Endurance Training Adaptations

Why does low intensity and therefore, slower training improve race times?

Simple question. Long answer.

Time to look at what adaptations occur to endurance training. To do so requires a couple of brief definitions of basic concepts.

Adaptation to training will only occur if the person exercises at a level above their normal habitual level of activity on a frequent basis. It is generally accepted that endurance training is performed at 50-80% VO2max for prolonged periods several times per week to induce adaptations that will improve functional capacities. Adaptations to endurance training are transient and reversible. Sufficient time for recovery is required to allow morphological adaptations to occur. The adaptations can be defined as central (cardiovascular, respiratory) and peripheral (muscle, cellular).

Adenonside triphosphate (ATP) is a high energy compound that is the immediate source for energy requiring processes in cells such as muscle contraction. The ability to maintain prolonged dynamic exercise (ie. running) is dependant on the rate of ATP utilisation in active muscle being matched by the rate of ATP supply. Failure leads to fatigue (reduced power output, reduced running speed).

With the above in mind, lets look at the specific changes induced through endurance training.

Muscle Adaptations

  • Selective hypertrophy of Type I fibres
  • Increased number of capillaries per fibre
  • Increased myoglobin content
  • Increased capacity of mitochondria to generate ATP by oxidative phosphorylation
  • Increased size and surface area of mitochondria
  • Increased number of mitochondria
  • Increased capacity to oxidise lipid and carbohydrate
  • Increased use of lipid as fuel
  • Increased glycogen and triglyceride content
  • Increased endurance capacity

Metabolic Adaptations

Increased contribution of lipid, uses more fat and less carbohydrate not only for given absolute intensity, but also per relative intensity of exercise. Because of the increased ability to use lipid there is a reduction in the use of muscle glycogen and blood glucose. The increased lipid oxidation is mainly fueled from intramuscular triacylglycerol stores with only a mild increase from the free fatty acids (FFA) circulating in the blood.

Decreased uptake and utilisation of blood glucose by the active muscle leads to decreased liver glycogenolysis and better maintenance of blood glucose levels during exercise. Increased lactate clearance. Decreased lactate production

Physiological Adaptations

  • Increased plasma volume
  • Increased total haemoglobin
  • Increased stroke volume of the heart due to ventricle enlargement and increase myocardial contractility
  • Increased total muscle blood flow during exercise
  • Increase oxygen extrication by the muscle

What Does It All Mean?

To simplify things lets accept that supplying ATP by aerobic means is, for the most part, the key factor in long distance racing. I know anaerobic contributions are important too, but in reality these are like the icing on the cake, and the cake is your aerobic abilities. More oxidation of fats and carbohydrate means less generation of anaerobic byproducts such as lactic acid which lead strongly to fatigue.

In a previous post (Limitations of Measurement) I mentioned that total oxygen consumption (VO2) of any intensity is the product of Cardiac Output and Oxygen Utilised At A Cellular Level. That is VO2 = (Heart Rate x Stroke Volume) x (CaO2 - CvO2). If you combine this knowledge with the adaptations listed above, then you have your answer as to why low intensity training improves higher intensity racing.

Looks a bit confusing in the above paragraph, so I'll break it down a bit more.

More oxygen is able to be delivered to the working muscles by:

  • Increased pumping of oxygen and nutrient rich blood
  • Increased volume of blood that also has a higher capacity to transport oxygen
  • Better redistribution and direction of blood flow

Once at the muscle the blood spends more time travelling through the larger capillary network allowing better extraction of all the goodies needed by the muscle.

The muscle can now able to use even more oxygen and at a faster rate through:

  • Increased number and size of mitochondria
  • Increased availability of fuel sources

All of this is supported by the metabolic adaptations through better balancing and response of various hormones, plus increased oxidative and fuel mobilising enzymes. Basically it is the oil that keep the machinery running smoothly on the cleaner fuel that is being provided.

While onto the topic of machinery, the actual muscles themselves through hypertrophy of Type I fibres, and enhancement of structures (ie. stronger actin-myosin bonding), better regulation of calcium release etc. lead to both stronger and fatigue resistant muscles. Add to this enhanced neuromuscular facilitation (the nerves better recruit motor units), or simply put the muscles now contract more efficiently.

All these adaptations can be developed through relatively low intensity training. As hopefully I demonstrated above, the adaptations lead to better delivery of O2, increased availability of fuels, better use of O2 and fuels plus stronger and more fatigue resistant musculature. All important regardless of the intensity you are actually performing at. The advantage of developing all this through low intensity training is that you can gain the benefits at a training level that is likely to be below that which causes injury in the connective structures, particularly tendons.


  1. Jason, thanks for this very interesting description of the advantages of low intensity training. I have a question.
    For marathons (or Tri events of Olympic distance or longer) a high capacity to burn lipids be expected to be very valuable as it should allow conservation of glycogen. However, as I understand it, lipid utilization is inhibited as lactic acid concentration rises, and hence lipid utilization tends to be switched off as lactate threshold is approached. Since a marathon is run a pace not far below lactate threshold pace, it seems to me that the crucial requirement is to be able to continue to utilise lipids almost up to lactate threshold. It might be expected that this capacity is best achieved by training near to the upper end of the aerobic range. Is there any evidence that enhancing the ability to use lipids at the lower end of the aerobic range (lets say 50-65% of VO2max) produces a substantial gain in the ability to utilize lipids in the upper part of the aerobic range?

    The first time I tried to submit this comment it did not appear, so I am trying again. My apologies if it comes through twice

  2. Jason, I've just found your blog, from a link sent to me by Canute1 (above). This is a great article you've written, and one that I think I need to apply to my own training.


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