Essay on the Underlying Mechanisms of Increased Vo2 Max in Mary
Ann
As mentioned above, a 27-year-old sedentary female named Mary Ann improved her VO2 max
from 38 ml/kg/min to 52 ml/kg/min. She achieved this milestone by adhering to the American
College of Sports Medicine (ACSM) guidelines for a six-month period. To the extent of my
knowledge, this notable improvement and enhancement in her aerobic capacity can be attributed
to a number of several factors and adaptations. These adaptations may affect both the
components of the Fick equation VO2 = Q x (a-vO2 diff):
The cardiac output (Q)
The arteriovenous oxygen difference (a-vO2 diff).
1) Biochemical Mechanisms: The Energetics of Exercise
Due to consistent aerobic exercise, there may have been several mitochondrial
adaptations at the cellular level. Frequent and consistent aerobic exercise has been suggested to
increase the size and number of mitochondria in the body. An increase in mitochondrial density
and number may enhance the muscle’s capacity for oxidative phosphorylation. This means that
Mary Ann’s muscles may have become more efficient at utilizing oxygen to produce ATP
through aerobic metabolism.
Furthermore, aerobic training has been observed to improve the intramuscular transport
of Free Fatty Acids (FFA) and carbohydrates in the body. Aerobic exercise may have promoted
the production of glucose transporter proteins and fatty acid transport proteins in the body Mary
Ann which may have facilitated better substrate availability for energy production. Additionally,
these changes in the biochemical mechanisms may collectively reduce the reliance of the body
on anaerobic metabolism to produce energy. Therefore, this may have further facilitated in
delaying fatigue and enhance the rate of ATP generation using oxygen by muscles in Mary
Ann’s body.
2) Physiological Mechanisms: Cardiovascular and Respiratory Adaptations
With respect to physiological mechanisms, the body adopts to two major adaptations as a
result of aerobic exercise that include cardiovascular and respiratory adaptations. For
cardiovascular adaptation, one of the most profound adaptations Mary Ann would have
experienced is an increase in stroke volume. VO2 max is heavily dependent on the ability of the
cardiovascular system to deliver oxygen to working muscles. Whereas, regular aerobic training
enhances left ventricular volume and myocardial contractility that allows more blood to be
pumped per beat. This may eventually increase the cardiac output (Q) in the body. This resultant
increase in maximal cardiac output plays a key role in elevating VO2 max.
On the other hand, for respiratory adaptations, aerobic training improves pulmonary
ventilation efficiency and increases tidal volume. While the lungs are not usually a limiting
factor in healthy individuals, improved respiratory muscle endurance and alveolar ventilation can
reduce the work of breathing and improve oxygen exchange at the pulmonary capillaries.
3) Training Adaptations: Musculoskeletal and Haematological Changes
Mary Ann’s aerobic training would also trigger musculoskeletal changes that contribute
to improved oxygen utilization. These include a shift in muscle fibre type from fast-twitch
glycolytic (Type IIx) to more oxidative fibres (Type IIa), which are better suited for sustained
aerobic activity. Additionally, increased myoglobin content within muscle fibres facilitates more
effective oxygen storage and transport within the cell.
Haematological adaptations include an increase in plasma volume and red blood cell
mass, which collectively enhance blood flow and oxygen-carrying capacity. The increase in
haemoglobin concentration further improves the efficiency of oxygen transport, increasing the
arteriovenous oxygen difference (a-vO2 diff). This expanded a-vO2 diff reflects Mary Ann’s
improved ability to extract and use oxygen from the blood at the muscular level.
Application of the Fick Equation to explain the improvement in Vo2 max
The improvement in Mary Ann’s VO2 max can be directly explained by both terms of the Fick
equation:
Cardiac Output (Q = HR x SV):
Increased stroke volume (due to cardiac hypertrophy and improved contractility)
Slight reduction or maintenance of maximal heart rate
Overall increase in maximal cardiac output
Arteriovenous Oxygen Difference (a-vO2 diff):
Increased capillary density
Enhanced mitochondrial function
Higher myoglobin content
Increased red blood cell count and haemoglobin content
In conclusion, together, all these adaptations may enhance both the delivery and extraction of
oxygen, leading to the significant improvement in VO2 max observed in Mary Ann.
