Ilaria Croci

Fat oxidation over a range of exercise intensities: fitness versus fatness

Maximal fat oxidation (MFO), as well as the exercise intensity at which it occurs (Fatmax), have been reported as lower in sedentary overweight individuals but have not been studied in trained overweight individuals. The aim of this study was to compare Fatmax and MFO in lean and overweight recreationally trained males matched for cardiorespiratory fitness (CRF) and to study the relationships between these variables, anthropometric characteristics, and CRF. Twelve recreationally trained overweight (high fatness (HiFat) group, 30.0% ± 5.3% body fat) and 12 lean males (low fatness (LoFat), 17.2% ± 5.7% body fat) matched for CRF (maximal oxygen consumption (V̇O2max) 39.0 ± 5.5 vs. 41.4 ± 7.6 mL·kg(-1)·min(-1), p = 0.31) and age (p = 0.93) performed a graded exercise test on a cycle ergometer. V̇O2max and fat and carbohydrate oxidation rates were determined using indirect calorimetry; Fatmax and MFO were determined with a mathematical model (SIN); and % body fat was assessed by air displacement plethysmography. MFO (0.38 ± 0.19 vs. 0.42 ± 0.16 g·min(-1), p = 0.58), Fatmax (46.7% ± 8.6% vs. 45.4% ± 7.2% V̇O2max, p = 0.71), and fat oxidation rates over a wide range of exercise intensities were not significantly different (p > 0.05) between HiFat and LoFat groups. In the overall cohort (n = 24), MFO and Fatmax were correlated with V̇O2max (r = 0.46, p = 0.02; r = 0.61, p = 0.002) but not with % body fat or body mass index (p > 0.05). Fat oxidation during exercise was similar in recreationally trained overweight and lean males matched for CRF. Consistently, substrate oxidation rates during exercise were not related to adiposity (% body fat) but were related to CRF. The benefits of high CRF independent of body weight and % body fat should be further highlighted in the management of obesity.

A Pilot Randomised Study of the Metabolic and Histological Effects of Exercise in Non-alcoholic Steatohepatitis

Aims: Type 2 diabetes is a risk factor for the development and progression of non-alcoholic fatty liver disease (NAFLD). Lifestyle intervention is the principal treatment for NAFLD however the effects of exercise alone on the histological and metabolic severity of NAFLD are unclear. This study assessed the effects of 6 months exercise training and diet-induced weight loss on insulin resistance and liver histologyin overweight patients with NAFLD. Methods: 21 patients were randomised to circuit exercise (EX) training (60 min×3/week) or dietary induced weight loss (DIWL) (-500 kcal/d). Insulin sensitivity (euglycaemic-hyperinsulinemic clamp with tracer), adiposity (CT scan) and histology (liver biopsy) were assessed at 0 and 6 months. Results: Weight decreased by 9.7 ± 4.6% (-6.7 ± 6.3 kg p=0.02) with DIWL but was unchanged after EX. Both groups equivalently reduced visceral fat (DIWL -22 ± 24% p=0.06 and EX -18 ± 18% p<0.05) while only EX increased lean mass (+3% p<0.01). DIWL markedly reduced steatosis (73 ± 36% to 23 ± 32%, p<0.05) and NAFLD activity score NAS (median (range) 5 (1-7) to 1 (0-5), p<0.05). After EX, there was no change in steatosis or NAS. A decrease in steatosis was associated with weight loss (r s =0.82, p<0.0001). An improvement in fibrosis was associated with a decrease in steatosis (r s =0.64, p=0.02). Small improvements in fasting hepatic insulin resistance were similar in both groups while changes in muscle insulin resistance were not significant. Conclusions: Circuit exercise is safe and efficacious for improving cardiometabolic risk factors in patients with NAFLD, however this dose of circuit training, without concomitant weight loss, was insufficient for histological improvements in NAFLD. The pilot study outcomes should stimulate further development of different exercise protocols (type, frequency and intensity) to address disease-specific conditions in those with severe insulin resistance.

Effect of 1-h moderate-intensity aerobic exercise on intramyocellular lipids in obese men before and after a lifestyle intervention

Intramyocellular lipids (IMCL) are depleted in response to an acute bout of exercise in lean endurance-trained individuals; however, it is unclear whether changes in IMCL content are also seen in response to acute and chronic exercise in obese individuals. We used magnetic resonance spectroscopy in 18 obese men and 5 normal-weight controls to assess IMCL content before and after an hour of cycling at the intensity corresponding with each participants maximal whole-body rate of fat oxidation (Fatmax). Fatmax was determined via indirect calorimetry during a graded exercise test on a cycle ergometer. The same outcome measures were reassessed in the obese group after a 16-week lifestyle intervention comprising dietary calorie restriction and exercise training. At baseline, IMCL content decreased in response to 1 h of cycling at Fatmax in controls (2.8 ± 0.4 to 2.0 ± 0.3 A.U., -39%, p = 0.02), but not in obese (5.4 ± 2.1 vs. 5.2 ± 2.2 A.U., p = 0.42). The lifestyle intervention lead to weight loss (-10.0 ± 5.4 kg, p < 0.001), improvements in maximal aerobic power (+5.2 ± 3.4 mL/(kg·min)), maximal fat oxidation rate (+0.19 ± 0.22 g/min), and a 29% decrease in homeostasis model assessment score (all p < 0.05). However, when the 1 h of cycling at Fatmax was repeated after the lifestyle intervention, there remained no observable change in IMCL (4.6 ± 1.8 vs. 4.6 ± 1.9 A.U., p = 0.92). In summary, there was no IMCL depletion in response to 1 h of cycling at moderate intensity either before or after the lifestyle intervention in obese men. An effective lifestyle intervention including moderate-intensity exercise training did not impact rate of utilisation of IMCL during acute exercise in obese men.

Impact of a brief exercise program on the physical and psychosocial health of prostate cancer survivors: A pilot study

It is well established that exercise is beneficial for prostate cancer survivors. The challenge for health professionals is to create effective strategies to encourage survivors to exercise in the community. Many community exercise programs are brief in duration (e.g. <5 exercise sessions); whilst evidence for the efficacy of exercise within the literature are derived from exercise programs ≥8 weeks in duration, it is unknown if health benefits can be obtained from a shorter program. This study examined the effect of a four‐session individualized and supervised exercise program on the physical and psychosocial health of prostate cancer survivors.

Independent effects of diet and exercise training on fat oxidation in non-alcoholic fatty liver disease

AIM To investigate the independent effects of 6-mo of dietary energy restriction or exercise training on whole-body and hepatic fat oxidation of patients with non-alcoholic fatty liver disease (NAFLD). METHODS Participants were randomised into either circuit exercise training (EX; n = 13; 3 h/wk without changes in dietary habits), or dietary energy restriction (ER) without changes in structured physical activity (ER; n = 8). Respiratory quotient (RQ) and whole-body fat oxidation rates (Fatox) were determined by indirect calorimetry under basal, insulin-stimulated and exercise conditions. Severity of disease and steatosis was determined by liver histology; hepatic Fatox was estimated from plasma β-hydroxybutyrate concentrations; cardiorespiratory fitness was expressed as VO2peak. Complete-case analysis was performed (EX: n = 10; ER: n = 6). RESULTS Hepatic steatosis and NAFLD activity score decreased with ER but not with EX. β-hydroxybutyrate concentrations increased significantly in response to ER (0.08 ± 0.02 mmol/L vs 0.12 ± 0.04 mmol/L, P = 0.03) but remained unchanged in response to EX (0.10 ± 0.03 mmol/L vs 0.11 ± 0.07 mmol/L, P = 0.39). Basal RQ decreased (P = 0.05) in response to EX, while this change was not significant after ER (P = 0.38). VO2peak (P < 0.001) and maximal Fatox during aerobic exercise (P = 0.03) improved with EX but not with ER (P > 0.05). The increase in β-hydroxybutyrate concentrations was correlated with the reduction in hepatic steatosis (r = -0.56, P = 0.04). CONCLUSION ER and EX lead to specific benefits on fat metabolism of patients with NAFLD. Increased hepatic Fatox in response to ER could be one mechanism through which the ER group achieved reduction in steatosis.

Temporal Changes in a Novel Metric of Physical Activity Tracking (Personal Activity Intelligence) and Mortality: The HUNT Study, Norway

BACKGROUND Personal Activity Intelligence (PAI) is a novel activity metric that translates heart rate variations during exercise into a weekly score. Weekly PAI scores assessed at a single point in time were found to associate with lower risk of premature cardiovascular disease (CVD) mortality in the general healthy population. However, to date, the associations between long-term longitudinal changes in weekly PAI scores and mortality have not been explored. PURPOSE The aim of the present study was to prospectively examine the association between change in weekly PAI scores estimated 10 years apart, and risk of mortality from CVD and all-causes. METHODS We performed a prospective cohort study of 11,870 men and 13,010 women without known CVD in Norway. By using data from the Nord-Trøndelag Health Study (HUNT), PAI was estimated twice, ten years apart (HUNT1 1984-86 and HUNT2 1995-97). Mortality was followed-up until December 31, 2015. Adjusted hazard ratios (AHR) and 95% confidence intervals (CI) for death from CVD and all-causes related to temporal changes in PAI were estimated using Cox regression analyses. RESULTS During a mean (SD) of 18 (4) years of follow-up, there were 4782 deaths, including 1560 deaths caused by CVD. Multi-adjusted analyses demonstrated that participants achieving a score of ≥100 PAI at both time points had 32% lower risk of CVD mortality (AHR 0.68; CI: 0.54-0.86) for CVD mortality and 20% lower risk of all-cause mortality (AHR 0.80; CI: 71-0.91) compared with participants obtaining <100 weekly PAI at both measurements. For participants having <100 PAI in HUNT1 but ≥100 PAI in HUNT2, the AHRs were 0.87 (CI: 0.74-1.03) for CVD mortality, and 0.86 (CI: 0.79-0.95) for all-cause mortality. We also found an inverse linear relationship between change in PAI and risk of CVD mortality among participants with 0 PAI (P < 0.01), and ≤50 PAI (P = 0.04) in HUNT1, indicating that an increase in PAI over time is associated with lower risk of mortality. Excluding the first three years of follow-up did not substantially alter the findings. Increasing PAI score from <100 PAI in HUNT1 to ≥100 PAI in HUNT2 was associated with 6.6 years gained lifespan. CONCLUSION Among men and women without known CVD, an increase in PAI score and sustained high PAI score over a 10-year period was associated with lower risk of mortality.