**3. Relationship between GH and exercise**

Increases in GH secretion due to stress, such as fasting, or exercise contributes to lead increases in circulating FFAs [34]. Stokes et al. [35] showed that FFA levels may also regulate GH throughout a negative feedback control, as nicotinic acid-mediated suppression of lipolysis, and consequently reducing circulating FFAs, led to an important GH response. This finding may help further explain why individuals with obesity and reduced cardiorespiratory fitness (CRF), who on average have elevated levels of FFAs [36, 37].

Regular aerobic exercise enhances the ability of the body in the transportation and oxidization of FFAs during exercise [38]. This is also found in individuals with impaired fatty acid oxidation, such as those with obesity and diabetes [38–40], and it has been suggested that these improvements may be mediated through exerciseinduced increases in mitochondrial and fatty acid transporter content, carnitine shuttle activity, and CRF [41, 42].

It is reported that low CRF may be a greater predictor of metabolic dysfunction than VAT [43], and as such, improving CRF has emerged as a therapeutic target for individuals with obesity-related disease. Moreover, acute exercise would temporarily increase the GH release, and such responses would be mediated by CRF [4]. Furthermore, although both aerobic and resistance exercise elicit a GH response, the relative contribution of aerobic exercise on GH response and action arguably is not totally understood. In this context, the evaluation of factors that contribute to aerobic exercise-induced GH response and how these changes influence VAT and cardiometabolic health more broadly have been studied [4].

GH promotes lipolysis within AT and increases mitochondrial oxidative capacity [44, 45] Although obesity decreases the exercise-induced GH response, CRF, which, at least, partly, is related to the muscle oxidative capacity, would be a more relevant determinant of exercise-induced GH secretion [4, 46].

Although the exercise and GH eliciting similar effects on AT and lipid metabolism, it is unclear whether exercise induced desirable effects in central adiposity are mediated by changes in physiologic GH response or if these effects in central adiposity and GH response are independent of exercise adherence [33, 47].

Acute aerobic exercise has been shown to increase GH levels, and these changes have been shown to be strongly associated with exercise intensity and volume, a function of exercise duration and frequency [48, 49]. It is suggested that exerciseinduced GH responses may only be elicited at, or above, specific exercise volume and intensity parameters. Sasaki et al. [50] reported that with high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT), the magnitude of GH response to exercise did not increase from pre-intervention measures in sedentary but otherwise healthy men for both interventions. Zhang et al. [51] reported, in a randomized controlled trial with young women with obesity, that when compared to energy-matched MICT, HIIT or supramaximal aerobic exercise led to greater VAT reduction but not greater changes from pre-intervention levels in serum GH measured immediately or 4 h after exercise. In fact, all groups showed elevated GH responses to exercise; however, only the higher-intensity interventions decreased VAT, suggesting that other factors likely contributed to these improvements. In addition, Calixto et al. [52] reported that the velocity of eccentric muscle action alters the acute responses following bench press exercises performed by resistancetrained men with a slow velocity leading to greater metabolic stress and GH response. Jørgensen et al. [53], previously, have pointed out that GH stimulates lipolysis and

### *Obesity: The Relationship between Growth Hormone and Exercises DOI: http://dx.doi.org/10.5772/intechopen.110785*

lipid oxidation during basal and fasting conditions and investigated whether GH also regulates substrate metabolism during exercise. The GH-deficient individuals were studied during exercise with and without GH administration as compared to untreated healthy subjects. It was verified that the GH predominantly stimulated the turnover of free fatty acids in the recovery phase after exercise. Then, it is possible to verify that aerobic and anaerobic exercises influence of GH secretion [51–53] and, consequently, these exercises could have positive effects on the CO.

Whole-body vibration exercise (WBVE), used in systemic vibratory therapy [54], is a type of physical exercise. In the WBVE, mechanical vibration (MV) generated in the vibrating platform is transmitted to the body of an individual that is in contact with this platform. Some publications have reported that the WBVE can alter the release of GH [55–58]. The potential physiological effects of WBVE on various organs/tissues would be also related to possible neuromuscular responses and the tonic vibratory reflex [59–61]. Moreover, the interaction of the MV with the mechanosensory system would be also involved in the effects described by the WBVE. The mechanosensors in the body cells, once stimulated by the MV, modulate the biological activity through specific signaling pathways, such as releasing hormones, like GH, and other substances (e.g., amino acids, proteins, lipids, ions) [54]. In consequence, several biological effects might be observed in several organs and tissues due to the WBVE [59, 61]. Furthermore, it is relevant to highlight that WBVE, depending on the parameters used in the protocols of the interventions and posture, can be considered aerobic or anaerobic exercises [62, 63].

The mechanisms driving the exercise-induced improvements in cardiometabolic outcomes and the relation with the GH is not fully clear yet. But, due to the various metabolic impacts of the exercise and GH, it is presented in **Figure 2** a possible relationship among GH and exercise, VAT and obesity.

Like GH, exercise exerts potent lipolytic effects, particularly on VAT [59]. Furthermore, exercise elicits improvements in ectopic fat in the absence of body

#### **Figure 2.**

*The proposed relationship among growth hormone, physical exercises, adipose tissue, and cardiometabolic outcomes. Green lines represent positive effects from physical exercise to visceral adipose tissue.*

mass loss [4]. As exercise induced GH response occurs in an intensity-dependent manner, and appears to be mediated by CRF, this may explain why HIIT can lead to similar improvements in WC and VAT than in higher-volume MICT despite requiring less time and expending less energy [60]. Moreover, considering the physiological adaptations and general health benefits of HIIT, individuals with obesity would be encouraged to perform such exercise.
