Abstract
Exercise training which meets the recommendations set by the National Physical Activity Guidelines ensues a multitude of health benefits towards the prevention and treatment of various chronic diseases. However, not all individuals respond well to exercise training. That is, some individuals have no response, while others respond poorly. Genetic background is known to contribute to the inter-individual (human) and -strain (e.g., mice, rats) variation with acute exercise and exercise training, though to date, no specific genetic factors have been identified that explain the differential responses to exercise. In this review, we provide an overview of studies in human and animal models that have shown a significant contribution of genetics in acute exercise and exercise training-induced adaptations with standardized endurance and resistance training regimens, and further describe the genetic approaches which have been used to demonstrate such responses. Finally, our current understanding of the role of genetics and exercise is limited primarily to the nuclear genome, while only a limited focus has been given to a potential role of the mitochondrial genome and its interactions with the nuclear genome to predict the exercise training-induced phenotype(s) responses. We therefore discuss the mitochondrial genome and literature that suggests it may play a significant role, particularly through interactions with the nuclear genome, in the inherent ability to respond to exercise.
Highlights
Attention is yet to be directed on how the mitochondrial genome influences such adaptations
Given that genetic background strongly contributes to exercise training-induced responses, and that other lines of work hint towards a significant contribution of the mitochondrial genome, it is of interest to know whether mitochondrial–nuclear interactions exist to predict mitochondrial adaptations/responses to exercise training
We suggest that future work investigating the relationship between exercise and genetics consider employing animal models such as the Collaborative Cross (CC) or diversity outbred (DO) mice that are designed to control for the genetic diversity inherent in human models (Roberts et al 2007; Threadgill and Churchill 2012; Threadgill et al 2002, 2011)
Summary
Regular daily exercise has multiple beneficial health outcomes including reductions in risk for cardiovascular disease (Manson et al 1999), diabetes (LaMonte et al 2005), several forms of cancer (Campbell and McTiernan 2007), stroke (Alevizos et al 2005), neuro-cognitive dysfunctions (Verghese et al 2003), all-cause mortality rates (Iestra et al 2005), quality of life (Belardinelli et al 1999), and lifespan (Moore et al 2012; Paffenbarger et al 1986). With treadmill aerobic capacity testing, Desai et al (1997) have shown in four inbred and two outbred mouse strains that a linear increase in heart rate, VO2, VCO2, and RER occurs with an increase in exercise intensity indicative of an escalation in metabolic cost of workload, which is similar to humans These effects have been observed in several other studies that have measured responses to treadmill running in mice (Fluckey et al 1996a, b). While the RFLP technique is limited in terms of fully uncovering the contribution of mtDNA sequence and polymorphisms to the inter-individual responses to exercise training, this study did indicate that the mitochondria genome may have a role in determining V O2max responses which warrants further investigation Challenging this previous finding, Scott et al (2005) considered mtDNA haplogroups in a general Ethiopian population and an elite athlete runner Ethiopian population. Together with the recent techniques such as next-generation ultra-deep sequencing, such methods have enabled multiple avenues for future research regarding interactions between the mitochondrial and genomes that may associate with exercise traininginduced phenotypes
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