Three months of ice baths left the redox and mitochondrial adaptations intact

The acute arm put 9 men through one resistance session followed by 10 minutes of cold water immersion or active recovery. Plasma F isoprostanes, a marker of lipid peroxidation, were lower after immersion at 1 hour (p=0.006), 2 hours (p=0.005) and 24 hours (p=0.002), and plasma glutathione peroxidase activity was higher at 2 hours (p=0.008).

The redox genes NRF2, SRXN1 and HMOX1 all rose after exercise (time effect p<0.001), as did GCLM (p=0.034), while KEAP1 did not change (p=0.50). None of them differed between cold water immersion and active recovery, with every time by trial interaction above 0.05.

In the training arm, 21 men trained twice a week for three months. Citrate synthase activity rose (p=0.044), along with complex I (p=0.005) and complex IV (p=0.023). None of the three differed between the groups, with time by group interactions of 0.81, 0.68 and 0.83.

One measure did diverge. Total muscle oxygen consumption during isokinetic contractions showed a time by group interaction of p=0.001, increasing in the cold water immersion group (p=0.001) but not in the active recovery group (p=0.15), and sitting higher in the cold group after training (p=0.023).

The numbers

Plasma F isoprostanes, cold vs active at 24 h	lower with cold, p=0.002
Redox gene response, cold vs active	no difference, all time by trial p>0.05
Citrate synthase after three months, cold vs active	no difference, time by group p=0.81
Complex I and complex IV, cold vs active	no difference, p=0.68 and p=0.83
Muscle oxygen consumption after training, cold vs active	higher with cold, p=0.023

Why this might happen

Shown in this study The study measured this step directly.

The authors measured the mechanistic step rather than inferring it, tracking redox gene transcription, mitochondrial enzyme activity and muscle oxygen kinetics directly.

Their reading is that the physiological responses to cold water immersion, meaning reduced venous oxygen saturation, reduced muscle blood flow and altered perfusion, do not modify systemic oxidative stress, redox related gene expression or mitochondrial adaptations after acute or chronic resistance exercise.

On the lower F isoprostanes they are deliberately careful. They write that the change might suggest reduced oxidative stress, but might equally reflect altered antioxidant activity or lipid peroxidation dynamics rather than a simple reduction in oxidative stress.

For the higher muscle oxygen use they point to previously reported increases in type IIa fibre proportion and capillaries per fibre in these same participants. That is an explanation they offer rather than one they tested here.

Drawn from Discussion, PMC13394430.

What this does not show

It does not show that cold water immersion is neutral for every kind of training. This was resistance training twice a week for three months in young men. It says nothing about endurance blocks, high volume weeks, or training phases where hypertrophy is the goal.
It does not show what happened to redox state inside the muscle itself. The authors write that the blood based markers they measured might not fully capture local oxidative stress responses within muscle. The gene expression was measured in muscle, the oxidative stress markers were measured in blood.
It does not apply to women. Both arms recruited only male participants, which the authors flag as a limit on generalisability.
The higher muscle oxygen use is not shown to be a benefit. It is a measured difference in oxygen consumption during contractions. No strength, power or endurance outcome was attached to it.

Where this leaves us

The concern that post exercise cold water immersion blunts the redox signalling behind training adaptation is less well supported than it was, and this refines rather than overturns the earlier work that raised it.

Young men doing supervised resistance training twice a week for three months, with 10 minutes of immersion after each session.

The authors point to high resolution respirometry and direct measurement of oxidative stress within the muscle, in both sexes, as what would settle whether the local redox picture matches the blood.

Caveats worth holding

Nine participants in the acute arm and 21 across the two training groups, so every comparison rests on a small sample.
The authors note that enzyme activity assays might not reflect functional changes detectable by high resolution respirometry.
Correlation analyses were exploratory and not adjusted for multiple comparisons.
The paper reports an effect size beside each p value, but the retrieved text did not resolve which statistic it is, so those values are not quoted here.