Beyond Protein Synthesis - Here's What's Really Driving 'ur Gainz | Plus: Exercise & NAFLD, Telomere Length + More

Unless it's done in excess, exercise is a universal health booster ... and it can make you look great naked ;-)

In the latest edition of the short news, I am going to address recently published papers from Exercise and Sport Science Reviews that shed a new light on the way(s) your muscle grow and suggest that exercise is able to cure NAFLD at least partly due to its ability to activate hepatic autophagy.

In conjunction with three studies from the July issue of Medicine & Science in Sports & Exercise that dealt with the link between leisure-time physical activity and telomere length, the underlying reason grandpa (and -ma) are at a very high risk of fall (hint: it's a neuromuscular weakness) and the validity of "use it or lose it" when it comes to the cartilage tissue in your knee.

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• "Interactions between muscle stem cells and protein turnover facilitate both hypertrophic and nonhypertrophic muscle remodeling," Burd and De Lisio write in their paper "Skeletal Muscle Remodeling: Interconnections Between Stem Cells and Protein Turnover" in Exercise and Sport Science Reviews.

  

  Figure 1: Illustration of the interaction between exercise and nutrition signals are sensed at the sarcolemma to augment rates of hypertrophic and non-hypertrophic muscle fiber remodeling (Burd 2017).

  In their review, the scientists from the Universities of Illinois and Ottawa, respectively, emphasize that the gains you're striving for are not a simple result of pumping protein into the muscle. Rather than that, continuous growth requires (as you've learned in the Intermittent Thoughts on Building Muscle | read more) protein synthesis and muscle remodeling to maintain (or expand) the composition of a healthy proteome.
  
  

  

  Figure 2: Graphical illustration of what you could have learned about this interaction back in 2012 if you'd read the corresponding SuppVersity article | more

  This remodeling requires the recruitment of muscle stem cells (aka satellite cells) and has hitherto often been thought of being independent of the classic hypertrophy via increases in net protein balance. Burd and De Lisio do now suggest that "muscle stem cells and protein turnover are interconnected and thus collaborate to improve rates of muscle remodeling in response to anabolic stimuli to ultimately facilitate muscle adaptations" (Burd 2017). Only if both processes are activated by training and nutrition, you will see maximal gains.

Finally officially published: "Endurance Exercise Training and Male Sexual Libido" - I discussed this paper by Anthony Hackney and colleagues back in February when it was published ahead of print. The title of the post is "Training Volume, Intensity, and Your Libido - How Bad is It? Who Read the Study Knows: It's not Just About Cardio ...! " - if you missed it or cannot remember it, I suggest you reread this important article.

• Exercise repairs NAFLD liver via autophagy, Chun et al. hypothesize. In their paper in Exercise and Sport Science Reviews, the researchers from the University of Florida propose a hypothesis that activation of autophagy through exercise ameliorates cellular defects underlying the pathogenesis of non-alcoholic fatty liver disease (NAFLD).
  
  In his editorial comment, Dasarathy confirms that "preclinical and consistent but very limited data in patients with NAFL suggest impaired hepatic autophagy in NAFLD" (Dasarathy 2017). Part of this evidence points to increases in irisin and "potentially other myokines" as driving motors of the browning of body fat and inhibitors of hepatocyte triglyceride accumulation.
  
  

  

  There's a whole arsenal of vitamins & herbals that are supposed to either protect you from or even cure NAFLD. Learn more about a dirty dozen of nutrient and supplement suggestions.

  Dasarathy does yet also highlight that "the beneficial effects of exercise cannot be ascribed only to stimulation of autophagy". Rather, ...

  "Exercise also improves oxidative stress and insulin sensitivity, both of which are beneficial in NAFLD. Exercise also improves microcirculatory and endothelial dysfunction, major contributors to morbidity and mortality in NAFLD" (Dasarathy 2017).

  In other words, even if autophagy takes care of the liver problems, it will not take care of the various non-hepatic accompaniments of NAFLD.
• "Greater engagement in vigorous [leasure time physical acticity] LTPA and exceeding the PA recommendation may have a protective effect against telomere shortening", Elisa F. Ogawa et al. write in their latest paper in Medicine & Science in Sports & Exercise.
  
  

  

  Do you remember the link between coffee and telomere length? If not, reread "Coffee Lengthens, While Caffeine Shortens Your Telomeres: An Essential Paradox? The Latest Evidence Reviewed"

  In their study, the researchers examined the associations between different physical activity (PA) domains, PA recommendations, and leukocyte telomere length (LTL) using data from a nationally representative sample of U.S. adults in the National Health and Nutrition Examination Survey, 1999–2002.
  
  The results of their data analyses leave little doubt: On average, an increase of 1 h/wk of vigorous LTPA was associated with a 0.31% (P < 0.001) longer LTL, and an increase of 1 h/wk of household/yard work PA was associated with a 0.21% (P = 0.03) shorter LTL while adjusted for sociodemographic and health behavior covariates.
  
  Quite interesting that house- and yardwork, on the other hand, seems to shorten one's telomeres. Well, be that as it may, other factors, such as transportation PA nor moderate LTPA were not significantly associated with the subjects' telomere length. In addition, compared with not meeting the PA recommendation (<150 min/wk), exceeding the recommended PA levels (≥300 min/wk) was positively associated with longer LTL (P = 0.04), whereas there was no difference in telomere length between those not meeting versus those meeting the PA recommendation (150–299 min/wk).
• Slow, not just weak -- "[N]euromuscular factors [...] influence the age-related reductions in [rate of torque development] RTD" of elderly subjects, a recent paper by Gerstner et al. highlights and explains why muscular function and performance in older adults sucks.
  
  In the study, thirty-two young (20.0 ± 2.1 yr) and 20 older (69.5 ± 3.3 yr) recreationally active men performed rapid plantarflexion isometric muscle actions to examine absolute and normalized RTD and muscle activation using EMG at early and late time intervals. Ultrasonography was used to examine medial gastrocnemius muscle size, echo intensity (EI), and muscle architecture (fascicle length [FL] and pennation angle [PA]).
  

  

  Figure 3: Absolute (A) and normalized (B) RTD for 0–50 and 100–200 ms for the young and older men during rapid plantarflexion isometric contractions. *P <= 0.05, significant difference between the young and the older men. Data are presented as mean ± SD (Gerstner 2017).

  Analyses of the data revealed (1) the obvious: the older men were weaker (23.9%, P < 0.001) and had lower later absolute and normalized RTD (P = 0.001–0.034) variables when compared with the young men; and the (2) the expected: the older men also had higher EI (P < 0.001), smaller PA (P = 0.004), and lower later EMG amplitude values (P = 0.009–0.046).
  What the study did not show, however, were the significant differences in early RTD and EMG amplitude values, muscle size, or FL between groups (P = 0.097–0.914) you may have expected.

If you premix it with vitamin C, any form of gelatin will work just as well as the mix the scientists used in a recent study which showed. And if it contains 15g + of gelatin, consuming this stuff before a workout could indeed make a significant difference for your tendon health and stability/resilience.

What else is worth reporting? Well, maybe that "you snooze, you lose" applies to the knee cartilage tissue of 87 volunteer postmenopausal women, age 60 to 68 yr, with mild knee OA (Kellgren Lawrence I/II and knee pain), too.

Over a period of 12 months, a group of Finnish researchers observed a "significant linear relationship between higher LTPA [leasure time physical activity] level and increased dGEMRIC index [a proxy for cartilage density] changes in the posterior region of interest (ROI) of the lateral (P = 0.003 for linearity) and medial (P = 0.006) femoral cartilage" (Munukka 2017). Ah, and the vitamin C + gelatin stack, I discussed in my 2016 article "100% Increase in Exercise-Induced Collagen Synthesis With Cheap, Yet Effective 15g Gelatin + 200mg Vitamin C Stack" (read it) may even have augmented these results | Comment!

References:

• Burd, Nicholas A.; De Lisio, Michael. "Skeletal Muscle Remodeling: Interconnections Between Stem Cells and Protein Turnover." Exercise & Sport Sciences Reviews . 45(3):187-191, July 2017.
• Chun, Sung Kook, et al. "Exercise-Induced Autophagy in Fatty Liver Disease." Exercise & Sport Sciences Reviews: July 2017 - Volume 45 - Issue 3 - p 181–186
• Gerstner, Gena A., et al. "Neural and Muscular Contributions to the Age-Related Reductions in Rapid Strength." Medicine & Science in Sports & Exercise: July 2017 - Volume 49 - Issue 7 - p 1331–1339
• Munukka, Matti. "Physical Activity Is Related with Cartilage Quality in Women with Knee Osteoarthritis." Medicine & Science in Sports & Exercise: July 2017 - Volume 49 - Issue 7 - p 1323–1330
• Ogawa, Elisa F., et al. "Physical Activity Domains/Recommendations and Leukocyte Telomere Length in U.S. Adults." Medicine & Science in Sports & Exercise: July 2017 - Volume 49 - Issue 7 - p 1375–1382.
• Dasarathy, Srinivasan. "Are Exercise Benefits in Nonalcoholic Fatty Liver Disease Due to Increased Autophagy?" Exercise & Sport Sciences Reviews: July 2017 - Volume 45 - Issue 3 - p 125