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N Leenders

Publications and source records attributed to N Leenders.

5 recordsLinked to original sources
PubMed1998

Evaluation of a commercial accelerometer (Tritrac-R3 D) to measure energy expenditure during ambulation.

This study evaluated the ability of a commercially available accelerometer (Tritrac-R3 D) to measure energy expenditure in 16 subjects at rest (pre- and post-exercise) and during three different intensities of steady-state exercise (40-70% of peak oxygen consumption [VO2peak]) while ambulating on a treadmill (no grade). Oxygen consumption and the respiratory exchange ratio from indirect calorimetry and the vector magnitude of triaxial accelerations were used to estimate energy expenditure using the manufacturers' equations. There was a significant relationship between indirect calorimetry-derived energy expenditure and the energy expenditure derived from the accelerometer (r=0.96). Using analysis of variance, there was no difference in the energy expenditure derived by the two methods at rest before exercise and during the three different intensities of ambulatory exercise. There was a significant difference between energy expenditure derived via indirect calorimetry and with the accelerometer during rest after exercise, probably due to the failure of the accelerometer to accurately estimate the energy expenditure associated with the progressive decline in post-exercise oxygen consumption. Thus, this commercially available accelerometer appears to provide statistically acceptable estimates of energy expenditure at rest and during zero-grade treadmill ambulation up to about 70% VO2peak. This may indicate its acceptable utility for large-scale population studies of physical activity involving this mode of movement. The failure of the accelerometer to accurately estimate energy expenditure during recovery from exercise may contribute to an underestimation of energy expenditure in some physically active individuals.

Adult↗
PubMed1996

Exercise training and the glucose transport system in obese SHHF/Mcc-fa(cp) rats.

The effects of a similar exercise training stimulus on maximal insulin-stimulated (MIS) plasma membrane glucose transporter number and glucose transport were determined in lean and obese SHHF/Mcc-facp rats. Six-week-old lean and obese male rats were randomly divided into four groups: lean sedentary (LSed), obese sedentary (OSed), lean exercise (LEx), and obese exercise (OEx). An 8- to 12-wk treadmill running program equalized daily muscular work for LEx and OEx. Plasma membranes were isolated from control and MIS muscles of mixed fiber types. MIS significantly increased glucose transport (3.4- and 2.8-fold) in LSed and OSed, respectively. MIS significantly increased glucose transporter number (2.5-fold) in LSed, but there was no increase in glucose transporter number in OSed. Peak oxygen uptake and citrate synthase activity were increased a similar amount for LEx and OEx groups, demonstrating a similar training stimulus. MIS significantly and similarly increased glucose transport in LEx and OEx (4.4- and 5.1-fold, respectively). The effects of MIS on plasma membrane glucose transporter number in the exercise-trained rats were similar to the responses observed in the sedentary lean and obese groups. MIS significantly increased glucose transporter number (2.6-fold) in LEx, whereas there was no increase in glucose transporter number in OEx. The reduction in MIS glucose transport in OSed appears to be related to a defect in the processes associated with the translocation of glucose transporters to the plasma membrane. Exercise training of the obese rats apparently did not alter this defect. Similar increases in peak oxygen uptake, citrate synthase, and MIS glucose transport in LEx and OEx groups suggest that insulin resistance does not limit the ability of the glucose transport system to adapt to exercise training in the obese male SHHF/Mcc-facp rats.

4-Nitrophenylphosphatase↗
PubMed1995

Fat loading: the next magic bullet?

The depletion or reduction of bodily carbohydrate reserves is associated with fatigue during endurance exercise. Various carbohydrate supplementation and exercise regimens have been used experimentally to increase carbohydrate reserves before exercise or to maintain the availability of carbohydrate for oxidation during exercise. On the other hand, the improved endurance capability observed after aerobic training has been attributed to an increased oxidation of fat relative to carbohydrate; this carbohydrate sparing presumably delays the point at which reduced carbohydrate reserves cause fatigue. This effect has led to the suggestion that a greater availability of fat during exercise can improve performance via the carbohydrate-sparing effect of "fat loading." Although this is a plausible hypothesis, it is not supported by a sufficient number of valid, credible, and replicated studies. Thus, it appears prudent to advise endurance athletes to consume a diet that is largely carbohydrate to optimize training and competitive performance and, more importantly, to promote optimal health.

Carbohydrate Metabolism↗