Building a Bigger Engine: Resistance After Endurance Training Increases Mitochondrial Biogenesis & Protein Synthesis and Ramps Up Fat Metabolism

Image 1: There is nothing wrong with some "classic cardio" training, especially if you spike it up to build your mitochondrial engine

In a recent review of the literature, J.M. Wilson from the University of Tampa analyzed the results of 27 studies to determine whether and to which extend concomitant endurance training does / could have detrimental effects on the outcomes of resistance training (Wilson. 2011). And I suspect that it will not surprise you that Wilson found negative correlations "between frequency (-.26 to -.35) and duration (-.29 to -.75) of endurance training [and] hypertrophy, strength, and power." What is yet also noteworthy is a similarly significant (p<0.05) correlation with lower body fat levels and maximal heart rates on part on those strength athletes who did some sort of endurance exercises. Now, a more recent study which is soon going to be published in Journal of Applied Physiology sheds some more light on the complex interplay of endurance and resistance training and the potential benefits of combining both to build a "bigger mitochondrial engine" (Sahlin. 2011).

Interestingly, the Swedish scientists started out with a diametrically opposed hypothesis. Sahlin et al. expected that the signaling of mitochondrial biogenesis, of which it is common knowledge that it is promoted by "classic" low(er) intensity endurance exercise, would be impaired by resistance exercise. To validate their hypothesis, the scientists had a group of ten healthy subjects (7 males and 3 females; age, 26 ± 1.2 (mean ± SE) yr; height, 177 ± 2.9 cm; weight, 72 ± 3.5 kg) perform either 60min of endurance exercise (65% of VO2Max on a cycle ergometer) alone (E), or in combination (R+E) with a subsequent bout of 6 sets of leg presses at workloads corresponding to 70, 75, 80, 80, 75 and 70 % of the individual 1RM with 3 min rest between each set (cf. figure 1)

Figure 1: Graphical overview of the study outline (based on Sahlin. 2011).

Muscle biopsies were taken before and after the exercise protocol, to which the subjects had been randomly assigned and which was repeated 2 weeks (4 weeks in the female participants to avoid any influence of the menstrual cycle) later with subjects from the E group performing E + R and vice versa. The results, I'll say so much, were by no means what the researchers had expected.

Figure 2: Changes in lactate and muscle glycogen content in response to endurance (E) and combined endurance and resistance (E+R) training (calculated based on Sahlin. 2011).

While there were the expected differences in lactate levels, and glycogen content of the biopsied legs (cf. figure 2), the increase in the phosphorylation of mTOR and its upstream regulator Akt (you should know these promoters of protein synthesis from the posts in the Intermittent Thoughts series and my dissertations on other studies, by now ;-) was not only exclusive to the endurance + resistance training group (E+R), it was probably also much more pronounced than one might expect with 6 sets of leg presses and lead to an almost dramatic increase in p56Sk1 phosphorylation (do I have to mention that this happened "although" the subjects trained >12h fasted and remained fasted for the whole study period?) - a relatively reliable marker for protein synthesis (cf. figure 3).

Figure 3: Changes of key enzymes envolved in the phosphorylation of key enzymes in the protein synthetic cascade in response to endurance (E) and combined endurance and resistance (E+R) training (calculated based on Sahlin. 2011).

Morover, and totally contrary to what the scientists had expected, the expression of the key enzyme for mitochondrial biogenesis and increased fatty acid oxidation, PDK4 was significantly elevated, not suppressed, in response to the additional leg training (cf.  figure 4).

Figure 4: PDK4 phosphorylation (arbitrary units) in response to endurance (E) and combined endurance and resistance (E+R) training (calculated based on Sahlin. 2011).

The research hypothesis that a (relatively short, but intense) bout of resistance training subsequent to a mitogenic "classic" cardio regimen would blunt the beneficial effects of the latter on mitochondrial biogenesis is thusly more than falsified. As it turns out, the 6% increase in total work-load due to the addition of the 6 sets of leg presses makes a huge and desirable (!) difference (way beyond what an over-simplified workload = output equation would explain) in terms of "building a bigger engine" - an engine that will keep you lean on a bulk and help you lean out while your dieting.

If you are no powerlifter, it is thus probably no mistake to keep some "classic cardiovascular" exercise in your regimen, especially if you spice it up with a subsequent short bout resistance exercise - another option, and I am repeating myself here, would obviously be a high intensity cardio session (cf. HIIT). That being said, change has time and again proven to be the key to continuous improvements in exercise performance, muscular growth and strength, to incorporate both spiced up "classic cardio" and HIIT in your routine could not only improve your results (in view of the protein synthetic response, you could even "grow" on such an E+R day), it will also prevent you from getting bored with performing the same routine day in and day out and if you asked me, that is an even more fundamental key to success than a X% increase in the phosphorylation of whatever key enzyme ;-)