Effects of High-Intensity Training on Anaerobic and Aerobic Contributions to Total Energy Release During Repeated Supramaximal Exercise in Obese Adults

Several studies have recently focused on determining energetic system contributions in several sports practices, with the objective of understanding the energetic demand related to these events in order to develop improved training recommendations [1, 2]. In the context of obesity, exercise energy metabolism is impaired [3, 4]. Aerobic energy release during peak exercise is reduced by excessive fat mass, which imposes an unfavorable burden on cardiac function and on oxygen uptake by working muscles [5]. Evaluation of aerobic energy release has become part of routine clinical assessments of this population, as the degree of its reduction is a strong predictor of an individual’s health [6]. By contrast, anaerobic metabolic pathways have received less attention. Studies involving obese individuals are more focused on evaluating anaerobic aptitude (e.g., maximal power output). These studies describe lower values of peak power output in obese subjects compared with normal-weight subjects [7, 8]. This reduced parameter has been linked to excessive fat mass, which may reduce motor-unit activation and the ratio of muscle strength to units of muscle mass [8]. However, no data are available regarding anaerobic energetic yield during exercise. Therefore, studying energetic muscle interactions for a given exercise may be the best approach to describing the true metabolic energy of the muscles of obese individuals and understanding the metabolic adaptations that occur in response to an exercise intervention in obese individuals.

Regarding intervention strategies and their impact on metabolic profiles, high-intensity training, such as supramaximal exercise, is gaining popularity in the context of obesity management. Based on data provided by post-intervention metabolic measures, this model of exercise appears to be a valuable approach for managing obesity [9]. Indeed, Whyte et al. [10] demonstrated that very high-intensity sprint interval training [2 weeks, comprising 6 sessions of 4 to 6 repeats of 30-s Wingate anaerobic sprints on an electromagnetically braked cycle ergometer, with a 4.5-min recovery period between each repetition] improved several metabolic risk factors: 1) an increase in resting fat oxidation rate in the fasted state and 2) a decrease in resting carbohydrate oxidation in the fasted state compared with baseline. This high-intensity training also decreased waist and hip circumferences in overweight and obese sedentary men and illustrated the potential of this alternative exercise model to improve lipid utilization in individuals with excess body weight. However, no information describing true metabolic adaptations during exercise is available. More importantly, a simultaneous evaluation of the maximal activation of both energetic systems (e.g., anaerobic vs. aerobic) may allow us to better understand anaerobic/aerobic interactions during exercise and provide information regarding the factor(s) that limit performance in obese individuals, as well as for other populations (normal-weight individuals, athletes).

Accumulated oxygen deficit (AOD) is a descriptor of the maximal amount of energy obtained from anaerobic metabolism [11] and makes it possible to directly measure maximal anaerobic energy release during supramaximal effort. This concept makes it possible to simultaneously evaluate the maximal activation of both anaerobic and aerobic metabolic systems and obtain a complete and coherent description of exercise energy demands in obese individuals. Based on the Oxygen consumption (VO₂) predicted from the individual VO₂-intensity relationship determined from the graded exercise test, the AOD can be determined during supramaximal exercise protocol [12]. It has been admitted that AOD measures are generally accepted as the criterion measure of anaerobic energy expenditure as a result of flaws in the use of blood lactate concentration as a quantitative tool for the measurement of anaerobic energy supply [13].

The aim of the present study is to evaluate the relative anaerobic and aerobic contributions to total energy release during repeated bouts of supramaximal cycling exercise in obese adults undergoing 6 weeks of supramaximal exercise training. Therefore, the examination of muscle metabolism and power output profiles in response to repeated bouts of cycling sprinting with a short recovery interval may enable us to better understand the regulation of these metabolic pathways.

Anaerobic energy contributions (calculated using the AOD method) increased significantly for the training group following HIT (p < 0.01) and were also significantly higher during SCE during the first, second, third, and fourth repetitions compared with values obtained for the control group during visit 1 (p < 0.01) and visit 2 (p < 0.01). During the third and the fourth repetitions, the control group and the trained group demonstrated significant decreases in anaerobic contributions compared with values obtained during the first repetition, decreases that were accompanied by increases in the values of the aerobic contributions, before HIT (Table 2).

Lactate concentrations measured at rest did not differ between the groups during visit 1 and visit 2. Following HIT, lactate concentrations increased significantly in the trained group compared with visit 1 (~6 mmol.kg ⁻¹, p < 0.01) and were significantly higher than those observed for in the control group during visit 1 and visit 2 (p < 0.01).

In this study, the increased power output levels observed for the trained group following HIT and during the SCE bouts correlated positively with anaerobic contribution increases (r = 0.9, p < 0.01, respectively). However, no relationships were observed between anaerobic contribution increases and VO_2max (r = 0.08, p = 0.7).

To the best of our knowledge, this study is the first to examine the effects of HIT on relative anaerobic and aerobic contributions to total energy release in obese adults during repeated bouts of supramaximal cycling exercise. The primary finding of this study was that relative anaerobic and aerobic contributions to total energy release during repeated bouts of SCE differed in untrained obese adults compared with the obese group following HIT. Indeed, anaerobic contributions to energy release increased significantly in the trained group following HIT. These higher anaerobic contributions were accompanied by both greater AOD deficits and larger decreases in oxygen uptake during SCE repetitions. Our results revealed that for the same relative work (at maximal power output), HIT may be an appropriate approach for enhancing anaerobic capacity, reasonable given that this type of exercise training improves glycolytic activity [25].

The performances demonstrated by our experimental subjects during SCE satisfied the criteria for supramaximal testing. Indeed, the PO exhibited by our groups during SCE was much closer to their maximal power output values (PO_max), which were obtained during the force-velocity test (p = 0.1). Moreover, the PO exhibited by our groups did not differ during the fourth repetition. The AOD values obtained in our study were similar between the groups before HIT (74.4 vs. 73.4 ml.kg⁻¹). Ten seconds of SCE may be considered a brief event during which subjects pedaled at maximal velocities against resistances determined during a force-velocity test [26, 27]. To meet the high ATP demand of SCE (e.g., adenosine diphosphate [ADP]), phosphorylation from PCr hydrolysis and glycolysis is necessary to overcome the oxygen deficit at the onset of exercise [28]. Several studies indicate that for events lasting 6–15 s, anaerobic contributions in sprinters are estimated to be 98 % of these individuals’ total energy expenditure [29]. Although AOD is a useful tool for determining anaerobic energy release [11], the present study demonstrated in the control group that the energy supply needed to perform 6 s during the first repetition of SCE results from anaerobic contributions (~83 %), as well as a small aerobic supply (~15 %). Therefore, contrary to the above findings, aerobic contributions to 6 s of SCE performance in obese adults represent a significant portion of the energy supply, which may result in lower rates of anaerobic glycolysis. The same tendency was also previously reported in normal-weight subjects, suggesting that this incompatibility between anaerobic energy release and power output during supramaximal exercise is sometimes compensated for by the increased contributions of aerobic metabolism, as reflected by the increase in oxygen consumption [26]. It is likely that the relative contributions of different energy systems during repeated-sprint exercises depend on the exercise protocol (duration, number of repetitions, recovery duration, passive or active recovery) and training status. In the context of obesity, we also speculate that other factors such as reduced motor-unit activation [8], premature fatigue and reduced activation of type II muscle fibers [7] may affect the energy contribution profile. Unfortunately, none of these factors were assessed in the present study.

During the second, third, and fourth repetitions, there were decreases in anaerobic contributions, which became significant during the third and fourth SCE bouts. Conversely, aerobic energy contributions increased and reached a value of participation of approximately 22 %. We speculate that examinations of repeated-sprint exercises may offer supplement information concerning changes in muscle metabolism and other factors affecting performance. In the present study, there was an increase in aerobic solicitation in both the control group and the trained group before HIT, during the second, the third, and the fourth repetitions. Given that our exercise was a model of intermittent exercise with 2 min of recovery between each repetition, it may be that the synthesis capacity of muscle was modified by obesity. In normal-weight subjects, several studies have indicated that the resynthesis of substrates such as PCr depends on several factors (endurance fitness, training status) [26, 30], factors that may affect the energy profile of muscle during subsequent exercise. Despite the absence of data regarding muscle recovery rates during supramaximal exercise in the obese population, the probable impact of obesity on the capacity of muscle resynthesis cannot be ruled out as an explanation for our results.

Following HIT, there was an 11 % reduction in calculated aerobic contributions to SCE, primarily as a result of an 11 % increase in anaerobic energy contributions. Moreover, the lactate response to the fourth SCE bout increased significantly following HIT. In the present study, the lactate concentrations were used to compare the anaerobic potential processes between subjects during this type of exercise [31]. Our results demonstrated that anaerobic capacity may improve after only 6 weeks of HIT, reflecting enhancements in glycolysis activation. Anaerobic capacity responses to HIT have typically been assessed by measuring blood lactate levels in response to standardized exercise load or by measuring anaerobic performance via a Wingate test. A number of studies have demonstrated that HIT lasting between 2 and 15 weeks results in significant increases in anaerobic capacity, increases ranging between 5 and 28 % in untrained males [21, 32, 33], as well as in overweight and obese men [10].

The mechanism(s) underlying these adaptations are likely the result of skeletal muscle adaptations involving marked increases in skeletal muscle capacity for glycolytic enzyme content [34], increases in anaerobic fitness, and increased insulin sensitivity. Additionally, it should be noted that obesity does not appear to negatively affect intrinsic muscle contractility properties (“muscle quality”) [35]. For Maffiuletti et al. [36], the presence of factors such as the handicapping effects of excess fat mass and impaired motor coordination may account for the poor physical performances of obese people of all ages. In the present study, a positive relationship between PO and both anaerobic contributions and lactate concentrations was noted. Concerning the lactate concentrations, which obtained via capillary blood samples using the LactatePro analyzer, higher values obtained after HIT may probably reflect amelioration in glycolysis activity in trained obese group. Although enhancements in anaerobic contributions were associated with PO enhancements, it is possible that the improvements in muscle coordination induced by HIT may also have contributed to PO and to lactate improvement.

From a clinical point of view, our results are valuable in understanding the interaction between intensity and energy contributions during high-intensity exercise. This study demonstrates that incompatibilities in energy balance during SCE bouts may reflect lower anaerobic contributions or poor skeletal muscle function in obese adults. This may, in turn, help clarify why obese people require high-intensity training as part of their multicomponent treatment for obesity.

The Wingate test (30 s of all-out sprint) has been the protocol utilized most often in the context of high-intensity training. This protocol consists of 3 to 4 min of cycle exercise per session, and each session typically occurs three times per week. This protocol, although remarkably short in duration, is extremely rigorous, and subjects must tolerate significant discomfort. Our study is the first to demonstrate that 6 weeks of very short repeated bouts of SCE may improve muscle power, improvements associated with increased anaerobic system contributions. In spite of these adaptations, more studies are necessary in order to understand the effects of such protocols on other health parameters. Finally, although the cardiovascular and metabolic consequences of obesity have been studied extensively over the last two decades, less attention has been paid to investigating the impact of obesity on muscle-energetic interactions for a given exercise. The present study has forced us to consider muscle energy potential during exercise in order to describe the true energetic adaptations that occur during exercise and following a training program for obese individuals.

However, there are some limits in the current study. Firstly, the missing post-intervention measure in several metabolic (e.g., lactate) and hormonal (e.g., catecholamines) parameters, besides psychological variables, may allow us to better understand the effect of such exercise training on metabolic and hormonal adaptations. Secondly, the physical activity and dietary level 48 h prior to the test were not directly controlled, and then we cannot be sure if our instructions were fully respected. Finally, the results obtained in the present study included men and women in the same study group. Given that gender could have affected our results, further studies are needed to address this effect.

In conclusion, this study demonstrated the existence of a disparity in relative anaerobic and aerobic metabolism contributions to total energy release during supramaximal effort in obese adults, before and after HIT. Increased anaerobic contributions after HIT were associated with increased power output, although no changes in fat-free mass were observed. Such results highlight the importance of HIT in enhancing muscle tolerance to exercise by improving anaerobic capacity. Thus, the present findings provide an important first step towards an evidence-based approach for the utilization of HIT as a strategy for the obese sedentary population. However, the role of other training model (e.g., aerobic training) on improving several health parameters (e.g., cardiovascular and metabolic adaptations) cannot be excluded in the context of obesity management.

Finally, the evaluation of energy interactions during exercise must be examined in obese individuals.