The aim of this study was to investigate whether 6 weeks' high intensity interval training (HIIT; 6 × 30 s sprints at 40% peak power, once every five days) following 6 weeks' of aerobic preconditioning could favourably affect fasting insulin, glucose, and the homeostatic model assessment of insulin resistance (HOMA1-IR) in sedentary older men compared with masters athletes. A secondary aim was to establish whether lifelong exercisers (LEX) exhibited improved fasting insulin, glucose, and HOMA1-IR, compared to sedentary older males (SED). Twenty-two males (62 ± 2 years) comprised the SED group and 17 males (60 ± 5 years) were enrolled as LEX. Participants were tested at phase A (baseline), B (after preconditioning), and C (post-HIIT). There was no effect of time (P = 0.116) or interaction (P = 0.727) on insulin. However, there was an effect of group (P < 0.001). In terms of magnitude, HIIT induced a small decrease in SED insulin compared to baseline (15.8 ± 8.1 uIU·ml⁻¹ at baseline and 14.0 ± 7.8 uIU·ml⁻¹ post-HIIT; Cohen's d = 0.23) and compared to post-preconditioning (17.5 ± 9.7 uIU·ml⁻¹; Cohen's d = 0.40). LEX insulin was unchanged throughout (all differences were trivial). Insulin was lower in LEX than SED at phase A (P < 0.001, Cohen's d = 1.31), B (P = 0.023, Cohen's d = 0.78), and C (P = 0.004, Cohen's d = 1.01). There was no effect of time (P = 0.290), group (P = 0.166), or interaction (P = 0.153) for glucose. In terms of magnitude, HIIT produced a small reduction in SED glucose compared to baseline (5.7 ± 1.3 mmol·l⁻¹ at baseline and 5.3 ± 0.9 mmol·l⁻¹ post-HIIT; Cohen's d = 0.36), and compared to phase B (5.6 ± 0.8 mmol·l⁻¹, Cohen's d = 0.35). LEX glucose was unchanged throughout (all changes were trivial). SED had moderately higher blood glucose than LEX at phase A (Cohen's d = 0.49), and B (Cohen's d = 0.63), but only a trivial difference existed at phase C (Cohen's d = 0.15). There was no effect of time (P = 0.110), or interaction (P = 0.569) on HOMA1-IR. However, there was an effect of group (P = 0.002). In terms of magnitude, SED HOMA1-IR was unchanged from phase A to B (4.2 ± 3.0 and 4.5 ± 2.9 arbitrary units respectively [Cohen's d = 0.10]). However, at C (3.5 ± 2.6) there was a small decrease compared to B (Cohen's d = 0.36), and A (Cohen's d = 0.25). LEX experienced a small increase in HOMA1-IR from phase A to B (1.6 ± 1.3 and 2.3 ± 2.8 respectively [Cohen's d = 0.32]), followed by a small decrease from B to C (1.7 ± 1.1 at phase C [Cohen's d = 0.28]), and a trivial change from A to C (Cohen's d = 0.08). HOMA1-IR was lower in LEX than SED at baseline (P = 0.002, Cohen's d = 1.12), after preconditioning (P = 0.024, Cohen's d = 0.77), and post-HIIT (P = 0.014, Cohen's d = 0.90). Results of this study provide preliminary evidence that HIIT preceded by preconditioning can induce small improvements in fasting insulin, glucose, and HOMA1-IR in sedentary older men compared with masters athletes.

这项研究的目的是研究在进行6周的有氧预处理后，进行6周的高强度间歇训练（HIIT；在40％峰值功率下进行6×30 s冲刺，每五天一次）是否可以对空腹胰岛素，葡萄糖，和久坐的老年男子与熟练运动员的胰岛素抵抗（HOMA1-IR）稳态模型评估。第二个目的是确定与久坐的老年男性（SED）相比，终身运动者（LEX）是否表现出改善的空腹胰岛素，葡萄糖和HOMA1-IR。SED组为22位男性（62±2岁），其中LEX为17位男性（60±5岁）。在阶段A（基线），阶段B（预处理后）和阶段C（HIIT之后）测试参与者。时间（P = 0.116）或相互作用（P = 0.727）对胰岛素没有影响。然而，有一个组的影响（P <0.001）。就数量级而言，HIIT诱导的SED胰岛素与基线水平相比有小幅下降（15.8±8.1 uIU·ml^-1在基线和14.0±7.8 UIU·毫升^-1后HIIT; Cohen的d  = 0.23），并与后置预处理（17.5±9.7 uIU·ml ^-1； Cohen的d  = 0.40）进行比较。LEX胰岛素始终保持不变（所有差异均很小）。在阶段A（P <0.001，Cohen's d  = 1.31），阶段B（P = 0.023，Cohen's d  = 0.78）和阶段C（P = 0.004，Cohen's d  = 1.01），胰岛素的LEX浓度低于SED 。对于葡萄糖，时间（P = 0.290），组（P = 0.166）或相互作用（P = 0.153）没有影响。就数量级而言，HIIT与基线相比，SED葡萄糖有少量降低（基线为5.7±1.3mmol·l ^-1，基线为5.3±0.9mmol·l ^-1HIIT后；Cohen d  = 0.36），并与B相（5.6±0.8mmol·l ^-1，Cohen d = 0.35）。LEX葡萄糖始终保持不变（所有变化都是微不足道的）。SED在A期（Cohen d = 0.49）和B期（Cohen d = 0.63）比LEX中度有较高的血糖，但在C期（Cohen d = 0.15）只有微不足道的差异。时间（P = 0.110）或交互作用（P = 0.569）对HOMA1-IR没有影响。但是，有一个小组的影响（P = 0.002）。就幅度而言，SED HOMA1-IR从A阶段到B阶段没有变化（分别为4.2±3.0和4.5±2.9个任意单位[Cohen d = 0.10]）。但是，在C（3.5±2.6）下，与B（Cohen's d = 0.36）和A（Cohen's d = 0.25）相比，下降很小。LEX的HOMA1-IR从A阶段到B阶段有小幅增加（分别为1.6±1.3和2.3±2.8 [Cohen d = 0.32]），然后从B阶段变为C的小幅下降（1.7±1）。在阶段C [科恩d = 0.28]时为1，从A到C的微小变化（科恩d = 0.08）。基线时，HOMA1-IR在LEX时低于SED（P = 0.002，Cohen's 预处理（P = 0.024，Cohen d  = 0.77）和HIIT后（p = 0.014，Cohen d  = 0.90），d = 1.12 ）。这项研究的结果提供了初步的证据，表明与先驱者相比，久坐的HIIT可以使久坐的老年男性的空腹胰岛素，葡萄糖和HOMA1-IR有所改善。