<i>Estimation of Lean Body Mass and Body Fat From Basal Oxygen Consumption and Creatinine Excretion</i>

Miller, A. T.; Blyth, Carl S.

doi:10.1152/jappl.1952.5.2.73

Cited by 127 publications

(24 citation statements)

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“…Lean body mass and %LBM were derived using the regression equation of Miller and Blyth (11); LBM = 20.97 + 0.5161 (mg creatinine excreted/h). It is notable that creatinine levels and consequently creatinine coefficients and LBM estimates in this study were low in comparison with several other studies (e.g., 11,12). This could have been due either to the method of assay or to restrictions placed on the activity levels and dietary intake of the subjects.…”

Section: Methodscontrasting

confidence: 83%

Effect of Physical Fitness and Body Composition on Sleep and Sleep-Related Hormone Concentrations

Paxton¹,

Trinder²,

Shapiro³

et al. 1984

Sleep

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Summary: The study assessed the effect of physical fitness and body composition on sleep and the nighttime secretion of the hormones, human growth hormone (hGH), prolactin, and cortisol. Two groups of 17 subjects, one of fit athletes and the other of unfit nonathletes, were selected so that the groups were matched for weight, height, lean body mass (LBM), and fat levels. Subjects slept in a sleep laboratory for 3 nonconsecutive nights: 1 adaptation night and 2 experimental nights. On 1 experimental night blood samples were collected; on the other, baseline sleep was assessed and the catheter was not inserted. Weight and height were measured and LBM assessed by 24 h urinary creatinine. The effect of physical fitness was tested by a comparison of the two groups; body composition was assessed by correlation analyses. Physical fitness did not have a significant effect on either sleep or hormone levels, although in the latter case the results were marginal. In contrast, body composition was related to both sleep and hGH. Percentage LBM was negatively correlated with slow-wave sleep and positively correlated with hGH levels. These results were significant for all subjects combined and for the fit group, although not the unfit group alone. Key Words: Sleep--Physical fitness-Body composition-Hormones.Numerous studies have examined the effects of daytime exercise and physical fitness on electroencephalographic sleep patterns. Two studies have investigated the effects of exercise on sleep period hormone secretions. In one study human growth hormone (hGH) levels were found to be significantly elevated whereas corticosteroid levels were depressed (1). In contrast, the second experiment failed to find increased peak hGH secretion (2). The present study was designed to assess the relationship between physical fitness and the nighttime secretion of hGH, prolactin, and cortisol.In addition to these variables lean body mass (LBM) and fat levels were assessed in all subjects. This was because there is evidence to suggest that hGH, slow-wave sleep (SWS),

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Section: Methodscontrasting

confidence: 83%

Effect of Physical Fitness and Body Composition on Sleep and Sleep-Related Hormone Concentrations

Paxton¹,

Trinder²,

Shapiro³

et al. 1984

Sleep

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“…Ntutritional evaluation of' the 14 hylpocarnitinemiic eirrlhoties, as compared to the 16 normals (Table V'I), showed severely redtuced creatinine/lheiglht index, MANIC, and TSF, consistenit with advanced proteincalorie starvation (14,15,17). The hypocarniitiniemic cirrlhotics also hlad severe hepatocelltular disease, as revealed by the plasmua levels of albunminl, bilirtubin, and prothrombin (Table VI (Table VI).…”

Section: Resultsmentioning

confidence: 96%

“…In the cirrhotics, serum concentration declined from the 6th-day value of 28/18 (total/free) to 20/10 ,uM on day 12; the reduction however was not significant (P > 0.05). Urine total carnitine remained in the range [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] ,umol/day during days [6][7][8][9][10][11][12] Table II1. body weight 105-140% of ideal, and history negative for recent anorexia or weight loss) wlho died after an acute illness of a 1-3-day duration. In the cirrhotic patients' pectoral muscle, heart, liver, kidney, and brain, concentrations of both total and free carnitine wTere only 16-40% as great as in the nonhepatic, normiially nourished cases (P < 0.05).…”

Section: Resultsmentioning

confidence: 99%

“…They then received for 6 days carnitine-free oral and parenteral nutrition providing two to three times the recommended daily allowance (RDA)' of lysine and methionine, while serum concentration and urinary excretion of carnitine continued to be monitored. During days 13 (14), midarm muscle circumference (MAMC) and triceps skin-fold thickness (TSF) (15,16), creatinine/height ratio (17), and serim albumin level and hematocrit.…”

Section: Methodsmentioning

confidence: 99%

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Deficiency of Carnitine in Cachectic Cirrhotic Patients

Rudman¹,

Sewell²,

Ansley³

1977

J. Clin. Invest.

173

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A 3 S T RA C T Carnitine is synthesized from lysine and metlhionine. In the rat, inade(quiate intake of either of these essential amino acids cauises carnitinie depletioIn 14 of' 36 hospitalized cirrhotics hald subnormal valtues for seruim carnitine. The creatinine/height index, midarm munscle circumference, and triceps skin-fold thickness indicated protein-calorie starvation in the 14 hypocarnitinemic liver patients. In six of the hypocarnitinemic cirrhotics (average seruim level 50% of normal), spontaneouis dietary intakes of' carnitine, lysine, and methionine were measuired and foulnd to be only 5-15% as great as in six normocarnitinemiic, healthy controls. When these six cirrhotic anuI six normnal stil)jects were given the same lysine-rich, methioninle-ricl, and carnitine-free nultritionaitl intake, the normaiitls mnain tained n oi-'matl serumiii camr iti ne levels and exeretedl 100 tLmol/day, wvhereas the cirrlhoties' sertum level fell to 25% of noimatl, and(l uirinary excretion dec ined to 15 Lmol/day. Seven lhypocarniitiniemic cirrhotics dlie(l. P'ostmlortemn concentratioons of' carnitine in liver, musele, heart, kidney, and brain averagedl only one-fouirtlh to onethir(d those in corresponding tisstues of eight normally noutrished nonhepatic patients who died after an actute illness of a 1-3-day duiration.These data show that carn-itine depletion is common in pattients hospitalized for advanced cirrhosis, and that it resuilts from three factors: stubstandard intake of dietary carnitine; substandard intake of lysine and methionine, the prectursors ftor endlogenouis carnitine synthesis; acnd loss of' cappacity to syntlhesize carnitine from lysine and methiioniine.

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“…Lean body mass was calculated from the daily creatinine excretion during the control periods by the formula of Miller and Blyth (21). Changes in total body water were derived from the formula of Peters (17).…”

Section: Results: Derivedmentioning

confidence: 99%

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

Huth¹,

Squires²,

Elkinton³

1959

J. Clin. Invest.

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In the preceding paper (1) experimental depletion of potassium in normal human subjects did not produce an extracellular metabolic alkalosis of the severity which usually occurs in patients with comparable potassium deficits. Much investigative study has been applied to this association but, because of the many factors involved in such patients, the relative importance of such factors in the etiology of this association in man remains unclear.Most of our knowledge of the metabolic derangements induced in mammals by potassium depletion has come from studies in rats (2-12). The depletion in rats is usually accompanied by metabolic alkalosis of varying severity. A hypothesis accounting for the alkalosis has been formulated by Darrow, Cooke and coworkers (2-4) and has been given additional support by the studies of Orloff, Kennedy and Berliner (9). In brief, the loss of potassium from cells is replaced in part by hydrogen ion from extracellular fluid, the latter shift resulting in an intracellular acidosis and an extracellular alkalosis. This primary cellular distortion of acid-base equilibrium is then maintained by the kidney by an enhancement of tubular reabsorption of bicarbonate over that of chloride and the excretion of a relatively acid urine. In these rat studies the absence or presence and degree of alkalosis appear to be related to many variables including the duration and severity of the depletion, the protein content of the diet, the acidbase composition of the diet and the use of desoxycorticosterone in promoting depletion.

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Estimation of Lean Body Mass and Body Fat From Basal Oxygen Consumption and Creatinine Excretion

Cited by 127 publications

References 0 publications

Effect of Physical Fitness and Body Composition on Sleep and Sleep-Related Hormone Concentrations

Effect of Physical Fitness and Body Composition on Sleep and Sleep-Related Hormone Concentrations

Deficiency of Carnitine in Cachectic Cirrhotic Patients

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

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