fbpx
  • /Home
  • /Blog
  • /Strength
  • /Why are higher intensities better for strength: PART 2 – Morphological adaptations
28 May 2020

Why are higher intensities better for strength: PART 2 – Morphological adaptations

by Brian Minor 0

In part 1 of this series I laid down the framework to discuss why/how higher intensities of load are generally more beneficial for maximal strength development. One of the two primary categories of adaptations associated with expression of strength are ‘morphological’ adaptations, which is what we will explore in this part of the article series….

In part 1 of this series I laid down the framework to discuss why/how higher intensities of load are generally more beneficial for maximal strength development. One of the two primary categories of adaptations associated with expression of strength are ‘morphological’ adaptations, which is what we will explore in this part of the article series.

Morphological adaptations are simply changes to factors within the mechanical supply line for force production; the actual structural changes. Due to their considerable importance to maximal strength, the two areas we will place our focus on are:

  1. Increases in muscle size (muscle hypertrophy) and 
  2. Changes within connective tissue.

1. Muscle Hypertrophy

Perhaps the most obvious adaptation to resistance training is building muscle. However, it’s role in strength is often misunderstood. Does building muscle build strength? Or does building strength build muscle? Is it both? Is it technically neither?…

Many people have probably heard the following analogy when discussing this relationship: Muscle is like a cup, and strength as what fills it. The size of the cup ultimately constrains the amount of liquid in it, just as muscle size ultimately constrains the amount of force that can be produced (12). Additionally, just as a cup can be filled below its capacity, 1 RM strength can fall well below it’s capacity based on muscular development alone (14). The ability to reach one’s strength potential (and fill the cup to its capacity) is therefore largely dictated by additional improvements within specific neurological adaptations (discussed in more detail in Part 3). 

How does muscle hypertrophy impact strength?

In short, larger muscle fibers, all else equal, are able to produce more force.

Our skeletal muscle is made up of a bunch of fascicles, which are just bundles of individual muscle fibers. These individual fibers are made up of smaller myofibrils, arranged into repeating segments called sarcomeres.  Each sarcomere contains the contractile machinery of the muscle, thin protein filaments called actin which surround thicker protein filaments called myosin. Each myosin filament has multiple ratcheting heads (often referred to as motors) that when active, grab a hold of the actin filaments and pull them over the myosin, shortening the entire sarcomere. This action is called cross-bridging, and it is where force is generated. When it occurs within a bunch of sarcomeres, within a bunch of myofibrils, within a bunch of muscle fibers, within a number of fascicles, the whole muscle shortens and produces force. Since each end of the muscle is attached to the tendon, which is attached to bone (hopefully), we get movement!

Increases in whole muscle size is influenced primarily by an increase in individual fiber cross sectional area. This cross sectional area increases via an addition of myofibrils in parallel to an existing fiber(s). With an increase in myofibrils comes an increase in contractile proteins/“machinery” for cross-bridging. When activated, more cross-bridging means more total force for muscular contraction (8).

So how much of a role does hypertrophy play in 1 RM strength, and does that role change with time? 

A 2007 study showed that in trained lifters, up to 76% of the increases in squat 1 RM could be attributed to hypertrophy (increase in vastus lateralis CSA) (5).

Greg Nuckols wrote an excellent article covering the role of muscle size on strength, which showed that muscle size accounts for up to ~ 65% of the strength variability in experienced lifters. The article gets into some of the finer details in terms of relative contributions so if you are interested, I highly recommend checking it out.

What about in less experienced athletes? A 2019 study (1) took men with different levels of training experience (none, 12 weeks, and 4 years), and looked at the EMG-torque relationship when performing leg extensions. EMG-torque is basically a measure of how much muscle activation is occurring relative to the torque produced at a joint. What they found was similar amounts of agonist muscle activation between the 12 week and 4 year groups, despite a greater torque produced in the 4 year group. In addition, the 4 year group had greater quadricep cross sectional area (CSA). This data suggests that the increase in torque generated in the 4 year group was driven primarily by morphological adaptations, since activation levels were the same. Considering the increase in CSA that also occurred, hypertrophy likely played a significant (and perhaps primary) role in the strength increase that occurred sometime between 12 weeks and 4 years, with neurological adaptations primarily driving the increases inside 12 weeks. 

That being said, despite the relative importance of hypertrophy appearing to increase over time, the absolute importance is high at any time point in a training career as development ultimately both establishes, and can constrain your capacity to produce force (12)

Does absolute intensity influence muscle hypertrophy?

A bunch of evidence points to no. Unlike 1 RM strength (14), when it comes to hypertrophy, there has been substantial research demonstrating that hypertrophy is not load specific (14). Similar hypertrophy can across a spectrum of loading ranges so long as volume (# sets) and relative effort are sufficient. As many readers may be aware, simply counting the number of hard sets has been shown to be a practical way to quantify training volume when it comes to hypertrophy (2).

Before we move on,let’s discuss why loading doesn’t really matter for hypertrophy, as it’s a convenient way to introduce some neuromuscular physiological concepts that are fundamental to future discussion.

The Size Principle

A motor unit is a motor neuron and all of the muscle fibers that it controls. The larger the motor unit, the more muscle fibers it controls, and the more overall force it can produce. The size principle is the observation that the central nervous system recruits motor units on an as needed basis to meet and/or maintain an imposed force demand. When the brain receives the message that the force demand is greater than the current “supply” of muscular force provided by existing motor units, then more force is brought to the table through the recruitment of progressively “higher threshold” motor units (HTMU). Once activated, all of the muscle fibers are controlled by the MU contract, contributing additional force.

Now, full MU recruitment occurs “out of the gate” to meet the demand of lifting heavy loads (~70-90% depending on muscle and lift (9,15), and as fatigue sets in and force output must be maintained (4,11). Light loads performed relatively close to failure fall into the latter category. As fatigue sets in, more MUs are called into action contributing force through cross-bridging, and velocity begins to slow. This is where the force-velocity relationship comes into play. 

The Force-Velocity Relationship

The force-velocity relationship is the observation that force and velocity share an inverse relationship during concentric contractions. A simple way to think of this is that the heavier the weight, the more muscular force is required to lift it, but the slower (lower velocity) the rep will be. 

Now going back to low load sets taken to relatively close proximity to failure. As fatigue sets in within existing MUs, larger MUs are recruited, and velocity begins to slow.  The amount of cross-bridging occurring and subsequently force produced within an active fiber increases (up until the fiber itself begins to fatigue anyway).  The combination of HTMU recruitment in conjunction with the increase in cross-bridging results in high degrees of mechanical tension on the HTMUs, and similar hypertrophy with light loads.

2. Connective Tissue

While force is generated at the level of the sarcomere, that force ultimately needs to be applied across a joint to our bones to generate movement. This force is transferred via connective tissue within the muscle itself and then through the tendons connecting our muscle to bone. So it should come as no surprise that morphological changes to connective tissue could impact our ability to generate force through movement. 

Two of the primary changes that occur which positively influence our ability to generate force are increases in lateral force transmission and increases in tendon stiffness. 

How do these changes in connective tissue impact strength?

When force is generated within the sarcomere of a myofibril, it transfers force both longitudinally (down the length of the fiber) as well as laterally across adjacent myofibrils out to the fiber’s cell membrane sheath (sarcolemma) via structures called costameres (3,13).  This force is then transmitted laterally across the extracellular connective tissue matrix (endomysium) to the nearby muscle fibers. These lateral connections ultimately allow for a more efficient transfer of force down to the tendon.

So now we are at the tendon. Since the muscle is exerting force on the tendon, the tendon properties also influence the amount of force that is ultimately applied to the bone. Think of it like the muscle and bone playing a game of tug-war. Would the muscle be able to transfer more of its force through a rubber band or through a steel cable? Unsurprisingly, a stiffer tendon allows the muscular force to be transferred more efficiently. There is another reason it works though, one I hadn’t thought of until reading some of Chris Beardsley’s work. A stiffer tendon is also going to resist the actual muscle from shortening as easily upon contraction. Contraction velocity slows and there is a greater degree of cross bridging that occurs within each active fiber, increasing force production. This is a prime example of the force-velocity relationship.

Does absolute intensity influence connective tissue adaptations?

As we discussed previously, changes in muscle size (hypertrophy) are not intensity specific primarily because it’s dependent on tension experienced at the fiber level, rather than tension experienced at the whole muscle level. However, in the case of connective tissue, increases in tendon stiffness (6,7,10) and lateral force transmission are more likely a result of increased loading on the whole muscle level (which heavy loads provide).

Morphological Summary

When thinking about morphological adaptations to training, it’s easy to only consider muscle hypertrophy. It appears to play an increasingly important role in strength progression over time, and accounts for most of the strength variability in experienced athletes. Since we know hypertrophy isn’t load dependent, it can therefore be easy to assume high intensities play minimal to no role in morphological adaptations. However, high intensity loading appears to elicit adaptations related to whole muscle tension more so than tension at the fiber lever (which is what’s more important for hypertrophy). Connective tissue adaptations conducive to strength can be improved to a greater degree with high(er) intensity loading, and play an important role in efficient force transfer and getting the most out of the force produced at the myofibril level.

References

1. Balshaw, TG, Massey, GJ, Maden-Wilkinson, TM, Lanza, MB, and Folland, JP. Neural adaptations after 4 years vs 12 weeks of resistance training vs untrained. Scand J Med Sci Sports 29: 348–359, 2019.

2. Baz-Valle, E, Fontes-Villalba, M, and Santos-Concejero, J. Total Number of Sets as a Training Volume Quantification Method for Muscle Hypertrophy: A Systematic Review. J Strength Cond Res , 2018.

3. Bloch, RJ and Gonzalez-Serratos, H. Lateral force transmission across costameres in skeletal muscle. Exerc Sport Sci Rev 31: 73–78, 2003.

4. Conwit, RA, Stashuk, D, Suzuki, H, Lynch, N, Schrager, M, and Metter, EJ. Fatigue effects on motor unit activity during submaximal contractions. Arch Phys Med Rehabil 81: 1211–1216, 2000.

5. Cribb, PJ, Williams, AD, Stathis, CG, Carey, MF, and Hayes, A. Effects of whey isolate, creatine, and resistance training on muscle hypertrophy. Med Sci Sports Exerc 39: 298–307, 2007.

6. Eriksen, CS, Svensson, RB, Gylling, AT, Couppé, C, Magnusson, SP, and Kjaer, M. Load magnitude affects patellar tendon mechanical properties but not collagen or collagen cross-linking after long-term strength training in older adults. BMC Geriatr , 2019.

7. Grosset, J-F, Breen, L, Stewart, CE, Burgess, KE, and Onambélé, GL. Influence of exercise intensity on training-induced tendon mechanical properties changes in older individuals. Age 36, 2014.Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4082599/

8. Huxley, AF. Muscle structure and theories of contraction. Prog Biophys Biophys Chem , 1957.

9. Król, H and Gołaś, A. Effect of Barbell Weight on the Structure of the Flat Bench Press. J Strength Cond Res 31: 1321–1337, 2017.

10. Kubo, K, Komuro, T, Ishiguro, N, Tsunoda, N, Sato, Y, Ishii, N, et al. Effects of low-load resistance training with vascular occlusion on the mechanical properties of muscle and tendon. J Appl Biomech 22: 112–119, 2006.

11. Looney, DP, Kraemer, WJ, Joseph, MF, Comstock, BA, Denegar, CR, Flanagan, SD, et al. Electromyographical and Perceptual Responses to Different Resistance Intensities in a Squat Protocol: Does Performing Sets to Failure With Light Loads Produce the Same Activity? J Strength Cond Res 30: 792–799, 2016.

12. Maden-Wilkinson, T, Balshaw, T, Massey, G, and Folland, J. What makes long-term resistance-trained individuals so strong? A comparison of skeletal muscle morphology, architecture, and joint mechanics. J Appl Physiol , 2019.

13. Peter, AK, Cheng, H, Ross, RS, Knowlton, KU, and Chen, J. The costamere bridges sarcomeres to the sarcolemma in striated muscle. Prog Pediatr Cardiol 31: 83–88, 2011.

14. Schoenfeld, B, Grgic, J, Ogborn, D, and Krieger, J. Strength and hypertrophy adaptations between low- versus high-load resistance training: A systematic review and meta-analysis. J Strength Cond Res , 2017.

15. Yavuz, H and Erdağ, D. Kinematic and Electromyographic Activity Changes during Back Squat with Submaximal and Maximal Loading. Appl Bionics Biomech Volume 2017 (2017): 8 pages, 2017.

Your email address will not be published. Required fields are marked *

Send this to a friend