Thermal responses to cardiovascular fatigue: measuring the response to prolonged exercise.
The response of the skin temperature to the generation of fatigue during exercise is an indicator of the nature of the effort. As we saw in the article on local fatigue, during isolated neuromuscular exercise, the temperature of the region increases. We will now discuss what happens with cardiovascular exercise.
Differences between central and local fatigue and their physiological processes.
As occurred with muscular fatigue (local), central fatigue implies a multifactorial response related to physical exercise, where central and peripheral mechanisms interact, characterized by a decrease in the capacity or ability to generate muscular strength or power, which causes physiological, mechanical and psychological modifications, and a reduction in performance as a bodily strategy to preserve cellular integrity and function” (1).
The fundamental characteristics of fatigue lie in the decrease in the capacity for effort or performance and the decrease in the capacity to generate maximum muscle force (2).
This complex response of central and peripheral mechanisms has traditionally been divided into local or peripheral and general or central fatigue (2-4):
- Central fatigue can be understood as the alteration in the ability or capacity of the central nervous system (CNS) to recruit motor units at a discharge rate higher than the tetanic fusion frequency, where the decrease in central activation during exercise can be originated from several factors at the spinal and/or supraspinal level (4). The causes of this type of fatigue are diverse in nature, as the mechanisms of fatigue are multifactorial and include psychological, homeostatic and metabolic aspects that affect the musculoskeletal, cardiovascular, respiratory and nervous systems (3).
- Local or peripheral fatigue refers to changes that take place locally in the muscles, hindering the execution of downward central commands (3).
Therefore, central fatigue attends to changes in the function of the nervous system, and peripheral fatigue to modifications at the muscular level, being interdependent in the mediation of peripheral afferents (4).
While strength exercise requires peripheral effort, cardiovascular exercise presents a combination of both types of central and peripheral fatigue. While it is true that some types of strength training, where low to high repetition loads are used (also defined as strength endurance) can have similar metabolic behavior to cardiovascular training, they demand a more pronounced peripheral fatigue, which will be the final limiting factor of the exercise.
The studies by Garnacho-Castaño et al. (5), compare the effect of two types of training with the same lactate threshold: a half squat training at 23% 1RM and a constant cycle ergometer test at 126.9 W, to analyze the cardiovascular and muscular responses.
At the cardiovascular level, the cycle ergometer test is the one that significantly increases cardiovascular values (Figure 1).
However, at the peripheral level, the response varies being only strength training the one that sees a significant decrease in its mechanical capabilities to develop power in a jump test, since it is the peripheral fatigue that is dependent on the generation of fatigue (Figure 2).
Cardiovascular exercise as a fatigue generator
Both cardiovascular exercise and multi-joint strength exercise request large muscle groups in multiple combinations, so there is a significant increase in blood flow.
As we saw in previous sections, in strength exercise, mechanical behavior and peripheral factors play a large role in the generation of fatigue in strength training. While in cardiovascular training we need the interaction of many factors for fatigue generation.
For many years, the model that explained the onset of fatigue in cardiovascular training was that the heart was not able to provide sufficient oxygen to the muscle at the rate necessary to maintain the intensity during the contraction processes. Today, we know that increased blood flow is one of the limiting factors in cardiovascular endurance exercise. But there are other factors, such as muscle capillarization, the state of energy depletion, the accumulation of metabolites in the muscle membrane or even motivation. Figure 3 summarizes the factors.
Therefore, to understand fatigue, it is necessary to know how all these systems are affecting the muscle and its contraction. To this end, analyzing the type of response and the differences in the type of thermal pattern allows us to know what the character of the effort has been and which fatigue-generating pathways have predominated during training (more mechanical or more metabolic).
Thermography as a tool to measure the response to cardiovascular exercise.
A recent review by Hillen et al. (7) investigated the role of thermography in the study of exercise physiology. The authors noted three types of thermal response to exercise depending on the type of exertion performed, which are depicted in Figure 5:
- Local fatigue pattern, as described in this article.
- The pattern of fatigue of large muscle groups.
- Cardiovascular fatigue pattern.
In this article, we will focus on the third type: the thermal response to cardiovascular exercise. As Fernandez-Cuevas describes in his 2012 thesis (8), aerobic exercise presents a very characteristic response (a Dalmatian, or hot spot pattern as the author names in the thesis). While other authors, such as Merla et al. (9) call it “tree-shaped hyperthermic spots” and are a consequence of the body’s attempt to thermoregulate through the circulatory system and perforating vessels. A real example of this pattern can be seen in Figure 6.
As with the sensation of heat perceived by the system, with increasing duration of exertion and the onset of fatigue, cutaneous vasodilation occurs with the aim of warm blood flow radiating through the perforating vessels to the skin surface to cool the body by convection (10).
In the scientific literature, increased core body temperature has been highlighted as one of the limiting factors of performance during aerobic exercise, being a major cause of fatigue (11). The need to shunt blood to the perforating vessels to thermoregulate when fatigue increases create a blood flow disadvantage in the muscles and brain during exertion, which seems to give rise to the Dalmatian or hot spot pattern, and makes sense of the thermoregulation model of fatigue.
As we have seen, the musculature loses vascularization as a reactive measure to thermoregulation. Therefore, during exercise, the main muscle groups and synergists lower their temperature (Figure 7).
In contrast to strength exercise, skin temperature progressively decreases in aerobic exercise in the exercised regions, as noted in the literature (7,8).
In a review of the literature, most studies find a large variability between subjects, but none point to an increase in temperature during cardiovascular exercise (7). Of note, Duc et al. (12) note that the decrease in temperature has a high positive correlation with the decrease in pedaling efficiency and a moderate negative correlation with heart rate (p<0.001), as we see in Figure 8.
Although, no research reports increases in temperature, all the articles point out that near the end or at the end of the cardiovascular tests or exercises a Dalmatian or hot spot pattern is presented.
The thermal response to cardiovascular exercise in successive hours results in an increase in the temperature of the exercised regions and in secondary regions as compensation for physiological processes, as pointed out by Fernandez-Cuevas (8) research, summarized in Figure 9.
Finally, it should be noted that joints such as the ankle or knee, after running at moderate intensity and with a duration of 45 minutes, increase their temperature as a response possibly to their lower capacity to thermally regulate themselves and the mechanical demand during exercise.
The thermal response to fatigue produced by cardiovascular exercise has a decreasing trend that is intensity-dependent. This response is induced to a greater extent by the body’s thermoregulatory system which, through noradrenergic sympathetic activity (with the release of norepinephrine and neuropeptide Y), produces cutaneous arterial vasoconstriction.
Consequently, there is a redistribution of blood volume to the organs demanded during exercise. All these processes are necessary to adjust the hemodynamic state and meet the oxygen requirements of the brain, heart and muscles demanded during exercise.
It should be noted that thermography is more accurate in detecting vasomotor changes than sweating, as these are the most efficient option as they are less costly for the body to deal with the increase in internal temperature. The appearance of tree-shaped hot spots (9) supports this assertion.
As exercise progresses, and fatigue begins to accumulate, heat production in active organs and core temperature thermal equilibrium are altered.
Another way in which the sympathetic system acts to try to dissipate the heat appears is the neurogenic reflex of vasodilation (non-adrenergic vasodilator system), which acts when the internal temperature of the exercised muscle tissue exceeds a certain level and by means of cholinergic neurotransmitters causes active vasodilation of the perforating vessels of the skin, which ends up producing the Dalmatian or hot spot pattern (7).
As we have seen, the nervous system plays an important role in skin temperature control. And it may be one of the factors affecting the large variability of responses to exercise. In future posts, we will delve deeper into the role of the nervous system in body temperature and exercise.
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