Paul A. Molé

Evaluation of a new air displacement plethysmograph for measuring human body composition.

A new air displacement plethysmograph, the BOD POD (BP), was evaluated in comparison to hydrostatic weighing (HW). Sixty-eight adult subjects (26 F, 42 M) varying widely in age (range 20-56 yr), ethnicity, and fatness participated in this study. Same-day test-retest reliability was assessed in a subsample of 16 subjects (9 F, 7 M) and validity was assessed in all subjects (N = 68). The test-retest coefficients of variation (CV) for %FAT measured by BP (%FATBP) and HW (%FATHW) were not significantly different (1.7% +/- 1.1% and 2.3% +/- 1.9% for BP and HW, respectively (mean +/- SD)), indicating excellent reliability for both methods. Validity of percent fat measured by the BP (%FATBP) was also excellent. The mean difference in %FAT (BP - HW) was -0.3 +/- 0.2 (SEM), with a 95% confidence interval of -0.6 to 0 %FAT. The regression equation (%FATHW = 1.86 + 0.94 %FATBP; r2 = 0.93, SEE = 1.81) was not significantly different from the line of identity (%FATHW = %FATBP), and did not differ by gender. These findings indicate that the BOD POD is a highly reliable and valid method for determining %FAT in adult humans in comparison to HW. This new method has several advantages over HW in that it is quick, relatively simple to operate and may be able to accommodate special populations such as the obese, elderly, and disabled.

Comparative analysis of NMR and NIRS measurements of intracellular PO2 in human skeletal muscle.

1H NMR has detected both the deoxygenated proximal histidyl NδH signals of myoglobin (deoxyMb) and deoxygenated Hb (deoxyHb) from human gastrocnemius muscle. Exercising the muscle or pressure cuffing the leg to reduce blood flow elicits the appearance of the deoxyMb signal, which increases in intensity as cellular[Formula: see text] decreases. The deoxyMb signal is detected with a 45-s time resolution and reaches a steady-state level within 5 min of pressure cuffing. Its desaturation kinetics match those observed in the near-infrared spectroscopy (NIRS) experiments, implying that the NIRS signals are actually monitoring Mb desaturation. That interpretation is consistent with the signal intensity and desaturation of the deoxyHb proximal histidyl NδH signal from the β-subunit at 73 parts per million. The experimental results establish the feasibility and methodology to observe the deoxyMb and Hb signals in skeletal muscle, help clarify the origin of the NIRS signal, and set a stage for continuing study of O2regulation in skeletal muscle.1H NMR has detected both the deoxygenated proximal histidyl NdeltaH signals of myoglobin (deoxyMb) and deoxygenated Hb (deoxyHb) from human gastrocnemius muscle. Exercising the muscle or pressure cuffing the leg to reduce blood flow elicits the appearance of the deoxyMb signal, which increases in intensity as cellular PO2 decreases. The deoxyMb signal is detected with a 45-s time resolution and reaches a steady-state level within 5 min of pressure cuffing. Its desaturation kinetics match those observed in the near-infrared spectroscopy (NIRS) experiments, implying that the NIRS signals are actually monitoring Mb desaturation. That interpretation is consistent with the signal intensity and desaturation of the deoxyHb proximal histidyl NdeltaH signal from the beta-subunit at 73 parts per million. The experimental results establish the feasibility and methodology to observe the deoxyMb and Hb signals in skeletal muscle, help clarify the origin of the NIRS signal, and set a stage for continuing study of O2 regulation in skeletal muscle.

Myoglobin desaturation with exercise intensity in human gastrocnemius muscle

The present study evaluated whether intracellular partial pressure of O(2) (PO(2)) modulates the muscle O(2) uptake (VO(2)) as exercise intensity increased. Indirect calorimetry followed VO(2), whereas nuclear magnetic resonance (NMR) monitored the high-energy phosphate levels, intracellular pH, and intracellular PO(2) in the gastrocnemius muscle of four untrained subjects at rest, during plantar flexion exercise with a constant load at a repetition rate of 0.75, 0.92, and 1.17 Hz, and during postexercise recovery. VO(2) increased linearly with exercise intensity and peaked at 1.17 Hz (15. 1 +/- 0.37 watts), when the subjects could maintain the exercise for only 3 min. VO(2) reached a peak value of 13.0 +/- 1.59 ml O(2). min(-1). 100 ml leg volume(-1). The (31)P spectra indicated that phosphocreatine decreased to 32% of its resting value, whereas intracellular pH decreased linearly with power output, reaching 6.86. Muscle ATP concentration, however, remained constant throughout the exercise protocol. The (1)H NMR deoxymyoglobin signal, reflecting the cellular PO(2), decreased in proportion to increments in power output and VO(2). At the highest exercise intensity and peak VO(2), myoglobin was approximately 50% desaturated. These findings, taken together, suggest that the O(2) gradient from hemoglobin to the mitochondria can modulate the O(2) flux to meet the increased VO(2) in exercising muscle, but declining cellular PO(2) during enhanced mitochondrial respiration suggests that O(2) availability is not limiting VO(2) during exercise.The present study evaluated whether intracellular partial pressure of O2 ([Formula: see text]) modulates the muscle O2 uptake (V˙o 2) as exercise intensity increased. Indirect calorimetry followedV˙o 2, whereas nuclear magnetic resonance (NMR) monitored the high-energy phosphate levels, intracellular pH, and intracellular[Formula: see text] in the gastrocnemius muscle of four untrained subjects at rest, during plantar flexion exercise with a constant load at a repetition rate of 0.75, 0.92, and 1.17 Hz, and during postexercise recovery.V˙o 2 increased linearly with exercise intensity and peaked at 1.17 Hz (15.1 ± 0.37 watts), when the subjects could maintain the exercise for only 3 min.V˙o 2 reached a peak value of 13.0 ± 1.59 ml O2 ⋅ min-1 ⋅ 100 ml leg volume-1. The31P spectra indicated that phosphocreatine decreased to 32% of its resting value, whereas intracellular pH decreased linearly with power output, reaching 6.86. Muscle ATP concentration, however, remained constant throughout the exercise protocol. The 1H NMR deoxymyoglobin signal, reflecting the cellular[Formula: see text], decreased in proportion to increments in power output andV˙o 2. At the highest exercise intensity and peakV˙o 2, myoglobin was ∼50% desaturated. These findings, taken together, suggest that the O2 gradient from hemoglobin to the mitochondria can modulate the O2flux to meet the increasedV˙o 2 in exercising muscle, but declining cellular [Formula: see text]during enhanced mitochondrial respiration suggests that O2 availability is not limitingV˙o 2 during exercise.

Exercise reverses depressed metabolic rate produced by severe caloric restriction

The effects of caloric restriction and exercise on resting metabolic rate (RMR) were studied in five obese humans. Subjects consumed a 500 kcal.d-1 diet for 4 wk, with the subjects remaining sedentary during the first 2 wk and then exercising 30 min daily at 60% VO2max during the last 2 wk of caloric restriction. After 2 wk of dieting, RMR decreased to approximately 87% of the pre-dieting control value. Over the last 2 wk of dieting with the addition of daily exercise, the fall in RMR was reversed as it returned to the pre-dieting level. In summary, daily exercise reversed the drop in RMR associated with severe caloric restriction.

Impact of energy intake and exercise on resting metabolic rate.

SummaryResting metabolic rate is modulated by the amount of calories consumed in the diet relative to energy expenditure. Excessive consumption of energy appears to increase resting metabolic rate while fasting and very low calorie dieting causes resting metabolic rate to decrease. Since the metabolic rate at rest is the primary component of daily energy expenditure, its reduction with caloric restriction makes it difficult for obese individuals to lose weight and to maintain weight that is lost.Whether exercise has a carry-over effect on resting metabolic rate remains controversial, even though this question has been studied extensively during the last 90 years. Reasons for contradictory results include variations in control of prior diet and exercise patterns, inadequate exercise frequency, intensity and duration, and the possibility of response to exercise varying between individuals. Several lines of evidence suggest exercise may modulate resting metabolic rate. Bed rest in sedentary individuals leads to a reduction in resting metabolic rate. Similarly, in highly trained runners, cessation of daily exercise training lowers resting metabolic rate by about 7 to 10%. Resting metabolic rate is depressed in previously sedentary obese individuals on a very low calorie diet, but it quickly returns to the predicting level when exercise of sufficient frequency, intensity and duration is undertaken while dieting.These findings suggest caloric intake and daily exercise can modulate resting metabolic rate. Exercise of adequate intensity and duration may also enhance resting metabolic rate.

Effect of suspending exercise training on resting metabolic rate in women

We tested the hypothesis that enhanced resting metabolic rate (RMR) in highly trained endurance athletes is an acute effect of prior exercise induced by catecholamines and not serum thyroxine. RMR and energy-regulating hormones were studied in nine highly trained women runners during habitual training (period I), and suspension of training (period II). Data were collected during the follicular phase of two consecutive menstrual cycles, confirmed by serum progesterone and estradiol. Subjects maintained training between the two periods. Total energy intake and diet composition, body weight, and oral temperature did not change from period I to period II (P greater than 0.05). With suspension of training, urinary epinephrine and nonrepinephrine excretion dropped (P less than 0.022) while serum TSH rose (P = 0.011) and free T4 did not change (P = 0.182). RMR (mean +/- SEM) was 274 +/- 6.2 and 252 +/- 7.8 kJ.h-1 for periods I and II, respectively, with repeated measures ANOVA indicating a drop in RMR occurred with cessation of exercise (P = 0.048). The augmentation of RMR by exercise lasted more than 15 h but less than 39 h post-exercise. The results suggest that the drop in catecholamines may partly explain the lower RMR following suspension of training.

Dilution of body fluid electrolytes affects bioelectrical impedance measurements

This study was designed to assess how acute perturbation in electrolyte concentration of body fluids affects the bioelectrical impedance analysis (BIA) measurement of resistance (R) and derived total body water (TBW) in humans. After an initial measurement of R, subjects drank either water (group W: n = 8, 1211 ± 119 ml) or a hypotonic rehydration beverage (group H: n = 8, 1211 ± 118 ml, 18 mEq/L) or an isotonic solution composed of the rehydration beverage supplemented with 209 mEq/L sodium chloride (group I: n = 8, 1196 ± 118 ml, 308 mEq/L) to produce a 3% increase in TBW. R was measured approximately 3 to 5 minutes following fluid intake, and three additional times at 30‐minute intervals. In all groups, R increased significantly immediately following fluid intake (p ≤0.05). However, the subsequent changes in R were dependent on beverage electrolyte concentration. Ninety minutes after fluid ingestion, the mean R for groups W and H remained elevated, whereas R for group I had decreased significantly (p <...

Myoglobin and O2 consumption in exercising human gastrocnemius muscle.

The regulation of oxygen transport to the mitochondria in exercising muscle is a key issue in biology, since oxygen demand can increase dramatically from the resting state. As the oxygen consumption (VO2) increases, a coordinate set of controls must enhance the oxygen delivery from the lung to the cell. As VO2 approaches its maximum rate (VO2max), convection, diffusion or enzymatic activity must also become limiting. Identifying the rate- determining step is then a central issue (Sutton, 1992).

Daily exercise enhances fat utilization and maintains metabolic rate during severe energy restriction in humans

Whether daily exercise initiated with dieting can increase resting energy expenditure and fat utlization while minimizing loss of lean tissue is equivocal. Therefore, the effect of a 4‐week program of food restriction and daily exercise on resting metabolic rate (RMR) and body composition was studied and compared with the effect of the same diet program without exercise on moderately obese humans. Following a 7‐day control period, 13 subjects consumed a diet providing 600 Kcal/day (2510 kJ/day) for 4 weeks; eight subjects exercised 30 to 45 minutes daily at 60 to 65% maximum oxygen uptake (DE group) and five subjects remained sedentary throughout the study (D group). RMR was measured by indirect calorimetry between 5 and 8 AM each morning after an overnight fast and a weekly average was calculated for each subject. Body composition was determined by hydrodensitom‐etry each week. RMR decreased significantly, amounting to 88% of the predietary control after 4 weeks of dieting in the D group. In contrast, RM...

Physiological adaptation to 6 weeks of specific training of intercollegiate soccer players

The purpose of this study was first to examine selected anthropometric and physiological characteristics of the outfield players of a soccer team according to playing position, and secondly to study the effects of a six week soccer training regimen on peak aerobic power (VO2peak), treadmill run‐time to exhaustion (TTE), percent body fat (%BF), and sum of skinfold thicknesses (SST). Twenty four outfield players of an intercollegiate soccer team [9 defenders (DF), 8 midfielders (MF), and 7 forwards (FW)] participated in the first part of the study, whereas only 17 players completed the training. Body weight and height were not different among playing positions. Also, no difference was found between player positions for: (a) %BF [DF = 9.9 ± 2.2(SD) MF=10.2 ± 5.7; FW=10.6 ± 4.1%], (b) VO2peak [DF = 55.9 ± 3.3; MF = 56.4 ± 5.2; FW = 52.9 ± 4.3ml · min−1 · kg−1], and (c) maximal ventilation rate [DF= 127.8 ± 11.8; MF= 119.1 ± 13.0; FW= 117.1 ±7.3 1·min−1]. The TTE was not different among groups. The VO2peak before training was 55.3 ± 4.3 ml · min−1· kg−1 and it increased (p≤.05) to 57.5±5.8 ml · min−1· kg−1 after training. TTE also increased (p≤.05) from 22.8 ± 3.0 min before to 25.2 ± 1.6 min after training. Although body mass (74.0 ± 6.4 kg) and % BF (9.8 ± 4.4%) remained unchanged during the training period, the SST decreased (p ≤ .05) from 60.9 ± 17.4 to 55.4 ± 14.0 mm. The results indicated no difference in selected anthropometric and physiological variables among playing positions. The loss of subcutaneous fat without a change in the total fat after six weeks of training in all players suggests there was a redistribution of fat storage.