Determinants of metabolic cost during submaximal cycling.

The metabolic cost of producing submaximal cycling power has been reported to vary with pedaling rate. Pedaling rate, however, governs two physiological phenomena known to influence metabolic cost and efficiency: muscle shortening velocity and the frequency of muscle activation and relaxation. The purpose of this investigation was to determine the relative influence of those two phenomena on metabolic cost during submaximal cycling. Nine trained male cyclists performed submaximal cycling at power outputs intended to elicit 30, 60, and 90% of their individual lactate threshold at four pedaling rates (40, 60, 80, 100 rpm) with three different crank lengths (145, 170, and 195 mm). The combination of four pedaling rates and three crank lengths produced 12 pedal speeds ranging from 0.61 to 2.04 m/s. Metabolic cost was determined by indirect calorimetery, and power output and pedaling rate were recorded. A stepwise multiple linear regression procedure selected mechanical power output, pedal speed, and pedal speed squared as the main determinants of metabolic cost (R(2) = 0.99 +/- 0.01). Neither pedaling rate nor crank length significantly contributed to the regression model. The cost of unloaded cycling and delta efficiency were 150 metabolic watts and 24.7%, respectively, when data from all crank lengths and pedal speeds were included in a regression. Those values increased with increasing pedal speed and ranged from a low of 73 +/- 7 metabolic watts and 22.1 +/- 0.3% (145-mm cranks, 40 rpm) to a high of 297 +/- 23 metabolic watts and 26.6 +/- 0.7% (195-mm cranks, 100 rpm). These results suggest that mechanical power output and pedal speed, a marker for muscle shortening velocity, are the main determinants of metabolic cost during submaximal cycling, whereas pedaling rate (i.e., activation-relaxation rate) does not significantly contribute to metabolic cost.     

Serum and saliva adrenocortical hormones in obese diabetic men during submaximal exercise

The aim of this study was to evaluate serum and saliva adrenocortical hormones and their relationships at rest and during submaximal exercise and recovery in 9 obese diabetic middle-aged men (BMI: 35.2 ± 1.6 kg/m (2)). Blood and saliva samples were taken at rest, every 10 min of a 30-min cycling exercise at 70% of maximal heart rate, and after 10 min of recovery in order to analyze cortisol, dehydroepiandrosterone sulfate (DHEA-S) and dehydroepiandrosterone (DHEA). Serum and saliva cortisol increased significantly during recovery (p<0.05), but no significant difference was observed between the rest, exercise, and recovery DHEA-S and DHEA concentrations. A strong correlation was found at rest between both serum and saliva cortisol (r=0.72, p<0.001) and DHEA-S and DHEA (r=0.93, p<0.001). Serum DHEA-S and saliva DHEA remained strongly correlated during and after the submaximal exercise (r=0.81, p<0.001), whereas a weaker but still significant relationship was observed between serum and saliva cortisol during and after the exercise (r=0.52, p<0.001). In conclusion, these results suggest that saliva adrenocortical hormones, and especially saliva DHEA, may offer a practical surrogate for serum concentrations during both rest and exercise in obese diabetic men.     

Norepinephrine spillover at rest and during submaximal exercise in young and old subjects

Mazzeo, Robert S., Chakravarthi Rajkumar, Garry Jennings,and Murray Esler. Norepinephrine spillover at rest and during submaximal exercise in young and old subjects. J. Appl. Physiol. 82(6): 1869-1874, 1997.Aging isassociated with elevations in plasma norepinephrineconcentrations. The purpose of this investigation was toexamine total body and regional norepinephrine spillover as anindicator of sympathetic nerve activity. Eight young (26 ± 3 yr)and seven old (69 ± 5 yr) male subjects were studied at rest andduring 20 min of submaximal cycling exercise at 50% of peak workcapacity. Norepinephrine spillover was determined by continuousintravenous infusion of[³H]norepinephrine.Arterial norepinephrine concentrations were significantly greater atrest for old vs. young subjects (280 ± 36 vs. 196 ± 27 ng/ml,respectively). Whereas total norepinephrine spillover did not differbetween groups at rest, hepatomesenteric norepinephrine spillover was50% greater in old subjects compared with their young counterparts (51 ± 7 vs. 34 ± 5 ng/min, respectively). Additionally,norepinephrine clearance rates at rest were significantly lower for theold subjects (23%). During exercise, plasmanorepinephrine concentrations increased compared with rest, with oldsubjects again demonstrating greater values than the young group.Hepatomesenteric norepinephrine spillover was significantly greater(+36%) during exercise for old subjects compared with young; however,no difference was found for whole body spillover rates between agegroups. Norepinephrine clearance rates remained depressed(30%) in the old subjects during exercise. Clearance ofepinephrine mirrored that for norepinephrine both at rest and duringexercise across age groups. It was concluded that in old subjects, areduction in norepinephrine clearance and an increase in regionalnorepinephrine spillover can account for the higher plasmanorepinephrine concentrations observed at rest. This relationship isnot exacerbated by the stress imposed during an acute bout of exercise.

     

Persistent sympathoexcitation long after submaximal exercise in subjects with and without coronary artery disease

There is an increased risk of cardiac events after exercise, which may, in part, be mediated by the sympathoexcitation that accompanies exercise. The duration and extent of this sympathoexcitation following moderate exercise is unknown, particularly in those with coronary artery disease (CAD). Twenty control subjects (mean age, 51 years) and 89 subjects with CAD (mean age, 58 years) underwent two 16-min bicycle exercise sessions followed by 30-45 min of recovery. Session 1 was performed under physiological conditions to peak workloads of 50-100 W. In session 2, parasympathetic blockade with atropine (0.04 mg/kg) was achieved at end exercise at the same workload as session 1. RR interval was continually recorded, and plasma catecholamines were measured at rest and selected times during exercise and recovery. Parasympathetic effect, measured as the difference in RR interval with and without atropine, did not differ between controls and CAD subjects in recovery. At 30 and 45 min of recovery, RR intervals were 12% and 9%, respectively, shorter than at rest. At 30 and 45 min of recovery, plasma norepinephrine levels were 15% and 12%, respectively, higher than at rest. A brief period of moderate exercise is associated with a prolonged period of sympathoexcitation extending >45 min into recovery and is quantitatively similar among control subjects and subjects with CAD, with or without left ventricular dysfunction. Parasympathetic reactivation occurs early after exercise and is also surprisingly quantitatively similar in controls and subjects with CAD. The role of these autonomic changes in precipitating cardiac events requires further evaluation.     

Determinants of resting energy expenditure in obese and non-obese children and adolescents

Resting energy expenditure (REE) is the largest component of total daily energy expenditure. Objectives of this study were to examine whether differences in REE exist after obesity develops in a group of children and adolescents, and to determine the effects of body composition, gender, age, pubertal development and parental obesity on REE. In 116 Caucasian children and adolescents (57 obese and 59 non-obese), aged 7.8 to 16.6 years, REE was assessed by open-circuit indirect calorimetry and different anthropometric variables and bioelectrical impedance were obtained (weight, height, skinfold thicknesses, waist and hip circumferences). Anthropometric indices and body compartments were calculated: the body mass index, surface area (SA), fat-free mass (FFM), fat-mass (FM) and percentage of FM. Differences between obese and non-obese subjects were tested and stepwise multiple regression analysis was performed with REE as dependent variable. Results show that REE was significantly higher in obese than in non-obese children and adolescents but REE/FFM ratio was not significantly different between these groups. In the non-obese group, FFM explained 73.1% of the variability in REE and gender, age and SA added 3.8%, 2.6%, and 2.6% to it, respectively. In the obese group, FFM was also the most powerful predictor of REE with 72.3%, followed by waist circumference and age with 2.5% and 2.1%, respectively. These results show that REE differences between obese and lean children do not seem to justify the maintenance of obesity. The main determinant of REE is FFM in both groups. No significant contribution of FM, pubertal development or parental obesity in REE was found in children and adolescents.     

Plasma visfatin concentrations in severely obese subjects are increased after intestinal bypass

Objective: Visfatin has shown to be increased in obesity and in type 2 diabetes. The aim of this study was to determine the change in plasma visfatin in severely obese (SO) persons after weight loss following bariatric surgery in relation to glucose concentration. Research Methods and Procedures: Visfatin and leptin were studied in 53 SO persons (BMI, 54.4 ± 6.8 kg/m²) before and 7 months after bariatric surgery and in 28 healthy persons (BMI, 26.8 ± 3.8 kg/m²). All of the patients underwent bariatric surgery with biliopancreatic diversion or gastric bypass. Results: The pre‐surgery levels of visfatin in the SO group were greater than in the control group (55.9 ± 39.9 vs. 42.9 ± 16.6 ng/mL, p = 0.024). This increase was significant in the SO group with impaired fasting glucose (63.4 ± 36.6 ng/mL) and diabetes (60.0 ± 46.0 ng/mL). SO patients with normal fasting glucose had similar levels of visfatin to the controls. Seven months after surgery, visfatin levels were significantly increased (84.8 ± 32.8 ng/mL, p < 0.001). This increase was independent of the pre‐surgical glucose levels. The type of bariatric surgery had no influence on visfatin levels. Post‐surgical visfatin was significantly correlated with the post‐surgery plasma concentrations of leptin (r = 0.39, p = 0.014). Discussion: Plasma levels of visfatin in the SO group were increased but only when accompanied by high glucose levels, even in the range of impaired fasting glucose. Bariatric surgery causes an increase in visfatin, which is correlated mainly with the changes produced in the leptin concentration.     

Attenuated thermoregulatory responses with increased plasma osmolality in obese subjects during two seasons

Obese subjects may be more vulnerable to injury from heat stress, and appear to be less efficient at thermoregulation. Sweat rate, tympanic temperature and osmolality in obese subjects were investigated in Japan during two seasons. The purpose of this study was to examine the relationship between obesity, thermoregulatory response and season. Five obese (BMI, 32.0?±?4.9 kg/m²) and five non-obese (BMI, 23.2?±?2.9 kg/m²) men participated in this experiment at latitude 35°10′ N and longitude 136°57.9′E. The average atmospheric temperature was 29.1?±?1.0 °C in summer and 3.3?±?1.4 °C in winter. Tympanic temperature and sweat rate were measured during leg water immersion at 42 °C for 30 min. Blood samples were analyzed for plasma osmolality. The relationship between tympanic temperature and sweat rate decreased significantly in obese compared to in non-obese subjects in both seasons, there being a lowered sweat rate for any core temperature in obese subjects. Plasma osmolality was significantly higher in obese than in non-obese subjects in both seasons. Thermal sensation increased significantly in non-obese than in obese in winter but not in summer. Our data show that thermoregulatory responses are attenuated in obese subjects compared with controls, suggesting that obese people are at increased risk of heat-related illnesses.     

Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure

Isnard, Richard, Philippe Lechat, Hanna Kalotka, HafidaChikr, Serge Fitoussi, Joseph Salloum, Jean-Louis Golmard, Daniel Thomas, and Michel Komajda. Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heartfailure. J. Appl. Physiol. 81(6):2571-2579, 1996.Blood flow to working skeletal muscle is usuallyreduced during exercise in patients with congestive heart failure. Anintrinsic impairment of skeletal muscle vasodilatory capacity has beensuspected as a mechanism of this muscle underperfusion during maximalexercise, but its role during submaximal exercise remains unclear.Therefore, we studied by transcutaneous Doppler ultrasonography thearterial blood flow in the common femoral artery at rest and during asubmaximal bicycle exercise in 12 normal subjects and in 30 patientswith heart failure. Leg blood flow was lower in patientsthan in control subjects at rest [0.29 ± 0.14 (SD) vs. 0.45 ± 0.14 l/min, P < 0.01], at absolute powers and at the same relative power (2.17 ± 1.06 vs. 4.39 ± 1.4 l/min, P < 0.001). Because mean arterial pressure was maintained, leg vascularresistance was higher in patients than in control subjects at rest (407 ± 187 vs. 247 ± 71 mmHg ^· l^{1 ·} min,P < 0.01) and at thesame relative power (73 ± 49 vs. 31 ± 13 mmHg ^· l^{1 ·} min,P < 0.01) but not at absolutepowers. Although the magnitude of increase in leg blood flow correctedfor power was similar in both groups (31 ± 10 vs. 34 ± 10 ml ^· min^{1 ·} W¹),the magnitude of decrease of leg vascular resistance corrected forpower was higher in patients than in control subjects (5.9 ± 3.3 vs. 1.9 ± 0.94 mmHg ^· l^{1 ·} min ^· W¹,P < 0.001). These results suggestthat the ability of skeletal muscle vascular resistance to decrease isnot impaired and that intrinsic vascular abnormalities do not limitvasodilator response to submaximal exercise in patients with heartfailure.

     

Prolonged submaximal exercise and L-carnitine in humans

Changes in the main physiological parameters and circulating indicators of carbohydrate, protein, lipid (and ketone body) metabolism were measured in ten exercising subjects before L-carnitine (L-carn) loading, after 4 weeks of daily loading with 2 g L-carn, and 6-8 weeks after terminating L-carn administration. Measurements were made on venous blood samples collected during each experiment at fixed time intervals over an initial rest of 45 min, 60 min bicycle exercise performed near 50% VO2max and 120 min recovery. Free and total plasma carnitine levels reached a plateau corresponding to an average rise of 25% for both fractions, 9-10 days after the beginning of the L-carn diet. These levels returned to their initial values 6-8 weeks after cessation of the supply. Generally L-carn supplementation did not significantly modify the physiological parameters and circulating metabolites. No distinct increase of the relative participation of endogenous lipids in the fuel supply of prolonged submaximal exercise was observed. In normal human subjects the increased demand for fatty acid oxidation resulting from exercise seems to be adequately supported by endogenous levels of carnitine.     

External load can alter the energy cost of prolonged exercise

The present study was undertaken to examine the energy cost of prolonged walking while carrying a backpack load. Six trained subjects were tested while walking for 120 min on a treadmill at a speed of 1.25 m.s-1 and 5% elevation with a well fitted backpack load of 25 and 40 kg alternately. Carrying 40 kg elicited a significantly higher (p less than 0.01) energy cost than 25 kg. Furthermore, whereas carrying 25 kg resulted in a constant energy cost, 40 kg yielded a highly significant (p less than 0.05) increase in energy cost over time. The study implies that increase in load causes physical fatigue, once work intensity is higher than 50% maximal work capacity. This is probably due to altered locomotion biomechanics which in turn lead to the increase in energy cost. Finally, the prediction model which estimates energy cost while carrying loads should be used with some caution when applied to heavy loads and long duration of exercise, since it might underestimate the actual energy cost.     

Effect of acute exercise on glycogen synthase in muscle from obese and diabetic subjects

Insulin stimulates glycogen synthase (GS) through dephosphorylation of serine residues, and this effect is impaired in skeletal muscle from insulin-resistant [obese and type 2 diabetic (T2DM)] subjects. Exercise also increases GS activity, yet it is not known whether the ability of exercise to affect GS is impaired in insulin-resistant subjects. The objective of this study was to examine the effect of acute exercise on GS phosphorylation and enzyme kinetic properties in muscle from insulin-resistant individuals. Lean normal glucose-tolerant (NGT), obese NGT, and obese T2DM subjects performed 40 min of moderate-intensity cycle exercise (70% of Vo(2max)). GS kinetic properties and phosphorylation were measured in vastus lateralis muscle before exercise, immediately after exercise, and 3.5 h postexercise. In lean subjects, GS fractional activity increased twofold after 40 min of exercise, and it remained elevated after the 3.5-h rest period. Importantly, exercise also decreased GS K(m) for UDP-glucose from ≈0.5 to ≈0.2 mM. In lean subjects, exercise caused significant dephosphorylation of GS by 50-70% (Ser(641), Ser(645), and Ser(645,649,653,657)), and phosphorylation of these sites remained decreased after 3.5 h; Ser? phosphorylation was not regulated by exercise. In obese NGT and T2DM subjects, exercise increased GS fractional activity, decreased K(m) for UDP-glucose, and decreased GS phosphorylation as effectively as in lean NGT subjects. We conclude that the molecular regulatory process by which exercise promotes glycogen synthesis in muscle is preserved in insulin-resistant subjects.     

Physical activity and energy expenditure in lean and obese adult human subjects.

We compared the physical activity of 11 lean and 11 obese men and women over a 7-day period. There were no significant differences in either the amount of movement recorded with an accelerometer (9.5 (SD 3.9) vs 9.9 (SD 2.6) kcounts.day-1), or in the energy expenditure due to physical activity reflected by the difference between the average daily metabolic rate measured by the doubly labelled water technique and the sleeping metabolic rate measured in a respiration chamber and adjusted for fat-free mass: 112 (SD 33) vs 118 (SD 22) kJ.kg-1.day-1. The obese showed a non-significant loss of body mass of 0.5 (SD 1.1) kg, probably due to reduced intake during the 7-day intake recording period.