For a long time we treated heat mainly as a problem to be managed — something that degrades performance and has to be defended against. That framing is increasingly out of date. A growing body of work, including studies from my own group, points to the same conclusion: a controlled dose of heat is a genuine physiological stimulus in its own right, capable of driving adaptation from the whole-body oxygen-transport system all the way down to the regenerating muscle fibre. In this post I want to bring together two recent papers on the systemic side and connect them to what we have learned about heat at the muscle level.

The through-line is simple. If we stop thinking of heat as merely a stressor to survive and start treating it as an additional training input — layered on top of, or alongside, the usual mechanical and metabolic load — we open up practical ways to enhance adaptation without adding more hard training. That matters for athletes managing fatigue, for those returning from injury, and for anyone trying to hold on to hard-won gains.

The systemic story, part 1: passive heat and VO₂max

The first study I want to write about, from Jenkins and colleagues at Cardiff Metropolitan University and published in The Journal of Physiology, asked a clean question: can passive heat — hot-water immersion, which lets athletes keep training normally rather than compromising session quality — reproduce the haematological and aerobic benefits usually attributed to exercise-in-the-heat? Ten well-trained runners completed five weeks of hot-water immersion (5 × 45 min per week at ≥ 40 °C) in a within-subject, counterbalanced crossover against a time-matched control, alongside their habitual training.

The results are striking for a passive intervention. Hot-water immersion increased haemoglobin mass by 33 g, expanded blood volume by 284 mL, and raised left-ventricular end-diastolic volume by 10 mL — without altering systolic or diastolic strain mechanics. Those coordinated changes drove a 2.7 mL·kg⁻¹·min⁻¹ improvement in VO₂max and a 0.8 km/h increase in the treadmill speed at VO₂max. Crucially, haemoglobin mass was the strongest independent predictor of the VO₂max gain, with cardiac adaptation adding further explanatory value. The take-home is that passive heat acts on multiple convective links of the oxygen-transport chain at once — more blood, more of it carrying oxygen, and a heart filling a little more with every beat.

The systemic story, part 2: locking in altitude gains

The second study, from the same group in Experimental Physiology, tackles a problem every altitude-camp practitioner knows too well: the haemoglobin mass you build at altitude tends to melt away within about a week of coming down. If heat can expand haemoglobin mass, could it also preserve an altitude-induced expansion after descent? Twenty-one adults spent 14 days at 3800 m and, on descending to 1250 m, were assigned either to hot-water immersion (45 min at 40 °C for four days) or to a control condition.

The divergence after descent is the headline. Haemoglobin mass rose by 24 g at altitude across the whole cohort. Back at low elevation, the control group lost 18 g — the familiar wash-out — while the hot-water group actually held on, drifting up by 9 g. Interestingly, this preservation was not explained by sustained erythropoietin: EPO declined similarly in both conditions, and plasma-volume expansion was comparable. So heat protected the red-cell expansion through a route we have not yet pinned down. Mechanism aside, the applied message is immediate: a few days of hot-water immersion after an altitude block is a low-impact, practical way to defend the adaptation athletes travelled a long way to earn.

From the bloodstream to the muscle fibre

If those two papers make the case for heat as a systemic stimulus, our own recent work makes the complementary case at the tissue level. In a study led by colleagues at Aspetar and published in The Journal of Physiology, we examined how different thermal treatments influence human muscle regeneration after a simulated injury. Thirty-four participants underwent an electrically stimulated eccentric-contraction protocol that triggers genuine myofibre necrosis and regeneration, then completed ten days of daily lower-body immersion in cold (12 °C), thermoneutral (32 °C), or hot (42 °C) water, with muscle biopsies before and at five and eleven days post-damage.

The findings ran against the reflex to reach for ice. Hot-water immersion produced lower perceived muscle pain and lower circulating creatine kinase and myoglobin than both thermoneutral and cold water. It up-regulated heat-shock proteins 27 and 70 and raised the anti-inflammatory cytokine interleukin-10, while blunting the rise in nuclear factor-κB seen in the other conditions. Cold-water immersion, by contrast, did not improve pain or reduce markers of damage, and appeared to dampen the heat-shock-protein response. In short: heat supported the muscle’s own regenerative machinery; cold did not. This is a muscle-level adaptation — a shift in the molecular environment toward repair — driven by the same physical stimulus that, systemically, expands haemoglobin mass and cardiac filling.

Why this matters: heat as an additional stimulus

Read together, these three studies tell a coherent story. At the systemic level, passive heat expands haemoglobin mass, blood volume and cardiac filling to lift VO₂max, and can preserve the haemoglobin expansion won at altitude. At the muscle level, heat tilts the local environment toward regeneration through heat-shock proteins and a more favourable inflammatory profile. The common thread is that heat is not merely a comfort measure or a stressor to be tolerated — it is a controllable physiological input that produces real, measurable adaptation on two fronts at once.

For practitioners, that reframing is the point. Heat can be programmed deliberately: to add an aerobic-adaptation stimulus in athletes who cannot absorb more mechanical load, to protect red-cell mass in the days after an altitude camp, and to support tissue repair during return-to-play rather than reflexively cooling everything down. The doses in these studies were modest and passive — 45 to 60 minutes of hot-water immersion — which makes them realistic to implement. As always, individual responses vary and heat carries its own cardiovascular and hydration considerations, so it should be dosed and monitored like any other training variable. But the direction of travel is clear, and I suspect we are only beginning to map what a well-designed heat stimulus can do.

I will keep writing about this as the evidence develops. If you are applying heat with your athletes and seeing effects — systemic or muscular — I would be glad to hear about it.

References

• Jenkins EJ, Killick JA, Zerilli O, Douglas AJM, Corr L, Hughes MG, Tremblay JC, Stembridge M. Long-term passive heat acclimation enhances maximal oxygen consumption via haematological and cardiac adaptation in endurance runners. The Journal of Physiology, 2025. DOI: 10.1113/JP289874 (via PubMed).
• Jenkins EJ, Koep JL, Douglas AJM, Maier LE, Howe CA, Sheitelman S, Corr LD, Siebenmann C, Hughes MG, Tremblay JC, Ainslie PN, Gibbons TD, Stembridge M. Daily hot-water immersion preserves altitude-induced haemoglobin mass expansion following descent independent of erythropoietin. Experimental Physiology, 2026. DOI: 10.1113/EP093944 (via PubMed).
• Dablainville V, Mornas A, Normand-Gravier T, et al., Cardinale M, Candau R, Bernardi H, Racinais S. Muscle regeneration is improved by hot water immersion but unchanged by cold following a simulated musculoskeletal injury in humans. The Journal of Physiology, 2025;603(23):7603-7625. DOI: 10.1113/JP287777 (via PubMed).