An examination of current methods to prescribe exercise intensity: validity of different approaches and effects on cell signalling events associated with mitochondrial biogenesis

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Jamnick, Nicholas (2019) An examination of current methods to prescribe exercise intensity: validity of different approaches and effects on cell signalling events associated with mitochondrial biogenesis. PhD thesis, Victoria University.


While seemingly simple, the underlying exercise prescription to bring about the desired adaptations to exercise training is as complicated as that of any drug. Prescribing the frequency, duration, or volume of training is relatively simple as these factors can be altered by manipulating the number of exercise sessions per week, the duration of each session, or the total work performed in a given time frame (e.g., per week). However, prescribing exercise intensity is more complex and there is controversy regarding the reliability and validity of the many methods used to determine and prescribe intensity. Despite their common use, it is apparent V̇ O2 and HR based exercise prescription has no merit to elicit a homogeneous and explicit homeostatic response. Alternatively, the use of submaximal anchors has been employed and perceived to represent shifts in the metabolic state of the working muscle and represent a demarcating point to define training zones. Whereas, the domains of exercise are independent of these anchors and defined by their distinct homeostatic responses, and offer a valid concept for normalising exercise intensity (Chapter 1; Review 1). Furthermore, the relationship between graded exercise test (GXT) derived anchors and constant work load derived anchors is at this point non sequitur and we discourage using submaximal anchors interchangeably (Chapter 2; Study 1). Mitochondria are organelles found inside skeletal muscle cells and their main role is the production of adenosine triphosphate (ATP) which is necessary for skeletal muscle contractions. The bioenergetics demands associated with aerobic exercise lead to a homeostatic perturbation, activating sensor proteins that initiates gene expression through transcriptional and translational processes leading to the development of mitochondrial proteins. The source of ATP production modulates the homeostatic perturbations that activate the sensor proteins which include: an increase in the redox state of the cell (NAD+/NADH), an increase in ATP turnover (measured via AMP/ATP), increased calcium flux and mechanical stress and these are largely influenced by the source of ATP production. These perturbations act as signals to activate sensor proteins that ultimately modulate transcriptional coactivators associated with mitochondrial biogenesis (Chapter 3; Review 2). Despite the relationship between exercise intensity and mitochondrial biogenesis, submaximal exercise intensity is almost exclusively prescribed relative to maximal oxygen uptake or maximal work rate. The well-established limitation of these methods is the inability to normalise exercise intensity; specifically, to elicit a homogenous homeostatic perturbations. Thus, employing methodology that normalises exercise intensity based on homeostatic perturbations may modulate the activation of signalling kinases and the extent of gene expression (Chapter 4; Study 2).

Item type Thesis (PhD thesis)
Subjects Historical > FOR Classification > 1106 Human Movement and Sports Science
Current > Division/Research > Institute for Health and Sport
Current > Division/Research > College of Sports and Exercise Science
Keywords exercise; exercise intensity; mitochondrial biogenesis; oxygen; lactate; muscle; VO2max
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