Coach's Corner - Lift Heavy & Bike (or run?) Strong!

Here’s another one for you science keeners! Ever wonder if hitting the gym is going to make you less efficient of a runner, cyclist, cross-country skier, snow shoe-er, or aqua-jogger? Well, think again!

Basically, it looks like your muscles adapt to the lack of blood flow that can reach them (bigger muscles = some tissue gets farther away from the source) and they become efficient in other means of metabolism! So if you’re thinking you can’t hit the gym because you’ll become inefficient, there is an amount of muscle mass that can be gained (from a recreational athlete’s perspective) that will mitigate the negative aspect of increased weight, by improving both overall strength and efficiency of movements! And although it’s not discussed in this article, there is then the added bonus of injury prevention/mitigation!

Maybe you should start adding some weight training to your program! Just make sure it’s sport specific and include your mobility/stretching.

The authors of Salvadego et al. (2013) set out to determine the effect of resistance training and hypertrophy on the oxidative capacities of muscle fibers in endurance performance. Theorizing that an increase muscle mass and density would negatively affect the muscle’s oxidative capacity. The study addresses the conflicting logics surrounding increased muscle mass due to resistance training and it’s influence on oxidative function in aerobic performance, the authors cite confounding principles, those relating to performance enhancement include: increased cross-sectional area of skeletal muscle fibers enhance force-generating potential, require recruiting fewer motor units, and more oxidative muscle fibers, increase skeletal muscle efficiency, and increase metabolic stability of the muscle tissue; potentially performance inhibiting include: “unchanged or lower mitochondrial volume density, oxidative enzyme activity, and capillary density in the hypertrophic muscles.” This variance in the literature leading up to this study inconclusive and requiring further clarity.

The study included 22 competitive athletes who are of National-caliber in Slovenia. 11 athletes were recruited for each group, because Resistance Trained Athletes (RTA) and non-resistance trained Control group. (CTRL) Those in the RTA group were athletes who took part in regular aerobic as well as intense strength training regimens as part of their sport, the CTRL group had no strength training programs, though similar or great aerobic training to the RTA’s. A qualification for the RTA group was to have a thigh circumference >60cm and a fat thickness <10mm. An 8 week training diary was supplied by each athlete to ensure adequate criterion qualification. This cohort could be considered fairly substantial, including 22 National level currently competing athletes, and each producing muscle biopsies, provides a highly difficult population to acquire. I highly regard the ability of the authors to recruit, and athlete’s willingness to participate in this study. An interesting note from the pretesting procedures, although peak KE was greater in the RTA group, after normalizing for cross-sectional area of the quadriceps femoris muscle group, there was no significant difference, I would postulate this being due to the ability of trained athletes to maximally contract tissue due to training activity, i believe this would have not been the case if CTRL group was not comprised of athletically trained individuals.

To determine oxidative capacity, athletes were all subjected to two incremental effort tests, a Cycle Ergometer (CE) and Knee Extension (KE) testing protocol, testing conditions were based off preliminary peak effort tests. The KE tests was completed as a knee-extension specific cycle-ergometer apparatus, this machine ensured only the quadriceps femoris muscle group would be active in this testing condition. Subjects data were recorded during protocols, these data included: Pulmonary ventilation (V̇E), tidal volume (VT), respiratory frequency (f), O2 uptake (V̇O2), and CO2 output (V̇CO2), heart rate (HR), stroke volume (SV), and local Oxygen saturation (Δ[deoxy(Hb+Mb)]). At 5 hours following the protocol, athletes provided 2 muscle biopsies for ex vivo observation. Mitochondrial respiratory function and Citrate Synthase activity was calculated and observed using these tissue samples. The data sets and figures provided in this article are well displayed and provide a clear and concise image of the results obtained. Given the quantity of data acquired, I believe these data tables to be of great value to the article.

The results acquired are extensive, due to the quantity of data recorded. Rejecting their hypothesis, that increased muscle mass due to strength training would inhibit aerobic oxidative capacities, the results indicated that, mean peak VO2 was equal between RTA and CTRL groups during the CE testing. An interesting result though was the value in oxygenation of the vastus lateralis, indicated by Δ[deoxy(Hb+Mb)]  (an ischemic measure), although a similar sigmoid pattern was observed, the difference in relative ischemia (%) was shocking to me. At the same workload, and relative workload (ie. peak effort), there existed a difference in the Δ[deoxy(Hb+Mb)]. The authors discuss this phenomena in their discussion, stating “The main impairment could then reside in the diffusing capacity of the muscle for O2 and/or in the intramuscular matching between O2 delivery and O2 utilization, which could be altered as a consequence of the marked muscle hypertrophy.” Further, results from the muscle biopsies indicated an increased mitochondrial respiration function in RTAs, which the authors hypothesize to be due to the impaired peripheral O2 diffusing capacity previously mentioned, this causes mitochondria to adapt to this environment of repeated-hypoxia, and improve the mitochondrial coupling process.

Lastly, the authors pose an interesting question to the scientific community; the whole body peak oxidative function was observed to be enhanced in the RTA compared to CTRL athletes, despite the anthropometric differences between groups, this is contrary to literature regarding subjects categorized as obese, where there also exists a significantly larger body mass, previous studies indicate “the VO2 vs work rate relationship is shifted upward… indicating a higher O2 cost of CE exercise derived from the excess in body mass”. The authors conclude that young RTAs exhibiting significant skeletal muscle hypertrophy seem to compensate for the impaired peripheral O2 diffusion, and display equal efficiency to non-RTAs though have increased peak whole body oxidative function.

In my personal experience, I would anticipate these data be of value to the realm of track cycling, where muscular hypertrophy and aerobic oxidative function are highly prevalent in top athletes. Considering athletes such as Robert Förstemann and Chris Hoy, where marked skeletal muscle hypertrophy is obvious, these athletes are required to perform highly strenuous aerobic and anaerobic efforts, events ranging in duration from the 10km Scratch Race to the Flying 200m, these athletes function with high metabolic and oxidative function requirements

Refs:

Salvadego, D., et al. (2013). Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training. Journal of Applied Physiology, 114(11), 1527-1535.