The purpose of this study was to examine the validity of the SC-StepMX pedometer for measuring step counts. A convenience sample of 40 participants wore 4 SC-StepMX pedometers, 2 Yamax DigiWalker pedometers, and 2 Actical accelerometers around their waist on a treadmill at 4 speeds based on each participant's self-paced walking speed (50%, 100%, 180%, and 250%; range: 1.4-14.1 km·h(-1)). The SC-StepMX demonstrated lower mean absolute percent error (-0.2%) compared with the Yamax DigiWalker (-20.5%) and the Actical (-26.1%). Mean measurement bias was lower for the SC-StepMX (0.1 ± 9.1; 95% confidence interval = -17.8 to 18.0 steps·min(-1)) when compared with both the Yamax DigiWalker (-15.9 ± 23.3; 95% confidence interval = -61.6 to 29.7 steps·min(-1)) and the Actical (-22.0 ± 36.3; 95% CI = -93.1 to 49.1 steps·min(-1)). This study demonstrates that the SC-StepMX pedometer is a valid tool for the measurement of step counts. The SC-StepMX accurately measures step counts at slower walking speeds when compared with 2 other commercially available activity monitors. This makes the SC-StepMX useful in measuring step counts in populations that are active at lower intensities (e.g., sedentary individuals, the elderly).

Prolonged overeating and the resultant weight gain are clearly linked with the development of insulin resistance and other cardiometabolic abnormalities, but adaptations that occur after relatively short periods of overeating are not completely understood. The purpose of this study was to characterize metabolic adaptations that may accompany the development of insulin resistance after 2 weeks of overeating. Healthy, nonobese subjects (n = 9) were admitted to the hospital for 2 weeks, during which time they ate ∼4000 kcals·day(-1) (70 kcal·kg(-1) fat free mass·day(-1)). Insulin sensitivity was estimated during a meal tolerance test, and a muscle biopsy was obtained to assess muscle lipid accumulation and protein markers associated with insulin resistance, inflammation, and the regulation of lipid metabolism. Whole-body insulin sensitivity declined markedly after 2 weeks of overeating (Matsuda composite index: 8.3 ± 1.3 vs. 4.6 ± 0.7, p < 0.05). However, muscle markers of insulin resistance and inflammation (i.e., phosphorylation of IRS-1-Ser(312), Akt-Ser(473), and c-Jun N-terminal kinase) were not altered by overeating. Intramyocellular lipids tended to increase after 2 weeks of overeating (triacylglyceride: 7.6 ± 1.6 vs. 10.0 ± 1.8 nmol·mg(-1) wet weight; diacylglyceride: 104 ± 10 vs. 142 ± 23 pmol·mg(-1) wet weight) but these changes did not reach statistical significance. Overeating induced a 2-fold increase in 24-h insulin response (area under the curve (AUC); p < 0.05), with a resultant ∼35% reduction in 24-h plasma fatty acid AUC (p < 0.05). This chronic reduction in circulating fatty acids may help explain the lack of a robust increase in muscle lipid accumulation. In summary, our findings suggest alterations in skeletal muscle metabolism may not contribute meaningfully to the marked whole-body insulin resistance observed after 2 weeks of overeating.

Both acute exercise and excessive training can cause oxidative stress. The resulting increase in free radicals and the inadequate response from antioxidant systems can lead to a framework of cellular damage. An association between affected tissue and the biomarkers of oxidative stress that appear in plasma has not been clearly established. The aim of this study was to evaluate the source of oxidative stress biomarkers found in the plasma of untrained rats after a single bout of swimming exercise at 2 different intensities: low intensity (SBLIE) or high intensity (SBHIE). Immediately after the exercise, aspartate transaminase (AST), alanine transaminase (ALT), γ-glutamyltransferase (GGT), and lactate dehydrogenase (LDH) were measured in plasma to characterize cell damage. Oxidative stress was assessed using protein carbonylation (PC), total antioxidant capacity (TAC), and thiobarbituric acid reactive substances (TBARS) quantified by malondialdehyde concentration. SBHIE raised levels of plasma AST (93%) and ALT (17%), and both exercise regimens produced an increase in GGT (7%) and LDH (∼55%). Plasma levels of PC and TBARS were greater in the SBHIE group; there were no changes in TAC. SBLIE caused only a modest increase in TBARS. In muscle, there were no changes in TAC, PC, or TBARS, regardless of exercise intensity, In the liver, TAC and TBARS increased significantly in both the SBLIE and SBHIE groups. This indicates that the oxidative stress biomarkers measured in the plasma immediately after a single bout of swimming exercise were generated primarily in the liver, not in muscle.

Acute mental stress can impair brachial artery (BA) flow-mediated dilation (FMD) in response to reactive hyperemia (RH) induced increases in shear stress. Handgrip exercise (HGEX) is emerging as a useful tool to increase shear stress for FMD assessment; however, the impact of acute mental stress on HGEX-FMD is unknown. The purpose of this study was to determine whether acute mental stress attenuates RH- and HGEX-induced BA-FMD to a similar extent. In 2 counterbalanced visits, 16 healthy males (19-27 years of age) performed RH-FMD or HGEX-FMD tests after a counting control task (prestress FMD) and a speech and arithmetic stress task (poststress FMD). BA diameter and mean blood velocity were assessed with echo and Doppler ultrasound, respectively. Shear stress was estimated using shear rate (SR = BA blood velocity/BA diameter). Mean arterial pressure (MAP), heart rate (HR), and salivary cortisol were used to assess stress reactivity. Results are expressed as mean ± SE. The stress task elevated MAP (Δ24.0 ± 2.6 mm Hg) and HR (Δ15.5 ± 1.9 beats·min(-1)), but not cortisol (prestress vs. poststress: 4.4 ± 0.7 nmol·L(-1) vs. 4.7 ± 0.7 nmol·L(-1); p = 0.625). There was no difference between the pre- and poststress SR stimulus for RH (p = 0.115) or HGEX (p = 0.664). RH-FMD decreased from 5.2% ± 0.6% prestress to 4.1% ± 0.5% poststress (p = 0.071); however, stress did not attenuate HGEX-FMD (prestress vs. poststress: 4.1% ± 0.6% vs. 5.3% ± 0.6%; p = 0.154). The pre- to poststress change in FMD was significantly different in the RH-FMD vs. the HGEX-FMD test (-1.1% ± 0.6% vs. +1.1% ± 0.8%; p = 0.015). In conclusion, acute mental stress appears to have a disparate impact on FMD stimulated by RH vs. HGEX induced increases in shear stress.

Reductions in active joint range of motion (ROM) are responsible for decreased work-generating capacity during fatiguing repetitive isotonic shortening contractions. Factors responsible for impairing the joint-angle-specific net torque developed during muscle shortening could include fatigue-induced torque loss, shortening-induced torque depression in the agonist muscle, and opposing passive tension of the antagonists, but these have not been systematically explored. Nine men (aged 25.8 ± 2.0 years) performed a maximal-effort fatiguing task that consisted of repetitive loaded shortening dorsiflexions through a 40° ankle joint ROM until active ROM decreased by 50%. Torque developed during contractile shortening, as well as passive opposing tension, was quantified before and after the reduction in active ROM. Before fatigue, and compared with maximum voluntary isometric contraction torque at the terminal ROM, shortening-induced torque depression in the agonist muscle and passive tension from the antagonists reduced net torque developed at the end of contractile shortening by ∼42% and ∼19%, respectively. After fatigue, a steepened ascending joint torque-angle relationship remained during contractile shortening, but neither muscle coactivation nor contractile slowing contributed to the fatigue-induced torque loss. Fatigue-induced torque loss, shortening-induced torque depression in the agonist, and passive tension in the antagonist greatly depressed net torque developed at the end of contractile shortening. These contributed to the fatigue-induced reduction in active ROM by impairing the ability of the dorsiflexors to generate sufficient torque to overcome the imposed load at the end of contractile shortening.

Candy bar-like protein supplements are sometimes consumed for their sugar alcohol content, which lowers the glycemic response. The purpose of this study was to determine the acute glycemic and blood lipid response to the ingestion of a candy bar-like protein supplement compared with its candy bar counterpart. In a crossover design, 5 males and 5 females (N = 10; age, 24 ± 5.5 years; height, 174 ± 8.3 cm; weight, 80 ± 21.9 kg) consumed a candy bar (CBR) or a similar protein bar (PBR) after a 10-h fast. Blood draws occurred at baseline and at 15, 30, 45, and 60 min after consumption and were analyzed for blood glucose, insulin, and lipid profiles. A 2×5 ANOVA was used, with Student's t tests for significant interactions. A significant (p < 0.05) blood glucose time effect occurred in both groups, with a more profound glucose response from the CBR at 15 min (CBR: 6.2 ± 0.8 mmol·L(-1); PBR: 4.9 ± 0.5 mmol·L(-1)). Triglycerides increased significantly (p < 0.05), independent of group, peaking at 60 min (Δ CBR: 0.8 ± 0.3 mmol·L(-1); Δ PBR: 1.3 ± 0.3 mmol·L(-1)). Insulin increased significantly (p < 0.05), independent of group, peaking at 15 min (Δ CBR: 42 ± 27 μIU·mL(-1); Δ PBR: 25 ± 11 μIU·mL(-1)). No significant change (p > 0.05) was observed in total cholesterol. Blood glucose, triglycerides, and insulin all increased significantly in response to both CBR and PBR consumption. The CBR elicited a greater effect on blood glucose; however, the PBR had a strong impact on serum triglycerides and insulin.

The objective of this study was to examine the combined associations between time spent in moderate- to vigorous-intensity physical activity (MVPA) and time spent sedentary in relation to cardiometabolic risk factors in a cohort of Canadian children. A cross-sectional study was conducted on 536 white children aged 8-10 years with at least 1 obese biological parent. Time spent in MVPA and sedentary behaviour over 7 days was measured using accelerometry and participants were stratified by tertiles. Daily screen time over 7 days was also self-reported by the child. Outcomes included waist circumference, systolic and diastolic blood pressure, fasting triglycerides, high-density lipoprotein cholesterol, and glucose concentrations. Analyses of covariance comparing tertiles of sedentary time/MVPA showed that higher levels of MVPA were associated with lower waist circumference, fasting triglycerides and diastolic blood pressure, and higher high-density lipoprotein (HDL) cholesterol, irrespective of sedentary time. In linear regression, MVPA was inversely associated with waist circumference and diastolic blood pressure and positively associated with HDL cholesterol, independent of covariates including sedentary time. In contrast, sedentary time was positively associated with diastolic blood pressure but after adjustment for MVPA the association was no longer statistically significant. Self-reported screen time was positively associated with waist circumference and negatively associated with HDL cholesterol independent of covariates including MVPA. Overall, a high level of MVPA was associated with reduced cardiometabolic risk in this sample of children, regardless of their amount of sedentary behaviour. The type of sedentary behaviour (i.e., screen time) might be more important than overall sedentary time in relation to cardiometabolic risk.