The article below leads on from the first article Understanding Intervals
There are two major points I want to draw from Dr. Astrand’s experiments:
1) Intermittent exercise allows a higher total volume of high intensity work. Performed continuously, the subject could only manage 9 minutes at 350 watts. Performed in 3 minute intervals, he could accumulate over 3 times as much total work (30 minutes, with great effort).
2) When the intervals were 3 minutes in length, the desired work could be accomplished within one hour, at great effort. However, when the work and rest periods were shortened, the physiological strain was dramatically reduced, even though total oxygen uptake during the hour was not markedly reduced. Specifically, if the intervals are less than 2 minutes in length, the physiological workload/stress is severely reduced despite the same total accumulated time (30 minutes here) and same interval intensity (350 watts workload here). If you compare the peak oxygen consumption, HR, and lactic acid concentration achieved during 1 minute intervals with 2 minute intervals in the table above, this difference is easily observed.
Why are the responses so different?
I think the best explanation for the difference was put forward by Astrand. He suggested that during very brief intervals, oxygen bound to myoglobin served as an effective buffer against the accumulation of an oxygen deficit (and lactic acid) during the exercise bout. Therefore after a 30 second bout, myoglobin oxygen stores were repleted during the rest period, and the peak demand on oxygen delivery was not severe. By analogy, the body manages to live expensively, and briefly deplete cash reserves, then always repay the small debt during a subsequent “debt recovery period”. No long term debt accumulates. As the exercise bout lengthens, the capacity of the small buffering myoglobin oxygen store is outstripped, lactic acid production and accumulation becomes significant, and the burden of greater oxygen delivery during the work interval falls on the cardiovascular system.
Subsequent experiments by Astrand showed that if you shortened the work period and rest periods to smaller and smaller intervals, it was possible to perform at even higher power outputs without accumulating lactic acid or severely stressing the cardiovascular system.
Conclusions So Far
For a period of intermittant exercise that approximates a max VO2 workload to overload the cardiovascular system effectively, it needs to be of at least 2 minutes duration due to 1) lag time in the cardiovascular response and 2) the oxygen buffering effect of myoglobin
Now, lets go back to my master’s thesis. The question I set out to address with that study was this: “What is the impact of interval training and steady state training on the performance of the rat heart?” I wanted to evaluate the heart independent of the muscles, and make direct measurements, so I had to use rats. I bred a group of rats in the laboratory, meaning they were litter-mates and therefore, presumably quite similar genetically (they sure looked the same). After they reached adulthood, I divided them into three groups. One group sat around in cages, ate rat chow and got weighed periodically. A second group was gradually adapted over 4 weeks (several months in rat years) to running on a treadmill until they were running for 60 minutes, 5 days a week at an intensity that was equal to about 75% of VO2 max. The third group was adapted to an interval running program. These guys would run two minute bouts at a speed that required just over 100% of VO2 max, then slow down for two minutes, and so on for 10 bouts (after four weeks of buildup). The total running distance was the same for the two groups, only the intensity differed. To evaluate cardiac performance, I develped a surgical procedure under anesthesia (the rats, not me) that allowed me to directly and constantly measure cardiac output, intraventricular pressure development, heart rate etc., while subjecting the heart to a volume overload with saline infusion. What I found and reported at a meeting of the American College of Sports Medicine was this. In these previously untrained rats, 8 weeks of interval training was superior to 8 weeks of steady state training as an inducer of enhanced maximal cardiac performance. Interval trained hearts achieved higher peak stroke volumes during overload.
OK, So What?
Remember VO2 max? We have established that cardiac performance is a primary determinant of the VO2 max. The results of my thesis study suggested that interval training was the best way to enhance maximal cardiac performance, and therefore, presumably, VO2max. In fact, in a study by a different laboratory, a significant increase in VO2 max occurred in previously untrained rats subjected to 5, very high intensity 1 minute bouts of exercise a day. That’s 5 minutes of exercise. This improvement occured without any change in skeletal muscle oxidative capacity. There are other studies, on humans, that demonstrate the same finding.
Interval training allows us to accumulate a greater volume of stress on the blood pumping capacity of the heart. By using a large muscle mass, we promote maximal stroke volume responses. A high heart rate also is achieved as a function of the intensity. Finally, the periodic elevations and decreases in intensity may create special loading stresses on the heart that are adaptive. For example, during an interval, heart rate climbs high, then at the moment you stop the interval, heart rate immediately starts to drop, but venous return remains high. These exposures to additional ventricular stretch may help trigger ventricular remodeling (bigger ventricle volume). In addition, interval training may create a greater signal for changes in the compliance in the arterial system, but that is just more speculation.
Followed by the article : Interval Intensity of Understanding Intervals
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