exercise/training in general.

SECTION IV
Exercise Biochemistry Relative to Health Through the Lifespan

Peter M. Tiidus

The last number of years have seen a tremendous increase in understanding and appreciation for the influence of exercise and physical activity on chronic and lifestyle-related diseases, ageing, and obesity. The positive effects of exercise have been firmly established for both the reduction in incidences and progression of chronic diseases such as cancers, cardiovascular conditions, type 2 diabetes, and osteoporosis. In addition, exercise has been demonstrated to improve the quality of health and life for individuals living with or being actively treated for these conditions.

The incidence and progression of childhood obesity, as well as the quality of life and functional capacity of those with childhood-onset type 1 diabetes, are also positively influenced by exercise and physical activity. Exercise has also been shown to have important positive influence on processes of ageing, longevity, and functional capacity of older adults. Physical activity plays a vital role in delaying ageing-related morbidity and is a likely factor in prolonging life. Exercise has a critically positive influence on mitochondrial function, vitality, and density in muscles, as well as other tissues, which contributes to many of these benefits, as well as being an important factor in influencing the progression of a number of other disease conditions.

This section deals specifically with important new understanding of how exercise influences the biochemistry of a number of chronic disease conditions, as well as ageing and some related c-morbidities such as osteoporosis as well as the propensity for obesity in children. This relatively new appreciation for the importance influence of regular exercise on disease incidence, severity, and progression and our growing understanding of the biochemical and cellular mechanisms involved in physiological adaptations to various forms of resistance, endurance, power, and movement-based exercise help to inform new therapeutic interventions and prophylactics for these diseases via exercise and lifestyle modifications. In addition, this research contributes significantly to understanding the basic science of such diseases and conditions, which can also inform investigations into other forms of treatments as well as pharmacological interventions. Understanding the biochemistry of exercise effects will also inform the efficacy of these treatments and how they contribute to improvements in individuals’ quality of life in general as well as during active treatment.

The new and cutting-edge research outlined in the chapters in this section form a sound basis for understanding the complex and important biological effects of physical activity as preventive medicine as well as treatment for various diseases and other health-related issues, as well as enhanced-ageing related functionality and will prove to be a vital basis in moving forward with further research.

26
MITOCHONDRIAL DYSFUNCTION IN CHRONIC DISEASE

Christopher Newell, Heather Leduc-Pessah, Aneal Khan, and Jane Shearer

Introduction

Present in almost all eukaryotic cells, the mitochondrion is the organelle responsible for aerobic energy production via cellular respiration. Proper mitochondrial function is vital for metabolic homeostasis of the human body, whereas dysfunctional mitochondria, characterized by loss in the efficiency of the electron transport system and therefore a reduction in energy synthesis, has been linked to the ageing process (12) and a multitude of chronic disease states. These include neurodegenerative diseases (62), cardiovascular diseases (113), diabetes (112), cancers (109), musculoskeletal diseases (96), and gastrointestinal disorders (40), among others. Exercise is a well-known intervention proven to maintain mitochondrial function and density. This chapter highlights our current understanding of how mitochondria are affected by both exercise and chronic disease. There are also primary mitochondrial diseases that are a group of rare diseases which can be caused by mutations to either mitochondrial or nuclear DNA (mtDNA or nDNA) (106); however, these are beyond the scope of this chapter.

Mitochondrial Physiology

Anatomy of Mitochondria

The “bean-shaped” mitochondrion consist of outer and inner membranes made of proteins and phospholipid bilayers. The inner mitochondrial membrane (IMM) is folded into cristae which increase surface area, enabling increased capacity for energy production. The outer mitochondrial membrane (OMM) regulates the bidirectional movement of proteins, cellular signalling molecules, and metabolic intermediates. Between the IMM and OMM is the intermembrane space, whereas the innermost compartment surrounded by the IMM is called the matrix.

Inner Mitochondrial Membrane

Acting as a tight barrier to all ions and molecules from the matrix and intermembrane space, the IMM utilizes a proton gradient to drive ATP synthesis. Embedded in the IMM are a series of large enzyme complexes, which generate this proton gradient, collectively termed the electron transport system (ETS) (Figure 26.1). Once liberated from metabolic substrates, electrons are shuttled through the ETS via NADH dehydrogenase (Complex I) or succinate dehydrogenase (SDH; Complex II). Electrons are then carried by the mobile electron carrier ubiquinone (coenzyme Q or CoQ) to cytochrome c reductase (Complex III) before being transferred to cytochrome c, with cytochrome c oxidase (COX; Complex IV) eventually receiving the electrons. Complex IV enables O₂ to accumulate four electrons, which generates one molecule of H₂O. The drop in free energy that occurs drives proton pumping at Complexes I, III, and IV from the matrix into the mitochondrial intermembrane space. Complex II only transfers electrons to coenzyme Q and does not help generate the proton gradient. The proton redistribution established by mitochondrial respiration maintains and modulates the IMM proton gradient, which drives the f...