Medicine & Science in Sports & Exercise:
SPECIAL COMMUNICATIONS: Letters to the Editor-in-Chief
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom
Helgerud et al. (1) demonstrate that high-intensity interval training improves V˙O2max to a greater extent than moderate continuous training. However, the approach of using heart rate to prescribe, quantify, and monitor training intensity during continuous and interval training programs is not without limitations.
In relation to the continuous training protocols, the authors report that when heart rate started to drift during exercise, running velocity was reduced to maintain intensity in the target heart rate zones. I question the suitability of this approach when training in controlled conditions, as lowering running velocity will lower the absolute workload and subsequently affect muscle recruitment patterns (3). Is it not more suitable to maintain running velocity and absolute workload at a percentage of V˙O2max during such interventions? Moderately trained subjects can readily perform 45 min of continuous running exercise (approximately 70% V˙O2max), despite significant cardiovascular drift (2). In employing this approach, the researchers can be more confident that the degree of signaling (e.g., fiber recruitment, glycogen depletion, AMPK activation, intracellular calcium, hypoxia) is better controlled within and between subjects.
This is particularly important when peripheral adaptations such as mitochondrial biogenesis are of interest. The interval training groups consisted of "15/15" (15-s intervals at 90-95% HRmax with active resting periods at 70% HRmax) or "4 × 4" protocols (4 min at 90-95% HRmax with 3-min active resting periods at 70% HRmax). Examination of the heart rate trace for the 4 × 4 group indicates that approximately only 50% of each exercise bout was in the designated heart rate zone of 90-95% HRmax (this is obviously not unexpected, because of the lag in oxygen delivery), despite a fixed running velocity during the 4-min exercise period. In contrast, examination of the 15/15 trace reveals this group to be in the target 90-95% heart rate zone for the majority of the training session. In this regard, the 15/15 group results in a greater overall training stress (as demonstrated by time in the designated heart rate zones) compared with the 4 × 4 group, despite running velocity during each period of exercise and recovery likely being the same between protocols.
Relying solely on heart rate to prescribe, quantify, and monitor training intensity therefore provides a somewhat "noisy" model, in which the reader may be misinformed or misinterpret the physiology of the particular intervention. I therefore suggest that we place more emphasis on exercising at a percentage of running velocity at V˙O2max during differing interval running programs, as opposed to target heart rate zones. In this way, the total time spent at a particular workload during both exercise and recovery can be readily matched. We should also report the average V˙O2 and heart rate during each interval and recovery period, so as to provide a more informative account to the reader. The major challenge should now be to elucidate and understand the signaling pathways activated by each intervention and to examine how potential differences in signaling may translate into differing performance adaptations.
Research Institute for Sport and Exercise Sciences
Liverpool John Moores University
Liverpool, United Kingdom
1. Helgerud, J., K. Hoydal, E. Wang, et al. Aerobic high-intensity intervals improve V˙O2max
more than moderate training. Med. Sci. Sports Exerc.
2. Morton, J. P., D. P. M. MacLaren, N. T. Cable, et al. Time-course and differential expression of the major heat shock protein families in human skeletal muscle following acute non-damaging treadmill exercise. J. Appl. Physiol.
3. Saltin, B., and P. D. Gollnick. Skeletal muscle adaptability: significance for metabolism and performance. In: Handbook of Physiology (Section 10): Skeletal Muscle
, L. D. Peachey, R. H. Adrian, and S. R. Geiger (Eds.). Bethesda, MD: American Physiological Society, pp. 540-555, 1983.