A number of readers have asked my opinion on the recent study by Lundberg et al. (2013), which showed that adding cardio to a resistance training routine actually increased muscle growth. I actually wrote a critique of this study several months ago for Alan Aragon’s Research Review. Alan was kind enough to grant me permission to reprint the critique on my blog. So without further ado, here’s what we can take away from the study by Lundberg et al.:



Background Info

A large body of research indicates that combining aerobic training with resistance training (i.e. concurrent training) has a negative effect on gains in muscular strength and size (9). There is evidence that aerobic exercise mediates catabolic pathways while anaerobic exercise mediates anabolic pathways. This has led to the “AMPK-PKB switch” hypothesis, which professes that the two types of exercise are incompatible (2). It has been shown, however, that considerable overlap exists in signaling responses to mechanical stimuli, calling into question the validity of this hypothesis (5).

Recently, Lundberg et al. (6) found that acute anabolic signaling markers (mTOR and p70S6K) were actually greater with concurrent training compared to resistance exercise alone. This seemingly contradicts the majority of previous research, and raises the possibility that aerobic exercise may in fact be beneficial to muscle hypertrophy. However, such results must be taken with caution as the response of translational signaling components to an acute exercise bout are often unrelated to the degree of myofiber hypertrophy seen after long-term resistance training (1). Hence, the current study was conducted by the same lab as a follow-up to this previous work, with the objective of assessing the chronic impact of concurrent training on muscular hypertrophy, strength, power, and endurance.

Study Specifics

Subjects were 10 “moderately trained” college students. The study employed a within-subject design, where participants performed resistance training on one leg while performing concurrent training (both aerobic and resistance exercise) on the other leg. The limb chosen to receive concurrent exercise was counterbalanced between subjects, meaning that for every subject who performed concurrent training on the right leg another would perform the condition on the left leg. This type of design has the inherent advantage of negating any inter-individual differences in response to training, thereby improving statistical power. Thus, the low sample size was not as big an issue as it would have been had the researchers evaluated two independent groups (although the study was still likely underpowered nevertheless).

The training program was carried out over the course of 5 weeks. Aerobic training consisted of 40 minutes of one-legged cycle ergometer exercise per session at 70 percent of peak power output. Immediately following each 40 minute aerobic bout, the workload was bumped up to near maximum peak power and subjects continued pedaling until failure (which occurred, on average, after approximately 2 minutes 30 seconds). Aerobic sessions were performed 3 non-consecutive days a week. Resistance exercise comprised 4 sets of 7 reps of unilateral leg extensions with 2 minutes rest between sets. Resistance sessions were performed 6 hours after the aerobic bout and took place 2-3 days a week (2 days/week in weeks 1, 3, and 5; 3 days/week in weeks 2 and 4). Maximal strength was assessed via isokinetic dynamometry; peak muscle torque, power, and endurance were assessed by flywheel ergometry; muscle hypertrophy was assessed by MRI as well as muscle biopsy.

The study produced some interesting findings. To no one’s surprise, the concurrent training leg showed a strong trend for greater muscular endurance as determined by time to exhaustion. Aerobic exercise requires local endurance and it therefore stands to reason that consistent cycle ergometry training would mediate specific adaptations to enhance this variable. Somewhat surprisingly, measures of strength and power were not different between conditions. Given that a preponderance of evidence seems to indicate that concurrent training interferes with strength-related gains (9), one might have assumed that the resistance-only leg would have shown greater improvements in strength/power. The most surprising finding was that muscle volume and cross sectional area in the concurrent leg was almost double that of the resistance-only leg (13.6% vs. 7.8%, respectively)! Muscle biopsy indicated that these results were primarily attributable to increases in type I fiber hypertrophy. This led researchers to conclude that aerobic exercise may provide synergistic hypertrophic benefits when incorporated into a resistance training routine without compromising functional gains attained from resistance exercise.

A Critical Analysis of Results

So what to make of these results? Should aerobic exercise be included as part of any hypertrophy protocol? Let’s dig a little deeper and see what can be ascertained from a practical standpoint…

The first thing to evaluate in any scientific study is its theoretical rationale; in other words, does the data make sense? In this case, we need to consider why hypertrophic adaptations take place in muscle tissue. The principle of specificity dictates that adaptations are specific to the stimulus applied. With respect to hypertrophy, muscles grow larger in an effort to respond to strength-related challenges. When an overload stimulus is repeatedly imposed on a muscle (such as during resistance training), it will synthesize proteins in order to meet this challenge in the future. By its very nature, aerobic exercise does not challenge the muscle in a strength-related manner, so there would be little reason for the muscle to respond by hypertrophying. In fact, hypertrophy is detrimental to lengthy aerobic-endurance exercise as it requires the body to continually support a greater load during performance. So although we should not dismiss the results of the study outright, we nevertheless must be skeptical as to their validity.

A couple of things stand out upon close scrutiny of the findings. For one, subjects were classified as “moderately trained.” By the authors’ definition, this meant that participants were involved in recreational activities such as skiing and team sports, but had not performed resistance training in the past year. So in essence, the subjects were actually untrained from a resistance training standpoint. Why is this an issue? Well, in those without training experience, virtually any stimulus will be a challenge to the musculature and thus cause hypertrophy. On the other hand, well-trained subjects have already adapted to lower-level stresses, and it therefore remains questionable whether aerobic training would provide enough of a stimulus for further muscular adaptation. It stands to reason that it would not.

Another interesting finding was that while muscle hypertrophy was deemed to be substantially greater in the concurrent leg compared to the resistance-only leg, muscle strength and power was not different between the two conditions. This seems to defy logic. Studies show a direct correlation between muscle strength and muscle CSA: a greater cross sectional area is strongly associated with greater strength (4). The fact that a greater increase in muscle mass did not lead to greater strength therefore sends up a red flag. It would seem that this contradiction is due, at least in part, to the fact that hypertrophic differences were primarily attributed to type I fiber growth. Type I fibers are endurance-related fibers with a limited force-producing capacity; it’s the type II fibers that are primarily responsible for strength and power, and these fibers showed no significant difference between groups. It seems reasonable to question whether such type I fiber hypertrophy is sustainable over the long-term. Since these fibers are highly fatigue-resistant, it could be speculated that they’d be increasingly stubborn to continued growth after an initial period of conditioning. This theory remains to be elucidated.

It also should be noted that MRI signal intensity was markedly increased with concurrent exercise but not with resistance exercise. The significance here is that an increased MRI signal intensity is consistent with an increase in tissue water content. This suggests that the greater muscle volume seen with combined aerobic and resistance exercise may well have been related to intramuscular fluid accumulation, presumably mediated by edema pursuant to muscle damage. The researchers tried to minimize this possibility by obtaining MRI scans 48 hours after completion of the final exercise session. However, peak swelling has been shown to occur approximately 5 days post-exercise (3), raising serious questions as to whether edema in fact played a role in results. The researchers downplayed any potential confounding effects from muscle damage by stating that no subject reported any soreness at the time of testing. But studies show that DOMS is not necessarily well correlated to various markers of muscle damage including maximal isometric strength, ROM, upper arm circumference, and plasma CK levels (7), making it a poor gauge of both the presence and magnitude of tissue trauma. Taking all factors into account, it appears likely that a good portion of the hypertrophic differences between conditions were related to sarcoplasmic elements rather than an increase in contractile muscle proteins.

A major limitation of the study was its short duration. One of the biggest detriments of concurrent training with respect to strength and hypertrophy is that hastens the onset of overtraining syndrome (OS). OS causes the body to shift into a catabolic state, leading to decrements in performance and impaired muscular adaptations (8). The chronic interference hypothesis suggests that the addition of aerobic exercise to a resistance training program results in long-term competing adaptations that ultimately brings about OS and thus interferes with strength-related muscular adaptations (9). Thing is, the effects of OS take time to manifest–certainly more than the five week time-course of this study. Moreover, the volume and frequency of the resistance routine employed was not very demanding, to say the least. 4 sets of knee extensions performed 2-3 days a week is no way representative of the type of routine used by most serious lifters. A higher volume routine, similar to what is customarily employed in a hypertrophy-oriented program, would place greater demands on recuperative abilities and thereby increase the potential for overtraining when combined with frequent aerobic exercise. All things considered, it is impossible to extrapolate the results of this study to long-term, higher volume training programs.

Another limitation is that the study is that a single type of aerobic exercise (cycling) was evaluated for a single muscle group (quadriceps). We cannot conclude that other forms of aerobic exercise (i.e. jogging, treadmill, stepmill, stairmaster, elliptical training, etc) provide the same effects for the quadriceps, nor can we conclude that the same effects will occur in the other lower body muscles, such as the glutes, hamstrings, or calves. In fact, evidence shows that running interferes with strength-related gains to a greater extent than cycling (9). Finally, we cannot conclude that the upper body muscles would respond similarly to upper body aerobics such as swimming or arm ergometry.

In conclusion, this study provided interesting data that challenges existing beliefs with respect to concurrent training. However, the inherent limitations of the study make it far too premature to draw any definitive conclusions on the topic. Future research should seek to examine the chronic effects of concurrent training on muscular hypertrophy over longer time periods and employing routines consistent with what lifters actually perform in real-world situations.

References

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2. Atherton PJ, Babraj J, Smith K, Singh J, Rennie MJ, Wackerhage H. Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation. FASEB J. 2005; 19(7):786-8.

3. Clarkson PM, Nosaka K, Braun B. Muscle function after exercise-induced muscle damage and rapid adaptation. Med Sci Sports Exerc. 1992; 24(5):512-20.

4. Frontera WR, Hughes VA, Fielding RA, Fiatarone MA, Evans WJ, Roubenoff R. Aging of skeletal muscle: a 12-yr longitudinal study. J Appl Physiol. 2000; 88(4):1321-6.

5. Gibala M. Molecular responses to high-intensity interval exercise. Appl Physiol Nutr Metab. 2009; 34(3):428-32.

6. Lundberg TR, Fernandez-Gonzalo R, Gustafsson T, Tesch PA. Aerobic exercise alters skeletal muscle molecular responses to resistance exercise. Med Sci Sports Exerc. 2012; 44(9):1680-8.

7. Nosaka K, Newton M, Sacco P. Delayed-onset muscle soreness does not reflect the magnitude of eccentric exercise-induced muscle damage. Scand J Med Sci Sports. 2002; 12(6):337-46.

8. Schoenfeld BJ. The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res. 2010; 24(10):2857-72.

9. Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP, Anderson JC. Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. J Strength Cond Res. 2012; 26(8):2293-307.