Kinetics of catecholamines and potassium,
and heart rate during exercise
testing in obese subjects

Salvadori, Alberto; Fanari, Paolo; Giacomotti, Emanuela; Palmulli, Patrizia; Bolla, G.; Tovaglieri, Ilaria; Luzi, Livio; Longhini, E

doi:10.1007/s00394-003-0409-3

Cited by 27 publications

(31 citation statements)

References 30 publications

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“…Hypertrophy may depend on an increased amount of work that is required to move heavier bodies. In agreement with data from a previous study [26], lower maximal plasma K + levels were observed in the obese subjects during maximal exercise. It is conceivable that a difference of K + , if any, should be in the opposite direction than that observed, due to the larger muscular mass of obese subjects releasing K + (increased FFM, higher values of creatine kinase [27]).…”

Section: Discussionsupporting

confidence: 82%

Ventilation and Its Control during Incremental Exercise in Obesity

et al. 2006

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Background: In obesity, the addition of mass loading of the chest wall by adipose tissue decreases compliance, but its ventilation does not seem to be a limiting factor to physical performance. Plasma K⁺ and lactic acid are considered important determinants of ventilation during exercise. Obesity is characterized by insulin resistance. Objectives: The aim of this study was to assess ventilatory adaptations to sustained effort and the effects of lactic acid and potassium in young obese subjects. Methods: Twelve obese subjects with a body mass index of 40 (mean age 27 years, 6 males) and 12 normal subjects with a body mass index of 22 (aged 28 years, 6 males) performed a progressive cycloergometric test with increases of 20 W every 4 min to exhaustion while minute ventilation, oxygen consumption, carbon dioxide production, end-tidal oxygen pressure, and end-tidal carbon dioxide pressure were measured. Blood samples were collected at the end of every step to determine plasma K⁺. Lactic acid was measured at rest, 40, 80, 120 W and peak exercise (or only at peak exercise if <120 W). Before each exercise, we tested insulin sensitivity using the quantitative insulin sensitivity check index. Results: Obese subjects had lower insulin sensitivity (0.318 vs. 0.345, p < 0.01). Peak exercise was not significantly different between both groups (125 W in the obese group vs. 137 W in the control group), but the ventilatory threshold was at lower power output in the obese group compared to the controls (76 vs. 107 W, p < 0.05). Ventilation increased less in the obese group but oxygen saturation of hemoglobin remained within normal limits up to exhaustion in both groups. Ventilation was appropriate for the CO₂ increase but less appropriate for the increased O₂ consumption. Both K⁺ and lactic acid increased less in the obese group. Conclusions: In our obese subjects, ventilation was not a limiting factor during exercise. Its lower increase may be due, in addition to the characteristics of their chest walls, to insulin resistance which may limit the increase in lactic acid during effort, and to the hypertrophy of muscle fibers previously noted, which may be linked to a lower increase in plasma K⁺ during physical exercise.

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Section: Discussionsupporting

confidence: 82%

Ventilation and Its Control during Incremental Exercise in Obesity

et al. 2006

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“…36 On the other hand, other studies show that although many obese individuals have normal "resting" levels of NE, they exhibit significant differences in NE induction following stress. 37 In addition, obesity has been associated with cellular resistance to NE and other adrenergic agonists. 38 In some tissues, this is due to decreased adrenoceptor expression.…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine regulates hepatic innate immune system in leptin-deficient mice with nonalcoholic steatohepatitis

Oben

Yang

et al. 2004

Hepatology

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It is not known why natural killer T (NKT) cells, which modulate liver injury by regulating local cytokine production, are reduced in leptin-deficient ob/ob mice. NKT cells express adrenoceptors. Thus, we hypothesize that the low norepinephrine (NE) activity of ob/ob mice promotes depletion of liver NKT cells, thereby sensitizing ob/ob livers to lipopolysaccharide (LPS) toxicity. To evaluate this hypothesis, hepatic NKT cells were quantified in wild-type mice before and after treatment with NE inhibitors, and in dopamine ␤-hydroxylase knockout mice (which cannot synthesize NE) and ob/ob mice before and after 4 weeks of NE supplementation. Decreasing NE activity consistently reduces liver NKT cells, while increasing NE has the opposite effect. Analysis of hepatic and thymic NKT cells in mice of different ages demonstrate an age-related accumulation of hepatic NKT cells in normal mice, while liver NKT cells become depleted after birth in ob/ob mice, which have increased apoptosis of hepatic NKT cells. NE treatment inhibits apoptosis and restores hepatic NKT cells. In ob/ob mice with reduced hepatic NKT cells, hepatic T and NKT cells produce excessive T helper (Th)-1 proinflammatory cytokines and the liver is sensitized to LPS toxicity. NE treatment decreases Th-1 cytokines, increases production of Th-2 cytokines, and reduces hepatotoxicity. Studies of CD1d-deficient mice, which lack the receptor required for NKT cell development, demonstrate that they are also unusually sensitive to LPS hepatotoxicity. In conclusion, low NE activity increases hepatic NKT cell apoptosis and depletes liver NKT cells, promoting proinflammatory polarization of hepatic cytokine production that sensitizes the liver to LPS toxicity. (HEPATOLOGY 2004;40:434 -441.)

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“…Others have described higher resting heart rate but decreased maximal heart rate in overweight adults, 38,40 which may be attributable to decreased maximal catecholamine responses. 21,41 To our knowledge, this is the first report of a significant relationship between HRR and fitness and performance in overweight adolescents. Additional study, including detailed measurement of cardiac function, is needed to clarify whether cardiac impairment (or the initial stages of impairment) may exist in severely overweight adolescents.…”

Section: E694mentioning

confidence: 99%

“…Other reports have suggested that both deconditioning and obesity may reduce maximal heart rate. 21,27,39,40,41 Because of their higher resting heart rate and lower maximal …”

mentioning

confidence: 99%

Influence of Excess Adiposity on Exercise Fitness and Performance in Overweight Children and Adolescents

et al. 2005

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ABSTRACT. Objective. Relatively little is known about how excess body mass affects adolescents' capacity to perform sustained exercise. We hypothesized that most of the difficulty that severely overweight adolescents have with sustained exercise occurs because the metabolic costs of moving excess mass result in use of a high proportion of their total oxygen reserve.Methods. We compared results from a maximal cycle ergometry fitness test in 129 severely overweight adolescents who had BMIs of 41.5 ؎ 9.7 kg/m 2 and ages of 14.5 ؎ 1.8 years (range: 12.1-17.8 years) and 34 nonoverweight adolescents who had BMIs of 20.1 ؎ 2.9 kg/m 2 and ages of 14.5 ؎ 1.5 years (range: 12.0 -18.1 years). Oxygen uptake (V O 2 ) was compared at 3 times: during a 4-minute period of unloaded cycling (ULV O 2 ), at the lactate threshold estimated by gas exchange (LTV O 2 ), and at maximal exertion (V O 2 max). Heart rate was obtained at rest and at V O 2 max. Participants also completed a 12-minute walk/ run performance test to obtain distance traveled (D12) and heart rate. Results. Absolute LTV O 2 and V O 2 max and LTV O 2 as a percentage of V O 2 max were not different in overweight and nonoverweight adolescents during the cycle test.However, absolute ULV O 2 was significantly greater in overweight adolescents: ULV O 2 accounted for 35 ؎ 8% of V O 2 max (and 63 ؎ 15% of LTV O 2 ) in overweight adolescents but only 20 ؎ 5% of V O 2 max (and 39 ؎ 12% of LTV O 2 ) in nonoverweight adolescents. Resting heart rate before initiating the cycle test was significantly greater in overweight than nonoverweight adolescents (94 ؎ 14 vs 82 ؎ 15 beats per minute). However, maximal heart rate during the cycle test was significantly lower in overweight adolescents (186 ؎ 13 vs 196 ؎ 11 beats per minute). During the walk/run test, mean D12 was significantly shorter for overweight than for nonoverweight adolescents (1983 ؎ 323 vs 1159 ؎ 194 m). D12 was negatively related to BMI SDS (r ‫؍‬ ؊0.81) and to ULV O 2 (r ‫؍‬ ؊0.98).Discussion. Overweight and nonoverweight adolescents had similar absolute V O 2 at the lactate threshold and at maximal exertion, suggesting that overweight adolescents are more limited by the increased cardiorespiratory effort required to move their larger body mass through space than by cardiorespiratory deconditioning. ABBREVIATIONS. V o 2 max, maximum oxygen uptake; SDS, SD score; ULV o 2 , unloaded oxygen uptake; LTV o 2 , oxygen uptake at the lactate threshold; V o 2 max, oxygen uptake at maximal exertion; HRR, heart rate reserve; RPE, rating of perceived exertion; bpm, beats per minute; D12, distance achieved at 12 minutes during walk/run test; ANCOVA, analysis of covariance. O verweight during childhood has been identified as a major health problem in the United States. 1-4 Pediatric overweight commonly presages adult obesity 5 and is associated with the development of weight-related comorbid conditions and increased morbidity. [6][7][8] Decreased physical activity and a more sedentary lifestyle have been implicated as importan...

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Kinetics of catecholamines and potassium, and heart rate during exercise testing in obese subjects

Cited by 27 publications

References 30 publications

Ventilation and Its Control during Incremental Exercise in Obesity

Ventilation and Its Control during Incremental Exercise in Obesity

Norepinephrine regulates hepatic innate immune system in leptin-deficient mice with nonalcoholic steatohepatitis

Influence of Excess Adiposity on Exercise Fitness and Performance in Overweight Children and Adolescents

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