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| I have to admit, I cannot answer the question about the effects of muscle damage on glycemia once and for all, but for the average workout, it's probably irrelevant and the overall effect beneficial. |
The reason that I write "probably", is that we do now have one study that suggests beneficial (Ho 2016) and one that found detrimental effects (Asp 1995) - and a couple of reasons why neither of the studies is fully convincing.
One important determinant of your 24h insulin levels is your meal frequency:
Grazin' Bad For the Obese!
Largest Meal For Lunch = Winner!?
Regularity is Key to Leanness
Optimal Meal Freq. 4 Kids?
8 Meals = Stable, But High Insulin
Are 6 Meals Better Than 2?
- 5 sets of barbell front squat for 20 repetitions at 30 pounds a day and
- 100-meter downhill sprinting consisted of 5 repetitions...
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| Figure 1: Plasma levels of muscle creatine kinase (Ho 2016); as a SuppVersity reader you shouldn't be surprised to see "high-" and "low-responders" as discussed in a 2014 article on CK elevations w/ exercise. |
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| Figure 2: Oral glucose tolerance test (OGTT), blood glucose levels and area under the curve - Pre: before exercise challenge; Post: ca. 24h after exercise challenge. *Significantly different against Pre, P < 0.05 (Ho 2016). |
So, it's 'hit it hard and don't care about muscle damage'? Not so fast... as previously pointed out, the study at hand shows that muscle damage has a less sign. effect on your muscles' ability to suck up glucose than the earlier studies by Asp et al. suggested. The reason(s), it does not fully refute the notion that muscle damage may promote temporary insulin resistance are...
(A) the, in my humble opinion, questionable time-frame within which the glucose tolerance test was conducted (24h post) - while it is true that it takes time for the CK levels to rise and testing them 48h after the last workout may be sensible, there's no logical reason not to test the effect on glucose uptake immediately after the workout;
(B) the nonreflective use of CK-MB as a marker of muscle damage that becomes obvious when the scientists divide their subjects into two groups - what the authors believe to be a division in subjects with high and low muscle damage is (as discussed previously) rather a division in genetic high- and low-responders (an analysis of the correlation between CK and glycemia, as you would expect it in view of the research question, is missing);
(C) the probably relatively low(er) degree of muscle damage which is, as one can speculate, significantly less pronounced than in the Asp study, in which the subjects did one-legged eccentric exercise on a motor-driven device and saw ~2-times greater mean elevations in CK
The good news, however, is that the effect on the GLUT4 expression and glycogen flux in the Asp study (Figure 3) looks more relevant than it actually is - the sign. difference between the pre- and the late muscle glycogen measurements also raise the question how accurate the latter was actually measured; after all, the fractional velocity of the glycolytic flux (not shown in Figure 3) changed only non-significantly from 34.1 ± 3.6% to a short-lived minimum of 29.8 ± 2.8% on day 1 after the muscle damaging leg workout in the Asp study. Eventually, it's thus unlikely that hard workouts will turn you into a type II diabetic (i.e. have health relevant effects on your glucose levels) - that harder is not necessarily better (for glucose management), however, is also something worth remembering, I guess | Comment on Facebook!
References: |
| Figure 3: While there was a sign. reduction in GLUT4 (top) and a correspondingly reduced glycogen resynthesis (bottom) in exercised (full circles) vs. control leg (open circles) in the Asp study, it's not likely that the subjects' suffered from physiologically relevant insulin resistance. |
(B) the nonreflective use of CK-MB as a marker of muscle damage that becomes obvious when the scientists divide their subjects into two groups - what the authors believe to be a division in subjects with high and low muscle damage is (as discussed previously) rather a division in genetic high- and low-responders (an analysis of the correlation between CK and glycemia, as you would expect it in view of the research question, is missing);
(C) the probably relatively low(er) degree of muscle damage which is, as one can speculate, significantly less pronounced than in the Asp study, in which the subjects did one-legged eccentric exercise on a motor-driven device and saw ~2-times greater mean elevations in CK
The good news, however, is that the effect on the GLUT4 expression and glycogen flux in the Asp study (Figure 3) looks more relevant than it actually is - the sign. difference between the pre- and the late muscle glycogen measurements also raise the question how accurate the latter was actually measured; after all, the fractional velocity of the glycolytic flux (not shown in Figure 3) changed only non-significantly from 34.1 ± 3.6% to a short-lived minimum of 29.8 ± 2.8% on day 1 after the muscle damaging leg workout in the Asp study. Eventually, it's thus unlikely that hard workouts will turn you into a type II diabetic (i.e. have health relevant effects on your glucose levels) - that harder is not necessarily better (for glucose management), however, is also something worth remembering, I guess | Comment on Facebook!
- Asp, Sven, Jens R. Daugaard, and Erik A. Richter. "Eccentric exercise decreases glucose transporter GLUT4 protein in human skeletal muscle." The Journal of physiology 482.3 (1995): 705-712.
- Ho, Chien-Te, Machiko Otaka, and Chia-Hua Kuo. "Improving glucose tolerance by muscle-damaging exercise." Journal of Traditional and Complementary Medicine (2016).