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. 2023 Jul 18;28(6):721–729. doi: 10.1007/s12192-023-01364-7

Influence of body composition and cardiorespiratory fitness on plasma HSP72, norepinephrine, insulin, and glucose responses to an acute aerobic exercise bout performed in the fed state

Carlos Henrique de Lemos Muller 1, Cesar Eduardo Jacintho Moritz 2,5, Helena Trevisan Schroeder 1, Ana Maria Oliveira Battastini 3, Alvaro Reischak-Oliveira 2, Paulo Ivo Homem de Bittencourt Júnior 1, Giuseppe De Vito 4, Maurício Krause 1,✉
PMCID: PMC10746641  PMID: 37462825

Abstract

Being overweight is already considered a metabolic risk factor, which can be overcome by increasing cardiorespiratory fitness (CRF). Acute exercise is known to induce changes in plasma hormones and heat shock proteins release. However, there is a lack of studies investigating the impact of body composition and CRF on these variables following acute aerobic exercise. To assess the influence of body composition and cardiorespiratory fitness on plasma heat shock protein 72 kDa (HSP72), norepinephrine (NE), insulin, and glucose responses to an acute aerobic exercise bout in the fed state. Twenty-four healthy male adults were recruited and allocated into three groups: overweight sedentary (n = 8), normal weight sedentary (n = 8), and normal weight active (n = 8). The volunteers performed an acute moderate exercise session on a treadmill at 70% of VO2 peak. Blood samples were drawn at baseline, immediately post-exercise, and at 1-h post-exercise. The exercise session did not induce changes in HSP72 nor NE but changes in glucose and insulin were affected by body mass index. Also, subjects with elevated CRF maintain reduced NE through exercise. At baseline, the overweight sedentary group showed elevated NE, insulin, and glucose; these last two impacting the HOMA-IR index. Thirty minutes of aerobic exercise at 70% VO2 peak, in the fed state, did not change the levels of plasma NE and HSP72. Elevated body composition seems to impact metabolic profile and increase sympathetic activity. Conversely, subjects with increased cardiorespiratory fitness seem to have attenuated sympathetic activity.

Keywords: HSP72, Norepinephrine, Aerobic exercise, Overweight, Physically active, Fed state

Introduction

Overweight and obesity have increased in the last decades around the world (Collaborators 2018). Projections show that, by 2030, the prevalence of obesity will reach 1 billion people globally (Lobstein and Jewell 2022). However, even overweight is already considered a metabolic risk factor (Collaborators 2018). It has been demonstrated that overweight people have an increased risk for diabetes (Twig et al. 2014) and cardiovascular disease (Opio et al. 2020), even in the absence of metabolic abnormalities.

Subjects with elevated adipose tissue often have low cardiorespiratory fitness (CRF) (Laukkanen et al. 2009), which is also associated with premature mortality (Global et al. 2016). In the same way, the improvement in CRF is related to reduced mortality risk (de Lannoy et al. 2019) and can be achieved by increasing the level of physical activity (PA) (Ross et al. 2016). Especially, higher levels of PA during leisure time and performing a sport were also associated with higher CRF (Bahls et al. 2021).

Following an exercise bout, adaptations in the cardiovascular, endocrine, and autonomic nervous system happen to provide an appropriate energy supply for working muscles (Vettor et al. 1997). In this way, the sympathetic nervous system (SNS)–derived norepinephrine (NE) is involved in increasing heart rate, cardiac contractility, and in substrate mobilization and utilization during exercise (Zouhal et al. 2013). As a counterregulatory hormone, NE also reduces insulin secretion by pancreatic beta cells (Zouhal et al. 2008), which implicates a diminished blood insulin concentration (Lobstein and Jewell 2022). The exercise-induced response of these hormones directly impacts blood glucose concentration. This fuel source is tightly regulated by hepatic glucose production and glucose peripheral uptake, then maintaining blood glucose homeostasis (van Vliet et al. 2020).

Beyond the hormonal response, an exercise session also culminates in the induction of heat shock proteins (HSPs) (Noble et al. 2008). In particular, exercise induces an increase in the circulation of the 72 kDa member of the 70 kDa family of heat shock proteins (HSP70) (Noble et al. 2008). During exercise, this protein is released to the extracellular environment by peripheral blood mononuclear cells (PBMC) (de Lemos Muller et al. 2018), but mainly from hepatosplanchnic viscera (Febbraio et al. 2002), through a NE-dependent mechanism, activating immunological responses (Asea et al. 2002), exerting an anti-inflammatory response post-exercise (Ortega et al. 2012), and participating on the motoneurons protection (Krause and Rodrigues-Krause Jda 2011).

Exercise produces changes in metabolic, hormonal, and HSP72 responses, but studies investigating how body composition and CRF modulate these responses are scarce, particularly in the feed state. Regarding NE, studies have investigated differences between trained and untrained subjects in this response (Zouhal et al. 2008) or the effect of obesity only (Zouhal et al. 2013). For insulin and glucose, studies have assessed the effect of BMI, but not CRF (Vettor et al. 1997; Yale et al. 1989). In addition, studies investigating plasma HSP72 have seen how obesity impact in basal release of this protein (Rodrigues-Krause et al. 2012) or the effect of physical activity (Simar et al. 2007) as well as training (Fehrenbach et al. 2000) in the HSP72 expression in leukocytes.

Therefore, this study aimed to assess the influence of body composition and cardiorespiratory fitness on plasma HSP72, norepinephrine, insulin, and glucose responses to an acute aerobic exercise bout performed in the fed state. We choose to test the effects of 30 min of exercise considering the type of population involved (sedentary and overweight adults) and following the recommendation of The American College of Sport Medicine’s (ACSM—general exercise guidelines), which suggests a minimum of 30 min, five times a week, for moderate-intensity aerobic activity.

Methods

Participants

Volunteers in the study were participants of a previous study into the effect of acute exercise on the activity of soluble purinergic enzymes (Moritz et al. 2021). All participants were aged between 18 and 30 years, non-smokers, had no previous cardiovascular, orthopedic, or metabolic disorders, and had not received pharmacological treatment for at least 30 days. A history of alcohol abuse (≥ 2 doses per day) was considered an exclusion criterion. The participants were instructed to abstain from caffeine for ≥ 12 h before the test.

Twenty-four healthy male adults were recruited and divided into three groups: overweight sedentary (n = 8), normal weight sedentary (n = 8), and normal weight active (n = 8). For each group, the following inclusion criteria were adopted: (1) overweight sedentary (OWS): body mass index (BMI) 25–29.9 km/m2, had not been involved in any exercise program for at least 6 months and peak oxygen uptake (VO2 peak) < 40 ml/kg/min; (2) normal weight sedentary (NWS): BMI 18.5–24.9 km/m2, had not been involved in any exercise program for at least 6 months and VO2 peak 40–45 ml/kg/min; (3) normal weight active (NWA): BMI 18.5–24.9 km/m2, had been performing at least 3 h of exercise per week for a minimum of 6 months, and VO2 peak > 45 ml/kg/min. All participants signed the written informed consent statement containing the research proposal. The study was approved by the Ethics Committee of the Universidade Federal do Rio Grande do Sul (protocol number 79422417.2.0000.5347) and was conducted according to the Declaration of Helsinki, except for registration in a database.

Study design

The volunteers attended the Exercise Research Laboratory of the Universidade Federal do Rio Grande do Sul (Porto Alegre, Brazil) on two different occasions to perform the experimental protocol. On the first day, all participants were clinically assessed, and data about disease history, pharmacological treatment, diet, and usual exercise activities were collected. Then, subjects with a previous or familial condition that could affect the results were excluded from the study. Likewise, all participants answered the Physical Activity Readiness Questionnaire (PAR-Q) (Shephard 1988), which was applied to ensure that only individuals with a proper health conditions were included in the study. The body composition was assessed using the five-components method, based on the anatomical site markings and the technique of measuring skinfolds, according to the standards of the International Society for the Advancement of Kinanthropometry (ISAK) (Clarys et al. 2006).

The workload of our acute exercise protocol was determined through an incremental cardiopulmonary exercise test performed on a treadmill. VO2 peak was determined by the breath-by-breath method, using an open-circuit spirometry system (Quark CPET, Cosmed, Rome, Italy). Heart rate (HR) was continuously measured by a telemetric band (Polar Electro Oy, Kempele, Finland). The warm-up consisted of 3 min of walking at 5 km/h and was followed by increases of 1 km/h every minute until exhaustion. The recovery period consisted of 3 min of walking at 5 km/h. Volunteers were verbally encouraged to perform at maximum effort during the test.VO2 peak was identified as the highest value in a line of tendency plotted against time (Dekerle et al. 2003; Wasserman and McIlroy 1964).

On the second day of the experimental protocol, 1 week after the first assessment, participants arrived fasted at the laboratory for a basal sample collection (pre-exercise). Afterward, they received a standard meal composed of 0.5 g/kg carbohydrates (overweight sedentary: total calories 329.15 ± 26.25 kcal, carbohydrates 42.46 ± 4.02 g, proteins 21.02 ± 1.83 g, fats 8.37 ± 0.31 g; normal weight sedentary: total calories 304.69 ± 11.98 kcal, carbohydrates 38.71 ± 1.83 g, proteins 19.31 ± 0.83 g, fats 8.07 ± 0.14 g; normal weight active: total calories 299.8 ± 29.35 kcal, carbohydrates 37.96 ± 4.5 g, proteins 18.97 ± 2.05 g, fats 8.02 ± 0.35 g) and remained at rest for 30 min. Then, the participants performed 30 min of aerobic exercise on a treadmill at 70% of VO2 peak, which was continuously monitored by the open-circuit spirometry system. Blood samples were obtained again immediately and 1 h after the exercise session.

Blood sample collection

Venous blood samples (10 ml) were collected from the antecubital vein with heparin anticoagulant tubes. This was done pre-exercise, after at least 8 h of fasting, immediately post-exercise, and 1 h after the exercise session. The blood was centrifuged at 4 °C, 1500 g for 10 min. Then, the plasma sample was collected and stored at − 80 °C for subsequent analysis.

General biochemistry

Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), and glucose were assessed using an automated enzymatic colorimetric method (Cobas C111, Roche Diagnostics, Basel, Switzerland). Low-density lipoprotein cholesterol (LDL-C) was calculated by the Friedewald equation (Friedewald et al. 1972). The homeostatic model of insulin resistance index (HOMA-IR) was calculated by the formula: HOMA-IR = fasting plasma insulin (µU/ml) × fasting plasma glucose (mmol/l) / 22.5 (Matthews et al. 1985).

Plasma HSP72 (eHSP72), insulin, and NE quantification

Plasma HSP72 protein was quantified using a highly sensitive, enzyme-linked immunosorbent (ELISA) assay method, according to the manufacturer’s instructions (EKS-715 Stressgen, Victoria, Canada). Insulin was evaluated by enzyme-linked immunosorbent assay, according to the manufacturer’s instructions (90,095 Crystal Chem, Elk Grove Village, IL, USA). NE was determined by ELISA method according to the manufacturer’s instructions (EU2565 Fine Test, Wuhan, Hubei, China). HSP72, NE, and insulin were analyzed in a microplate reader (Multiskan Go, Thermo Scientific, Waltham, USA).

Total area under the curve estimation

HSP72, NE, insulin, and glucose responses during the experimental session were assessed by the estimation of the total area under the curve (AUC), using the trapezoidal method (Tai 1994).

Statistical analysis

The possible distributions for dependent variables were normal and gamma. These two distributions were compared using the goodness of fit, the Akaike information criteria (AIC) for generalized linear model (GZLM), or quasi-likelihood under independence model criteria (QIC) for generalized estimating equation (GEE). The distribution was defined according to the lower value in AIC or QIC, which means that model has better adherence to the data. Then, the variables age, weight, body mass, BMI, muscle mass, fat mass, waist and hip circumference, maximum heart rate, V̇O2 peak, TC, TG, and LDL were analyzed by GZLM with normal distribution. Also, basal measurements of glucose, NE, and plasma HSP72 were assessed by GZLM with the same distribution. The GZLM with gamma distribution was used to analyze the variables heart rate rest, HDL, HOMA-IR, basal insulin, glucose AUC, insulin AUC, NE AUC, and plasma HSP72 AUC. The variables related to the exercise session were assessed by GEE. As a result, glucose, NE, and insulin were assessed with gamma distribution, but plasma HSP72 was evaluated with normal distribution. For all variables, post hoc comparisons were done with Bonferroni test. Pearson’s correlation was used to determine the correlation between rest heart rate (HR) and basal NE. Results are expressed as means and 95% confidence interval (CI) and differences were considered to be significant when p ≤ 0.05.Statistical Package for Social Sciences (IBM SPSS v.25.0, Armonk, NY, USA) was used for data analysis and graphs were done with GraphPad Prism Software (v.8.0, San Diego, CA, USA).

Results

Participant’s characteristics

As depicted in Table 1, there are no differences regarding volunteers’ age, height, muscle mass, and maximum heart rate among groups. However, body mass and BMI were higher in OWS in comparison to NWS and active groups. Likewise, the OWS group had higher waist and hip circumferences than the other two groups. Fat mass was also higher in OWS, compared to both normal weight groups. Interestingly, the body fat percentage was only higher in OWS than NWA individuals. The rest heart rate was also higher in OWS in comparison to NWA, but not compared to NWS. The VO2 peak values were higher for NWA, compared to both sedentary groups, and in NWS the values were also higher in comparison to OWS.

Table 1.

Subjects characteristics (n = 24)

Overweight sedentary
(n = 8)		 Normal weight sedentary
(n = 8)		 Normal weight active
(n = 8)		 GZLM
GROUP
Age (years) 25.75 [23.31–28.19] 26.37 [23.89–28.86] 23.12 [20.46–25.79] p = 0.051
Height (m) 1.75 [1.70–1.80] 1.78 [1.72–1.83] 1.78 [1.72–1.83] p = 0.558
Body mass (kg) 85.02 [80.05–90.00] *# 74.16 [62.02–82.31] 75.01 [68.66–83.09] p = 0.010
BMI (kg/m2) 27.75 [26.69–28.82] *# 23.40 [21.72–25.11] 23.65 [22.77–25.03] p < 0.001
Muscle mass (kg) 37.87 [36.03–39.72] 33.20 [28.40–38.00] 35.50 [30.28–40.72] p = 0.142
Fat mass (kg) 27.41 [24.08–30.74] *# 19.65 [15.22–24.08] 18.21 [14.84–21.59] p < 0.001
Fat mass (%) 31.92 [29.47–34.38] * 27.09 [22.46–31.74] 25.01 [20.27–29.75] p = 0.008
Waist circumference (mm) 91.24 [86.36–96.11] *# 79.39 [73.97–84.91] 79.18 [75.41–82.94] p < 0.001
Hip circumference (mm) 102.4 [99.26–105.6] *# 95.48 [87.62–103.3] 95,69 [91.68–99.69] p = 0.008
HR rest (beats/min) 73.75 [66.47–81.03] * 66.87 [61.79–71.96] 64.50 [58.62–70.38] p = 0.021
HR max (beats/min) 183.5 [173.5–193.5] 187.5 [178.3–196.7] 192.6 [187.2–198.0] p = 0.153
VO2 peak (ml/kg/min) 38.82 [36.75–40.91] *# 43.96 [43.04–44.88] * 50.30 [48.35–52.27] p < 0.001
Cholesterol (mg/dl) 172 [151.4–192.9] 171.7 [143.5–199.8] 153.6 [126.3–181.0] p = 0.338
Triglycerides (mg/dl) 108 [94.01–123.9] *# 67.11 [56.72–77.51] 71.31 [55.70–86.93] p < 0.001
HDL-C (mg/dl) 50.34 [44.96–55.73] 53.05 [41.66–64.44] 50.93 [43.41–58.45] p = 0.839
LDL-C (mg/dl) 98.64 [71.31–120] 103.9 [78.23–129.7] 89.85 [67.83–111.9] p = 0.545
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Descriptive data as reported as mean and 95% confidence interval. BMI, body mass index; HR, heart rate; HDL, high-density lipoprotein cholesterol; LDL, low-density lipoprotein cholesterol; VO2 peak, peak oxygen uptake. * Difference from normal weight active (p < 0.05). # Difference from normal weight sedentary (p < 0.05)

Biochemical parameters

Table 1 also shows the results for the lipid profile. For total cholesterol, HDL-C, and LDL-C, no differences were found among the groups. On the other hand, triglycerides and basal glucose levels were higher in overweight sedentary in comparison to both normal weight groups.

Basal measurements

The basal values for NE, insulin, glucose, HOMA-IR, and plasma HSP72 are shown in Table 2. In OWS, NE and glucose values were elevated in comparison to NWS and active group. Insulin and HOMA-IR were higher in OWS than NWS, but not compared to NWA group. For plasma HSP72, no differences were found among groups. The correlation analysis between rest HR and basal NE was not significant (r = 0.365, p = 0.124).

Table 2.

Basal measurements

Overweight sedentary
(n = 8)		 Normal weight sedentary
(n = 6)		 Normal weight active
(n = 6)		 GZLM
GROUP
Norepinephrine (pg/ml) 312.00 [226.5–397.6] *# 192.00 [58.23–325.9] 85.72 [26.69–144.7] p < 0.001
Glucose (mg/dl) 101.2 [96.17–106.30] *# 89.62 [84.08–95.17] 92.73 [87.95–95.51] p < 0.001
Insulin (µU/ml) 8.25 [3.57–12.94] # 4.17 [3.08–5.27] 5.80 [3.56–8.05] p = 0.024
HOMA-IR 2.09 [0.82–3.53] # 0.90 [0.67–1.13] 1.33 [0.80–1.86] p = 0.006
eHSP72 (ng/ml) 0.27 ± 0.28 0.97 ± 1.16 1.85 ± 2.06 p = 0.084
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Descriptive data as reported as mean and 95% confidence interval for all groups with exception for eHSP72 reported as mean and standard deviation. eHSP72, extracellular heat shock protein 72; HOMA-IR, homeostasis model assessment for insulin resistance. For glucose (n = 8) for all groups. * Difference from normal weight active (p < 0.05). # Difference from normal weight sedentary (p < 0.05)

Experimental protocol

Results of HSP72, NE, insulin, and glucose and their AUC are shown in Figs. 1 and 2. In this study, neither NE (p = 0.311) nor insulin (p = 0.088) nor glucose (p = 0.848) were considered good predictors for HSP72 release. For NE, there was no time effect (p = 0.058) or group x time interaction (p = 0.990). However, a group effect was observed (p < 0.001), with lower levels of NE for normal weight active in comparison to both sedentary groups. Concerning NE AUC, this same difference was verified among groups. Different from what we expected, no differences were observed in plasma HSP72 for any of the parameters evaluated (effect of time, group, or time x group interaction). Similarly, no differences among groups were found in HSP72 AUC.

Fig. 1.

Fig. 1

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Plasma HSP72 concentration (a), norepinephrine concentration (c), and the respective area under the curve (AUC) (b, d) in response to an aerobic exercise bout. Representative data are reported as mean with 95% confidence interval. * (p < 0.05), ** (p < 0.01), *** (p < 0.001)

Fig. 2.

Fig. 2

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Plasma insulin concentration (a), glucose concentration (c), and the respective area under the curve (AUC) (b, d) in response to an aerobic exercise bout. Representative data are reported as mean with 95% confidence interval. Significant difference: * (p < 0.05), ** (p < 0.01), *** (p < 0.001)

In contrast, there was a time effect (p < 0.001) for insulin levels, which was increased post-exercise and remained increased at 1-h post-exercise. Moreover, there was a group effect (p = 0.029), with higher insulin levels observed in OWS than NWS. A group x time interaction (p = 0.011) was also found, with differences observed in OWS group between pre- and post-exercise. In insulin AUC, differences among groups were verified, with OWS having higher levels in comparison to both normal weight groups. For glucose levels, no group effect (p = 0.169) was observed. Nonetheless, a time effect (p < 0.001) was found, with an increase post-exercise, but reducing at 1-h post-exercise. Also, a group x time interaction (p < 0.001) was found. This showed a difference between overweight and normal weight sedentary groups at pre-exercise; in overweight sedentary group among pre and post-exercise in comparison to 1-h post-exercise; in normal weight sedentary between pre and post-exercise; in normal weight active among pre-exercise with immediate post and 1-h post-exercise. In glucose AUC, no difference was observed among groups.

Discussion

The main finding of this study was that exercise, in the fed state, did not induce an increase in plasma HSP72 and NE, irrespective of BMI or CRF. Although NE did not augment, participants with elevated CRF maintain reduced plasma NE in the aerobic exercise session. Another finding was that, following exercise, subjects with reduced BMI (lower fat mass) showed an increase in glucose levels and those in the overweight sedentary group exhibited augmented insulin concentration. Finally, subjects with elevated BMI (higher fat mass) and reduced cardiorespiratory fitness had higher NE, glucose, and insulin levels at rest, which also impacted an elevated HOMA-IR.

In this study, we did not observe an exercise-induced eHSP72 elevation. The result is in contrast to earlier findings that demonstrated an increase of eHPS72 after exercise (Febbraio et al. 2002; Walsh et al. 2001). However, different from our protocol, the subjects were exercised in the fast state. As Febbraio and co-workers previously showed, glucose ingestion attenuates plasmatic HSP72 increase caused by exercise (Fehrenbach et al. 2005). According to the authors, this result is partially explained by diminished hepatosplanchnic HSP72 liberation because hepatic stress is reduced when glucose is ingested (Febbraio et al. 2004; Fehrenbach et al. 2005). Another possible explanation is the insufficient duration of exercise to elicit an eHSP72 increase. Studies have shown a plasmatic increase of this protein using exercise protocols ranging from 60 to 180 min (Febbraio et al. 2002; Lancaster et al. 2004; Walsh et al. 2001). This response appears to be intensity and duration-dependent (Fehrenbach et al. 2005). Thus, in our study, the meal consumption, as well as the exercise duration (30 min), may explain the incapacity of exercise to induce eHSP72 elevation.

In our hands, 30 min of aerobic exercise at 70% VO2 peak did not change the levels of plasma NE. It is expected that exercise increases circulating NE with intensities higher than 50% VO2 max (Peinado et al. 2014). Then, the intensity used in the present study would be expected to elicit an increase in NE. However, volunteers who performed exercise in a fed state (2 h after receiving a meal) had attenuated NE response than those who exercised in a fast state (Pequignot et al. 1980). Thus, it may be possible that the meal given 30 min before exercise affected the NE response.

Glucose and insulin responses were also investigated during the aerobic exercise session in a fed state. We verified that differences in BMI seem to affect the glucose and insulin response. Using meta-regression, a systematic review and meta-analysis verified that BMI did not impact in insulin and glucose response after exercise (Frampton et al. 2021). However, this analysis was performed with studies that used fed and fast state together. Then, it is possible that by assessing only studies in the fed state this response could be different. Exercise in the fed state induces hyperglycemia and hyperinsulinemia at the onset of exercise, which is reduced through exercise (Gillen et al. 2021). Regarding glucose response, it was still elevated in normal weight subjects at the end of exercise and reduced 1 h after exercise for OWS participants. Since blood glucose was not measured immediately before the exercise, it is possible that we did not see glucose fall during exercise. Also, this difference in normal weight subjects may be related to the timing between the meal and exercise. In different studies, the interval between meals and exercise is more than 60 min (Vieira et al. 2016), different from our protocol which used 30 min. Regarding the OWS, the glucose reduction may be linked to an increase of contraction-mediated muscle glucose uptake, which remains for some hours after exercise (Gillen et al. 2021). Also, this group showed elevated insulin concentration at the end of the exercise. Obesity is related to increased basal and post-prandial insulin secretion even without significant insulin resistance (van Vliet et al. 2020). Although insulin secretion was not measured, OWS may have already augmented insulin levels.

In our study, it was observed that the OWS group had elevated basal concentrations of NE. Even though plasma, NE is not the best marker of sympathetic nervous activity (Grassi et al. 2015); our results agree with a systematic review and meta-analysis that found increased muscle sympathetic activity in overweight subjects (Grassi et al. 2019). However, despite the higher resting HR in the overweight group, HR was not correlated with plasma NE concentration. The increased basal HR is an interesting finding because studies on obese people have not found a difference in this variable when comparing this group with normal weight subjects (Grassi et al. 1995; Rumantir et al. 1999; Vaz et al. 1997). Then, the rise in basal HR would not be a characteristic of sympathetic overdrive in obesity. The elevated sympathetic tone may be related to the elevated plasma insulin and leptin concentrations in obese people, both known inductors of sympathetic elevations. Despite not being tested in the present work, we suggest that the augmented sympathetic efficiency due to better cardiorespiratory fitness is reflected in reduced plasma NE concentration in physically active volunteers. Otherwise, in the overweight group, the reduced cardiorespiratory fitness also contributes to augmented sympathetic tone. However, we cannot reject the possibility that sedentary subjects performing exercise at 70% VO2 peak were working at higher intensity and, consequently, increasing NE concentration (Greiwe et al. 1999).

In the present study, we verified that overweight subjects had increased plasma insulin and glucose levels, which affected HOMA-IR index. Moreover, this group has higher insulin AUC than the other two groups. These results are in accordance with previous studies that showed overweight individuals with increased HOMA-IR (Kaur et al. 2016), fasting glucose, and insulin concentrations (Janssen et al. 2004) than those normal weight individuals. Furthermore, it has been hypothesized that hyperinsulinemia and insulin resistance could contribute to sympathetic overactivity (Thorp and Schlaich 2015). Thus, it is possible that the altered metabolic profile seen in our sample of overweight subjects already put them at risk for metabolic disorders.

Conclusions

In conclusion, the present work demonstrated that a 30-min bout of exercise performed in the fed state does not cause significant elevations in plasma HSP72 and NE. However, BMI seems to affect glucose and insulin response following exercise. The augmented rest HR and NE in the overweight group suggest a sympathetic overactivity which may be exacerbated by increased insulin levels. In addition, the elevated cardiorespiratory fitness, as seen in the physically active group, would indicate improved sympathetic activity. Finally, it is important to consider that our main limitation, the small sample size, may partially explain the lack of some cardiovascular and metabolic responses. Thus, further studies with a higher sample size are necessary to address these limitations.

Acknowledgements

C.H.L.M. and H.T.S. were supported by scholarships from Brazilian National Council for Scientific and Technological Development (CNPq, Brazil). C.E.J.M. was supported from scholarship from the Coordination for the Improvement of Higher Education Personnel (CAPES, Brazil). A.R.-O., A.M.O.B., P.I.H.B.J., and M.K. are Research Productivity Fellows of the Brazilian National Council for Scientific and Technological Development (CNPq, Brazil).

Abbreviations

AUC

Area under the curve

BMI

Body mass index

BP

Blood pressure

CRF

Cardiorespiratory fitness

GEE

Generalized estimated equations

GZLM

Generalized linear model

HDL-C

High-density lipoprotein cholesterol

HOMA-IR

Homeostatic model of insulin resistance index

HR

Heart rate

HSP72

Heat shock protein of 72 kilodaltons (kDa)

HSPs

Heat shock proteins

LDL

Low-density lipoprotein cholesterol

NE

Norepinephrine

NWA

Normal weight active

NWS

Normal weight sedentary group

OWS

Overweight sedentary group

PAR-Q

Physical activity readiness questionnaire

PBMC

Peripheral blood mononuclear cells

SNS

Sympathetic nervous system

TC

Total cholesterol

TG

Triglycerides

VO2 peak

Peak oxygen uptake

Author contribution

C.E.J.M., A.M.O.B., A.R-O., and M.K. conceived and designed the research. Funding acquisition: P.I.H.B.J., A.R-O., and M.K. Enrollment of subjects, testing, and data analysis: C.H.L.M., H.T.S., and C.E.J.M. Writing—original draft preparation: C.H.L.M. and M.K. Writing—review and editing: C.E.J.M., G.V. All authors read and approved the manuscript. The authors declare that all data were generated in-house and that no paper mill was used.

Funding

This work was supported by The State of Rio Grande do Sul Foundation for Research Support (FAPERGS; grant #30791.434.41354.23112017—CHAMADA FAPERGS/Decit/SCTIE/ MS/CNPq/SESRS n. 03/2017 – PPSUS, to M.K.) and The Brazilian National Council for Scientific and Technological Development (CNPq; grants #551097/2007–8, 563870/2010–9, 402626/2012–5 and 402364/2012–0, to P.I.H.B.J., and # 404707/2016–5 to A.R-O).

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval

The study was approved by the Ethics Committee of the Universidade Federal do Rio Grande do Sul (protocol number 79422417.2.0000.5347) and was conducted according to the Declaration of Helsinki, except for registration in a database.

Consent to participate

Informed consent was obtained from all individual participants included in the study.

Conflict of interest

The authors declare no competing interests.

Footnotes

Key Points

- Exercise-induced HSP72 release is blunted in feed state independently of body composition and cardiorespiratory fitness;

- Higher BMI and low cardiorespiratory fitness are associated with increased insulin responses and insulin resistance;

- Higher BMI and low cardiorespiratory fitness result in increased heart rate and noradrenaline responses (↑sympathetic tonus);

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Associated Data

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Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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