Physical training in obese women
Transcription
Physical training in obese women
European Journal of Eur J Appl Physiol (1984) 52:355-361 Applied Physiology and Occupational Physiology 9 Springer-Verlag 1984 Physical training in ,obese women Effects of muscle morphology, biochemistry and function Konstantinos Mandroukas, Marcin Krotkiewski, Marita Hedberg, Zet~on Wroblewski, Per Bj6rntorp, and Gunnar Grimby Department of Rehabilitation Medicine, MedicineI & Plastic Surgery, Sahlgren's Hospital, Universityof G~teborg, Ovre Husargatan 36, S-41314 G6teborg, Sweden Summary. Peripheral adaptations to 3 months of physical endurance training without food restrictions were studied in skeletal muscles of 14, middle-aged, physically untrained, obese women. In comparison to aged-matched controls of normal weight, the obese group showed significantly lower isometric endurance9 In the obese group, physical training resulted in a significant increase of maximal isometric and isokinetic strength. Isokinetic but not isometric endurance also increased after training. The isometric strength of obese women showed a positive correlation with the percentage of FTb fibres. The training (50 min/day, 3 days/w) did not result in any change in body weight, body fat, and the number and weight of fat cells. The 20% increase of VO 2 max after training was found to be significantly correlated with the increase in the number of capillaries around muscle fibres. The relative percentage of FTa fibres, the number of capillaries per fibre as well as the activities of citrate synthase, 3-hydroxy-acyl-CoA-dehydrogenase,and hexokinase showed a significant increase after training9 The concentrations of glucose during OGTT showed a trend to decrease with a significant decrease at the end glucose curve (120-min value). The concentration of insulin and C peptide and the insulin removal did not change after training9 The changes in the concentration of glucose during OGTT was significantly correlated with the increase in muscle capillarization and of dynamic endurance. Key words: Obesity - Muscle strength - Fibre composition - Capillarization - Enzymes - Physical training Offprint requests to: M. Krotkiewstd at the above address Introduction Physical training is widely recommended in the treatment of obesity. However, unless it is combined with food restrictions, in severely obese subjects training does not result in a decrease in body weight. The training causes, however, numerous metabolic adaptations (Bj6rntorp et al. 1970, 1973a, 1973b; Krotkiewski et al. 1979, 1980a, 1980b), which can be considered advantageous in the prevention of metabolic disorders associated with obesity (Sullivan et al. 1981). Skeletal muscles are important target organs for insulin and for glucose storage and utilization, while glucose utilization in adipose tissue is comparatively small. Neither the number nor weight of fat cells changes after training in severly obese subjects (Bj6rntorp et al. 1970, 1973a, 1973b; Krotkiewski et al. 1979, 1980a, 1980b), while numerous adaptations have been described in muscle tissue (Andersen and Henriksson 1977; Josenhans 1962; Petrofsky and Lind 1975). Physical training increases insulin sensitivity (Bj6rntorp et al. 1970; Sullivan 1976). This increase may be causally related to the metabolic, morphologic and/or microvascular adaptations in muscle tissue9 The aim of the present study was to examine in detail the adaptation occuring in obese subjects in skeletal muscles, and to relate them to general adaptations, such as changes in body composition, Vo2 max, blood pressure, heart rate, and metabolism. Material and methods Fourteen obese middle-agedwomenwere includedin the study. Their general characteristics are summarized in Table 1. All patients had sedentaryoccupations and had not been engagedin any regular physical training programme during the preceding year. During the period of physical training the patients were instructed to maintaintheir usualfoodintake and drinkinghabits. 356 No patients included in the study had any signs of cardiovascular or renal diseases or neurological disorders. There was no drop out during the training programme. Before starting the training programme, body weights of the patients were recorded at intervals during 2 months to ensure body weight stability. All the women had given their informed consent to the various parts of the experiments. The local ethical committee at the University of G6teborg had approved all details of the present study. Body composition and blood chemistry Body composition was calculated from 4~ measurements with a whole body counter. Lean body mass (LBM = whole body without adipose tissue mass) was calculated according to the formula by Forbes et al. (1961), which assumes a constant amount of potassium (68.1 mEq) per kilogram of lean body mass. Body fat was calculated by substraction of lean body mass from the total body weight. Subcutaneous fat biopsies were taken from the epigastric, hypogastric, femoral, gluteal, and upper arm regions (Krotkiewski et al. 1977). The total fat cell number and fat cell weight were determined according to Sj6str6m et al. (1971). Serum cholesterol was determined according to the method of Cram6r and Isaksson (1959), and serum triglycerides according to Carlson (1959). A glucose tolerance test was performed with 100 g glucose dissolved in 200 ml lemon flavoured water taken orally in the morning after overnight fasting. The subjects did not smoke that morning and moved about leisurely. From an indwelling needle in an antecubital vein blood samples were obtained in the supine position before and at 30, 60, 90, and 120 min after taking glucose for the determination of blood glucose (Levin et al. 1962) plasma insulin (Phadebas, Pharmacia, Uppsala, Sweden), and C peptide (Novo, Copenhagen, Denmark). These tests were preceded by 3 days of controlled diet containing 35 kcal/kg ideal body weight with the caloric per cent of protein, fat, and carbohydrate being exactly the same before and after the training period. Muscle biopsies Muscle biopsies were taken superficially before and after training from the right vastus lateralis under local anesthesia using a surgical technique. No complications were recorded. On each occasion two muscle specimens were taken from the patient. One was frozen immediately in liquid nitrogen for determination of enzyme activities and metabolite analyses, the other was trimmed, mounted, and frozen in isopentane (cooled by liquid nitrogen) for histochemical analyses. Both specimens were stored at - 8 0 ~ until analysed. Histochemical analyses Serial transverse sections (10 p,m) were cut with a cryotome at -21 ~ The myofibrillar ATP-ase (adenosine triphosphatase) method was used for muscle fibre classification (Gomori 1941; Padykula et al. 1955). The reactions were carried out at pH 9.4, following by alkaline preincubation at pH 10.3, to classify into slow twitch (ST, type I) and fast twitch (FT type II) fibres. The FT fibres could be further classified into types FTa and FTb by preincubation at pH 4.6 and 4.4 (Dubowitz et al. 1973). The mean number of fibres counted was 614 _+ 51 (mean + SD). Amylase-PAS-staining to visualize capillaries was used for capillary analyses. The capillary supply was calculated according to Andersen et al. (1977). The mean number of fibres counted for capillaries was 104 + 23 (mean + SD). As regards the methodological error for capillary analyses, see Aniansson et al. (1981). K. Mandroukas et al.: Physical training in obese women Measurements of fibre areas were made on photographs of transverse sections, stained for DPNH-activity (Novikoff et al. 1981). An optical illumination device ("particle size analyzer", Carl Zeiss, FRG), projecting muscle fibres as circles of varying sizes, was used, and the total fibre area was approximated as described by Aniansson et al. (1981). The mean number of fibres measured for fibre areas was 226 + 10 (mean + SD). Enzyme activity analysis Enzyme activity determinations were performed by means of fluorimetric techniques. The reactions catalyzed by the enzymes under investigation were coupled to NAD-NADP-linked reactions according to Lowry et al. (1972). The enzymes analyzed wer lactate dehydrogenase (LDH), citrate synthase (CS), 3-hydroxyacyl-CoA-dehydrogenase (HAD), triosephosphate dehydrogenase (TPDH), and hexokinase (HK). The assays were performed at 25~ C. The assay mixtures were somewhat modified from those described by Bass et al. (1969). The glycogen content was quantified according to Karlsson (1971) and the protein content according to Lowry et al. (1951). The methodological errors calculated from 15 duplicate determinations were: LDH 5.2%, CS 3.8%, TPDH 5.3%, protein 1.1%, HK 3.4%, and glycogen (n = 58) 4.2%. Testing procedure for force and velocity measurements Muscle strength of the right quadriceps was measured as the torque during maximal static contraction and at maximal knee-extension with constant angular velocities using an isokinetic dynamometer (Cybex II, Lumex Inc., NY, USA) modified with a strain gauge (Cykob, Stockholm, Sweden). Isometric strength was measured as the torque during maximal isometric contractions at knee extension with knee angles 60 and 90 degrees. Three tests were carried out at each angle and the highest values were recorded. Isokinetic strength was measured as the torque during maximal knee extension movement with constant angular velocities, which were preset at 30, 60,120, and 180 degrees per second. Three tests were carried out at each velocity. The highest value was registered. Torque output and knee angles were recorded on an x-y-recorder (Omnigraphic, Houston Instrument, USA). Isometric endurance was measured as the time the subject could hold 50% of the maximal isometric strength at a knee angle of 90 degrees. Isokinetic endurance was measured as the percentage decline in peak torque of 50 maximal isokinetic contractions at 180 degrees per second. To compare the pretraining values of muscle strength in obese women with a normal population, an additional group of 14 normal-weight (60.8 _+ 6.8 kg), age-matched (36.3 _+ 9.3 years), healthy women was tested on a Cybex dynamometer in an identical manner to that described above. Exercise test and determination of maximal oxygen uptake Heart rate was measured by continuous telemetry. A Monark (Varberg, Sweden) mechanically-braked bicycle ergometer was used for submaximal (50 and 100 W) and maximal exercise loads. The same submaximal exercise loads were used for pre- and posttraining measurements of expired air volume and analysis of O2-fraction using a Beckman OM-11. The measuring of maximal oxygen uptake 02o2 max) started with submaximal loads followed by stepwise increase in exercise loads until exhaustion. K. Mandroukas et al.: Physical training in obese women The criterion used for maximal oxygen uptake was a levelling of oxygen uptake despite further increase in exercise load, with blood lactate levels > 8 mM/l. A second determination of 12o2max was carried out on another day. Both determinations gave similar values (_+ 3%). The Rated Perceived Exertion (RPE) (Borg 1970) and the blood pressure were recorded at the 50- and 100-W work loads. Blood lactate concentration was determined from fingertip blood immediately after the maximal exercise and was analysed by an enzymatic method (Boehringer, Mannheim, FRG). Physical training programme The group was trained for 3 months, three times a week. The duration of the training session was 50min, starting with 10-15 min of warming-up exercises including walking, jogging, and calisthenics of light intensity, including exercise with all parts of the body. The programme then continued with alternating heavy and light periods. The heavy intervals were performed on a bicycle ergometer and lasted for 4 min. The work load was chosen individually, based on the maximal work load performance at the test before the training. The work during each heavy interval started with a submaximal work load. After 3 - 4 weeks of training the work load was gradually increased. The "light" intervals lasted 8 - 1 0 rain and consisted of walking and calisthenics affecting mainly muscle groups other than those utilized during the heavy intervals. The intensity of the training was followed in each patient by telemetry. In four patients, heart rate and oxygen uptake (by oxygen flowmeter) - Oxylog, Morgan, GB were continuously measured during the whole training period. The variations in oxygen uptake and heart rate during the training intervals are shown in Fig. 1. The oxygen uptake at the heavy intervals reached 8 0 - 8 5 % of 12o2max. Statistics The significance of intraindividual differences was tested using the paired t-test. A P value of < 0.05 was considered significant. 357 Results Three months of physical training gave no significant changes in body weight, body fat, lean body mass, fat cell weight, or fat cell number (Table 1). The concentration of plasma insulin and C peptide and blood glucose, both fasting values and values during OGTT, did not change after training. However, glucose values at 120 min after oral glucose load decreased significantly after training. The extraction of plasma insulin (calculated as the difference between the sum of C peptide and the sum of insulin values in nmoles/1) did not change after training (Table 1). Heart rate, systolic and diastolic blood pressure at rest, and systolic blood pressure at submaximal work load (100 W), decreased significantly after training Table 1. Body weight and composition and metabolic variables in obese women before and after physical training (n = 14) Before training Mean Age = (years) Height (cm) Body weight (kg) Body fat (kg) Lean body mass (kg) Cholesterol (mmol x 1-1) Triglycerides (mmol x 1-1) Fat cell weight (gg) Fat cell number (x 101~ 200 ////_ ZZ E "~ 150 ~Q = "r 100 l LA LJm z - - m a x , nr~ 9 m 9{ c / , ' 9 >. u /.>./ 'agl' x /.t~ o~ //',4,,, 100 r o .2~ E 50 "5 0 20 30 Time m~n Fig. I. Heart rate (upper panel) and percentage of m a x , 1 2 o 2 (lower panel) for one patient during different training intervals 10 Fasting glucose (mmol x 1-I) Fasting insulin (gU x 1-1) /c. ,1t /J// //// ////, Fasting C peptide (nmol x 1-1) Glucose at 120' during OGTT (mmol x 1-1) Insulin at 120' during OGTT (btU x 1-1) C peptide at 120' during OGTT (nmol • 1-1) Sum(Z) of glucose values during OGGT (mmol x 1-1) Sum of insulin values during OGGT (~U x 1-1) Sum of C peptide values during OGTT (nmoI x 1-1) N C peptide - Z insulin during OGTT in nmol x 1-1 38.6 166.7 96.6 45.26 51.3 5.75 After training SEM _+ +_ _+ + + • 3.10 1.47 3.91 3.35 2.9 0.30 Mean 98.5 47.87 50.6 6.03 SEM -+ + + • 3.97 3.20 2.7 0.30 1.44 + 0.19 1.64 _+ 0.20 0.66 _+ 0.01 7.48 • 0.12 0.69 _+ 0.01 7.52 _+ 0.10 4.5 + 0.1 4.5 19.9 + 2.0 0.62 • 0.06 6.5 + 0.2 89.4 + 8.4 1.75 • 0.16 34.8 + 2.6 414.1 _+ 29.2 7.03 _+ 0.4 4.38 • 0.6 _+ 0.2 24.3 • 2.1 0.56 • 0.03 6.0 + 0.3* 92.8 + 6.7 1.45 • 0.11 33.3 • 2.9 444.3 • 26.0 6.88 • 0.5 4.03 + 0.7 358 K. Mandroukas et al.: Physical training in obese women Table 2. Heart rate, systolic and diastolic blood pressure at rest and at 50-W and 100-W work loads. 12E and 12o2 at 50-W and 100-W work loads, before and after 3 months' training Rest 50 W Before training Mean Heart rate (beats x rain -I) Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) 12E (1 X min -1) 12o2 (1 X min -1) RPE After training SEM 100 W Before training After training Before training After training Mean SEM Mean SEM Mean SEM Mean SEM Mean SEM 86 4 77 4*** 116 4 115 4 147 5 141 4 140 4 131 4*** 150 3 145 4 179 5 157 6** 87 2 80 2* . . . . . . . . . . . . . . . . 23.32 0.98 10 . 1.11 0.05 0.4 22.95 1.05 10 0.78 0.04 0.4 . . 43.18 1.70 14 . 2.06 0.07 0.6 37.81 1.60 13 1.37 0.05 0.3 * P < 0.05; ** P < 0.005; *** P < 0.001 RPE denotes rated perceived exertion (Borg 1970) Table 3. Oxygen uptake (1202)' expiratory gas volume (12E), and plasma concentration of lactic acid at the maximal work load before and after 3 months' training Table 4. Fibre type distribution, fibre area, ratio of fibre area, and relative fibre areas of the vastus lateralis muscle before and after 3 months' training. Means + SEM for 14 obese patients Max. exercise Before training Heart rate (beats x min -1) 12E (1 X rain -1) 12o2 (1 X min -1) Lactate (mM x 1-1) Before training After training Mean Mean SEM Mean SEM 177 4.38 176 4.10 63.93 2.21 8.60 3.56 0.tl 0.37 78.05 2.62 9.54 2.77*** 0.10"** 0.30** * P < 0.05; ** P < 0.005; *** P < 0.001 SEM Mean SEM Fibre type distribution (%) ST 44.9 FTa 30.1 FTb 24.7 3.3 1.3 2.5 43.1 35.1 21.6 3.6 1.5" 4.0 Fibre area (~tmz x 103) ST FT FTa Fib 5.01 5.04 5.59 4.34 0.29 0.28 0.32 0.29 5.60 5.41 5.77 4.69 0.36 0.27 0.31 0.32 5.05 0.26 5.45 0.27 1.03 1.11 0.89 0.06 0.05 0.08 1.00 1.06 0.86 0.05 0.06 0.06 Mean fibre area (~tm2 x 103) 200" Nm [ ] Controls [ ] Obese before training 150" [ ] Obese after training After training Area ratio FT/ST FTa/ST FTb/ST Relative fibre area (%) ST FTa Fib 43.2 33.9 26.1 3.0 1.8 4.2 43.8 37.4 18.7 3.7 2.0 3.8 100" * P < 0.05 50- 120% 180% O~ A90~ 0% A60~ 30~ 60% Fig. 2. Maximal and isokinetic torque values at different angular velocities in 14 obese women and in the control group. Means _+ SEM before and after 3 months physical training are given ( T a b l e 1), w h i l e t h e R P E d i d n o t c h a n g e ( T a b l e 2). Maximal oxygen uptake and blood lactate acid c o n c e n t r a t i o n a f t e r m a x i m a l e x e r c i s e i n c r e a s e d sign i f i c a n t l y w i t h t r a i n i n g ( T a b l e 3). I s o m e t r i c s t r e n g t h i n c r e a s e d a f t e r t r a i n i n g a t a 90 ~ knee angle. Isokinetic strength increased significantly a t b o t h 30~ a n d 60~ a n g u l a r v e l o c i t i e s ( F i g . 2). K. Mandroukas et al.: Physical traMng in obese women Table 5. Capillary supply of the vastus lateralis muscle in 13 obese patients before and after training (Means + SEM) Before training Capillaries per mm2 After training Mean SEM Mean SEM 264 12 279 14 Capillaries per fibre 1.55 0.07 1.83 0.i1"* Capillaries around fibres ST FT FTa FTb 4.50 3.84 4.18 3.44 0.17 0.20 0.24 0.18 5.24 4.46 4.71 3.93 0.24** 0.29** 0.28* 0.31 Fibre type area per capillary (~tm2 X 103) ST 1.11 FT 1.29 FTa 1.34 FTb 1.26 0.05 0.07 0.07 0.09 1.05 1.21 1.20 1.21 0.05 0.05 0.05 0.05 * P < 0.05; ** P < 0.005 Table 6. Enzymatic activity and glycogen content in m. vastus lateralis Muscle glycogen (mMol x g-X) HK (~Mol x rain -1 x g protein -1) TPDH (~tMol x rain -1 x g protein -I) LDH (~tMol x rain -1 x g protein -1) CS (~tMol x rain -1 x g protein -1) HAD (~Mol x rain -1 x g protein -1) Before training After training Mean Mean SEM 89.81 6.i0 101.11 5.7 0.4 8.4 1,199.50 7 8 . 0 3 1,278.67 SEM 9.66 0.5*** 84.94 795.92 86.36 8 3 9 . 4 2 77.54 36.98 1.87 47.01 2.88** 40.85 1.76 48.26 2.25** ** P < 0.01; *** P < 0.001 LDH = lactate dehydrogenase, TPDH = triosephospate dehydrogenase, CS = citrate synthase, HAD = 3-hydroxy-acyl-CoAdehydrogenase, HK = hexokinase 359 In c o m p a r i s o n with a normal-weight control group, in this study the overweight w o m e n s h o w e d no significant differences in isokinetic and isometric maximal strength and isokinetic endurance. T h e time during which 50% of maximal isometric contraction was maintained a p p e a r e d to be significantly lower in obese w o m e n , 45.5 s ( S E M ) in c o m p a r i s o n with value of 63.7 s ( S E M ) for n o r m a l w o m e n (P < 0.05) 9 Isokinetic e n d u r a n c e (P < 0.01), but not isometric e n d u r a n c e , increased significantly after training, the decrease in t o r q u e values for 50 contractions at 180~ being 54% ( S E M ) before and 44% (SEM) after training 9 In spite of s o m e t e n d e n c y to increase, no statistically significant change in fibre area was o b s e r v e d in any of the fibre types (Table 4). T h e p e r c e n t a g e of F T a fibres increased significantly (P < 0.05) after training. T h e n u m b e r of capillaries a r o u n d each fibre increased mainly for the m o r e oxidative fibre types (ST 18%, F T a 14%). Generally, the n u m b e r of capillaries per fibre increased significantly ( P < 0 . 0 1 ) after training 9 H o w e v e r , the part of the fibre area supplied by one capillary did not increase significantly (Table 5). T h e c o n c e n t r a t i o n of glycogen per gram of muscle tissue did not change significantly after training. T h e activities of citrate synthase (P < 0.01) and hexokinase ( P < 0.001), as well as 3 - h y d r o x y - a c y l - C o A - d e h y d r o g e n a s e ( P < 0.01), increased (Table 6), while activities of lactate d e h y d r o g e n a s e and triosephosp h a t e d e h y d r o g e n a s e did not change. T h e trend to decrease of the sum of glucose values during O G T T after training was significantly correlated with the increase in the n u m b e r of capillaries a r o u n d ST type of muscle fibres, and to the increase of d y n a m i c e n d u r a n c e after training. T h e increase in the n u m b e r of capillaries a r o u n d all fibres (not shown), and particularly a r o u n d F T a type o f muscle fibres, was significantly correlated to the increase of Vo2 max. T h e changes (trend to increase) of the muscle fibre area of the F T b fibres were significantly correlated to the increase in isometric strength, and the changes in fibre area of the F F a fibres correlated significantly with the increase in d y n a m i c (isokinetic) strength (Table 6). Correlation analyses Difference before - after physical training in r-value P-value The number of capillaries in contact with ST type of muscle fibres Dynamic endurance The sum of glucose values during OGTI" 0.54 0.54 0.54 < 0.05 < 0.05 < 0.05 The capillaries in contact with FTa type of muscle fibres Vo2 0.58 < 0.05 The fibre area of Fib type of muscle fibres Isometric strength (90~ knee angle) 0.54 < 0.05 The fibre area of FFa type of muscle fibres Isokinetic strength (60~ 0.57 < 0.05 max 360 Discussion As previously reported in severely obese subjects (Bj6rntorp et al. 1973b; Krotkiewski et al. 1979, 1983c, 1983e), long-term physical training without restriction of food intake resulted neither in changes in body weight and composition nor in changes in fat cell weight or number. When maximal oxygen uptake was analyzed at the start of the experimental period, obese women showed values comparable with those of healthy non-obese women (Sullivan 1976; Sullivan e t a ! . 1981). In obese patients, physical training resulted in a normal cardiovascular adaptation with a 20% increase in maximal oxygen uptake, comparable to previously reported results in obese persons (Bj6rntorp et al. 1970; 1973a, 1973b). Overweight persons often have elevated lean body mass (Bj6rntorp et al. 1970; 1973a, 1973b). They are compelled to develop some extra force to mobilize the weight- supporting muscles in order to compensate their overweight. These factors may imply differences in the recruitment pattern and composition of muscle fibres. The obese women were normoglycemic and only slightly hyper-insulinemic before training. In a similar group of obese normoglycemic women we could not find any indications of insulin resistance and intensitivity in terms of insulin binding, insulin effects on glucose incorporation to triglycerides and on lipolysis (L6nnroth et al. 1983; Krotkiewski et al. 1983c, 1983d) and in terms of glucose disposal during euglycemic insulin clamp (Krotkiewski et al. 1983c, 1983d). The decrease in the 120-rain glucose value is also in accordance with repeated observations on the improvement of glucose tolerance (Krotkiewski 1983a) and glucose disposal during euglycemic insulin clamp (Krotkiewski et al. 1983c, 1983d) after training in obese normoglycemic women. The slight improvement noted at 120 rain during OGTT is also in harmony with the increased activity of hexokinase. In comparison with morphologic data reported for 54 healthy normal weight women by Nygaard (1981), the obese group generally showed large cross-sectional areas of muscle fibre. Furthermore, both the relative percentage distribution and the cross-sectional area of FTb fibres seem to be exceptionally high in obese persons. Physical training increased the relative proportion of FTa fibres, while a trend to decrease could be observed with respect to FTb fibres (Table 4) as expected from an endurance training programme in relatively untrained individuals (Saltin et al. 1977). In comparison with a population of normal-weight sedentary women described by Nygaard (1981), obese women have a somewhat higher K. Mandroukas et al.: Physical training in obese women number of capillaries around the various types of muscle fibres. The number of capillaries around different types of muscle fibres increased after training. As a similar increase took place concomitantly with respect to the fibre area, the proportion of cross-sectional area supplied by one capillary did not change significantly. This is in contrast with the results described by Aniansson et al. (1981) in older men and women, and in healthy men of normal weight (Andersen 1977), where the decrease in fibre area per capillary was treated as evidence of improved diffusion distance. It has been found that body weight correlates positively with maximum strength and negatively with muscular endurance (Elbel 1949; Joyes 1947; Josenhans 1962). More recently, however, a negative relationship between body weight and muscular endurance has been reported, and it is suggested that it is caused by the higher deep muscle temperature (Petrofsky et al. 1975) due to insulation by the subcutaneous fat layer around a limb. In the present study, isometric endurance also showed reduced values compared with the controls. Both training and weight reduction through a low caloric diet (Krotkiewski et al., unpubl, results) appeared to improve the reduced isometric endurance in obese women. In comparison with normal weight women, the overweight participants showed similar dynamic and isometric strength measured on an isokinetic dynamometer at different angular velocities and at different knee angles. The positive correlation between the improvement of glucose tolerance and the increased capillarization of muscle tissue has been reported previously (Krotkiewski et al. 1983e). The significant correlation between the changes in glucose concentrations and the increase in dynamic strength (Table 6) might reflect the importance of better substrate availability for the working muscle. In conclusion, obese women show a higher percentage and area of FTb fibres in comparison with data available in the literature for normal weight women. Physical training results in increased enzymatic activities and microvascular proliferation in muscles, but the increased number of capillaries is not sufficient to diminish the diffusion distance because of concimitant increase in fibre areas. The relative proportion of endurance and strength components in the training programme can, however, be responsible for such variations in training effects. The central and peripheral adaptations of physical training in obesity seem to be generally comparable to those observed in non-obese women. Acknowledgements. The study was supported by grants from Greta and Einar Asker's Foundation 1981 and 1982; Nordiska Samfundets Stiftelse f6r Vetenskaplig Forskning och Djurf6rs6k; the Sport K. Mandroukas et al.: Physical trai~aing in obese women Research Council 48/81; and the Swedish Medical Research Council (Project 03888). References Andersen P, Henriksson J (1977) Capillary supply of the quadriceps femoris muscle of man: adaptative to exericse. J Physiol 270:677-699 Aniansson A, Grimby G, Hedberg M, Krotkiewski M (1981) Muscle morphology, enzyme activity and muscle strength in elderly men and women. 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Clin Sci Molec Med 48:405-412 Saltin B, Henriksson J, Nygaard E, Andersen P, Jansson E (1977) Fibre types and metabolic potentials of skeletal muscles in sedentary man and endurance runners. Ann NY Acad Sci 301 : 3-29 Sj6str6m L, Bj6rntorp P, Vrana J (1971) Microscopic fat cell size measurement on frozen cut adipose tissue in comparison with automatic determinations of osmiumfixed fat cells. J Lipid Res 12 : 521-530 Sullivan L (1976) The effects of exercise in hyperplastic obesity with special reference to physical performance and hyperinsulinemia. Scand J Rehab Med [Suppl 5] pp 1-25 Sullivan L, Bjur6 T, Krotkiewski M (1981) Physical training in obese subjects. In: Bj6rntorp P, Cairella M, Howard AN (eds) Recent advances in obesity, Research III. London, pp 307-314 Accepted January 18, 1984