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Obese Patients Decrease Work Rate in Order to Keep a Constant Target Heart Rate

ZUCCARELLI, LUCREZIA1; SARTORIO, ALESSANDRO2,3; DE MICHELI, ROBERTA2; TRINGALI, GABRIELLA2; GRASSI, BRUNO1

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Medicine & Science in Sports & Exercise: May 2021 - Volume 53 - Issue 5 - p 986-993
doi: 10.1249/MSS.0000000000002551
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Abstract

Exercise intolerance is both a cause and a consequence of obesity (1,2), within a vicious circle characterized by obesity → early fatigue → reduced exercise tolerance → reduced physical activity → obesity. Thus, exercise training, in association with nutritional and psychological interventions, aimed at reducing body mass (BM) and exercise intolerance, is considered a cornerstone in obesity treatment (3,4). The positive aspects of exercise training in obese patients may go well beyond those related to a reduced BM. According to Gaesser and Blair (5), for example, a higher level of cardiorespiratory fitness may attenuate or eliminate the mortality risk associated with an elevated body mass index (BMI).

Although health benefits can be presumably gained by any regular exercise and physical activity, a targeted exercise prescription is needed to elicit specific physiological responses and/or adaptations (6). It has been recently shown that exercise prescription based on a fixed percentage of maximum values (i.e., pulmonary oxygen uptake (V˙O2), heart rate (HR), work rate) does not take into account the specific exercise-intensity domain metabolic responses (7). Exercise prescription, both in healthy and diseased populations, is indeed carried out with respect to variables such as the gas exchange threshold (GET) (7,8) or critical power (CP) (9). By doing so, exercise prescription takes into account the nonlinearity (higher slope) of the V˙O2 versus work rate relationship for constant work rate (CWR) exercises above GET, and particularly above CP, as a consequence of the appearance of the V˙O2 “slow component” (10). GET and CP are, however, difficult to determine outside an exercise physiology laboratory, and therefore, the identification of the training intensity is most often done by choosing a work rate corresponding to a fixed percentage of peak HR (11,12). Also the HR versus work rate relationship, however, shows a nonlinear behavior (higher slope) during CWR exercises above GET and above CP. The issue is further complicated by the recent observation by our group (13) of a slow component of the HR kinetics also for work rates below GET. In that study, moreover, the relative amplitude of the HR slow component was more pronounced than the relative amplitude of the V˙O2 slow component (13). Some mechanisms potentially responsible for the HR slow component are mentioned later in the Discussion section. In any case, as a consequence of the HR slow component, in order to keep HR constant at a value slightly above that corresponding to GET, the work rate had to be decreased by ~14% during a 15-min exercise task (13). In other words, the appearance of HR slow component makes exercise prescription based on some percentage of HR peak an inaccurate approach.

The study by Zuccarelli et al. (13) was carried out in young healthy physically active subjects. We hypothesize that the phenomena discussed previously could be more pronounced in diseased populations, such as obese patients. Obese patients are indeed characterized (vs healthy subjects) by lower exercise tolerance, by higher V˙O2 and HR values for the same submaximal work rate, and by a more pronounced slow component of the V˙O2 kinetics (14). Thus, the mentioned differences in the metabolic responses to exercise in the obese subjects versus healthy individuals lead us to hypothesize in obese patients a more pronounced slow component of HR kinetics as well. This would make exercise prescription based on a fixed submaximal HR even more questionable in these patients.

The aim of the present study was to test this hypothesis. More specifically, we hypothesized that in obese patients, as a consequence of a more pronounced slow component of the HR kinetics, in order to keep HR constant during a work rate slightly above GET, the decrease in work rate would be more pronounced than that observed in young healthy physically active subjects (13). We also hypothesize that in obese patients a standard 3-wk multidisciplinary BM reduction program, consisting of moderate-intensity exercise, caloric restriction, and psychological counseling would attenuate the work rate decrease aimed at keeping a constant HR, thereby improving exercise tolerance and facilitating exercise prescription, which is often done at work rates slightly above GET.

MATERIALS AND METHODS

Subjects

Sixteen male obese subjects, seven young adults and nine adolescents (mean ± SD: age, 22 ± 7 yr; height, 174 ± 7 cm; BM, 127 ± 19 kg; BMI, 41.6 ± 3.9 kg·m−2), were hospitalized (Division of Metabolic Diseases for young adults and Division of Auxology for adolescents, Istituto Auxologico Italiano, IRCCS, Piancavallo, Italy) and tested before and after a 3-wk multidisciplinary BM reduction program. The program included the following: constant and monitored physical activity (5 d·wk−1 training, including 1-h dynamic aerobic standing and floor exercise with arms and legs, at moderate intensity and under the guide of a therapist, and either 20- to 30-min cycle ergometer exercise at 60 W or 3- to 4-km outdoor walking on flat terrain, according to individual capabilities and clinical status), psychological counseling, and nutritional education and moderate energy restriction. The adult patients and both parents of the adolescents provided signed consent statements, after being fully advised about the purposes and testing procedures of the investigation, which were approved by the ethics committee of the Italian Institute for Auxology, Milan, Italy (reference code: 01C827; acronym: COLEESEROB-RC18). All procedures were in accordance with the recommendations set forth in the Declaration of Helsinki (15).

Inclusion criteria were as follows: 1) BMI SD score >2 for age and sex (adolescents), using the Italian growth charts (16) and BMI >30 kg·m−2 for young adults; 2) no involvement in structured physical activity programs (regular activity >20 min·wk−1) during the 8 months preceding the study; 3) absence of overt uncompensated diabetes; 4) absence of signs or symptoms referable to any major cardiovascular, respiratory, or orthopedic disease contraindicating or significantly interfering with the tests; and 5) absence of any kind of disease related to gastrointestinal tract (i.e., obstruction of the digestive tract, motility disorders, previously surgical procedures, swallowing disorders).

BMI was calculated as BM divided by height2, expressed in kilograms per square meter. Body composition was determined by bioelectrical impedance (Human-IM Scan; DS-Medigroup, Milan, Italy). Whole-body resistance to an applied current (50 kHz, 0.8 mA) was measured with a tetrapolar device, with electrodes placed on the right wrist and ankle of the supine subjects lying comfortably in bed with limbs abducted from the body. Fat-free mass (FFM) was calculated with equations derived with a two-compartment model (17). Fat mass (FM) was calculated as the difference between total BM and FFM; both variables were expressed as kilograms and as a percentage of BM (Table 1). The same investigators performed all examinations before and after the 3-wk intervention period (see discussion hereinafter).

TABLE 1 - Anthropometric characteristics and age of participants before (PRE) and after (POST) a 3-wk multidisciplinary BM reduction program.
PRE POST P
Age, yr 22 ± 7 22 ± 7
Height, m 1.74 ± 0.09 1.74 ± 0.09
BM, kg 127 ± 19.5 121 ± 19.3 <0.0001
BMI, kg·m−2 41.6 ± 3.9 39.8 ± 3.6 <0.0001
FFM, % BM 58.6 ± 8.27 61.8 ± 7.78 0.0006
FFM, kg 74.7 ± 20.32 75.1 ± 19.72 0.67
FM, % BM 43.6 ± 3.88 40.7 ± 3.96 0.003
FM, kg 55.6 ± 11.85 49.5 ± 10.74 <0.0001
Values are mean ± SD.

Exercise protocols

Before (PRE) and after (POST) the 3-wk multidisciplinary BM reduction program exercise tests were conducted in three separate occasions over a 4-d period. Exercise tests were carried out in a well-ventilated laboratory under continuous medical supervision.

During the first visit, the subjects completed an incremental exercise (INCR) up to voluntary exhaustion on an electronically braked cycle ergometer (Corival cpet, Lode, the Netherlands) to determine V˙O2peak and GET. The test started with 20 W for 2 min, and then 20-W increases of work rate were imposed every minute until voluntary exhaustion. Pedaling frequency was digitally displayed to the subjects, who were asked to keep a constant cadence throughout the tests at their preferred value (between 60 and 80 rpm). Voluntary exhaustion was defined as the incapacity to maintain the imposed load and pedaling frequency despite vigorous encouragement by the researchers. After the first visit, the subjects performed in two different days one repetition of a 10-min CWR submaximal exercise corresponding to 80% of GET determined in PRE (moderate-intensity, MODERATE), followed by one repetition of a 15-min exercise (or until exhaustion) at 120% GET determined in PRE (heavy-intensity, HEAVY) and one repetition of a 15-min “HR-controlled” exercise (HRCLAMPED). The HEAVY CWR exercise was performed when subjects reached again baseline values of the investigated variables (i.e., after ~30 min of recovery). Participants performed the CWR exercises (MODERATE + HEAVY) and the HRCLAMPED exercise in a randomized order.

During HRCLAMPED, a target HR corresponding to 120% of GET determined during the INCR in PRE was identified. The work rate was kept constant for the first 2 min or until HR reached its target value, and then it was adjusted by the operator every 5 s to maintain a constant HR at the target value (for more details, see Ref. [13]). Before the trial, the subjects were familiarized with the protocol. CWR exercises were carried out at the same absolute work rate in PRE and POST; the same was true for the initial work rate during HRCLAMPED.

Measurements

Pulmonary ventilation (V˙E), V˙O2, and CO2 output (V˙CO2) were determined breath-by-breath by a metabolic cart (Ergostick; Geratherm Respiratory, Bad Kissingen, Germany). Expiratory flow measurements were performed by a turbine flow meter, calibrated before each experiment by a 3-L syringe at different flow rates. V˙O2 and V˙CO2 were determined by continuously monitoring PO2 and PCO2 at the mouth throughout the respiratory cycle and from established mass balance equations. Calibration of O2 and CO2 analyzers was performed before each experiment by utilizing gas mixtures of known composition. Peak values of the main variables were taken as the highest 20-s mean values attained before the subject’s voluntary exhaustion. Gas exchange ratio (R) was calculated as V˙CO2/V˙O2. GET was determined by standard methods (18). In order to identify the work rate corresponding toV˙O2 at GET, the effect of the delayed V˙O2 adjustment (19,20) to the increased work rate during the incremental test was corrected by shifting the linear V˙O2 versus time (and work rate) relationship to the left, by an amount corresponding to the mean response time of the V˙O2 kinetics (21) previously determined by our group in an obese population (30 s) (14).

HR was determined continuously by a chest band (Polar Electro, Oulu, Finland); mean values were calculated every 5 s. Considering that only one repetition of each CWR exercise was carried out, a formal V˙O2 and HR kinetics analysis was not performed (22). The presence or absence of a steady state in V˙O2 and HR after the first minutes of CWR exercise was evaluated by fitting linear regressions on the data obtained from the third to the last minute of exercise (13).

Core body temperature was continuously monitored using ingestible telemetric temperature capsules (e-Celsius; BodyCap, Caen, France) during each CWR exercise in PRE. The validity and reliability of this device have been recently confirmed against a temperature-controlled water bath (23). Briefly, the ingestible core body temperature sensor (17.7-mm length, 8.9-mm diameter, and 1.7 g) wirelessly transmits signals by a radio frequency of 433–434 MHz through the body to the data recorder (e-Viewer; BodyCap), worn on the outside of the body. Each capsule was activated and then swallowed by the patients 3 h before the CWR exercises. Sampling rate was set at 5 s, and mean capsule temperature values were calculated during the last 30 s of every minute of CWR exercise.

RPE values were obtained every minute during exercise using the Borg’s 6–20 scale (24).

Statistical analysis

Results are expressed as mean ± SD values. Statistical significance of differences in PRE and POST for the main respiratory, cardiovascular, and metabolic variables during INCR, MODERATE, and HEAVY was checked using a two-tailed Student’s t-test for paired data. Linear regression line and correlation analysis were carried out by the last-squared residual method. A two-way ANOVA with repeated measures (intervention × time) was used to assess changes in V˙O2, HR, and work rate during CWR and HRCLAMPED exercises. When significant differences were found, a Bonferroni post hoc test was used to determine the exact location of the difference. The level of significance was set at P < 0.05. Statistical analyses were carried out by a commercially available software package (Prism 6.0; GraphPad). Power analysis was conducted a priori, taking the work rate decrement seen during HRCLAMPED exercise in our previous article (13) as the main variable. In order to identify significant differences, with an α error of 0.05 and a statistical power (1 − β) of 0.90, an n value of 11 subjects resulted to be necessary (G*Power 3.1).

RESULTS

All patients carried out the entire protocol except one, who did not complete the INCR exercise in POST for medical reasons (this subject was not taken into account for analyses related to the INCR exercise). The main anthropometric characteristics of the patients are reported in Table 1. BM (by ~6 kg, corresponding to ~5% of the initial BM), BMI, and FM were significantly lower in POST than in PRE.

Peak values of the main respiratory, cardiovascular, and metabolic variables determined during INCR are shown in Table 2. Patients attained peak HR values corresponding to ~89% and ~86% of the age-predicted maximum (calculated as 208 − 0.7 × age [25]), respectively, in PRE and POST. Taking into account also the R peak and RPE peak values, it can be assumed that exhaustion was indeed reached, although no validation test for determination of maximal V˙O2 (26) was carried out in the recovery phase. V˙O2 peak values were typical for obese subjects (27,28), and they were not significantly different (P = 0.44) in PRE (19.4 ± 3.0 mL·kg−1·min−1) versus POST (20.1 ± 4.3 mL·kg−1·min−1). In PRE, GET occurred at 59% of V˙O2 peak, corresponding to 1.395 L·min−1, not significantly different (P = 0.14) from the value in POST (61% of V˙O2 peak, corresponding to 1.487 L·min−1). Respiratory compensation point (RCP) was higher in POST than in PRE (1.942 ± 0.262 and 1.805 ± 0.300 L·min−1, respectively; P = 0.048).

TABLE 2 - Main respiratory, cardiovascular, and metabolic end-exercise or steady-state values, determined during INCR, CWR exercises (MODERATE and HEAVY), and HRCLAMPED exercise, before (PRE) and after (POST) a 3-wk multidisciplinary BM reduction program.
INCR MODERATE HEAVY HRCLAMPED
PRE POST P PRE POST P PRE POST P PRE POST P
Work rate, W 196 ± 28 205 ± 28 0.03 58 ± 13 58 ± 13 118 ± 18 118 ± 18 95 ± 23 112 ± 21 0.0002
V̇O2, L·min−1 2.400 ± 0.327 2.456 ± 0.380 0.52 1.146 ± 0.257 1.077 ± 0.264 0.14 1.854 ± 0.295 1.846 ± 0.310 0.88 1.566 ± 0.202 1.679 ± 0.307 0.04
V̇O2, mL·kg−1·min−1 19.4 ± 3.0 20.1 ± 4.3 0.43 9.2 ± 2.1 8.7 ± 1.9 0.17 15.0 ± 3.0 15.1 ± 3.1 0.84 12.6 ± 3.9 14.0 ± 3.5 0.04
V̇CO2, L·min−1 3.018 ± 0.397 2.990 ± 0.417 0.93 1.028 ± 0.228 0.940 ± 0.295 0.15 1.866 ± 0.317 1.837 ± 0.333 0.66 1.573 ± 0.217 1.641 ± 0.314 0.35
R 1.26 ± 0.06 1.25 ± 0.10 0.87 0.90 ± 0.04 0.88 ± 0.17 0.63 1.01 ± 0.07 1.00 ± 0.05 0.27 1.00 ± 0.09 0.99 ± 0.05 0.71
V̇E, L·min−1 101.2 ± 19.4 102.8 ± 20.1 0.57 31.2 ± 7.0 29.5 ± 8.5 0.32 63.7 ± 15.3 60.6 ± 14.1 0.23 47.6 ± 14.6 54.7 ± 12.1 0.06
fR, breaths·min−1 42 ± 6 44 ± 8 0.30 24 ± 4 24 ± 8 0.81 36 ± 8 34 ± 8 0.10 29 ± 9 34 ± 7 0.02
HR, bpm 176 ± 11 171 ± 14 0.06 118 ± 9 111 ± 10 0.0001 157 ± 15 147 ± 17 0.0001 148 ± 17 146 ± 15 0.17
RPE, 6–20 20 ± 1 20 ± 1 0.87 8 ± 3 8 ± 3 0.36 18 ± 3 16 ± 4 0.048 13 ± 3 13 ± 4 0.78
Time exercise, min 10.7 ± 1.4 11.3 ± 1.4 0.03 10.0 ± 0 10.0 ± 0 12.4 ± 4.3 13.5 ± 2.5 0.0043 14.8 ± 0.8 14.9 ± 0.5 0.33
Values are mean ± SD.
fR, breathing frequency.

Main respiratory, cardiovascular, and metabolic end-exercise or steady-state values, determined in PRE and POST during MODERATE and HEAVY CWR exercises, are also shown in Table 2. Work rates for MODERATE and HEAVY were set to be identical in the two conditions, and they were 29% ± 5% and 62% ± 9% of peak work rate, respectively. For MODERATE, all patients completed the imposed 10 min of exercise. No significant differences were found in V˙O2 end-exercise values in PRE versus POST, whereas HR values determined during the last 20 s were significantly lower in POST than in PRE (−6%; P = 0.005). As for HEAVY, 7 patients in PRE and 11 patients in POST completed the imposed 15-min exercise. Time to exhaustion was significantly higher in POST than in PRE (+8%; P = 0.004).

In Figure 1, HR (upper panel) and pulmonary V˙O2 (lower panel) mean values obtained during MODERATE and HEAVY in PRE and POST are plotted as a function of the time of exercise. To obtain this figure, individual values were grouped for discrete work rate intervals, which were determined in order to have, in each interval, each subject represented by one data point. When the subject had more than one “original” data point in the interval, mean individual values were calculated, both for the x and the y variables. Data were fitted by linear regression from the third minute to the end of exercise.

FIGURE 1
FIGURE 1:
Mean (±SD) values of HR (upper panel) and V˙O2 (lower panel), grouped for discrete time intervals, during CWR exercise at two investigated intensity domains, MODERATE and HEAVY, before and after a 3-wk multidisciplinary BM reduction intervention. Vertical lines indicate that exercise started at time 0. Horizontal lines indicate V˙O2peak in PRE, RCP in PRE and POST, and GET in PRE. The fitted linear regression lines are also shown. *Significantly different (P < 0.05) from PRE. See text for further details.

During MODERATE, the slopes of the linear regressions of HR versus time were significantly different from zero in PRE (0.408 ± 0.105 b·min−2; P = 0.008) but not in POST (0.166 ± 0.168 b·min−2; P = 0.36). Thus, HR was not in a steady state during the 10-min MODERATE exercise in PRE, suggesting the presence of a slow component (13), whereas a steady state was present in POST. HR values were lower in POST than in PRE (P = 0.008; F = 9.058) starting from the third minute of exercise. As for V˙O2, the slopes of the linear regressions were not significantly different from zero in both conditions (PRE and POST). In other words, in both conditions, V˙O2 values were in a steady state. At all time points, V˙O2 values were not different in POST versus PRE. In the lower panel of Figure 1, horizontal lines indicating V˙O2peak in PRE (no differences before vs after training were observed for this variable, as well as for GET (see previous discussion)), RCP in PRE and POST, and GET in PRE are shown. Steady-state V˙O2 values during HEAVY corresponded to RCP in PRE and were slightly below RCP in POST. In both cases, however, V˙O2 values seemed to be in a steady state between the 10th minute and the end of exercise.

During HEAVY, the slopes of the V˙O2 versus time regression lines were significantly different from zero both in PRE and in POST (P = 0.04 and P = 0.0008, respectively), and they were not significantly different in POST (0.012 ± 0.001 L·min−2) versus PRE (0.015 ± 0.004 L·min−2). The slopes of the HR versus time linear regressions were significantly different from zero both in PRE and in POST (P = 0.03 and P = 0.004, respectively), and they were lower (P = 0.001) in POST (1.103 ± 0.184 b·min−2) than in PRE (2.348 ± 0.567 b·min−2). HR values were lower in POST than in PRE (P = 0.0012; F = 15.73), starting from the fifth minute of exercise. The rate of HR and V˙O2 increases, calculated as the percentage increases with respect to the value obtained at the third minute of exercise, arbitrarily set at 100%, were greater for HR than for V˙O2, both in PRE (119% and 109% for HR and V˙O2, respectively; P = 0.001) and in POST (111% and 106% for HR and V˙O2, respectively; P = 0.047). The percent increases in V˙O2 were significantly correlated with the percent increases in HR (r = 0.57; r2 = 0.32; P = 0.0019).

Core body temperatures at the third and at the end of the exercise were 37.5°C ± 0.3°C and 37.6°C ± 0.3°C (P < 0.0001), respectively, during MODERATE and 37.5°C ± 0.2°C and 37.8°C ± 0.2°C (P < 0.0001) during HEAVY. A positive and significant correlation (r2 = 0.41; P = 0.0001) was found between the individual increases in HR and the corresponding increases in core body temperature, both calculated as end-exercise values minus values calculated at the third minute of exercise. As mentioned previously, core body temperature measurements were obtained only in PRE.

Figure 2 shows mean (±SD) HR, work rate, and V˙O2 values obtained during the HRCLAMPED exercise in PRE and POST. In the two conditions, the work rate imposed at the start of the exercise was the same, corresponding to HEAVY (GET +20%) determined in PRE; this work rate was imposed for the first 2 min, and then the work rate was adjusted to maintain HR constant (see Methods). Main respiratory, cardiovascular, and metabolic end-exercise values, determined in PRE and POST during HRCLAMPED exercise, are shown in Table 2. All patients but one (who terminated the exercise for voluntary exhaustion at the 12th minute in PRE and at the 13th minute in POST) completed the 15-min HRCLAMPED exercise. The HR target value was reached on average after 2 min in PRE and after 5 min in POST, and afterward, it remained substantially constant throughout the test (upper panel of the figure), indicating that the HR “clamp” was successful. In PRE, in order to maintain the target HR, work rate had to significantly decrease (middle panel of the figure) from the fifth minute until the end of exercise; at the end of the exercise (15 min), the percentage decrease in work rate versus the value obtained at the third minute was approximately 19%. On the other hand, in POST, the decrease in work rate was significantly (P = 0.0002) less pronounced (~5%), although it was still statistically significant (P = 0.005). From the fifth minute until the end of exercise, work rate was higher in POST than in PRE (P = 0.0023; F = 13.36). As shown in the lower panel of the figure, the reduced work rate in PRE and POST during HRCLAMPED was associated with a decreased V˙O2 (by ~10% and ~ 5%, respectively).

FIGURE 2
FIGURE 2:
Mean (±SD) values of HR, work rate, and V˙O2 during HR-controlled (HRCLAMPED) exercise before and after the 3-wk multidisciplinary BM reduction intervention. Vertical lines indicate that exercise started at time 0. The horizontal dashed line indicates the mean HR target value. *Significantly different from PRE (P < 0.05). See text for further details.

DISCUSSION

The main findings of the present study can be summarized as follows:

  1. Differently from V˙O2, during moderate-intensity (<GET) CWR exercise, HR increased significantly from the 3rd to the 10th minute of exercise, suggesting the presence of a slow component for this variable also in this exercise domain.
  2. During heavy-intensity exercise (>GET), from the 3rd to the 10th minute of exercise, the percentage increase in HR was greater than the percentage increase in V˙O2; thus, the HR slow component was more pronounced than the V˙O2 slow component.
  3. In order to keep a constant target HR value, slightly above that corresponding to GET, both work rate (by ~20% over a 15-min task) and V˙O2 had to decrease. Thus, in untrained obese patients, exercise prescription at a fixed submaximal HR translates into a work rate that must be progressively decreased during the training session; this obviously makes exercise prescription quite problematic. The work rate decrease was similar to that (~15%) observed in young healthy physically active subjects (13).
  4. A 3-wk multidisciplinary BM reduction program, including moderate-intensity exercise, eliminated the HR slow component during exercise <GET and reduced the amplitude of the HR slow component during exercise >GET, thereby increasing exercise tolerance (lower HR for the same work rate).
  5. After the BM reduction program, the decrease in work rate in order to keep HR constant at a value slightly above GET was substantially eliminated, confirming the increased exercise tolerance (29) and facilitating exercise prescription, by allowing to translate a fixed submaximal HR into a work rate slightly above GET.

To the best of our knowledge, this is the first study analyzing the relationship between HR and V˙O2 responses during CWR exercise carried out in different intensity domains in obese patients. In the present study, no formal analyses of the V˙O2 and HR kinetics and their different components (10) were carried out because only one repetition of each exercise was performed. The presence versus absence of a steady state (in other words, the absence vs the presence of a slow component) of the investigated variables was evaluated by a simplified approach, as proposed in previous studies by our group (see, e.g., Ref. [30]). We fitted a linear function to the data from the 3rd to the 10th minute of exercise: a significant positive slope suggests the absence of a steady state and therefore the presence of a slow component, whereas a slope not significantly different from zero suggests a steady state, and negates the presence of a slow component.

Whereas the slow component of the V˙O2 kinetics reflects a loss of efficiency of oxidative metabolism and is associated with fatigue (31), also in obese patients (14), the functional significance of the HR slow component, particularly during moderate-intensity exercise, is less clear (13). The results of the present study are, in this respect, of interest: the BM reduction program, which included exercise training, decreased (heavy-intensity exercise) or abolished (moderate-intensity exercise) the amplitude of the HR slow component, and increased exercise tolerance. This may indirectly suggest that also the HR slow component is associated with fatigue and a decreased exercise tolerance, as it occurs for the V˙O2 slow component.

Although HR responses during CWR exercises in relation to the physiological thresholds have been poorly studied so far, a slow component is known to occur also for the HR kinetics (13,32,33). Increases in core body temperature could have had a role in determining the HR increases during CWR exercise. In previous studies (34,35), 10 min of exercises at ~60% of V˙O2peak was associated with ~0.3°C increases in core body temperature. In the present study, we have similar data: the increases in core body temperature from the third to the end of exercise in PRE were indeed ~0.1°C during 10 min of moderate- and ~0.2°C during 15 min of heavy-intensity exercise. Core temperature increases were significantly correlated with the HR increases. Although a correlation does not imply a cause–effect relationship, it is legitimate to hypothesize that the slow component of the HR kinetics could be attributable, at least in part, to the increases in core temperature. Unfortunately, the measurements of core temperature could not be repeated in POST for logistic reasons, and thus, we miss information about the possible effects on this variable by the BM reduction program.

A causative role in determining the HR slow components could be attributed to blood catecholamine levels. Increments in catecholamine concentration were correlated with increments in HR (slow component) during short dynamic exercise at ~45% of V˙O2peak (32). On the contrary, no increase in norepinephrine occurred during very low intensity exercise (~23% of V˙O2peak), in which no HR slow component was identified (32). Obese patients, however, show lower plasma catecholamine concentrations compared with normal-weight individuals (36); this occurs at rest, during dynamic exercise, and after training interventions (36–39). A reduced epinephrine secretion has been described in obese patients (38), possibly because of higher plasma levels of leptin, insulin, and cortisol, and higher catecholamine elimination rate (36).

The different behavior of V˙O2 and HR during submaximal exercises was further confirmed during the HRCLAMPED exercise. In order to keep HR constant at the target value, the obese patients had to decrease the work rate to an extent at which V˙O2 not only did not present a slow component but actually decreased, confirming what previously observed by Zuccarelli et al. (13) in healthy physically active young subjects. This indirectly confirms that the slow component of the HR kinetics was more pronounced that the slow component of the V˙O2 kinetics.

Not confirming our hypothesis, the work rate decrease (−20%) during HRCLAMPED exercise observed in the present study was only slightly greater than that described by Zuccarelli et al. (13) in healthy physically active young subjects (−15%). Thus, the uncertainty in exercise prescription and the consequences on exercise tolerance deriving from the HR slow components are not more severe in obese patients compared with healthy controls. Further studies should be conducted on different patient populations. An interesting group would be represented by patients treated with β-blockers.

In the present study, the evidence of increased exercise tolerance after the BM reduction intervention, discussed previously, did not translate into an increased V˙O2peak. This seems to be in agreement with previous studies carried out in obese patients by our group, in which interventions that improved exercise tolerance during submaximal exercise (such as normoxic helium breathing [40] or respiratory muscles endurance training [27,30]) did not affect V˙O2peak. This variable, therefore, in obese patients may be more resistant to changes compared with other submaximal variables. GET was not significantly different in POST than in PRE, whereas RCP was higher in POST than in PRE; it cannot be excluded that the lack of a significant difference for GET could be related to a lack of statistical power. Moreover, V˙O2 values during HEAVY corresponded to RCP in PRE and were slightly below RCP in POST. In both cases, V˙O2 values seemed in a steady state during the last minutes of exercise, and they did not show the continuous increase that would characterize the severe exercise domain. Both in PRE and in POST, therefore, exercise was at upper boundary of the heavy-exercise domain. In any case, it should be stressed that even if changes in exercise domain had occurred after training, they would not have detracted from the message of the study: exercise training would improve exercise tolerance, as manifested (for the same absolute work rate) by a change in exercise domain, by less pronounced slow components of HR and V˙O2 kinetics, and by a less pronounced decrease in work rate for the same fixed HR.

To conclude, in untrained obese patients, exercise prescription at a fixed submaximal HR, slightly above that corresponding to GET (as it is often done for endurance exercise prescription), translates into a work rate that must be progressively decreased during the training session. A 3-wk multidisciplinary BM reduction intervention, including moderate-intensity exercise, increased exercise tolerance by eliminating (during moderate-intensity exercise) or by reducing (during heavy-intensity exercise) the slow component of HR kinetics. As a consequence, the decrease in work rate, occurring in order to maintain a constant HR slightly above that corresponding to GET, substantially disappeared after the BM reduction intervention, thereby facilitating exercise prescription, universally recognized as a cornerstone in the treatment of obesity.

The authors acknowledge the head nurses and the nursing staff at the Division of Auxology and at Division of Metabolic Diseases, Istituto Auxologico Italiano, IRCCS, Piancavallo (VB). Special thanks go to the subjects and their families for their willingness to participate in this research protocol.

The study was supported by Progetti di Ricerca corrente, Istituto Auxologico Italiano. Partial support from Italian Space Agency (ASI, MARS-PRE Project, Grant No. DC-VUM-2017-006) and Ministero dell’Istruzione dell’Universita’ e della Ricerca, PRIN Project 2017CBF8NJ, is also acknowledged.

The authors have no conflict of interest, and the results of the present study do not constitute endorsement by the American College of Sport Medicine. The results of this study are presented clearly, honestly, and without fabrication, or inappropriate data manipulation.

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Keywords:

HEART RATE; OBESITY; SLOW COMPONENT; EXERCISE TOLERANCE; EXERCISE PRESCRIPTION

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