Sedentary Individuals, Endurance & Strength Athletes: Their Fitness, Training & Hormones and How They Effect the Ratio of Fast- to Slow-Twitch Fibers

ATPase stained cross-section (100x magnification) of the quadriceps muscle of an untrained adult. Type 1 fibers are light, type 2 fibers are dark (McDonald. 2002). Can you change the make up? Is it genetically predetermined? Or is it determine by your hormones - and if so, which ones are responsible - "The Big T", again? Read more about testosterone's role in building muscle, here!

Wednesday, last week, I discussed the immediate effects of "cardio before strength training" vs. "cardio after strength training" and came to the conclusion that the prolonged yet acute elevation of "anabolism" (as measured by higher testosterone levels) in the "cardio before" group is of little significance with respect to the real-world effects the concomitant training regimen is going to have on the hypertrophy and strength gains of the average trainee.

Why I am telling you all that? Well, actually I wanted to post this news item last Thursday already, but then Adelfo's contest prep update appeared out of nowhere and I had to postpone the study on the "skeletal muscle myosin heavy chain isoform content in relation to gonadal hormones and anabolic-catabolic balance in trained and untrained men" I actually wanted to discuss as a follow-up to the Cardore study (cf. "Cardio First if You Want to Leave the Gym More "Anabolic" Than You Were When You Came in?").

Fast or slow muscles? Are your hormones to blame?

Contrary to the Brazilian researchers who put their study participants through two identical workouts, the scientists from the University School of Physical Education, the Jagiellonian University and the Cancer Institute in Krakow, Poland did an ex-post analysis of the influence of endurance and strength training on the gonadal hormones and anabolic-catabolic hormone balance as well as their influence on myosin heavy chain (MHC) transformation in humans and found that...

"[...] despite considerable dissimilarity in MHC content between endurance trained, sprint / strength-trained, and untrained men, there are no differences between them in regard to basal T concentration."(Grandys. 2012)

This may be in conflict with the bro-scientific notion that you just have to take your overpriced T-boosters (or better real gear) religiously and will convert all your (falsely) unloved type 1 into type 2 fibers, but is consistent with previous studies which compared the total testosterone levels of top-class sprinters with untrained subjects and were likewise unable to proof statistically significant difference between the two (Grandys. 2011).

Fit = more testosterone? No! If anything, fat and unfit = less testosterone

Moreover, the results clearly show that contrary to being fat and metabolically deranged, not working out alone does not have negative effects on your total testosterone levels (much contrary to overtraining, by the way). Now, this does certainly put another huge question-mark behind the "exercise induced increases in testosterone build muscle hypothesis". It stands to reason that the sprinters, were, just like the strength athletes in the study at hand more muscular than the sedentary men and had an increased amount of the hypertrophy prone MHC-II muscles (fast twitch, predominantly intermediate type), but if you look at the actual study outcome, you will have to concede that this appears to be a function of the training stimulus and the accommodation to either strength or endurance workouts and has little to nothing to do with the testosterone levels.

Figure 1: Conditioning parameters (PO2_max and VO2_peak; left) and MHC-fiber composition (right) of untrained (U), endurance trained (E) and strength / sprint (S) athletes (Grandys. 2012)

In fact, there were highly significant correlations between the fiber type distribution between the endurance-trained athletes (E), and sprint/strength-trained athletes (S) in the study at hand. For example, the scientists observed...

• statistically significant correlations between muscle fiber type and VO2_peak (r = -0.49, p < 0.01) , expressed both in absolute and relative terms, and power output observed at the VO2peak (POmax)  between the untrained (U; rel. VO2Peak 46ml/kg/min, p < 0.001), sprint training / strength training (S; rel. VO2Peak 47ml/kg/min, p=0.02) and endurance training (E; 55.9 ml/kg/min)
• even higher correlations between fiber type and PO2_max (r = -0.69, p < 0.01), which is the maximal power production when cycling at the VO2_peak

Now, while all that clearly indicates that what you do at the gym is the fundamental determinant of your MHC-fiber composition and with it at least to a certain degree your growth propensity (and obviously overall cardiovascular fitness), there is one thing that brings the hormonal response back to the forefront:

There is a statistically significant correlation (r = 0.69) between the MHC-II content of the muscle fibers and the free testosterone to cortisol ratio. 

Figure 2: Ratio of free testosterone to cortisol and MHC-2 content of the muscles. Given the fact that the fT levels did not show significant differences, the determining factor thus appears to be - once again - cortisol not testosterone.

With the baseline free testosterone levels being identical (~20nmol/L) and in the upper third of the normal range  (9-38nmol/L) the confounding variable here is yet - once again (!) - not testosterone but cortisol. In this case not as positive regulator of total increases in lean mass (cf. figure 2 in Wednessday's post), but as a modulator of skeletal muscle myosin heavy chain isoform composition, which is - and I would like to emphasis this - not a matter of losing one for the other, but rather a matter of expressing more of type A while keeping the total amount of the other relatively steady.  Please take another look at figure 1 in the "Intermittent Thoughts on Building Muscle" and take a mental note of the fact that bodybuilders have higher total MHC-1 fiber contents than endurance rowers and a higher ratio of MHC II (X) fibers to MHC I (II/I_ratio = 1.76) than rowers (II/I_ratio = 1.69).

So, what's the role of cortisol in this case and what are the implication for muscle-heads and endurance junkies?

With cortisol being increased in response to both extreme high volume and endurance training (long and "in the fat burning zone", which is basically also the "zone" in which you would be running a non-competitive 10k if you are well-trained), you better limit both these training types to a reasonable amount if you want to maximize your MHC-II fiber count and more importantly, don't want to overtrain.

That it's neither necessary nor feasible to totally neglect one type of training for the other should yet be obvious by (a) the necessity to keep some muscle as "metabolic currency" and life-insurance, for the time the average and extraordinary endurance athlete gets older, and (b) the fiber composition of bodybuilders, which is not half as MHC-II dominant as bro-science would have it. And even if you "only" want to get stronger - do you really want to have to drop the weight because you are running out of steam at the bottom of a 400lbs squat? I don't think so...

References:

• Grandys M, Majerczak J, Zapart-Bukowska J, Kulpa J, Zoladz JA. Gonadal hormone status in highly trained sprinters and in untrained men. J Strength Cond Res. 2011 Apr;25(4):1079-84.
• Grandys M, Majerczak J, Karasinski J, Kulpa J, Zoladz JA. Skeletal muscle Myosin heavy chain isoform content in relation to gonadal hormones and anabolic-catabolic balance in trained and untrained men. J Strength Cond Res. 2012 Dec;26(12):3262-9.
• McDonald W. Basic Histochemistry and Electron Microscopy of Normal Muscle. University of South Florida. 2002 < http://missinglink.ucsf.edu/lm/ids_104_musclenerve_path/student_musclenerve/normal2.html > retrieved on  01/06/2013