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VO₂Max

Lungs

Heart Rate Training

Your heart and the many blood vessels in your body make up your cardiovascular system. The purpose of the cardiovascular system is to circulate oxygen and nutrients through your whole body via an intricate network of blood vessels and to remove the waste products your body doesn’t need, such as carbon dioxide.  It’s a gas exchange system.  The system also assists with thermoregulation and helps to eliminate heat.

The fitness of the cardiovascular system is defined by the body’s ability to deliver oxygen to your muscles, based on demand.  The lungs take in oxygen from the air we breathe where it gets perfused into the blood stream, the heart and blood vessels deliver it into the working muscles, and the skeletal muscles utilize that oxygen to execute muscular contractions. 

Tip:  Keep in mind ‘If the pump don’t pump, you don’t go’.

Cardiorespiratory fitness (CRF), is often referred to as (VO2max). VO2 max is defined as the maximum rate of oxygen that can be delivered to and used by the working muscles, in other words, the aerobic capacity.  The more oxygen your body absorbs per minute, the higher your VO2 max, and the more fit your system is (Burtscher et al, 2019; Valenzuela et al, 2020).  VO2 max reflects the entire oxygen transport system – the lungs, cardiovascular, and active muscles- which transport and utilize the oxygen in the blood stream. 

VO2 max is measured in milliliters of oxygen used in one minute per kilogram of body weight (mL/kg/min). It is based on the premise that the more oxygen athletes consume during high-level exercise, the more the body will generate energy in the cells. 

VO2 max values can vary greatly between individuals, with untrained individuals typically having a range of 25-45 ml/kg/min while elite endurance athletes have values in the 80s or even 90s.  Males tend to have higher values than females.  After 30 years of age, VO2 max progressively decreases with age at a rate of about 10% per decade (Jansson & Kaijser, 1987; Simon et al, 1986; Levine, 2008), though appropriate training can slow the pace of decline (Haugen et al, 2018; Rønnestad et al, 1985; Weibel & Hoppeler, 2008). 

          Tip:  VO2 max is a function of pump capacity (stroke volume) and pumping rate

You can improve your cardio and go farther, faster.  Exercising and physical activity cause the cardiovascular system to adapt and improve, promoting cardiovascular fitness (Pinckard et al, 2019). During exercise, two major adjustments occur. First, cardiac output from the heart increases, as cardiac output is a major determinant of oxygen. There is also an increase in oxygen consumption by the lungs.  During strenuous exercise, heart rate can increase threefold and stroke volume can increase about 30-40%, up to about 90% of their maximum values. (Stroke volume is the volume of blood pumped out of the left ventricle of the heart during each contraction and heart rate refers to the number of heart beats per minute). When maximum stroke volume is increased, the heart can work more efficiently at a given pulse rate and increase the amount of blood that goes out to the rest of the body and muscles.

The second adjustment is blood flow from inactive organs and tissues is redistributed to active skeletal muscle. At rest, muscles receive approximately 20% of the total blood flow, but during exercise, the blood flow to muscles increases to 80-85%. During maximal exercise, almost all the available oxygen in the blood is extracted by skeletal muscle. (Joyner & Casey, 2015).  

Maximum heart rate (MHR) refers to the upper limit of what a person's cardiovascular system can handle during exercise.  The most common rule is simply '220 minus your age' – so, a 40-year-old would have a theoretical MHR of 180.  While the gold standard for finding your maximum heart rate is a treadmill stress test in a lab, you can simulate one on your own with a heart rate monitor. At a track, run or jog one or two miles as a warm-up, then run a mile at tempo pace, then gradually increase your speed over 400 meters before running a final 400 meters at an all-out effort. 

The Maximum Heart Rate can be increased through specific training, which releases  neurological and physiological restrictions holding you back from working at your maximum.  See the Heart Rate Training section to the right.

With repeated exercise, new blood vessels form in muscle, increasing skeletal muscle blood supply.  The increased vascular density coupled with greater dilation capacity of the vessels leads to enhanced oxygen extraction and perfusion capability, an important component of fitness.  This leads to higher heart rate over a longer period of time (Naik et al, 1999; Huonker et al, 2003; Saunders & Tschakovsky, 2004; Hoier et al, 2014; Joyner & Casey, 2015; Laughlin et al, 2017). 

Regular exercise also leads to a decreased resting heart rate, lower blood pressure, and increased cardiac muscle mass (Platt et al, 2015; Vega et al, 2017; Che & Li, 2017).  The more you exercise, the more efficient the heart becomes at this process, so you can work out harder and longer (Laughlin et al, 2012; Duncker & Bache, 2008). 

Athletes who pursue intense endurance exercise for five hours or more per week at high intensities may develop exercise-induced cardiac remodeling—often referred to as athlete's heart—a normal physiologic response where the heart becomes larger and more efficient than average as a natural response to intensive exercise.  Such cardiac adaptations are often reflected in the ECG and imaging studies.  It is regarded as a non-pathological condition. The changes are asymptomatic; signs include a lower resting heart rate, an enlarged heart, and a thickening of the muscular wall of the heart, specifically the left ventricle which pumps oxygenated blood to the aorta, and extra heart sounds.  During an intensive workout, more blood and oxygen are required for the peripheral tissues of the arms and legs in highly trained athletes' bodies. A larger heart results in higher cardiac output, which may allow it to beat more slowly at rest, as more blood is pumped out with each beat (Ellison et al, 2012; Weberruß et al, 2022; Fagard, 2003).

While athlete’s heart is not pathological, there are cardiac impairments that will impact cardiac function during exercise.  Folks diagnosed with hypertension and high blood pressure showed impaired skeletal muscle oxygenation. Even during submaximal exercise, those with cardiac issues can have their blood pressure increase 2-fold to achieve the similar muscle oxygenation that healthy folks could achieve (Dipla et al, 2017).  Studies of patients with heart failure have found under-perfusion to the skeletal muscle and lactic acidosis (Duscha et al, 2008; Gosker et al, 2000; Saltin & Calbet, 2006). 

Tip:  Think of it this way.  When you start training your engine (heart) is a 4 cylinder that runs at low RPM.  When you train you add cylinders and add RPM.

Nutrition
Your cardiovascular system, and specifically your heart rate, can be improved through specific training.  Also vital is your nutrition.  Data shows that your cardiovascular system benefits from nutrient support and we will discuss how the vitamin Ks, vitamin D, and astaxanthin all help heart function. 

Vitamin K
Vitamin K refers to a family of vitamins, best known for their role in helping the coagulation system to ensure that blood clots or coagulates properly.  However, we have learned that vitamin K has a much wider role in the body.  Research has identified numerous proteins in tissues throughout the body that depend on vitamin K to be active.  These proteins are found in the lungs, heart, vasculature, bones, muscles, and the brain to name a few.  Some of the most researched proteins include matrix Gla protein (MGP), growth arrest-specific protein 6 (Gas6), osteocalcin (OC), and Gla-rich protein (GRP) (Wen et al, 2018).  Through these proteins, vitamin K acts on almost every system in the body, and thus has a tremendous impact on movement and fitness (Willems et al, 2014; Beulens et al, 2013; Popa et al, 2021).

There are two types of vitamin K for human consumption. There is K1, also known as Phylloquinone, which is central to the coagulation system.  Vitamin K1 is mostly found in green plants, like spinach, broccoli, lettuces or parsley, and accounts for more than 50% of the dietary intake of vitamin K (Booth, 2012).

And there is K2, also known as Menaquinone.  There are at least 15 forms of menaquinones.  Two of the most widely researched are MK4 and MK7. Vitamin K2 is found in fermented products where bacteria are part of the production process, such as natto, hard cheeses, sauerkraut, egg yolk, sausages, and dairy products, etc, and it can also be produced by the gut bacteria (Shearer & Newman, 2008; Shearer et al, 2012; Vermeer et al, 2018).

Vitamin K2 insufficiency is very common in US adults. A recent study found K2 deficiency or insufficiency in 97% of older subjects in a mixed population (Bruno 2016).  Vitamin K insufficiency is also very common in athletes (Iwamoto et al, 2010; Sumida et al, 2012;

Ingesting enough vitamin K in your diet and/or through supplements is important to ensure you have a high functioning cardiovascular system, particularly as an athlete. 

Vitamin K and the Heart
Decades of research have shown that vitamin K supports heart health and could be an important intervention for exercise success.  Vitamin K helps prevent calcification, it keeps your vascular system from stiffening, it is anti-inflammatory, and it helps create maximum heart output (Crintea et al, 2021).

Vascular Calcification
Vascular calcification is when deposits of hydroxyapatite, a form of calcium, are deposited in the blood vessel walls (Wasilewski et al, 2019). This can lead to disease such as atherosclerosis, ischemia, PAD, peripheral artery disease, and CAD, coronary artery disease. Low levels of vitamin K2 can cause disruption in the binding between calcium and osteocalcin, leading to the buildup of calcium to other tissues such as arteries (Maresz, 2015).

Research has demonstrated that higher consumption of vitamin K2, reduces calcification and coronary heart disease (Geleijnse et al 2004; Gast et al, 2009). After monitoring 2987 participants during a median follow-up time of 11 years, intake of K2 was associated with a significantly lower risk of heart disease (Haugsgjerd et al, 2020), and a slowed progression of preexisting coronary artery calcification (CAC), in asymptomatic older men and women (Shea et al, 2009).

Cardiovascular tissues contain several key proteins that are dependent upon vitamin K to be active.  Matrix Gla protein is the most influential natural inhibitor of all types of calcification in the body and is closely associated with mortality, and cardiovascular disease (Barrett et al, 2018). Upon activation, MGP binds calcium, thereby inhibiting the calcification process, removing the calcium from circulation and leading it to the bones (Goiko et al, 2013; Cui et al, 2018; Jaminion et al, 2020).  Measures of MGP are regarded as markers of vascular health (Kumric et al, 2021).

When not activated by vitamin K, inactive MGP is associated with (peripheral) vascular calcification and carotid femoral/aortic pulse wave velocity, suggesting that it is a risk biomarker associated with mortality and the severity of vascular calcification and cardiac function (Ueland et al, 2011; Rennenberg et al, 2010; Dalmeijer et al, 2013; Liu et al, 2015; Roumeliotis et al, 2019). 

Additionally, Vitamin K modulates the Gas6 pathway which also inhibits the vascular calcification process (Jadhav et al, 2022). Gas6 has been shown to suppress vascular calcification and reduce coronary heart disease (Geleijnse et al, 2004; Vossen et al, 2015, Qiu et al, 2017).

Arterial Elasticity

Pulse wave velocity (PWV) is the velocity at which the blood pressure pulse propagates through the circulatory system.  The stiffer and harder the blood vessel walls, the wider the pulse pressure and the more the heart is working to pump blood into the arteries (Seals et al, 2006).  A study of patients with hypertension found that low intakes of vitamin K led to lower muscle mass and increased large artery stiffness (Vidula et al, 2022).

The vascular system is lined with smooth muscle cells.  Smooth muscle cells (SMCs) provide the main support for the structure of the vessel wall and maintain intravascular pressure and tissue perfusion (Qui, 2014).  Vitamin K promotes vascular smooth muscle differentiation, which is associated with better perfusion of muscle tissue (Chatrou et al, 2011).  

Anti-Inflammatory
Vascular calcification is a chronic inflammatory state mediated by the NF-кB, a transcription factor for inflammation and the immune response.  A high vitamin K status exerts anti-inflammatory effects and prevents calcification through antagonizing NF-кB signaling (Shioi et al, 2020). 

Interleukins are cell proteins that defend the body and ensure that our immune system is responsive.  High levels of IL-6 areassociated with chronic inflammation.  A lab study showed that of all the vitamin K forms K1, MK3, MK4, and MK7 were anti-inflammatory and suppressed IL-6, with MK4 having the most impact (Ohsaki et al, 2010).  

The Multi-Ethnic Study of Atherosclerosis (MESA), showed that low blood levels of vitamin K1 were associated with higher inflammatory markers, namely IL-6 and C-Reactive Protein (Shea et al, 2014). A cohort analysis of 1163 older adults in the Health ABC study, found that those with lower circulating levels of K1, also had higher circulating IL-6 levels, further supporting the anti-inflammatory effect of vitamin K at a systemic level (Shea et al, 2017). 

Maximal Cardiac Output
A recent study showed a powerful effect of MK7 on heart output during exercise in active athletes. MK7 was given to subjects during an 8- week period, while they maintained their typical exercise habits.  They found that MK7 intake was associated with a 12% increase in maximal cardiac output, using a graded cycle ergometer test.  This was the first study to report potential of vitamin K in active individuals. Cardiac output was defined as the maximum amount of blood (and therefore oxygen) that the heart can pump around the body each minute. The major finding was that cardiac output rose by a very significant 12% for the athletes receiving vitamin K2.  Cardiac output was defined as the maximum amount of blood (and therefore oxygen) that the heart can pump around the body each minute.  This increase translates to an increase in the maximum amount of blood and oxygen available to exercising muscles, which should improve endurance.  Research on elite runners and cyclists have confirmed that high cardiac outputs are associated with high levels of endurance performance (McFarlin et al, 2017). 

Osteocalcin
Osteocalcin (OC) is a widely researched vitamin K dependent protein.  Osteocalcin levels have been associated with a lower risk of coronary heart disease in Chinese adults (Zhang et al, 2016).  Fusaro (2016) has found lower osteocalcin levels in patients with aortic and iliac calcifications as compared to patients without calcifications. 

In a prospective study of 774 men aged 51–85 years from the MINOS cohort who were followed over 10 years, higher baseline total OC was associated with a lower aortic calcification progression rate and lower 10-year all-cause mortality (Confavreaux et al, 2013).  

Intake/Supplementation studies
In a study of a ten-year follow up of 4,500 elderly subjects (the Rotterdam study cohort) Geleijnse demonstrated that the more vitamin K in a person’s diet, the lower the rate of cardiovascular disease.  In the Rotterdam study, the highest quartile for K2 intake was 45 ug/day (Geleijnse et al, 2004).  In the Prospect study, a high intake of vitamin K2, menaquinones, especially MK7, MK8 and MK9 protected against coronary heart disease, and of those, vitamin MK7 turned out to have the most beneficial effects on cardiovascular disease with a mortality risk reduction of 9% for each 10 ug/day of extra intake (Gast et al, 2009). 

In the Hordaland Health Study, a higher intake of vitamin K2 was associated with lower risk of CHD (Haugsgjerd et al, 2020).  Beaulen also found that high intakes of menaquinone were associated with decreased risk of coronary calcification (Beulens et al, 2009).  In the LASA study (Longitudinal Aging Study Amsterdam), vitamin K insufficiency was significantly associated with a higher incidence of first cardiovascular events in a large group of healthy elderly people (Van den Heuvel et al, 2014). A study in Japan found that coronary artery calcification correlated with markers of chronic vitamin K insufficiency (Torii et al, 2016). 

Knapen (et al, 2015) showed that supplementing with 180 ug of MK7 over three years significantly improved arterial stiffness, and other vascular measures in healthy, postmenopausal women.  A second intervention trial was conducted with the same group of women, as well as men and carotid pulse wave velocity (the gold standard for arterial elasticity) were both favorably affected by MK7 after a year.  The effects of this modest dose of MK7 were mainly seen in the postmenopausal women (Vermeer & Vik, 2020). 

Brandenburg (et al, 2017) showed in a controlled trial, that men who received vitamin K over a twelve-month period had only a 10% progression in their aortic valve calcification score versus other men who had a 22% progression in their score.  A recent study showed that atherosclerotic cardiovascular disease (ASCVD) was inversely associated with diets high in vitamin K1 or K2.  In other words, there was a greater risk of disease if you had a low intake of vitamin K.   Folks with the highest K1 intake had a 14% lower risk of ischemic heart disease, a 17% lower risk of stroke, and a 34% lower risk of a PAD-related hospitalization. This was true for intakes of both K1 and K2 (Bellinge et al, 2021).  In the Danish Diet, Cancer, and Healthy Study, 53,372 Danish citizens were followed for 17-22 years of follow up.

In summary, there is extensive research establishing the benefit that vitamin K has on cardiovascular health. Since cardiovascular health is a key component of the oxygen delivery system when exercising, ensuring that you have sufficient intake of vitamin K could be a key advantage for your performance.

Vitamin D and the Heart
Vitamin D is critical for many physiological functions in humans. Vitamin D is naturally synthesized by the skin following exposure to the ultraviolet rays of the sun.  However, exposure to the sun depends on time outside, the amount of skin exposed, use of sunscreens, the season and your geographic location, so supplementing can provide a consistent dose.

Vitamin D receptors (VDR) are found in cells throughout the cardiovascular system. A variety of experimental studies indicate that these receptors may play an important role in controlling cardiac hypertrophy and fibrosis, regulating blood pressure, and suppressing the development of atherosclerosis. It also influences immunity within the body (Gardner et al, 2013). 

Over the last decade, vitamin D deficiency has emerged as a potential risk factor for cardiovascular diseases. (Wesley et al, 2017).  There are many observational studies which indicate a relationship, but intervention trials thus far have not been conclusive.

Heart Size
Vitamin D deficiency was first shown to negatively affect heart function about 30 years ago. Most research in this area has been done on the general population. Only one study has so far looked at its effect on the hearts of healthy athletes and what they found is alarming. The researchers found that athletes who were classed as severely Vitamin D deficient had significantly smaller hearts than athletes who were classed as being only slightly deficient or within normal ranges (Allison et al, 2015).

Blood Pressure
Men and women participating in health studies found that vitamin D deficiency, defined as <15 ng/mL had a 3 to 6 times increased risk of developing hypertension during a 4 year follow up, compared to those with optimal vitamin D status (Forman et al, 2007; Forman et al, 2008)

Vitamin D status was inversely associated with blood pressure in a large sample, representative of the US population.  The less vitamin D intake, the higher their blood pressure particularly in the group under 50 years of age (Scragg et al, 2007; Burgaz et al, 2011).

A meta-analysis of seven prospective studies, including a total of 48,633 participants with nearly 5,000 incident hypertension cases, found a 30% lower risk of hypertension in those in the highest level of serum 25-hydroxyvitamin D concentration.  It was estimated that every 10 ng/mL increase in serum 25-hydroxyvitamin D concentration was associated with a 12% lower risk of hypertension (Kunutsor, et al, 2013).   

Mortality
A longitudinal observational cohort of 1739 study participants, without prior cardiovascular disease, were followed for a mean of 5.4 years in the Framingham Offspring Study.  The results showed that low 25(OH)D3 levels were associated with increased rate of incident myocardial infarction (MI) (Wang et al, 2008).

Individuals with heart failure, hypertension, stroke, and other cardiovascular diseases (CVD) tend to have lower vitamin D levels than others (Liu et al, 2012).

In a study of 982 patients including 394 women from Northern Argentina serum 25(OH)D3 was a 2-year predictor of all-cause mortality, cardiac death, and sudden cardiac death in patients, especially in women (Naesgaard et al, 2012). 

Anti-Inflammatory
In a trial on 50 patients admitted with acute coronary syndrome, vitamin D supplementation at a dose of 4000 IU daily for 5 days stabilized the levels of inflammatory markers including interleukin (IL)-6, vascular cell adhesion protein 1 (VCAM-1) levels, and C-reactive protein (CRP). This suggested an anti-inflammatory effect of vitamin D on the vascular system mediating its possible cardio-protective properties after acute coronary event (Arnson et al, 2013).

Heart Health
There are mixed reviews as to whether vitamin D helps with heart health.  Multiple cross-sectional studies have shown an association between heart failure and 25(OH)D3 levels. In a small cross-sectional study of 101 subjects, 26% of subjects with heart failure had 25(OH)D3 levels below 15 ng/mL, with 17% of them having levels below 9 ng/mL (Shane et al, 1997). Similarly, the large National Health and Nutrition Examination Survey (NHANES) including data from 8531 participants showed that almost 90% of patients with heart disease and heart failure had low levels of vitamin D (Kim et al, 2008).  Anderson (et al, 2010) prospectively analyzed a large electronic medical records database of 41,504 patient records and found that vitamin 25(OH)D3 deficiency at low or very low levels was associated with significant increase in the prevalence of heart failure, as well as with incident heart failure.

A large observational study provided strong evidence that vitamin D supplementation reduces CVD risks (Acharya et al, 2021).  This was a retrospective, observational, nested case–control study of patients (N = 20,025) with low 25(OH)D concentrations (<50 nmol/L) who received care at the U.S. Veterans Health Administration from 1999 to 2018. Patients were divided into 3 groups: Group A (untreated, concentrations ⩽ 50 nmol/L), Group B (treated to concentrations 52-74 nmol/L), and Group C (treated to concentrations ⩾ 75 nmol/L). Among that cohort, the risk of myocardial infarction was significantly lower in Group C where the levels > 75 nmol/L.

However, a meta-analysis of 13 studies in women found no effect on vitamin D supplementation on the incidence of myocardial infarction events.  5108 adults subjects with a mean baseline 25(OH)D3 concentration of 25.3 ng/mL, randomized to receive monthly vitamin D supplementation, or placebo, and followed up for a median of 3.3 years, showed no significant difference for the incidence of heart failure (Scragg et al, 2017).  A more recent meta-analysis of 21 clinical trials also did not find an effect (Barbarawi, Kheiri et al, 2019). 

These findings of no effect are controversial and have been challenged as being based on flawed studies that did not consider health markers, vitamin D blood levels, and the very low dosages used in some of the research (Grant et al, 2023). Cited as more representative is a study of vitamin D and cardiovascular disease using a Mendelian randomization design, using genetic data from a UK Biobank cohort which found that the risk for cardiovascular disease decreased steeply as 25(OH)D concentrations increased to 25 nmol/L and leveled off as the D concentrations neared 50 nmol/L (Zhou et al, 2022).

Astaxanthin and the Heart
Astaxanthin is a red pigment found in certain microalgae which accumulates in many marine organisms, such as salmon, trout, and shrimp.  It is responsible for the reddish-pink color of flamingos, lobsters, and crawfish, due to the high amounts of astaxanthin they consume.

Heart Rate
A study of overweight people, under age 30, were given 12 mg of Asta or a placebo for 4 weeks.  They completed a graded exercise test on a cycling ergometer to examine changes in oxidation rates.  Those who received the Asta demonstrated a 7% decrease in heart rate on the exercise test.   A 2020 pilot study found that three months of astaxanthin supplementation suppressed oxidative stress and improved cardiac contractility and exercise tolerance in heart failure patients (Kato et al, 2020).

Heart Health
In one study, mice fed astaxanthin had a 36.5% reduction in the formation of plaque in the aorta, the main artery that leaves the heart.⁶

A group of 61 non-obese subjects with mild hypertriglycemia were given doses of 0,6, 12, or 18mg/day of Astaxanthin for 12 weeks.  Those who received the highest doses of 12 and 18 mg/day showed significant reductions in triglyceride levels.  The study showed a markedly positive correlation between the percentage change of adiponectin and that of the HDL-cholesterol level (Yoshida et al, 2009).

Reduced Oxidative Stress
Being overweight increases oxidative stress, which is closely associated with atherosclerotic disease. In one trial, researchers recruited 23 patients who were overweight or obese and tested whether astaxanthin could reduce oxidative stress (Choi, Kim et al, 2011).  After three weeks of daily astaxanthin intake, markers of oxidative stress decreased significantly.  At the same time, levels of superoxide dismutase (an enzyme that breaks down the harmful super-oxide free radical) and total antioxidants (which reduce oxidative stress) increased significantly compared to baseline. The same group of researchers conducted another trial on a different group of overweight or obese patients. This time, markers of lipids (fats) were also evaluated, and the trial was extended to 12 weeks. The results again showed beneficial reductions in oxidative stress. There were also decreased levels of LDL cholesterol and apolipoprotein B (a marker for LDL particle count), compared to a placebo group (Choi et al, 2011) .

Summary
Your cardiovascular system is core to athletic performance.  It is important for it to be healthy.  Cardio performance for athletes reflects the health of your overall system.  The good news is that cardio health can be supported through appropriate nutrition, and it can be improved through specific training. 

 

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