MRC/ARUK Centre for Musculoskeletal Ageing Research, ARUK Centre for Sport, Exercise and Osteoarthritis, NIHR Nottingham BRC, School of Life Sciences, The Medical School, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK.
Clinical Chemistry, Karolinska University Hospital, S-141 86 Huddinge, Sweden.
Clin Nutr. 2019 Apr;38(2):948-953. doi: 10.1016/j.clnu.2018.02.001. Epub 2018 Feb 15.
BACKGROUND & AIMS: Exercise activates muscle pyruvate dehydrogenase complex (PDC), but moderate intensity exercise fails to fully activate muscle PDC after high-fat diet [1]. We investigated whether maximal intensity exercise overcomes this inhibition.
Quadriceps femoris muscle biopsy samples were obtained from healthy males at rest, and after 46 and 92 electrically-evoked maximal intermittent isometric contractions, which were preceded by 3 days of either low- (18%) or high- (69%) isocaloric dietary fat intake (LFD and HFD, respectively).
The ratio of PDCa (active form) to total PDCt (fully activated) at rest was 50% less after HFD (0.32 ± 0.01 vs 0.15 ± 0.01; P < 0.05). This ratio increased to 0.77 ± 0.06 after 46 contractions (P < 0.001) and to 0.98 ± 0.07 after 92 contractions (P < 0.001) in LFD. The corresponding values after HFD were less (0.54 ± 0.06; P < 0.01 and 0.70 ± 0.07; P < 0.01, respectively). Resting muscle acetyl-CoA and acetylcarnitine content was greater after HFD than LFD (both P < 0.05), but their rate of accumulation in the former was reduced during contraction. Muscle lactate content after 92 contractions was 30% greater after HFD (P < 0.05). Muscle force generation during contraction was no different between interventions, but HFD lengthened muscle relaxation time (P < 0.05). Daily urinary total carnitine excretion after HFD was 2.5-fold greater than after LFD (P < 0.01).
A bout of maximal intense exercise did not overcome dietary fat-mediated inhibition of muscle pyruvate dehydrogenase complex activation, and was associated with greater muscle lactate accumulation, as a result of lower PDC flux, and increased muscle relaxation time.
运动可激活肌肉丙酮酸脱氢酶复合物(PDC),但高脂饮食后,中等强度运动未能充分激活肌肉 PDC[1]。我们研究了最大强度运动是否可以克服这种抑制。
在休息时、经过 3 天低(18%)或高(69%)等热量脂肪饮食(LFD 和 HFD)摄入后,分别取健康男性股四头肌活检样本,进行 46 次和 92 次电诱发最大间歇性等长收缩。
HFD 后,休息时 PDCa(活性形式)与总 PDCt(完全激活)的比值降低 50%(0.32±0.01 比 0.15±0.01;P<0.05)。在 LFD 中,该比值在 46 次收缩后增加到 0.77±0.06(P<0.001),在 92 次收缩后增加到 0.98±0.07(P<0.001)。而 HFD 后的相应值较低(0.54±0.06;P<0.01 和 0.70±0.07;P<0.01)。与 LFD 相比,HFD 后肌肉乙酰辅酶 A 和乙酰肉碱含量增加(均 P<0.05),但前者在收缩过程中的积累速度降低。HFD 后 92 次收缩后的肌肉乳酸含量增加 30%(P<0.05)。收缩过程中肌肉产生的力无干预差异,但 HFD 延长了肌肉松弛时间(P<0.05)。HFD 后每日尿总肉碱排泄量是 LFD 的 2.5 倍(P<0.01)。
一次最大强度运动未能克服饮食脂肪介导的肌肉丙酮酸脱氢酶复合物激活抑制,与肌肉乳酸积累增加有关,原因是 PDC 通量较低,肌肉松弛时间增加。