Real-time assessment of postprandial fat storage in liver and skeletal muscle in health and type 2 diabetes.

Liver and skeletal muscle triglyceride stores are elevated in type 2 diabetes and correlate with insulin resistance. As postprandial handling of dietary fat may be a critical determinant of tissue triglyceride levels, we quantified postprandial fat storage in normal and type 2 diabetes subjects. Healthy volunteers (n = 8) and diet-controlled type 2 diabetes subjects (n = 12) were studied using a novel 13C magnetic resonance spectroscopy protocol to measure the postprandial increment in liver and skeletal muscle triglyceride following ingestion of 13C-labeled fatty acids given with a standard mixed meal. The postprandial increment in hepatic triglyceride was rapid in both groups (peak increment controls: +7.3 +/- 1.5 mmol/l at 6 h, P = 0.002; peak increment diabetics: +10.8 +/- 3.4 mmol/l at 4 h, P = 0.009). The mean postprandial incremental AUC of hepatic 13C enrichment between the first and second meals (0 and 4 h) was significantly higher in the diabetes group (6.1 +/- 1.4 vs. 1.7 +/- 0.6 mmol x l(-1) x h(-1), P = 0.019). Postprandial increment in skeletal muscle triglyceride in the control group was small compared with the diabetic group, the mean 24-h postprandial incremental AUC being 0.2 +/- 0.3 vs. 1.7 +/- 0.4 mmol x l(-1) x h(-1) (P = 0.009). We conclude that the postprandial uptake of fatty acids by liver and skeletal muscle is increased in type 2 diabetes and may underlie the elevated tissue triglyceride stores and consequent insulin resistance.

Naturally occurring muscle pain during exercise: assessment and experimental evidence.

The objectives were: (i) to present a method for assessing muscle pain during exercise, (ii) to provide reliability and validity data in support of the measurement tool, (iii) to test whether leg muscle pain threshold during exercise was related to a commonly used measure of pain threshold pain during test, (iv) to examine the relationship between pain and exertion ratings, (v) to test whether leg muscle pain is related to performance, and (vi) to test whether a large dose of aspirin would delay leg muscle pain threshold and/or reduce pain ratings during exercise. In study 1, seven females and seven males completed three 1-min cycling bouts at three different randomly ordered power outputs. Pain was assessed using a 10-point pain scale. High intraclass correlations (R from 0.88 to 0.98) indicated that pain intensity could be rated reliably using the scale. In study 2, 11 college-aged males (age 21.3 +/- 1.3 yr) performed a ramped (24 W.min-1) maximal cycle ergometry test. A button was depressed when leg muscle pain threshold was reached. Pain threshold occurred near 50% of maximal capacity: 50.3 (+/- 12.9% Wmax), 48.6 (+/- 14.8% VO2max), and 55.8 (+/- 12.9% RPEmax). Pain intensity ratings obtained following pain threshold were positively accelerating function of the relative exercise intensity. Volitional exhaustion was associated with pain ratings of 8.2 (+/- 2.5), a value most closely associated with the verbal anchor "very strong pain." In study 3, participants completed the same maximal exercise test as in study 2 as well as leg cycling at 60 rpm for 8 s at four randomly ordered power outputs (100, 150, 200, and 250 W) on a separate day. Pain and RPE ratings were significantly lower during the 8-s bouts compared to those obtained at the same power outputs during the maximal cycle test. The results suggest that noxious metabolites of muscle contraction play a role in leg muscle pain during exercise. In study 4, moderately active male subjects (N = 19) completed two ramped maximal cycle ergometry tests. Subjects drank a water and Kool-Aid mixture, that either was or was not (placebo) combined with a 20 mg.kg-1 dose of powdered aspirin 60 min before exercise. Paired t-tests revealed no differences between conditions for the measures of exercise intensity at pain threshold [aspirin vs placebo mean (+/- SD)]: power output: 150 (+/- 60.3 W) versus 153.5 (+/- 64.8 W); VO2: 21.3 (+/- 8.6 mL.kg-1.min-1) versus 22.1 (+/- 10.0 mL.kg-1.min-1); and RPE: 10.9 (+/- 3.1) versus 11.4 (+/- 2.9). Repeated measures ANOVA revealed no significant condition main effect or condition by trial interaction for pain responses during recovery or during exercise at 60, 70, 80, 90, and 100% of each condition's peak power output. It is concluded that the perception of leg muscle pain intensity during cycle ergometry: (i) is reliably and validly measured using the developed 10-point pain scale, (ii) covaries as a function of objective exercise stimuli such as power output, (iii) is distinct from RPE, (iv) is unrelated to performance of the type employed here, and (v) is not altered by the ingestion of 20 mg.kg-1 acetylsalicylic acid 1 h prior to the exercise bout.