What we mean when we talk about training consistency

Endurance Coaches are often telling us that the key to performing well in triathlon, or in any sport for that matter, is consistency. Executing training consistently is what gets you to the podium, not erratic peaks and troughs in training structure with killer workouts scattered amongst misfire sessions and sessions missed altogether. The science clearly supports this message. In this blog, we are going to discuss the details for why achieving peak performance in endurance sport is about training consistently.

Training adaptation: Why we need to keep pushing the signal

 In an earlier blog, we discussed in some detail the basic principles of training adaptation – the supercompensation model of endurance training. We discussed how, when we train, we are challenging the ‘homeostasis’ of the body – that is, we put it under physiological stress. Our heart rate goes up, our fuel stores are depleted, and the pH of our blood and muscles can be reduced. The body wants to ensure that we can cope better with this stressor the next time we face it, so sends physiological signals that drive adaptive processes. We remodel our heart, blood, and muscles so that we can respond to that exercise challenge more effectively. We become fitter. The improvements in performance that we see after a solid block of endurance training are therefore cause by the amalgamation of these small adaptations we accrue in response to individual training sessions.

 I want to spend a little time in this blog discussing those physiological signals that are sent in response to individual training sessions to help us adapt, and how they relate to the need to train consistently. The primary signal that exercise physiologists research and measure in the laboratory is called PGC-1α, which has been called the ‘master regulator’ of endurance training adaptation, particularly mitochondrial adaptations in muscle (3, 4, 10). PGC-1α is by no means the only signal for endurance training adaptation, but it is the one we have, rightly or wrongly, and probably because of the relative ease of its measurement, tended to focus on (6). That being said, understanding how PGC-1α signalling works does give us a good insight into why training consistency is crucial from a physiological standpoint.

 PGC-1α is a protein that responds to metabolic stresses. When we are resting, most of the PGC-1α housed within our muscle cells is relatively inactive. However, when we stress our muscles with exercise, disturbing their internal homeostasis, we activate the PGC-1α we already have, and make more PGC-1α (5). Therefore, PGC-1α is a bit like an army; an army is ready but at ease until a war starts, when the troops become active and the government invests to increase the number of soldiers. An effect of more, more active PGC-1α is to send signals within the muscle to start producing more mitochondrial proteins – the powerhouses of the cells where aerobic metabolism takes place. This is good, and one of the primary adaptations we are seeking through endurance training.

 The time-course of the PGC-1α response to individual training sessions has been investigated, with a prominent study taking muscle biopsies from subjects before, immediately after, and then 2, 6, and 24 hours after three hours of exercise (7). I won’t get too far into the details, but they measured the what-is-called mRNA that stimulates the production of new PGC-1α. This increased as a result of exercise, rising to its peak two hours post-exercise, was still elevated after six hours, but back down to baseline 24 hours post-exercise.

 The important message here is that the ‘signal’ for adaptation lasted hours, not days, after a pretty-meaty exercise training session. If we want to maximise our adaptations, we need to back up training sessions and push the signalling response again and again. No signalling, no adaptation, and no further gains in fitness.

Overtraining: Why we don’t want to push the signal too hard

When we talk about producing a consistent signal for adaptation, we should acknowledge that the bigger risk for most committed athletes is pushing that signal too hard, rather than not producing signals often enough. We discussed in a previous blog the specific importance of low-intensity training (2), and why doing too much training at high intensity – to push for the biggest possible signal for adaptation (1) – might be a recipe for maladaptation, overreaching, and overtraining in the long-term (8, 9).

While providing a great adaptive signal when executed well, high-intensity training, by nature, is more stressful and more fatiguing than lower-intensity training. Too much of this stress mounted up over time will eventually suppress training quality and likely lead to missed training sessions when residual training fatigue becomes substantial. In turn, missing or failing to hit the mark in training sessions because of residual fatigue prevents us from generating any kind of signal for adaptation.

Consistency is key

Therefore, laying down training consistently allows us to keep pushing our adapting signalling, and prevents detraining, but we must guard against overtraining. What we are shooting for is the biggest, consistent training signal we can reasonably manage, rather than the biggest one we can achieve on each day or in each individual training session. Being consistent is therefore about managing the desire to do too much, with the need to keep pushing our adaptive response.

 Consistency is key!


1.       Fiorenza M, Gunnarsson TP, Hostrup M, Iaia FM, Schena F, Pilegaard H, Bangsbo J. Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle. J Physiol 596: 2823–2840, 2018.

2.       Granata C, Jamnick NA, Bishop DJ. Training-induced changes in mitochondrial content and respiratory function in human skeletal muscle. Sport Med 48: 1809–1828, 2018.

3.       Gurd BJ. Deacetylation of PGC-1α by SIRT1: importance for skeletal muscle function and exercise-induced mitochondrial biogenesis. Appl Physiol Nutr Metab 36: 589–597, 2011.

4.       Handschin C, Spiegelman BM. The role of exercise and PGC1α in inflammation and chronic disease. Nature 454: 463–469, 2008.

5.       Holloszy JO. Regulation by exercise of skeletal muscle content of mitochondria and GLUT4. J Physiol Pharmacol 59: 5–18, 2008.

6.       Islam H, Edgett BA, Gurd BJ. Coordination of mitochondrial biogenesis by PGC-1α in human skeletal muscle: a re-evaluation. Metabolism 79: 42–51, 2018.

7.       Pilegaard H, Saltin B, Neufer PD. Exercise induces transient transcriptional activation of the PGC-1α gene in human skeletal muscle. J Physiol 546: 851–858, 2003.

8.       Plews DJ, Laursen PB, Kilding AE, Buchheit M. Heart rate variability and training intensity distribution in elite rowers. Int J Sports Physiol Perform 9: 1026–1032, 2014.

9.       Plews DJ, Laursen PB, Stanley J, Kilding AE, Buchheit M. Training adaptation and heart rate variability in elite endurance athletes: Opening the door to effective monitoring. Sport Med 43: 773–781, 2013.

10.     Wu Z, Puigserver P, Andersson U, Zhang C, Adelmant G, Mootha V, Troy A, Cinti S, Lowell B, Scarpulla RC, Spiegelman BM. Mechanisms controlling mitochondrial biogenesis and respiration through the thermogenic coactivator PGC-1. Cell 98: 115–124, 1999.