A single high-fat, high-carbohydrate meal (HFHC) results in elevated postprandial glucose (GLU), triglycerides (TRG) and metabolic load index (MLI; TRG (mg/dL) + GLU (mg/dL)) that contributes to chronic disease risk. While disease risk is higher in older adults (OA) compared to younger adults (YA), the acute effects of exercise on these outcomes in OA is understudied. Twelve YA (age 23.3 ± 3.9 yrs, n = 5 M/7 F) and 12 OA (age 67.7 ± 6.0 yrs, n = 8 M/4 F) visited the laboratory in random order to complete a HFHC with no exercise (NE) or acute exercise (EX) condition. EX was performed 12 hours prior to HFHC at an intensity of 65% of maximal heart rate to expend 75% of the kcals consumed in HFHC (Marie Callender’s Chocolate Satin Pie; 12 kcal/kgbw; 57% fat, 37% CHO). Blood samples were taken at 0, 30, 60, 90 minutes, and then every hour until 6 hours post-meal. TRG levels increased to a larger magnitude in OA (Δ˜61 ± 31%) compared to YA (Δ˜37 ± 34%, p < 0.001), which were attenuated in EX compared to NE (p < 0.05) independent of age. There was no difference in GLU between OA and YA after the HFM, however EX had attenuated GLU independent of age (NE: Δ˜21 ± 26%; EX: Δ˜12 ± 18%, p = 0.027). MLI was significantly lower after EX compared to NE in OA and YA (p < 0.001). Pre-prandial EX reduced TRG, GLU and MLI post-HFHC independent of age.

The purpose of the present study was to determine fasting and high-fat meal (HFM)-induced post-prandial systemic inflammation and airway inflammation (exhaled nitric oxide (eNO)) in older adults (OAs) compared to younger adults (YAs) before and after acute exercise. Twelve YAs (23.3 ± 3.9 y n = 5 M/7 F) and 12 OAs (67.7 ± 6 y, n = 8 M/4 F) completed two HFM challenges. After an overnight fast, participants underwent an HFM session or pre-prandial exercise (EX, 65% VO2Peak to expend 75% of the caloric content of the HFM) plus HFM (EX + HFM) in a randomized order. Systemic inflammatory cytokines were collected at 0, 3, and 6 h, while eNO was determined at 0, 2, and 4 h after the HFM (12 kcal/kg body weight: 61% fat, 35% CHO, 4% PRO). TNF-α was higher in OAs compared to YAs (p = 0.005) and decreased across time from baseline to 6 h post-HFM (p = 0.007). In response to the HFM, IL-6 decreased from 0 to 3 h but increased at 6 h regardless of age or exercise (p = 0.018). IL-8 or IL-1β did not change over the HFM by age or exercise (p > 0.05). eNO was also elevated in OAs compared to YAs (p = 0.003) but was not altered by exercise (p = 0.108). There was a trend, however, towards significance post-prandially in OAs and YAs from 0 to 2 h (p = 0.072). TNF-α and eNO are higher in OAs compared to YAs but are not elevated more in OAs post-prandially compared to YAs. Primary systemic inflammatory cytokines and eNO were not modified by acute exercise prior to an HFM.

The acute effect of exercise on β-cell function during a high fat meal (HFM) in young (YA) vs. old (OA) adults is unclear. In this randomized cross-over trial, YA (n=5M/7F, 23.3±3.9y) and OA (n=8M/4F, 67.7±6.0y) underwent a 180 min HFM (12 kcal/kgbw; 57% fat, 37% CHO) after a rest or exercise (~65% HRpeak) condition ~12hr prior. After an overnight fast, plasma lipids, glucose, insulin, as well as FFA were determined for peripheral, or skeletal muscle, insulin sensitivity (Matsuda Index) as well as hepatic (HOMA-IR) and adipose (Adipose-IR) insulin resistance calculations. β-cell function was derived from C-peptide and defined as early (0-30min) and total phase (0-180min) disposition index (DI, glucose-stimulated insulin secretion (GSIS) adjusted for insulin sensitivity/resistance). Hepatic insulin extraction (HIE) body composition (DXA) and VO2peak were also assessed. OA had higher TC, LDL, HIE and DI across organs as well as lower adipose-IR (all, P<0.05) and VO2peak ( P=0.056) despite similar body composition and glucose tolerance. Exercise lowered early phase TC and LDL in OA vs. YA ( P<0.05). However, C-peptide AUC, total phase GSIS, and adipose-IR were reduced post-exercise in YA vs. OA ( P<0.05). Skeletal muscle DI increased in YA and OA after exercise ( P<0.05), while adipose DI tended to decline in OA ( P=0.06 and P=0.08). Exercise-induced skeletal muscle insulin sensitivity (r=-0.44, P=0.02) and total phase DI (r=-0.65, P=0.005) correlated with reduced glucose AUC180min. Together, exercise improved skeletal muscle insulin sensitivity/DI in relation to glucose tolerance in YA and OA, but only raised adipose-IR and reduced adipose DI in OA.

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