I was planning to review here an article, Resistance Training to Momentary Muscular Failure Improves Cardiovascular Fitness in Humans: A review of acute physiological responses and chronic physiological adaptations. It’s by James Steele, et al, in the Journal of Exercise Physiology (Vol. 15, No. 3, June 2012).
But it’s too technical for most of my readers. Heck, it’s too technical for me! Too much cell biology and cell metabolism. You’re dismissed now. Maybe “American Idol” or “Honey Boo Boo” is on TV.
I’m just going to pull out a few pearls from the article that are important to me. I ran across this in my quest for efficient exercise. By efficient, I mean minimal time involved.
The authors question the widespread assumption that aerobic and endurance training are necessary for development of cardiovascular fitness. Like Dr. Doug McGuff, they wonder if resistance training alone is adequate for the development of cardiovascular fitness. Their paper is a review of the scientific literature. The authors say the literature is hampered by an inappropriate definition and control of resistance training intensity. The only accurate measure of intensity, in their view, is when the participant reaches maximal effort or momentary muscular failure.
The authors, by the way, define cardiovascular fitness in terms of maximum oxygen consumption, economy of movement, and lactate threshold.
“It would appear that the most important variable with regards to producing improvement in cardiovascular fitness via resistance training is intensity [i.e., to muscle failure].”
The key to improving cardiovascular fitness with resistance training is high-intensity. These workouts are not what you’d call fun.
From a molecular viewpoint, “the adenosine monophosphate–activated protein kinase pathway (AMPK) is held as the key instigator of endurance adaptations in skeletal muscle. Contrastingly, the mammalian target of rapamycin pathway (mTOR) induces a cascade of events leading to increased muscle protein synthesis (i.e.,[muscle] hypertrophy).” Some studies suggest AMPK is an acute inhibitor of mTOR activation. Others indicate that “resistance training to failure should result in activation of AMPK through these processes, as well as the subsequent delayed activation of mTOR, which presents a molecular mechanism by which resistance training can produce improvement in cardiovascular fitness, strength, and hypertrophy.”
You’re not still with me, are you?
“… the acute metabolic and molecular responses to resistance training performed to failure appear not to differ from traditional endurance or aerobic training when intensity is appropriately controlled.”
Chronic resistance training to failure induces a reduction in type IIx muscle fiber phenotype and an increase in type I and IIa fibers. (Click for Wikipedia article on skeletal muscle fiber types.)
“It is very likely that people who are either untrained or not involved in organized sporting competition, but you have the desire to improve their cardiovascular fitness may find value in resistance training performed to failure. In fact, this review suggests that resistance training to failure can produce cardiovascular fitness effects while simultaneously producing improvements in strength, power, and other health and fitness variables. This would present an efficient investment of time as the person would not have to perform several independent training programs for differing aspects of fitness.” [These statements may not apply to trained athletes.]
Before listing their 157 references, the authors note:
“It is beyond the scope of this review to suggest optimal means of employing resistance training (i.e., load, set volume, and/or frequency) in order to improve cardiovascular fitness since there are no published studies on this topic.”
In conclusion, if you’re going to do resistance training but not traditional aerobic/cardio exercise, you may not be missing out on any health benefits if you train with intensity. And you’ll be done sooner.
PS: See Evidence-based resistance training recommendations by Fisher, Steele, et al.