Which Of The Following Adaptations Occurs With Exercise Training - T-Tees - Your Answers Await, Life's Questions Unraveled

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Normal (Acute) Adaptions

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Cardiovascular

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Changes in Cardiac Output

The ultimate goal of the cardiovascular response to acute aerobic exercise is to maximize cardiac output and match the metabolic demands of the musculoskeletal system.[1] In order to change cardiac output, there may be a change in either heart rate or stroke volume. During acute exercise, the main driver for augmentation is an increase in heart rate.[2] As aerobic exercise occurs, β-adrenergic stimulation by catecholamine release and vagal withdrawal leads to increased heart rate and oxygen delivery to tissues.[3] Additionally, changes in stroke volume also influence cardiac output.[1]

In the acute setting, adjustments in stroke volume are reflected by changes within the left ventricle. During exercise, an increase in primarily left ventricular (LV) end-diastolic volume augment stroke volume; however, a reduction in left ventricular end-systolic volume may also play a small role. Various factors have been shown to affect LV end-diastolic volume, including heart rate, intrinsic myocardial relaxation, ventricular compliance, ventricular filling pressures, atrial contraction, and pericardial and pulmonary constraints.[4] Alterations to any of these variables may result in additional alterations in stroke volume and, subsequently, cardiac output.

Changes in Blood Volume

Mechanisms inherent to blood volume and blood mass also allow the body to adapt following aerobic exercise. One way exercise may lead to increased blood volume is through activation of the renin-angiotensin-aldosterone cascade. Activation of this hormonal pathway causes water retention by the kidneys and increases plasma albumin, causing hypervolemia.[5][6] Studies have noted a single episode of exercise may augment blood volume 10% to 12% within a 24 hour period and may reach peak volumes between 10 and 14 days of training.[7][8] Additionally, over a 30 day period of exercise, both plasma and red blood cell volume may increase an additional 8 to 10% relative to pre-training levels.[8] Expansion in RBC volume is often accompanied by an increase in RBC mass as well. This is thought to improve the ability to buffer lactate and improve the body’s ability to produce energy through anaerobic metabolism.[9]

During blood volume expansion, it is hypothesized that exercise augments erythropoiesis by way of androgen production. Androgens cause an increase in catecholamine and cortisol levels, leading to further erythropoietin (EPO) release and reticulocyte production.[10] In efforts to optimize oxygen-carrying capacity and meet metabolic needs, changes in blood volume and mass are important and quick ways the body may adapt to aerobic training.

Blood Pressure

It has been well documented that consistent aerobic training reduces blood pressure in both the long and short term – in some cases as quickly as a few hours following one bout of exercise. A meta-analysis by Carpio-Rivera et al. demonstrated an average reduction of systolic blood pressure (sBP) by -4.8 mmHg and diastolic blood pressure (dBP) by -3.2 mmHg following one exercise session and continued reductions of sBP by -3.2 mmHg and dBP by -1.8 mmHg up to 24 hours after exercise.[11]

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The mechanism for this is likely due to aerobic exercise’s effect on parasympathetic and sympathetic nervous activity, nitric oxide (NO), the prostanoid system, the renin-angiotensin system, and vascular remodeling.[12][13] Immediately following exercise, the parasympathetic system (which was previously inactive before commencing exercise) reactivates, and the previously active sympathetic system inactivates. Collectively, this related activation/inactivation response results in decreased blood pressure.[14] Additionally, aerobic exercise increases the availability of NO by preventing its removal by reactive oxygen species.[2]

Consequently, greater amounts of nitric oxide induce more vasodilation and decrease blood pressure. Some studies have also shown exercise increases levels of prostacyclins, which may have an additional vasodilator effect. However, evidence supporting this is limited at the moment.[2][15] Lastly, blood pressure may also be impacted by decreased angiotensin levels found in exercise-trained individuals.[2][16] A decrease in angiotensin levels results in more vasodilation and less vascular dysfunction leading to lower blood pressure.[2]

Musculoskeletal

Changes in Mitochondria

Aerobic exercise has also been shown to initiate cellular and molecular changes to improve oxidative capacity. One of the main cellular modes of improving oxidative capacity is by increasing both the number and size of mitochondria.[17] Some studies have demonstrated growth in mitochondria density and capacity in as little as two weeks of aerobic exercise, while others suggest a longer time frame of about six weeks.[18][19]

The timing of adaptation is likely dependent on the training history of subjects and the type of aerobic exercise (endurance training versus high-intensity interval training (HIIT)) (Hughes 2018). In either case, the same mechanisms are thought to be responsible for these adaptations. Exercise has been shown to induce peroxisome proliferator-activated receptor-gamma coactivator (PGC)−1α transcription. During aerobic exercise, an increase in PGC-1α results in more mitochondria biogenesis and density, which subsequently improves glucose and fatty acid oxidation.[20] Additionally, newer research suggests that aerobic exercise may increase the activity of p53 in as little as three hours.[21]

Since being discovered as the original tumor suppressor protein, p53 has been shown to have additional roles in mitochondria biogenesis by modulating transcription factors and altering the mitochondrial genome.[19] These additional alterations may lead to further enhancements in mitochondrial density. By amplifying mitochondria volume within skeletal muscle, an individual has improved capacity to generate and supply the body with energy.

Muscle Capillary Characteristics

An increase in cardiac output would decrease the efficiency of oxygen uptake at muscle cells without muscle capillary growth. To accommodate for the drastic magnification in cardiac output, muscle capillaries undergo rapid growth. Most of the growth appears to occur within the first weeks of training before plateauing after about four weeks.[2] A study by Klausen et al. demonstrated that after 8 weeks of aerobic exercise, there was a 20% increase in capillary density, with much of the growth happening early in training.[22]

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Capillary growth is thought to occur mainly by shear stress and passive stretch. In shear stress, capillaries undergo longitudinal splitting resulting in two new parallel capillaries. With passive stretch, capillary growth occurs primarily through angiogenesis, where new capillaries sprout from existing capillaries.[23] Together, these mechanisms allow muscle capillaries to quickly adapt to the stress of aerobic exercise and optimize cardiac output and thus blood and oxygen delivery to skeletal muscle.

Glucose Metabolism In Muscle

Aerobic exercise has been linked to increased insulin sensitivity within skeletal muscle, which plays a large role in glucose metabolism as both a consumer of glucose and a storer of glucose (glycogen). Magkos et al. reported that a single episode of exercise improved insulin sensitivity from 12-48 hours after exercise.[24] One mechanism for this is through insulin signaling by increased GLUT4 transporter availability.[20]

GLUT4 is an insulin-stimulated transporter protein responsible for glucose uptake in muscle cells. On a molecular level, low to moderate aerobic exercise at <70% VO2 max has been linked to more production of AMP-activated protein kinase (AMPK) – a sign transducer involved in glucose uptake in skeletal muscle, possibly through increased GLUT4 translocation.[25] Studies have suggested that moderate aerobic training at 70% to 75% of VO2 max for 1 hour may increase GLUT4 concentrations in as little as one week.[20][26] Altogether, additional transmembrane GLUT4 allows for improved glucose translocation into the skeletal muscle and improved energy output and performance for the skeletal muscle.

Chronic Adaptations

Cardiovascular

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Structural Heart Changes

Over time, regular exercise causes the heart to undergo structural change and accommodate the homeostatic needs of the individual. In the cardiovascular system, this occurs through the increased end-diastolic right (RV) and left ventricular (LV) volume, LV hypertrophy and mass, and left atrium (LA) volume.[27] A study by Arbab-Zadeh et al. in 2014 demonstrated that previously sedentary individuals who underwent one year of endurance training experienced increases in LV mass and LV end-diastolic volume. Interestingly, these individuals initially experienced LV concentric hypertrophy from the 6-9 month period, followed by eccentric hypertrophy around the one-year period.[28] This form of cardiac remodeling results from the proliferation of myocytes in response to increased cardiac load. Ultimately, the goal of cardiac hypertrophy is to improve cardiac function by increasing oxygen delivery to muscles, reducing cardiac output at rest, and improving cardiac output during activity.[29]

Heart Rate Changes

At rest and submaximal exercise, a trained individual’s heart rate will be lower due to an increase in vagal tone and increased parasympathetic activity.[30] Studies have shown that maximal heart rate may be reduced by 3% to 7% due to the downregulation of β-adrenergic receptors.[31][32] This likely allows for increased left ventricular filling times, which preserves large end-diastolic volumes and stroke volumes in trained individuals.[2] Collectively, these changes continue to allow the cardiac output of an individual to continue to meet the body’s metabolic demands efficiently.

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Arterial Characteristics

As cardiac output increases, there is increased perfusion through the musculoskeletal system. In order to adapt to changes in blood flow, arteries and arterioles undergo remodeling in response to hemodynamic factors. As perfusion increases, arteries increase in diameter and reduce the wall thickness to augment blood volume carrying capacity.[33] This has been evidenced by an article by Dineno et al. 2001 which showed enhanced femoral artery diameter by 9% after 3 months of aerobic training in untrained individuals.[34]

Studies have shown that shear stress, the frictional force on the vascular endothelium, is the main driver that induces artery enlargement. One way it does this is through increased nitric oxide (NO) synthesis. NO acts directly on smooth muscle cells within arterial walls to cause vasodilation and can also promote vascular endothelial growth factor (VEGF), leading to angiogenesis and more arterial growth.[35] Capillary neogenesis has already been discussed.

Musculoskeletal

Muscle Hypertrophy and Myofibrillar Adaptations

Similar to resistance training, aerobic endurance training has been shown to elicit muscle hypertrophy and growth.[19] Konopka and Harbor explain that effective aerobic exercise, defined as maintaining heart rate reserve >70% for 30 to 45 minutes at least 4 days per week, has the potential to induce muscle growth. The large volume of low-load exercise initiates a large number of contractions within the desired muscle.[36]

Studies have shown that previously sedentary participants who performed cycling for 12 weeks using these protocols saw an increase in up to 11% muscle mass.[19] Additionally, slow-twitch type I fibers have been shown to increase in the cross-sectional area following aerobic training, but studies have not been consistent regarding adaptations of fast-twitch type IIa fibers. Coggan et al. reported a significant increase of 12% and 10% in type I and type IIa fibers, respectively, in older individuals undergoing 12 weeks of extensive endurance training.[37] However, Harber et al. only noted an increase in slow-twitch type I fibers in similar populations.[38] These hypertrophic changes and adaptations are thought to be driven by changes in muscle protein synthesis, which may increase by as much as 22%.[39] This is in part by the stimulation of anabolic pathways, creating a positive protein balance, and improving blood flow and amino acid delivery to the stimulated muscle.[37][39]

Lastly, there is thought to be a dampening of catabolic pathways from aerobic exercise, which may help create a positive muscle protein balance. Both FOXO3a and myostatin, regulators of intracellular protein degradation and skeletal muscle atrophy, have been shown to be significantly reduced following 12 weeks of aerobic exercise in older women. This suggests one possible molecular mechanism is to alter protein breakdown, although more studies need to be performed to determine further mechanisms.[37][39]

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