Sporting activity
Endurance
Resistance
5000–10,000 m run
Shot put
Half marathon—marathon
Discus throw
20–50 km race walk
Javelin throw
Olympic distance triathlon
Hammer throw
Ironman triathlon
Olympic style weightlifting
Cycling—road racing
Power lifting
Cycling—individual time trial
Wrestling
To aid in the clear and concise discussion of this topic, it is important to present some operational definitions of terms and concepts for the reader. Sport physiology is the application of the discipline of exercise physiology to the special demands of sport. Specifically, it involves applying the concepts derived from exercise physiology to optimize the training of athletes and enhance their physical performance (i.e., competition). Endocrinology is that branch of physiological–medical sciences that deals with the endocrine-related activities of glands and tissues that release hormones . In turn, a hormone is a chemical substance, formed in one gland/tissue of the body and carried in the blood to another gland/tissue where it exerts functional effects (i.e., endocrine function). Additionally, this definition of hormones has been recently broadened to include chemical substances formed by cells of the tissue, which in turn act on neighboring cells (i.e., paracrine function) or the same cells that produce them (i.e., autocrine function). In assessing and quantifying exercise training, it is critical to understand the concept of exercise dosage. Exercise dosage consists of “how much” exercise an individual is being exposed to in their training regime. The components which are manipulated to modulate the dosage are the duration (volume) of an exercise session, the frequency of exercise sessions per day–week, and the intensity of effort within a respective exercise session. The first two components of dosage are self-explanatory, but intensity is somewhat more complex. Classically, the perception of how difficult intense exercise is has been linked to cardiovascular responses, usually expressed as a percentage of maximal heart rate (HRmax) or maximal oxygen uptake (VO2max, which represents the amount of oxygen being utilized by body tissues which is proportional to overall energy expenditure; VO2 = (heart rate × stroke volume) × arteriovenous oxygen content differential; [4, 5]). For endurance-based sport activities (e.g., 10,000 m distance run), there is a high reliance on the cardiovascular system and aerobic energy metabolism to determine performance capacity. This means for such activities, the expressing of intensity relative to VO2max or HRmax is appropriate, although VO2max is recognized as the “gold standard.” On the other hand, resistance-based sport activities are highly explosive in muscular force–power output (e.g., shot put, hammer throw) and performance is far less dependent upon cardiovascular functioning and much more so on anaerobic energy production pathways. For such activities, the expression of intensity based upon VO2max or HRmax are far less valid (although, in some situations the intensity of some such activities is still expressed relative to VO2max; [5]). In the latter sporting activities, since resistance exercise training is a predominant component, the expression of exercise intensity is based upon percentage of maximal performance relative to a resistance task (i.e., the lifting of a specific amount of weight). The reference criterion here is the 1 repetition maximum (1 RM). This represents the maximal weight–force that can be generated for that task and signifies an intensity capacity of 100 %. Thus, submaximal intensity efforts are a percentage of the maximal weight–force generated (e.g., task, bench press → 1 RM = 120 kg; therefore, 60 % effort = 72 kg; [6]).
Table 5.2 presents some examples, explanation and terminology to aid in understanding the intensity concept and how this aspect of dosage is quantified in the sport physiology research literature [1, 7, 8]. On reviewing the table, it is obvious that team sport activities such as football (soccer) or field hockey are not represented. These sports activities are multidimensional in the demands that are placed on the physiology of the athlete and the intensity of their efforts (i.e., highly variable)—influenced by the position of play of the athlete, the competitiveness of the game, and action-events in the game. Thus, quantifying intensity in such sports gaming activities is extremely difficult. This difficulty makes it a highly complex area to study in sports physiology, and far more research is needed in the area of team sports.
Table 5.2
Examples of endurance and resistance exercise actives classified by different levels of intensity
Category term | Effort perception | Relative intensity | Energy pathway predominating | Representative duration (minute) | Other terminology | Sporting examples |
|---|---|---|---|---|---|---|
Endurance | ||||||
Light exercise | Easy | < 35 % VO2max | Aerobic | > 30 | Short term, submaximal | Warm-up activities |
Moderate exercise | Modest difficulty | < 70 > 35 % VO2max | Aerobic | 30–180 | Submaximal, prolonged | Cycle-run training |
Heavy exercise | Difficult | < 100 > 70 % VO2max | Aerobic–anaerobic | ≤ 120 | Submaximal, prolonged, high intensity | 10,000 m, marathon run, triathlons |
Maximal exercise | Strenuous | 100 % VO2max | Aerobic–anaerobic | < 15 | Maximal or max, high intensity | 1500–5000 m runs |
Supramaximal exercise | Extremely strenuous | > 100 % VO2max | Anaerobic | < 1 | All out, power | 100–400 m sprints |
Resistance | ||||||
Submaximal exercise | Modest—difficult | < 70 > 35 % 1 RM | Aerobic–anaerobic | ≥ 1 | Submaximal | Circuit resistance training |
Maximal exercise | Extremely strenuous | ~100 % 1 RM | Anaerobic | < 0.1 | All out, power | Shot put, javelin, Olympic lifts |
Supramaximal exercise | Extremely strenuous | > 100 % 1 RM | Anaerobic | ≤ 0.1 | Negatives | Eccentric resistance training |
Endocrine Responses
Acute Exercise
The acute responses of the major physiological systems to a single bout of exercise (training) or a sporting event (competition) can be large and robust and are usually proportional to the intensity of the exercise (most certainly for endurance events), although it is important to recognize that the relationship of this proportional response(s) is not always linear in nature [7]. Table 5.3 presents the major physiological systems and some of the key parameters reflective of the respective systems and how these parameters change in response to an exercise session/sports event based upon the emphasis of the activity being either endurance or resistance based in nature.
Table 5.3
Physiological responses to an acute exercise session based upon whether the activity is predominating involved with endurance or resistance forms of exercise activity. It is important to note that the changes in measure/parameter denoted here are relative to before versus immediately after the activity. It is well documented that as an athlete moves into the recovery period from exercise measure/parameter changes can be different from those observed at the completion of exercise [8, 9, 77]
Physiological systems | Measure/parameter | Exercise-sport activity predominating training component | |
|---|---|---|---|
Endurance | Resistance | ||
Cardiovascular | Heart rate | ↑ | ↑ |
Stroke volume | ↑ | ↑↓ | |
Cardiac output | ↑ | ↑↓ | |
Arteriovenous O2 difference | ↑ | ↑↓ | |
Respiratory | Tidal volume | ↑↑ | ↑ |
Breathing frequency | ↑↑ | ↑ | |
Minute ventilation | ↑↑ | ↑ | |
Metabolic | ATP → ADP + Pi + energy | ↑ | ↑↑ |
CP → creatine + phosphate + energy | ↑ | ↑↑ | |
Anaerobic glycolysis | ↑ | ↑↑ | |
Aerobic glycolysis | ↑↑ | ↑↓ | |
Tricarboxylic acid cycle | ↑↑ | ↑↓, nc | |
β-oxidation cycle | ↑↑ | ↑↓, nc | |
Muscle | Force | ↑ | ↑↑ |
Power | ↑ | ↑↑ | |
Endurance | ↑↑ | ↑ | |
Endocrine | Adrenocorticotrophic hormone (ACTH) | ↑ | ↑ |
Aldosterone | ↑ | ↑ | |
Angiotensin | ↑ | ↑ | |
Antidiuretic hormone (ADH) | ↑ | ↑↓ | |
Cortisol | ↑ | ↑ | |
Dehydroepiandrosterone (DHEA) | ↑ | ↑ | |
β-Endorphin | ↑ | ↑ | |
Epinephrine (adrenaline) | ↑↑ | ↑↑ | |
Estrogens | ↑ | ↑ | |
Follicle-stimulating hormone (FSH) | ↑↓, nc | ↑↓, nc | |
Glucagon | ↑ | ↑ | |
Growth hormone (GH) | ↑ | ↑ | |
Insulin | ↓ | ↑↓, nc | |
Insulin-like growth factor-1 (IGF-1) | ↑, nc | ↑, nc | |
Leptin | ↑↓, nc | ↑↓, nc | |
Luteinizing hormone (LH) | ↑↓, nc | ↑↓, nc | |
Norepinephrine (noradrenaline) | ↑↑ | ↑↑ | |
Progesterone | ↑ | ↑ | |
Prolactin (PRL) | ↑ | ↑ | |
Testosterone | ↑ | ↑ | |
Thyroxine (T4) | ↑ | ↑ | |
Triiodothyronine (T3) | ↑ | ↑ | |
Vitamin D | ↑ | ? | |
As noted earlier, the primary focus in this chapter is the endocrine system responses to exercise. Table 5.3 illustrates the general changes for a variety of hormones in response to endurance–resistance exercise. It is important to recognize, however, that many of these hormonal responses are and not independent of one another but highly interrelated. To illustrate this point, Dr. Henrik Galbo devised an explanatory model of the hormonal responses to exercise consisting of three interactive phases [9, 10]. The first phase of this model deals with the hormonal response immediately at the onset of exercise, with these responses taking just seconds to occur. These responses revolve around the increased sympathetic nervous system (SNS) activation that occurs with the onset of body motion. This increased SNS activity can also be a result of anticipation to the stress of the ensuing exercise, which is most certainly the case in sport competition scenarios. This increased SNS activity results in catecholamine (norepinephrine) release at target tissues directly as well as elevations in circulating catecholamine from so-called sympathetic spill-over effects [9–11]. This effect is further amplified by the sympathetic connection to the adrenal medullary gland, which in turn adds to the circulating catecholamine (epinephrine) response [10, 12]. Concurrent with these sympathetic–adrenal actions, pancreatic insulin secretion begins to be inhibited while glucagon secretion becomes stimulated [10]. This entire process involves a feed-forward mechanism of the central nervous system to drive these initial responses, although the events are also modified by peripheral afferent neural input from sensory receptors in particular those of skeletal muscle [12, 13].
The intermediate or secondary phase takes slightly longer to develop but is still typically very fast, beginning usually in much less than a minute from the onset of exercise. In this stage, the hypothalamus begins the process of releasing its hormones such as thyrotropin-releasing factor, corticotropin-releasing factor (CRF), and growth hormone-releasing factor (GHRF) in an attempt to provoke changes at the anterior pituitary gland to stimulate the release of select hormones. As the pituitary begins to respond to the hypothalamic stimulus, its “trophic hormones” begin to be added to the circulation, and these hormones begin to act upon their specific peripheral target glands to stimulate additional hormonal release. One of the most rapidly acting in this cascade of events is the hypothalamic–pituitary–adrenocortical interaction where CRF brings about adrenocorticotrophic hormone (ACTH) release and that in turn brings about cortisol release [8, 13, 14].
If the duration of an exercise session continues, there is a transition beyond the intermediate phase into a third phase of response which is a more prolonged state. In this third phase, the responses of the sympathetic–adrenal axis are being augmented by other hormones from the anterior and posterior pituitary (e.g., ADH, GH, PRL; see Table 5.3 for hormonal abbreviations) and the peripheral endocrine glands subordinated to pituitary regulation (testosterone, T4, T3, IGF-1; [7, 8]). Additionally, during this phase, the skeletal muscle begins to release select cytokines (e.g., interleukin-6, IL-6), hormonal-like agents, into the circulation, which affect other hormones to be released (IL-6 ⇒ cortisol; [15]).
Phase one and two of the model propose that neural factors are the primary stimuli regulating the hormonal responses to exercise; however, in the third phase of response, there is an ever-increasing influence of the humoral and hormonal factors that regulate the overall responses due to the changes in the “internal milieu” [10]. This shifting of primary regulatory factors allows an increasing reliance upon feedback rather than feed-forward control mechanism to determine the magnitude of the hormonal response. The influence of humoral and hormonal stimuli in modulating the hormonal levels are magnified as the exercise duration is extended, and energy substrate availability issues cause shifts in energy fuel usage (i.e., ↓ carbohydrate ⇒↑ lipid) or hydration issues (i.e., hemoconcentration and/or dehydration), which begin compromising the thermoregulatory ability and lead to greater heat storage within the body affecting hormonal responses (e.g., ↑ heat storage ⇒↑ norepinephrine, epinephrine; [4, 12, 13]). A need for conciseness does not allow for a more extensive discussion of all of the intricate details of hormonal responses to exercise, but the model of Galbo does illustrate that endocrine actions are highly interactive and complex [9, 10].
Chronic Exercise
The general responses of the body’s various physiological systems to an exercise bout/session after performing a progressive exercise training regime (chronic exposure) are similar to those as before such training. In other words, an acute bout of exercise after chronic training is still a stimulus to the physiology of the body. However, at all exercise intensities, less than the maximal level, such responses are typically attenuated to some extent. The greater the training adaption incurred due to the training regime, the greater is the attenuation of the response. The exception to this occurrence is maximal or supramaximal exercise. In such situations, the training adaptations result in a great level of workload performed at maximal/supramaximal efforts, for example, the athlete can run further or run faster over a fixed distance or lift a greater maximal amount weight, etc. The greater absolute maximal workload achievement in turn produces a greater physiological stimulus and thus comparable (or greater) maximal responses in the measures/parameters of the physiological systems, in other words, typically not an attenuation of responses. A noted allowance to this generalization is HRmax, as it is common for this parameter to be slightly lower or unchanged after a well-executed training regime even when there is substantial and further cardiovascular adaptation [4, 5, 13].
Relative to the endocrine system, typically after an adaptation and physical improvement to a training program, an exercise session (endurance or resistance based) still provokes a hormonal response. But, just as noted above, the responses tend to be attenuated. These attenuated responses come about by a greater sensitivity of target tissue to the hormonal stimulus and because the level of neural, humoral, and hormonal stimuli disturbances in the blood that influence the various endocrine glands become far less [13]. Also, relative to the former point (i.e., sensitivity), in response to an exercise training regime, many target tissues increase the expression of functional hormone receptors, receptor affinity for hormones become increased, and post-receptor amplification mechanisms in the cells of target tissues are typically increased. Essentially all these changes result in a target tissue needing less amount of a hormone to bring about a physiological outcome/change.
Maladaptation in the Exercise Training Process
Many athletes have met stagnation or decline of their performance in their career though they are training hard and pushing as much as possible . Athletes, especially elite athletes, wish to enhance their performance by constantly increasing their training loads. It has been estimated that the exercise training loads of athletes have increased on average by 20–25 % over the past decade [16–18]. The result of such training approaches is that sooner or later an athlete reaches the limit of his/her individual abilities. When this occurs, there are two possibilities, first an athlete’s training plan prescribes adequate amount of rest and the athlete develops due to supercompensation. Secondly, the athlete keeps on training with high loads and loses an optimal balance between training stressors (plus non-sport stressors affecting them) and recovery. The second way pushes the athlete in the direction of developing a state of overreaching and/or the overtraining syndrome (OTS).
Because there is a lack of common and consistent terminology in this research field, the following definitions are presented to aid the reader, as they are somewhat widely used definitions [19]:
Overreaching—an accumulation of training and/or non-training stress resulting in short-term decrement in performance capacity with or without related physiological and psychological signs and symptoms of maladaptation in which restoration of performance capacity may take several days to several weeks.
Overtraining—an accumulation of training and/or non-training stress resulting in long-term decrement in performance capacity with or without related physiological and psychological signs and symptoms of maladaptation in which restoration of performance capacity may take several weeks or months.
These definitions emphasize that the difference between overreaching and overtraining is the amount of time needed for performance restoration and not the type or duration of training stress or degree of impairment. This opinion was recently updated by leading sports science organization American College of Sports Medicine (ACSM) and European Congress of Sport Science (ECSS) Joint Consensus Statement [20].
According to the consensus statement, overtraining is used as a process of intensified training with possible outcomes of short-term overreaching (functional OR (FOR)), extreme overreaching (nonfunctional OR (NFOR)), or OTS. Overreaching is often used by athletes during a typical training cycle to enhance performance. Intensified training can result in a decline in performance; however, when appropriate periods of recovery are provided, a supercompensation effect may occur with the athlete exhibiting an enhanced performance compared with baseline levels.
This form of short-term OR can also be called FOR. When this intensified training continues, the athletes can evolve into a state of extreme OR or NFOR, which will lead to a stagnation or decrease in performance that will not resume for several weeks or months. At this stage, the first signs and symptoms of prolonged training distress such as performance decrements, psychological disturbance (decreased vigor, increased fatigue), and hormonal disturbances will occur, and the athletes will need weeks or months to recover. Several confounding factors such as inadequate nutrition, illness, and sleep disorders may be present. All of these factors combine to add to the total stress placed upon the athlete and in doing so can impact the effect of training process (Table 5.4 illustrates and summarizes these points).
Table 5.4
Development of functional overreaching (FOR), nonfunctional overreaching (NFOR), and overtraining syndrome (OTS)
The distinction between NFOR and OTS is very difficult and will depend on the clinical outcome and exclusion diagnosis. The athlete will often show the same clinical, hormonal, and other signs and symptoms. Therefore, the diagnosis of OTS can often only be made retrospectively when the time course can be overseen. The physiological cause to OTS is known—the exercise training load placed upon an athlete is too great, the stress level exceeds their ability to adapt [9, 18, 20]. Still it is difficult to determine on an individual basis how much is too much stress .
Some researchers have proposed there may be two discrete neuroendocrine varieties [21, 22], that is, OTS consists of a hyper-arousal and/or a hypo-arousal form. This conclusion is based upon the finding that in certain physiological parameters, diverging symptomology exists. The hyper-arousal form is also referred to as the “sympathetic” or “Basedow’s” OTS. It is commonly observed in “power” athletes (e.g., sprinters, jumpers, weight lifters) and occurs less frequently than the hypo-arousal disorder. The hypo-arousal form is more common and is also referred to as “parasympathetic” or “Addison’s” OTS. This form of the disorder is frequently observed in endurance-trained athlete (e.g., long-distance runners, rowers, cross-country skiers, cyclists, swimmers). Each form of the disorder has some similar characteristics and symptoms (i.e., in particular declining physical performance), but there also are obvious psychophysiological differences (see Table 5.5; [22]).
Table 5.5
Pathophysiologic findings in hyper-arousal versus hypo-arousal forms of the overtraining syndrome (OTS)
Parasympathetic, hypo-arousal | Sympathetic, hyper-arousal |
|---|---|
Decrease in physical performance | Decrease in physical performance |
Easily fatigued | Easily fatigued |
Depression | Hyperexcitability |
Normal sleep | Disturbed sleep |
Normal constant weight | Weight loss |
Low resting HR | Increased resting HR and blood pressure |
Hypoglycemia during exercise
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