Precautions
Introduction
There is wide consensus that exercise benefits older people. For example, just taking three research articles:
Izquierdo et al. (2021) argued that while every physiological function is diminished through ageing, the degradation in muscular and aerobic capacity is attenuated by adequate exercise. Specific conditions, such as sarcopenia, diabetes, cardiovascular disease, hypertension, cancer, osteoporosis, depression, and dementia, are also countered to one degree or another. The paper argued that physical activity should be prescribed so that it is individualised and framed to one’s own health state. — International Exercise Recommendations in Older Adults (ICFSR): Expert Consensus Guidelines Journal of Nutrition, Health & Aging 2021.
De Labra et al. (2021) reviewed 38 meta-analyses and found that resistance training improves muscle strength, balance and reduces the risk of falls in the over 65’s. — Exercise Interventions for Older Adults: A Systematic Review of Meta-Analyses Journal of Sport and Health Science / PMC
Cabo. C et al (2025) reports that a randomised controlled trial of 124 people aged 65 to 80 shows improvements caused by physical exercise across a wide range of parameters including psychological status. - Scientific Reports (2025) — The Role of Physical Exercise in Enhancing Health, Quality of Life and Joy Among Older Adults.
There is little point in citing more evidence. I don’t need convincing. However, a number of studies qualify the optimism that attends many research articles in this field. Di Lorito et al (2021) found ‘that exercise interventions for older adults are extremely diverse and that the findings from the included studies were mostly inconsistent.’ For example many studies had not taken into account important variables, such as the role of the carer.
Silva R.B. et al (2017) concluded that, despite positive evidence for exercise in frail older adults across cognition, physical functioning, and psychological wellbeing, there is no clear guidance regarding the most effective programme variables.
Franklin B.A. et al (2020) suggests that chronic training for extreme endurance events can cause transient acute volume overload of the right ventricle and, in some individuals over months to years, patchy myocardial fibrosis. So a flagging of the risk of high volume endurance training.
On balance, that exercise is good for older people seems undeniable. The more interesting question however is how hard and how frequently should older people exercise, or more specifically, how hard and how frequently should I exercise?
Before answering this question, I need to consider my own specific situation in the form of a self-audit.
Self-Audit
Firstly I’ll briefly mention family history as genetic possibilities are important. On my maternal side the over-riding condition that has eventually caused deaths in my family has been Diabetes. My maternal grandfather died of a stroke brought about by long-term Diabetes 2. As did my mother and my maternal uncle. My younger brother has it. I have escaped it so far but it would be conjecture to say why this is so. I have always been very careful about the food that I eat and I have always exercised. Perhaps that has helped but I don’t know for certain.
My father died of Leukemia. He was a heavy smoker, a factor that is implicated in this disease, but there might have been a genetic factor too. I don’t have the death records of my father’s family. My father also had congenital high blood pressure, not helped by smoking. I have a higher-than-optimal blood pressure which I take comes from my Dad. I am on medication for this and I try to observe eating habits that don’t exacerbate the condition. I will get onto my diet later in this post. I’m rigorous about taking my Blood Pressures several times each week. Currently it’s 128/78 (after medication). If it rises above 140/85 I act through diet, fasting and exercise and water intake.
Own history and present status
Exercised all my life - never had a long gap.
Diet is mainly vegetables, fish, chicken, pulses, cereals, nuts, seeds and fruit. I grow quite a few vegetables. I don’t eat ultra processed food and I enjoy cooking from basic natural ingredients.
Not overweight, Ectomorphic.
I can eat lots, but I don’t put weight on.
I’m on blood pressure medication: Statins and Beta blockers.
I care full-time for my wife who has Alzheimer’s Dementia. It can be very stressful and is presumably taking a toll on my health, part of the reason for this exercise programme.
Medication
I am on beta blockers, statins, and a calcium channel blocker (felodipine) for blood pressure management. These are not incidental to how I exercise — Here, I set out what the research says about each drug’s effects on exercise, how they interact, and what that means practically for someone who exercises vigorously in their seventies on these medications.
However, This is my personal interpretation. Any reader should always consult with a medical doctor before adjusting medication or exercise.
Beta Blockers
I was put onto beta blockers after experiencing an erratic heart rate when walking up a hill about five years ago. My doctor worked on a least-risk approach, suspecting a possible silent myocardial infarction. Since taking beta blockers, my resting heart rate has dropped from 65 to 45 bpm, and I struggle to elevate it beyond 115, no matter how hard I exert myself.
The idea behind the beta blockers is to reduce the work of the heart, thereby better safeguarding it. This raised two practical concerns for me as someone who exercises regularly.
First, I was accustomed to using target heart rate levels to gauge effort. For a 70-year-old man, the estimated maximum heart rate is roughly 150 bpm (220−70). Effective training zones include aerobic (75–128 bpm) for endurance and anaerobic (128–140+ bpm) for high-intensity work. Beta blockers have narrowed these ranges considerably, making this method impractical.
Second, I had assumed that a reduced heart rate meant less oxygen is transported to the muscles, therefore providing a cap on what I could achieve. But this doesn’t seem to be the case.
The Fick Equation and the Oxygen Pulse
The relevant framework is the Fick equation: VO₂ = HR × Stroke Volume (SV) × arterio-venous oxygen difference (a-vO₂).
The product of SV × a-vO₂ difference is known as the oxygen pulse. Beta-blockade reduces heart rate, but this only limits exercise capacity if there is no compensatory increase in oxygen pulse.
Priel et al. (2021) is perhaps the anchor research article examining beta blockers and exercise metrics. The key finding was that maximal heart rate was 19% lower in subjects taking beta-blockers (116 bpm vs 145 bpm), but oxygen pulse was greater by 19.5% in those taking beta-blockers. The compensatory increase in oxygen delivery per heartbeat offset the reduced heart rate, preserving exercise capacity.
Two mechanisms plausibly explain this compensation, and they are not mutually exclusive:
Increased stroke volume. Beta-blockade slows the heart, which allows longer diastolic filling time. By Frank-Starling mechanics, a more fully stretched ventricle contracts more forcefully, ejecting a larger volume per beat.
Increased a-vO₂ difference. When cardiac output is constrained, peripheral tissues may extract a higher proportion of the delivered oxygen. This can occur through improved capillary recruitment, slower transit time through capillaries (more time for diffusion), and mitochondrial adaptations from vigorous training.
Blood Pressure and the Self-Limiting Question
One might expect an increase in systolic blood pressure if the ventricle is ejecting blood harder. Surprisingly, the Priel paper found the opposite: beta blockade was associated with a modestly lower systolic blood pressure during exercise (−2.88 mmHg). The most plausible explanation is that beta-blockers reduce sympathetic tone, lowering peripheral vascular resistance (SVR). Since BP ≈ CO × SVR, the vasodilatory effect offsets any pressure-raising tendency from the larger stroke volume.
This also addresses the question of whether the compensatory mechanism is self-limiting. The rate-pressure product (HR × systolic BP) — the standard proxy for myocardial oxygen demand — is doubly reduced: heart rate is down 19% and systolic pressure is modestly lower too. The Frank-Starling compensation preserves exercise capacity without negating the cardioprotective effect.
Seemingly good news!
Statins
The most significant concern for active people is statin-associated muscle symptoms (SAMS) — ranging from mild myalgia to, rarely, myopathy or rhabdomyolysis (muscle breakdown). Vigorous exercise independently stresses muscle tissue, and statins can amplify this. Warning signs to watch for include:
Muscle fatigue or weakness during or after exertion that seems disproportionate to effort
Delayed onset muscle soreness that is worse than expected
In rare cases, dark urine — a warning sign requiring immediate medical attention
Statins can also reduce CoQ10 (coenzyme Q10) levels, which plays a role in mitochondrial energy production, potentially contributing to a sense of reduced exercise capacity or increased fatigue, though the evidence on supplementing CoQ10 is mixed.
I have not observed any adverse effects to date.
Felodipine: A Calcium Channel Blocker and Its Complications
More recently, I have been managing a complication arising from a medication change. My doctor increased my dose of felodipine (a calcium channel blocker prescribed for hypertension) from 2.5 mg to 5 mg. Within a few weeks I noticed that my ankles had become visibly swollen, though without pain.
The Haemodynamic Mechanism of Ankle Oedema
Felodipine is a calcium channel blocker (CCB). It blocks voltage-dependent calcium channels in smooth muscle cells, reducing cytosolic calcium, lowering peripheral vascular resistance, and thereby reducing blood pressure. More pointedly in this context, it selectively dilates arterioles and has no impact on venous vessels (StatPearls / NCBI, 2024).
This selectivity is possibly the source of the problem. The arteriolar dilation reduces resistance before the capillary bed while the venous side remains unconstricted — a haemodynamic mismatch. Capillary hydrostatic pressure rises, and fluid is pushed into interstitial tissue, particularly in dependent areas such as the ankles. Research has confirmed this mechanism directly: felodipine increases capillary hydrostatic pressure and causes net fluid filtration from blood to tissue, while also impairing the local vasoconstrictor responses that normally protect dependent vascular regions from enhanced fluid filtration (Gustafsson et al., J Hypertens, 1989).
The absence of pain is characteristic: this is not inflammatory oedema but a haemodynamic effect.
Dose-Dependence and Incidence
The oedema seems dose-related. With starting doses of felodipine, only approximately 5% of patients experience ankle swelling, but the incidence rises substantially with dose increases and may exceed 80% at very high doses of CCBs (Kakani et al., Am J Medicine, 2011). A network meta-analysis of randomised controlled trials ranked felodipine as having a 2.48 times greater risk of peripheral oedema compared to placebo (Comparative peripheral edema for DHPCCBs, PMC, 2022).
The timing of my swelling — appearing after the dose increase — seems to suggest that it has been caused by the increase in dosage.
Does Felodipine Affect Exercise Capacity?
Given the discussion above about beta blockers and the Fick equation, a pertinent question arises: does the haemodynamic mismatch caused by felodipine undermine the compensatory mechanisms that preserve exercise capacity on beta blockers?
The short answer is: probably not, and possibly slightly beneficial.
Felodipine reduces afterload (the resistance the ventricle ejects against) by lowering systemic vascular resistance. A lower afterload means the ventricle empties more completely per beat, which supports rather than undermines stroke volume. So the CCB does not sabotage the Frank-Starling compensation — if anything, it makes each contraction slightly more efficient.
A potential concern operates at the capillary level. The arteriolar dilation felodipine produces means blood arrives at capillary beds more rapidly and at higher pressure. Faster capillary transit time could reduce the time available for oxygen diffusion into tissues, potentially narrowing the a-vO₂ difference and partially undermining the peripheral extraction component of the oxygen pulse compensation. Conversely, increased capillary perfusion pressure might recruit more capillary beds, increasing the surface area for diffusion. The net effect is uncertain but likely to be small at typical exercise intensities.
From a cardiac protection standpoint, the combination of beta blocker and felodipine seems favourable. Both drugs independently reduce systolic blood pressure and the rate-pressure product (HR × systolic BP) — the myocardium’s oxygen demand at any given workload is lower still.
Managing the Oedema
My doctor has suggested switching from felodipine to amlodipine. Both are dihydropyridine CCBs working through an identical mechanism, so the class effect on oedema is shared. A meta-analysis found amlodipine has a higher oedema risk than felodipine (SUCRA 52.9% vs 47.3%), so switching does not obviously solve the problem, though individual responses vary. So I will probably decline my doctor’s suggestion.
What does more reliably reduce CCB-induced oedema is the addition of an ACE inhibitor or ARB. These counteract the venous-end haemodynamics. A meta-analysis of 15 studies showed that combining a CCB with a renin-angiotensin system blocker reduced the risk of oedema by 38% compared to CCB monotherapy (Kakani et al., 2011). This is a conversation worth having with my doctor.
The oedema also matters for exercise beyond mere discomfort: significant lower-limb oedema can impair venous return, which would affect preload and therefore the Frank-Starling mechanism if it became substantial. This is another reason to address it rather than simply manage it with compression stockings.
Conclusion
The evidence does not reveal red flags for vigorous exercise on this combination of medications. The Priel finding on beta blockers is reassuring: the reduction in heart rate appears to be compensated by an increase in oxygen pulse, preserving exercise capacity. Felodipine does not materially undermine this, and the combined effect on the rate-pressure product is actually cardioprotective.
What it does mean is that heart rate is no longer a reliable guide to effort. Rate of Perceived Exertion (RPE) — a subjective 1–10 scale based on how hard one actually feels one is working — becomes the primary instrument.
This is consistent with my broader philosophy of attentiveness for this web-site: listening to the body’s signals rather than peering at my exercise app.
The ankle oedema is the outstanding practical problem. It is mild but I would rather not have it. It is a haemodynamic side effect of the medication dose, well-established in the literature, and not a sign of cardiac or systemic pathology. But it requires resolution — both for comfort and to protect the venous return mechanisms that support exercise performance.
References
Priel, A. et al. (2021). Effects of beta-blockers on exercise metrics. [Anchor paper on beta blockers and exercise capacity.]
Gustafsson, D., Lanne, T., Bjerkhoel, P. et al. (1989). Microvascular effects and oedema formation of felodipine in man. J Hypertens, 7(Suppl 4): S161–S167.
Kakani, H., Bangalore, S., Romero, J. et al. (2011). Effect of Renin-Angiotensin System Blockade on Calcium Channel Blocker-Associated Peripheral Edema. The American Journal of Medicine, 124(2): 128–135.
Sica, D.A. (2003). Calcium Channel Blocker-Related Peripheral Edema: Can It Be Resolved? The Journal of Clinical Hypertension, 5(4): 291–297.
Comparative peripheral edema for dihydropyridine calcium channel blockers: A systematic review and network meta-analysis. (2022). PMC9106091.
StatPearls / NCBI Bookshelf (2024). Felodipine. National Center for Biotechnology Information.
NHS Specialist Pharmacy Service (2023). Managing peripheral oedema caused by calcium channel blockers.
