improve performance is by improving lactate utilisation. This significant effect on lactate metabolism leads to a


rightward shift of the blood lactate curve during increasing intensity exercise. This means that there is an increase in work intensity required to reach defined blood lactate concentrations, which is due in part to improved use of the available lactate. Following different HIT protocols it has been shown that blood lactate accumulation is greatly reduced at the same exercise intensity. There are a number of potential explanations for the decrease in blood lactate accumulation. It has been shown that following HIT skeletal muscle lactate accumulation is reduced. This decrease in lactate accumulation in the skeletal muscle could be due to either/or: i. a decreased rate of glycogenolysis post HIT; ii. an increased use of pyruvate in oxidative metabolism. Further, there is an increase in the amount of monocarboxylate transporter 1 (MCT1) in skeletal muscle after HIT and it has been shown that skeletal muscle lactate uptake is increased with increasing MCT1 content. Whatever the mechanisms that are causing the lowering of blood lactate levels, the reduced lactate accumulation is one of the major factors for the improved performance seen following HIT. We know that there is a really strong correlation between the absolute exercise intensity required to raise blood lactate concentration and endurance performance, and blood lactate accumulation has been suggested to be a more accurate measure of aerobic performance than VO2 max.


Oxidative metabolism An improvement in oxidative metabolism and an increased mitochondrial density in skeletal muscle is seen following traditional endurance training. Likewise two and six weeks of 30 second HIT have been shown to alter the oxidative potential of skeletal muscle (2). Peroxisome proliferator activated receptor a coactivator 1 alpha (PGC1a) is a key regulator of oxidative metabolism in skeletal muscle via promotion of oxidative gene transcription. When PGC1a is overexpressed in animals it results in a dramatic shift of fast to slow muscle fibre type with an increase in mitochondrial density. Indeed, the increase in expression of PGC1a following HIT was actually 30% greater than that seen with traditional endurance training. Along with the increase in PGC1a there is a dramatic increase in cytochrome C oxidase (COX4), a mitochondrial enzyme involved in electron transfer through the respiratory chain on the mitochondrial inner membrane and may be a rate limiting enzyme in oxidative metabolism. Further, other mitochondrial markers such as citrate synthase, which is involved in the TCA cycle, are up-regulated following HIT. All this suggests that improved skeletal muscle mitochondrial density and oxidative potential occurs rapidly, and potentially to a greater extent than with traditional endurance exercise, following HIT.


“the extremely low volume of exercise required with HIT may enhance adherence to training regimes”


16 16


120


100 80 60 40 20 0


Phosphocreatine (PCr) hydrolysis glycolysis


oxidative phosphorylation


200 175


150 0-6 sec


6-15 sec time duration


15-30 sec


125 100


Figure 1: Fuel utilisation during a 30-second all-out sprint with heart rate shown in the line graph


The health benefits associated with HIT Given the magnitude of the improvements in endurance performance following HIT it was speculated that it could also improve health outcomes. Metabolic adaptations associated with traditional endurance exercise training correlate with improved insulin action and glycemic control. These effects appear to be independent of changes in body composition (3), and more importantly endurance training of higher intensity elicits greater improvements in insulin sensitivity than moderate intensity training. The current guidelines* largely focus on the accumulation of time spent carrying out moderately intense activity (or total energy expenditure) and ultimately require many hours of exercise each week. However, the general population fails to follow such regimes due to exercise training being perceived as a major time commitment. This perception of time requirements is thus driving or contributing to low compliance with traditional exercise (4). This suggests that the current focus on time-consuming moderate intensity physical activity, aimed at increasing total energy expenditure, may not be the best strategy for reducing the risk of developing diseases associated with lifestyle such as obesity, cardiovascular disease or type 2 diabetes. Compared to traditional strategies for reduction of risk factors associated with these diseases, the extremely low volume of exercise required with HIT may enhance adherence to training regimes and thus represent a genuinely preventative public health strategy.


Insulin sensitivity Having a sedentary lifestyle is the major risk factor for a variety of lifestyle diseases and especially for type 2 diabetes. Therefore, in the first study to look at the health benefits associated with HIT we looked at whether this type of training can improve insulin sensitivity in a sedentary population (5). Utilising the oral glucose tolerance test, where a participant is asked to drink 75g of glucose and subsequent blood glucose and insulin levels are recorded, it was demonstrated that only a few minutes of high intensity interval exercise performed over two weeks is required to substantially improve insulin action and glucose homeostasis in healthy sedentary men. The findings of this study were remarkable, with the magnitude of the changes seen to the blood glucose profile following intake of carbohydrate being much greater than is seen with traditional endurance protocols. Following the same load there was a 12% reduction in the blood glucose response


The REPS Journal 2009;00(Month):00-00The REPs Journal 2012;24(May):14-19


heart rate bpm


% contribution to fuel


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