Posted on 04/26/2011 at 11:19:45 AM by Student BloggerBy: Jon C.
In this blog I hope to discuss training practices used by athletes in order to maximize the results seen from hours upon hours of aerobic training. Both running and cycling coaches often suggest occasionally training in the fasted state to their athletes. Also, several nutrition companies suggest very small meals or skipping breakfast on race day in order to maximize fatty acid oxidation during endurance racing. Thus my goal is to discuss the reliability of these suggestions, as well as propose an exciting potential mechanism.
During endurance exercise contracting muscle fibers rely on a mixture of metabolic substrates to provide energy. Different types of muscle fibers rely more heavily on different fuel sources. Glucose serves as the preferred energy source in type IIa (fast twitch) muscle fibers, while type I (slow twitch) muscle fibers rely more heavily on lipid metabolism (1). Submaximal endurance exercise in particular recruits mostly type I fibers, indicating that there is the potential to rely on fatty acid oxidation as an energy source for endurance sports (2). Intramyocellular triacylglycol (IMTG), lipoprotein-derived triacylglycerol (TG) and plasma free fatty acids (FFA) are proposed to be the source of lipids oxidized by type I fibers (3). Indeed, trained athletes accumulate IMTG and rely more heavily on fatty acids to provide energy if exercise is performed in the fasted state, rather than the postprandial state (1, 4).
Training in the fasted or glycogen depleted state has the potential to alter the metabolic machinery within type I muscle fibers. Several studies indicate that consistent training in a glycogen depleted state generally results in increased capacity of muscles to oxidize fatty acids through changes in enzyme activity, fatty acid transporter proteins, and gene expression resulting in increased fatty acid oxidation by mitochondria (1, 5). Interestingly, athletes utilizing carbohydrate depletion training methods also show improved ability to resynthesize muscle glycogen post-exercise (1). The implications to athletes are substantial, considering that this training may also facilitate glycogen sparing when carbohydrates are consumed during a race (6). Thus not only would an athlete start a race with optimal muscle glycogen content, but also be able to protect these stores until race conditions demand their use, such as a sprint finish.
Perhaps the most interesting studies examining the impact of increased fatty acid oxidation capacity on endurance exercise were performed using transgenic mice expressing a constitutively active form of the nuclear transcription factor peroxisome proliferation-activated receptor (PPAR) δ. These mice have been affectionately named “marathon mice” due to the fact that they are able to run twice as far and twice as long as their wild type littermates (7). PPARδ, also known as PPARβ, is the least studied of the PPAR isoforms, but is the predominate isoform expressed in muscle tissue and its expression is thought to be linked to increased capacity to oxidize fatty acids by mitochondria (7, 8). Most highly expressed in type I muscle tissue, targeted overexpression of this transcription factor in muscle leads to muscle fibers switching to a type I phenotype. Furthermore, treatment of wild type mice with a PPARδ agonist induces changes in gene expression similar to targeted overexpression of an active form of the transcription factor (8).
Endurance training as well as fasting has also been shown to upregulate PPARδ expression and in both mice and humans, resulting in increased capacity to metabolize fatty acids by skeletal muscle (7). This interesting PPAR provides at least one potential target to increase endurance capacity in both amateur and elite athletes as well as in individuals suffering from metabolic syndrome. PPARα and PPARγ agonsists are already used in the treatment of hyperlipidemia as well as insulin resistance, respectively. Interestingly, “marathon mice” are protected from high-fat-diet induced obesity and exhibit improved glucose tolerance compared to wild type controls. Because of the ability of PPARδ to induce a type I muscle fiber phenotype and enhance skeletal muscle fatty acid oxidation, pharmacological activators have the potential to be an “exercise pill” that can enhance beneficial metabolic gains acknowledged to be a result of endurance training.